50 results on '"Clavel, Jacqueline"'
Search Results
2. Breastfeeding and risk of childhood brain tumors: a report from the Childhood Cancer and Leukemia International Consortium.
- Author
-
Schraw JM, Petridou ET, Bonaventure A, Dockerty JD, Karalexi M, Ntzani E, Infante-Rivard C, Clavel J, Bracci PM, McKean-Cowdin R, Roman E, Kane E, Erdmann F, Schüz J, Mueller BA, and Scheurer ME
- Subjects
- Child, Female, Humans, Infant, Breast Feeding, Case-Control Studies, Risk Factors, Male, Astrocytoma epidemiology, Astrocytoma etiology, Brain Neoplasms epidemiology, Brain Neoplasms etiology, Cerebellar Neoplasms, Ependymoma epidemiology, Leukemia epidemiology, Medulloblastoma epidemiology, Neuroectodermal Tumors, Primitive epidemiology
- Abstract
Purpose: Studies report mixed findings regarding the association of breastfeeding with childhood brain tumors (CBT), the leading causes of cancer-related mortality in young people. Our objective was to determine whether breastfeeding is associated with CBT incidence., Methods: We pooled data on N = 2610 cases with CBT (including 697 cases with astrocytoma, 447 cases with medulloblastoma/primitive neuroectodermal tumor [PNET], 167 cases with ependymoma) and N = 8128 age- and sex-matched controls in the Childhood Cancer and Leukemia International Consortium. We computed unconditional logistic regression models to estimate the odds ratio (OR) and 95% confidence interval (CI) of CBT, astrocytoma, medulloblastoma/PNET, and ependymoma according to breastfeeding status, adjusting for study, sex, mode of delivery, birthweight, age at diagnosis/interview, maternal age at delivery, maternal educational attainment, and maternal race/ethnicity. We evaluated any breastfeeding versus none and breastfeeding ≥ 6 months versus none. We subsequently performed random effects meta-analysis to confirm our findings, identify potential sources of heterogeneity, and evaluate for outliers or influential studies., Results: Breastfeeding was reported by 64.8% of control mothers and 64.5% of case mothers and was not associated with CBT (OR 1.04, 95% CI 0.94-1.15), astrocytoma (OR 1.01, 95% CI 0.87-1.17), medulloblastoma/PNET (OR 1.11, 95% CI 0.93-1.32), or ependymoma (OR 1.06, 95% CI 0.81-1.40). Results were similar when we restricted to breastfeeding ≥ 6 months and in meta-analyses., Conclusion: Our data suggest that breastfeeding does not protect against CBT., (© 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.)
- Published
- 2023
- Full Text
- View/download PDF
3. Residential exposure to natural background radiation at birth and risk of childhood acute leukemia in France, 1990-2009.
- Author
-
Berlivet J, Hémon D, Cléro É, Ielsch G, Laurier D, Faure L, Clavel J, and Goujon S
- Subjects
- Background Radiation, Cities, France epidemiology, Humans, Infant, Newborn, Ultraviolet Rays, Leukemia epidemiology, Radiation Monitoring
- Abstract
Background: The role of natural background radiation (NBR) in childhood acute leukemia (AL) remains unclear. Several large record based studies have recently reported heterogeneous results. Differences in exposure assessment timing may explain this heterogeneity., Objectives: In a previous ecological study we did not observe any association between childhood AL incidence in France and NBR exposure at the time of diagnosis. With the same methodology, the present study focused on NBR exposure at the time of birth. Based on data from the French national registry of childhood cancer, we analyzed all AL together, and lymphoblastic and myeloid AL, separately., Methods: We included 6,059 childhood AL cases born and diagnosed in mainland France between 1990 and 2009. NBR levels in municipalities of residence at birth were estimated by cokriging models, using NBR measurements and precise geological data. The incidence rate ratio (IRR) per unit variation of exposure was estimated with Poisson regression models, with adjustment for socio-demographic indicators and ultraviolet radiation levels. NBR exposures were considered at the time of birth, and cumulatively from birth to diagnosis. We also estimated a total NBR dose to red-bone marrow (RBM)., Results: There was no evidence for an association between NBR exposure at birth and childhood AL incidence, neither overall (gamma radiation: IRR = 0.99 (0.94,1.05) per 50 nSv/h; radon: IRR = 0.97 (0.91,1.03) per 100 Bq/m
3 ) nor for the main AL types. The conclusions were similar with the cumulative exposures, and the total RBM dose., Conclusions: The study was based on high quality incidence data, large numbers of AL cases, and validated models of NBR exposure assessment. In all, the results further support the hypothesis that NBR are not associated to childhood AL in France., (Copyright © 2021 Elsevier Ltd. All rights reserved.)- Published
- 2021
- Full Text
- View/download PDF
4. Agricultural crop density in the municipalities of France and incidence of childhood leukemia: An ecological study.
- Author
-
Coste A, Goujon S, Faure L, Hémon D, and Clavel J
- Subjects
- Adolescent, Agriculture, Child, Child, Preschool, Cities, Crops, Agricultural, France epidemiology, Humans, Incidence, Infant, Infant, Newborn, Leukemia, Pesticides toxicity
- Abstract
Background: Pesticide exposure is suspected to play a role in the etiology of childhood leukemia (AL). Various sources of exposure have been explored, but few studies have investigated the risk of childhood AL in relation to residential exposure to agricultural pesticides. Since around 50% of France is agricultural land, with marked pesticide use, France is a suitable location to investigate for an association. We aimed to analyze the association between the agricultural crop density in the municipalities of France and the incidence of childhood AL between 1990 and 2014., Methods: 11,487 cases of AL diagnosed in children aged 0-14 years were registered by the French National Registry of Childhood Hematological Malignancies over 1990-2014. National agricultural census data for 1990, 2000 and 2010 were used to estimate the densities of the most common crops in France. The incidence of AL was estimated in the 35,512 municipalities, by age and gender, and 3 observation periods, and expressed as the standardized incidence ratio (SIR)., Results: We observed a moderate log-linear association between viticulture density and the incidence of AL, with a 3% increase in SIR for a 10% increase in viticulture density (SIRR = 1.03; 95%CI [1.00-1.06]). The association remained for lymphoblastic AL but not for myeloid AL. The association was stable after stratification by geographic area, age and period, and after adjustment on UV radiation and a French deprivation index. No consistent association was observed for other crop types., Discussion: This nationwide study shows a moderate increase in incidence of childhood AL in municipalities where viticulture is common. Future individual studies are needed to know whether this observation is confirmed and related to particular use of pesticides., Competing Interests: Declaration of competing interests The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)
- Published
- 2020
- Full Text
- View/download PDF
5. Proximity to overhead power lines and childhood leukaemia: an international pooled analysis.
- Author
-
Amoon AT, Crespi CM, Ahlbom A, Bhatnagar M, Bray I, Bunch KJ, Clavel J, Feychting M, Hémon D, Johansen C, Kreis C, Malagoli C, Marquant F, Pedersen C, Raaschou-Nielsen O, Röösli M, Spycher BD, Sudan M, Swanson J, Tittarelli A, Tuck DM, Tynes T, Vergara X, Vinceti M, Wünsch-Filho V, and Kheifets L
- Subjects
- Adolescent, Child, Child, Preschool, Female, Humans, Infant, Infant, Newborn, Leukemia etiology, Leukemia pathology, Male, Residence Characteristics, Risk Factors, Electric Power Supplies adverse effects, Environmental Exposure adverse effects, Leukemia epidemiology, Magnetic Fields adverse effects
- Abstract
Background: Although studies have consistently found an association between childhood leukaemia risk and magnetic fields, the associations between childhood leukaemia and distance to overhead power lines have been inconsistent. We pooled data from multiple studies to assess the association with distance and evaluate whether it is due to magnetic fields or other factors associated with distance from lines., Methods: We present a pooled analysis combining individual-level data (29,049 cases and 68,231 controls) from 11 record-based studies., Results: There was no material association between childhood leukaemia and distance to nearest overhead power line of any voltage. Among children living < 50 m from 200 + kV power lines, the adjusted odds ratio for childhood leukaemia was 1.33 (95% CI: 0.92-1.93). The odds ratio was higher among children diagnosed before age 5 years. There was no association with calculated magnetic fields. Odds ratios remained unchanged with adjustment for potential confounders., Conclusions: In this first comprehensive pooled analysis of childhood leukaemia and distance to power lines, we found a small and imprecise risk for residences < 50 m of 200 + kV lines that was not explained by high magnetic fields. Reasons for the increased risk, found in this and many other studies, remains to be elucidated.
- Published
- 2018
- Full Text
- View/download PDF
6. Residential exposure to solar ultraviolet radiation and incidence of childhood hematological malignancies in France.
- Author
-
Coste A, Goujon S, Boniol M, Marquant F, Faure L, Doré JF, Hémon D, and Clavel J
- Subjects
- Adolescent, Child, Child, Preschool, Female, France epidemiology, Humans, Incidence, Infant, Infant, Newborn, Leukemia etiology, Lymphoma etiology, Male, Registries, Leukemia epidemiology, Lymphoma epidemiology, Ultraviolet Rays adverse effects
- Abstract
Purpose: Few studies have investigated the relationship between solar ultraviolet radiation (UV) and childhood hematological malignancies (CHM). This study addresses the associations between residential UV exposure at diagnosis and the incidence of types and subtypes of CHM, by age and gender, in France, over a long period, on the fine scale of the 36,326 Communes that constitute mainland France., Methods: The 9,082 cases of acute leukemia and 3,563 cases of lymphoma diagnosed before the age of 15 years from 1990 to 2009 were provided by the French National Registry of Childhood Hematological Malignancies. The incidence of CHM was calculated by Commune, year, age and gender and expressed as the standardized incidence ratio (SIR). UV data from 1988 to 2007 were extracted from the EUROSUN database., Results: The annual daily average UV exposure of the children ranged from 85.5 to 137.8 J/cm(2). For each additional 25 J/cm(2), there was a significant increase in precursor B-cell acute lymphoblastic leukemia (PBC-ALL) in children aged less than 5 years (SIR 1.18; 95% CI 1.10-1.27). Further analysis of PBC-ALL in the young children suggested a better fit of models with a threshold, with the risk increasing above 100 J/cm(2), for which the SIR was 1.24 (95% CI 1.14-1.36) for a 25 J/cm(2) increase. The results remained stable in analyses stratifying by deprivation index or degree of urbanization of the Communes., Conclusion: The study suggests that higher residential UV exposure may be positively associated with a higher incidence of PBC-ALL in early childhood.
- Published
- 2015
- Full Text
- View/download PDF
7. Parental occupational pesticide exposure and the risk of childhood leukemia in the offspring: findings from the childhood leukemia international consortium.
- Author
-
Bailey HD, Fritschi L, Infante-Rivard C, Glass DC, Miligi L, Dockerty JD, Lightfoot T, Clavel J, Roman E, Spector LG, Kaatsch P, Metayer C, Magnani C, Milne E, Polychronopoulou S, Simpson J, Rudant J, Sidi V, Rondelli R, Orsi L, Kang AY, Petridou E, and Schüz J
- Subjects
- Adolescent, Case-Control Studies, Child, Child, Preschool, Female, Follow-Up Studies, Humans, Infant, Infant, Newborn, International Agencies, Male, Meta-Analysis as Topic, Pregnancy, Prognosis, Risk Factors, Leukemia etiology, Maternal Exposure adverse effects, Occupational Exposure adverse effects, Paternal Exposure adverse effects, Pesticides adverse effects, Pregnancy Complications, Neoplastic etiology, Prenatal Exposure Delayed Effects etiology
- Abstract
Maternal occupational pesticide exposure during pregnancy and/or paternal occupational pesticide exposure around conception have been suggested to increase risk of leukemia in the offspring. With a view to providing insight in this area we pooled individual level data from 13 case-control studies participating in the Childhood Leukemia International Consortium (CLIC). Occupational data were harmonized to a compatible format. Pooled individual analyses were undertaken using unconditional logistic regression. Using exposure data from mothers of 8,236 cases, and 14,850 controls, and from fathers of 8,169 cases and 14,201 controls the odds ratio (OR) for maternal exposure during pregnancy and the risk of acute lymphoblastic leukemia (ALL) was 1.01 [95% confidence interval (CI) 0.78, 1.30] and for paternal exposure around conception 1.20 (95% 1.06, 1.38). For acute myeloid leukemia (AML), the OR for maternal exposure during pregnancy was 1.94 (CI 1.19, 3.18) and for paternal exposure around conception 0.91 (CI 0.66, 1.24.) based on data from 1,329 case and 12,141 control mothers, and 1,231 case and 11,383 control fathers. Our finding of a significantly increased risk of AML in the offspring with maternal exposure to pesticides during pregnancy is consistent with previous reports. We also found a slight increase in risk of ALL with paternal exposure around conception which appeared to be more evident in children diagnosed at the age of 5 years or more and those with T cell ALL which raises interesting questions on possible mechanisms., (© 2014 UICC.)
- Published
- 2014
- Full Text
- View/download PDF
8. The Childhood Leukemia International Consortium.
- Author
-
Metayer C, Milne E, Clavel J, Infante-Rivard C, Petridou E, Taylor M, Schüz J, Spector LG, Dockerty JD, Magnani C, Pombo-de-Oliveira MS, Sinnett D, Murphy M, Roman E, Monge P, Ezzat S, Mueller BA, Scheurer ME, Armstrong BK, Birch J, Kaatsch P, Koifman S, Lightfoot T, Bhatti P, Bondy ML, Rudant J, O'Neill K, Miligi L, Dessypris N, Kang AY, and Buffler PA
- Subjects
- Adolescent, Child, Child, Preschool, Humans, Infant, Leukemia etiology, Leukemia genetics, Risk Factors, Leukemia epidemiology
- Abstract
Background: Acute leukemia is the most common cancer in children under 15 years of age; 80% are acute lymphoblastic leukemia (ALL) and 17% are acute myeloid leukemia (AML). Childhood leukemia shows further diversity based on cytogenetic and molecular characteristics, which may relate to distinct etiologies. Case-control studies conducted worldwide, particularly of ALL, have collected a wealth of data on potential risk factors and in some studies, biospecimens. There is growing evidence for the role of infectious/immunologic factors, fetal growth, and several environmental factors in the etiology of childhood ALL. The risk of childhood leukemia, like other complex diseases, is likely to be influenced both by independent and interactive effects of genes and environmental exposures. While some studies have analyzed the role of genetic variants, few have been sufficiently powered to investigate gene-environment interactions., Objectives: The Childhood Leukemia International Consortium (CLIC) was established in 2007 to promote investigations of rarer exposures, gene-environment interactions and subtype-specific associations through the pooling of data from independent studies., Methods: By September 2012, CLIC included 22 studies (recruitment period: 1962-present) from 12 countries, totaling approximately 31000 cases and 50000 controls. Of these, 19 case-control studies have collected detailed epidemiologic data, and DNA samples have been collected from children and child-parent trios in 15 and 13 of these studies, respectively. Two registry-based studies and one study comprising hospital records routinely obtained at birth and/or diagnosis have limited interview data or biospecimens., Conclusions: CLIC provides a unique opportunity to fill gaps in knowledge about the role of environmental and genetic risk factors, critical windows of exposure, the effects of gene-environment interactions and associations among specific leukemia subtypes in different ethnic groups., (Copyright © 2013 Elsevier Ltd. All rights reserved.)
- Published
- 2013
- Full Text
- View/download PDF
9. Childhood acute leukemia, maternal beverage intake during pregnancy, and metabolic polymorphisms.
- Author
-
Bonaventure A, Rudant J, Goujon-Bellec S, Orsi L, Leverger G, Baruchel A, Bertrand Y, Nelken B, Pasquet M, Michel G, Sirvent N, Bordigoni P, Ducassou S, Rialland X, Zelenika D, Hémon D, and Clavel J
- Subjects
- Acute Disease, Adolescent, Alcohol Dehydrogenase genetics, Arylamine N-Acetyltransferase genetics, Case-Control Studies, Child, Child, Preschool, Cytochrome P-450 CYP2E1 genetics, Female, Follow-Up Studies, France epidemiology, Humans, Infant, Infant, Newborn, Leukemia diagnosis, Leukemia epidemiology, Male, Pregnancy, Prognosis, Risk Factors, Alcohol Drinking adverse effects, Beverages adverse effects, Biomarkers, Tumor genetics, Coffee adverse effects, Leukemia etiology, Polymorphism, Genetic genetics, Tea adverse effects
- Abstract
Purpose: This study aimed to analyze the associations between childhood acute leukemia (AL) and maternal caffeinated beverage consumption during pregnancy, and to explore interactions between caffeinated and alcoholic beverage consumption and polymorphisms of enzymes involved in caffeine and ethanol metabolisms., Methods: The data were generated by the French ESCALE study, which included 764 AL cases and 1,681 controls in 2003-2004. The case and control mothers were interviewed on their consumption habits during pregnancy using a standardized questionnaire. Genotypes of the candidate alleles (NAT2*5 rs1801280, ADH1C*2 rs698 and rs1693482, CYP2E1*5 rs2031920 and rs3813867) were obtained using high-throughput genotyping and imputation data for 493 AL cases and 549 controls with at least two grandparents born in Europe., Results: Maternal regular coffee consumption during pregnancy was associated with childhood AL (OR = 1.2 [1.0-1.5], p = 0.02); the odds ratios increased linearly with daily intake (p for trend <0.001; >2 cups per day vs. no or less than 1 cup per week: AL: OR = 1.6 [1.2-2.1], lymphoblastic AL: OR = 1.5 [1.1-2.0], myeloblastic AL: OR = 2.4 [1.3-4.3]). The association was slightly more marked for children born to non-smoking mothers. Lymphoblastic AL was also associated with cola soda drinking (OR = 1.3 [1.0-1.5], p = 0.02). No significant gene-environment interactions with coffee, tea, cola soda, or alcohol drinking were observed., Conclusion: This study provides additional evidence that maternal coffee consumption during pregnancy may be associated with childhood AL. Coffee consumption is a prevalent habit and its potential involvement in childhood AL needs to be considered further.
- Published
- 2013
- Full Text
- View/download PDF
10. Fertility treatments, congenital malformations, fetal loss, and childhood acute leukemia: the ESCALE study (SFCE).
- Author
-
Rudant J, Amigou A, Orsi L, Althaus T, Leverger G, Baruchel A, Bertrand Y, Nelken B, Plat G, Michel G, Sirvent N, Chastagner P, Ducassou S, Rialland X, Hémon D, and Clavel J
- Subjects
- Case-Control Studies, Female, Humans, Leukemia etiology, Male, Pregnancy, Congenital Abnormalities epidemiology, Fetal Death epidemiology, Leukemia epidemiology, Mothers statistics & numerical data, Reproductive Techniques, Assisted adverse effects
- Abstract
Background: This study investigated the relationships between childhood acute leukemia (AL) and selective maternal and birth characteristics, including congenital malformations and the use of fertility treatment, for which the literature remains scarce., Procedure: The national registry-based case-control study ESCALE was carried out in France in 2003-2004. Population controls were frequency matched with cases on age and gender. Data were obtained from structured telephone questionnaires. Odds ratios (OR) and their 95% confidence intervals were estimated using unconditional regression models adjusted for potential confounders., Results: In all, 764 cases of AL (648 lymphoblastic AL (acute lymphoblastic leukemia, ALL) and 101 myeloblastic AL) and 1,681 controls were included. The AL cases' mothers reported congenital malformations more frequently than the controls' mothers (OR = 1.5 [1.0-2.4]). ALL was significantly associated with the use of fertility treatment for the index pregnancy (OR = 1.9 [1.3-2.8]). In particular, ALL was associated with ovulation induction only (OR = 2.6 [1.6-4.3]), but not with in vitro fertilization (IVF, OR = 1.0 [0.4-2.3]) or artificial insemination (OR = 1.3 [0.5-3.9]). A positive association was also observed for the difficulty of becoming pregnant without fertility treatment (OR = 1.5 [1.0-2.1]). AL was positively associated with a history of voluntary abortion (OR = 1.4 [1.1-1.8]) but not with a history of spontaneous (OR = 0.8 [0.7-1.0]) or therapeutic (OR = 0.7 [0.5-1.1]) abortion., Conclusion: The results suggest that subfertility in itself and ovulation induction may be associated with ALL, and support a positive association with congenital malformations. The links with the various types of fertility drugs and the underlying causes of infertility need to be investigated further., (Copyright © 2012 Wiley Periodicals, Inc.)
- Published
- 2013
- Full Text
- View/download PDF
11. Childhood leukemia around French nuclear power plants--the Geocap study, 2002-2007.
- Author
-
Sermage-Faure C, Laurier D, Goujon-Bellec S, Chartier M, Guyot-Goubin A, Rudant J, Hémon D, and Clavel J
- Subjects
- Adolescent, Case-Control Studies, Child, Child, Preschool, Cohort Studies, Female, Follow-Up Studies, France epidemiology, Humans, Incidence, Infant, Infant, Newborn, Leukemia epidemiology, Male, Nuclear Power Plants, Prognosis, Residence Characteristics, Risk Factors, Survival Rate, Environmental Exposure adverse effects, Leukemia etiology
- Abstract
The aim of this work is to study the risk of childhood acute leukemia (AL) around French nuclear power plants (NPPs). The nationwide Geocap case-control study included the 2,753 cases diagnosed in mainland France over 2002-2007 and 30,000 contemporaneous population controls. The last addresses were geocoded and located around the 19 NPPs. The study used distance to NPPs and a dose-based geographic zoning (DBGZ), based on the estimated dose to bone marrow related to NPP gaseous discharges. An odds ratio (OR) of 1.9 [1.0-3.3], based on 14 cases, was evidenced for children living within 5 km of NPPs compared to those living 20 km or further away, and a very similar association was observed in the concomitant incidence study (standardized incidence ratio (SIR)=1.9 [1.0-3.2]). These results were similar for all the 5-year-age groups. They persisted after stratification for several contextual characteristics of the municipalities of residence. Conversely, using the DBGZ resulted in OR and SIR close to one in all of the dose categories. There was no increase in AL incidence over 1990-2001 and over the entire 1990-2007 period. The results suggest a possible excess risk of AL in the close vicinity of French NPPs in 2002-2007. The absence of any association with the DBGZ may indicate that the association is not explained by NPP gaseous discharges. Overall, the findings call for investigation for potential risk factors related to the vicinity of NPP and collaborative analysis of multisite studies conducted in various countries., (Copyright © 2012 UICC.)
- Published
- 2012
- Full Text
- View/download PDF
12. Spatial variations of childhood acute leukaemia in France, 1990-2006: global spatial heterogeneity and cluster detection at 'living-zone' level.
- Author
-
Demoury C, Goujon-Bellec S, Guyot-Goubin A, Hémon D, and Clavel J
- Subjects
- Acute Disease, Adolescent, Age of Onset, Child, Child, Preschool, Cluster Analysis, Demography, France epidemiology, Humans, Incidence, Infant, Infant, Newborn, Registries, Time Factors, Leukemia epidemiology, Residence Characteristics statistics & numerical data
- Abstract
Childhood acute leukaemia (AL) accounts for a third of childhood cancers. Analysing the spatial distribution of the incidence of AL and its lymphoblastic and myeloblastic subtypes may contribute to the identification of risk factors. This national registry-based study aimed to evaluate global spatial heterogeneity in the incidence rates of AL and to detect clusters in France over the period 1990-2006 on the 'living-zone' scale. Between 1990 and 2006, 7675 cases of AL were registered in the National Registry of Childhood Haematopoietic malignancies. Their spatial distribution in the 1895 'living zone' was first evaluated with two tests for global spatial heterogeneity (Potthoff-Witthinghill and Rogerson's tests) and then with the SaTScan and FleXScan methods, which aim to locate spatial and space-time clusters. Over 1990-2006, no spatial heterogeneity of AL or its subtypes was evidenced. In addition, none of the most likely clusters identified with SaTScan and FleXScan over the whole period was significant, and the systematic search for space-time clusters yielded nonsignificant results. However, when three subperiods were considered, five statistically significant nonoverlapping spatial clusters were identified. This study did not find evidence of any global spatial heterogeneity of AL incidence rates in France over the period 1990-2006. Although no significant spatial cluster was detected over the whole period, the study identified a few significant spatial clusters in specific periods. Even though the significance levels of those clusters do not strongly support the existence of local risk factors, the clusters may still reflect a slight impact of shared risk factors, including background environmental exposures, which require further investigation.
- Published
- 2012
- Full Text
- View/download PDF
13. Detection of clusters of a rare disease over a large territory: performance of cluster detection methods.
- Author
-
Goujon-Bellec S, Demoury C, Guyot-Goubin A, Hémon D, and Clavel J
- Subjects
- Acute Disease, Child, Cluster Analysis, Epidemiologic Methods, France epidemiology, Humans, Monte Carlo Method, Disease Outbreaks statistics & numerical data, Leukemia epidemiology, Population Surveillance methods, Rare Diseases epidemiology
- Abstract
Background: For many years, the detection of clusters has been of great public health interest. Several detection methods have been developed, the most famous of which is the circular scan method. The present study, which was conducted in the context of a rare disease distributed over a large territory (7675 cases registered over 17 years and located in 1895 units), aimed to evaluate the performance of several of the methods in realistic hot-spot cluster situations., Methods: All the methods considered aim to identify the most likely cluster area, i.e. the zone that maximizes the likelihood ratio function, among a set of cluster candidates. The circular and elliptic scan methods were developed to detect regularly shaped clusters. Four other methods that focus on irregularly shaped clusters were also considered (the flexible scan method, the genetic algorithm method, and the double connected and maximum linkage spatial scan methods). The power of the methods was evaluated via Monte Carlo simulations under 27 alternative scenarios that corresponded to three cluster population sizes (20, 45 and 115 expected cases), three cluster shapes (linear, U-shaped and compact) and three relative risk values (1.5, 2.0 and 3.0)., Results: Three situations emerged from this power study. All the methods failed to detect the smallest clusters with a relative risk lower than 3.0. The power to detect the largest cluster with relative risk of 1.5 was markedly better for all methods, but, at most, half of the true cluster was captured. For other clusters, either large or with the highest relative risk, the standard elliptic scan method appeared to be the best method to detect linear clusters, while the flexible scan method localized the U-shaped clusters more precisely than other methods. Large compact clusters were detected well by all methods, with better results for the circular and elliptic scan methods., Conclusions: The elliptic scan method and flexible scan method seemed the most able to detect clusters of a rare disease in a large territory. However, the probability of detecting small clusters with relative risk lower than 3.0 remained low with all the methods tested.
- Published
- 2011
- Full Text
- View/download PDF
14. Road traffic and childhood leukemia: the ESCALE study (SFCE).
- Author
-
Amigou A, Sermage-Faure C, Orsi L, Leverger G, Baruchel A, Bertrand Y, Nelken B, Robert A, Michel G, Margueritte G, Perel Y, Mechinaud F, Bordigoni P, Hémon D, and Clavel J
- Subjects
- Air Pollutants toxicity, Child, Child, Preschool, Humans, Infant, Inhalation Exposure statistics & numerical data, Nitrogen Dioxide analysis, Nitrogen Dioxide toxicity, Risk Assessment, Vehicle Emissions toxicity, Air Pollutants analysis, Air Pollution statistics & numerical data, Automobiles statistics & numerical data, Leukemia epidemiology, Registries statistics & numerical data, Vehicle Emissions analysis
- Abstract
Background: Traffic is a source of environmental exposures, including benzene, which may be related to childhood leukemia., Objectives: A national registry-based case-control study [ESCALE (Etude Sur les Cancers et les Leucémies de l'Enfant, Study on Environmental and Genetic Risk Factors of Childhood Cancers and Leukemia)] carried out in France was used to assess the effect of exposure to road traffic exhaust fumes on the risk of childhood leukemia., Methods: Over the study period, 2003-2004, 763 cases and 1,681 controls < 15 years old were included, and the controls were frequency matched with the cases on age and sex. The ESCALE data were collected by a standardized telephone interview of the mothers. Various indicators of exposure to traffic and pollution were determined using the geocoded addresses at the time of diagnosis for the cases and of interview for the controls. Indicators of the distance from, and density of, main roads and traffic nitrogen dioxide (NO(2)) concentrations derived from traffic emission data were used. Odds ratios (ORs) were estimated using unconditional regression models adjusted for potential confounders., Results: Acute leukemia (AL) was significantly associated with estimates of traffic NO(2) concentration at the place of residence > 27.7 µg/m(3) compared with NO(2) concentration < 21.9 µg/m(3) [OR=1.2; confidence interval (CI), 1.0-1.5] and with the presence of a heavy-traffic road within 500 m compared with the absence of a heavy-traffic road in the same area (OR=2.0; 95% CI, 1.0-3.6). There was a significant association between AL and a high density of heavy-traffic roads within 500 m compared with the reference category with no heavy-traffic road within 500 m (OR=2.2; 95% CI, 1.1-4.2), with a significant positive linear trend of the association of AL with the total length of heavy-traffic road within 500 m., Conclusion: This study supports the hypothesis that living close to heavy-traffic roads may increase the risk of childhood leukemia.
- Published
- 2011
- Full Text
- View/download PDF
15. Increased frequency of hematopoietic malignancies in relatives of patients with lymphoid neoplasms: a French case-control study.
- Author
-
Villeneuve S, Orsi L, Monnereau A, Berthou C, Fenaux P, Marit G, Soubeyran P, Huguet F, Milpied N, Leporrier M, Hemon D, Troussard X, and Clavel J
- Subjects
- Adult, Aged, Case-Control Studies, Family, Female, Humans, Incidence, Leukemia epidemiology, Leukemia etiology, Lymphoma epidemiology, Lymphoma etiology, Male, Middle Aged, Leukemia genetics, Lymphoma genetics, Lymphoproliferative Disorders genetics, Multiple Myeloma genetics
- Abstract
Lymphoid neoplasms (LNs), including non-Hodgkin's lymphoma (NHL), Hodgkin's lymphoma (HL), lymphoproliferative syndrome (LPS) and multiple myeloma (MM), are among the most frequent cancers ( approximately 17,000 new cases per year in France), after those related to smoking. LNs were investigated using the data from the ENGELA study. ENGELA is a multicenter hospital-based case-control study that was carried out in France over the period September 2000-December 2004. In all, 822 cases (397 NHL, 149 LH, 168 SLP and 108 MM) and 752 controls were included and described 5,481 and 5,188 first-degree relatives, respectively. A positive association with a familial history of hematopoietic cancer was observed for LN (OR = 1.7 [1.0-2.8]) overall and for LPS (OR = 3.2 [1.4-6.8]). The associations with HL (OR = 10.4 [2.0-53.8]) and NHL (OR = 2.4 [1.0-5.9]) were stronger for men. The associations were also stronger when the disease had been diagnosed before the relatives were aged 45 years. The results mainly support the involvement of genetic factors and suggest that at least some of those factors may be sex-linked. However, the slight overrepresentation of affected spouses among the cases might also support the responsibility of environmental factors.
- Published
- 2009
- Full Text
- View/download PDF
16. Familial history of cancer and childhood acute leukemia: a French population-based case-control study.
- Author
-
Ripert M, Menegaux F, Perel Y, Méchinaud F, Plouvier E, Gandemer V, Lutz P, Vannier JP, Lamagnére JP, Margueritte G, Boutard P, Robert A, Armari-Alla C, Munzer M, Millot F, de Lumley L, Berthou C, Rialland X, Pautard B, and Clavel J
- Subjects
- Acute Disease, Adolescent, Case-Control Studies, Child, Child, Preschool, Family, Female, Humans, Infant, Infant, Newborn, Male, Leukemia genetics, Neoplasms genetics
- Abstract
A case-control study was conducted to investigate the role of a familial history of cancer in the etiology of childhood acute leukemia. The history of cancer in the relatives of 472 cases was compared with that of 567 population-based controls. Recruitment was frequency matched on age, sex and region. The familial history of cancer in each child's relatives was reported by the mother in response to a standardized self-administered questionnaire. A familial history of solid tumor in first or second-degree relatives was associated with an increased risk of acute lymphoblastic leukemia (odds ratio (OR)=1.6 [95% confidence interval, 1.2-2.1]), while a familial history of hematopoietic malignancies in first or second-degree relatives was associated with an increased risk of acute myeloid leukemia (OR=4.3 [1.4-13]). The ORs for the histories of cancer increased with the number of relatives with cancer (OR=1.5 [1.1-2.0] for one relative and OR=2.3 [1.3-3.8] for two relatives or more; Ptrend<0.0001). Significant associations between childhood acute leukemia and familial history of genital cancers and brain tumor were also observed (OR=2.7 [1.2-5.8] and OR=10.7 [1.3-86], respectively). This study supports the hypothesis that a familial history of cancer may play a role in the etiology of childhood acute leukemia. It also evidences some specific associations that require further investigation.
- Published
- 2007
- Full Text
- View/download PDF
17. Vaccination and the risk of childhood acute leukaemia: the ESCALE study (SFCE).
- Author
-
Mallol-Mesnard N, Menegaux F, Auvrignon A, Auclerc MF, Bertrand Y, Nelken B, Robert A, Michel G, Margueritte G, Perel Y, Méchinaud F, Bordigoni P, Leverger G, Baruchel A, Hémon D, and Clavel J
- Subjects
- Adolescent, Age Distribution, Case-Control Studies, Child, Child, Preschool, Drug Administration Schedule, Female, France epidemiology, Hepatitis B Vaccines administration & dosage, Hepatitis B Vaccines immunology, Humans, Infant, Leukemia epidemiology, Leukemia virology, Leukemia, Myeloid, Acute epidemiology, Leukemia, Myeloid, Acute immunology, Leukemia, Myeloid, Acute virology, Male, Precursor Cell Lymphoblastic Leukemia-Lymphoma epidemiology, Precursor Cell Lymphoblastic Leukemia-Lymphoma immunology, Precursor Cell Lymphoblastic Leukemia-Lymphoma virology, Risk Assessment methods, Sex Distribution, Vaccination adverse effects, Hepatitis B Vaccines adverse effects, Leukemia immunology
- Abstract
Background: In 2002, a poster alerted the French health authorities to the possibility that the risk of childhood leukaemia might be increased by hepatitis B vaccination. Elucidating the role of vaccination in the aetiology of childhood acute leukaemia (AL) was therefore included in the objectives of an ongoing national study., Methods: The ESCALE study was a French national population-based case-control study conducted in France in 2003 and 2004 in order to investigate the role of infectious, environmental and genetic factors in four childhood neoplastic diseases (leukaemia, lymphoma, neuroblastoma and brain tumour). The controls were randomly selected from the French population and age and gender frequency matched with the cases. A total of 776 cases of AL (91% of the eligible cases) and 1681 controls (71% of the eligible controls) were included. In a specific standardized telephone interview, which was the same for both the cases and controls, each mother was asked to read out her child's complete vaccination record., Results: No association between vaccination and the risk of childhood AL: acute lymphoblastic leukaemia or acute myeloblastic leukaemia was observed. No relationship between the risk of leukaemia and the type of vaccine, number of doses of each vaccine, total number of injections, total number of vaccine doses or number of early vaccinations was evidenced. No confounding factor was observed., Conclusion: The study did not show any evidence of a role of vaccination in the aetiology of childhood leukaemia.
- Published
- 2007
- Full Text
- View/download PDF
18. Childhood leukaemia, polymorphisms of metabolism enzyme genes, and interactions with maternal tobacco, coffee and alcohol consumption during pregnancy.
- Author
-
Clavel J, Bellec S, Rebouissou S, Ménégaux F, Feunteun J, Bonaïti-Pellié C, Baruchel A, Kebaili K, Lambilliotte A, Leverger G, Sommelet D, Lescoeur B, Beaune P, Hémon D, and Loriot MA
- Subjects
- Acute Disease, Adult, Alcohol Drinking adverse effects, Case-Control Studies, Child, Child, Preschool, Coffee, Female, Humans, Odds Ratio, Polymorphism, Genetic, Pregnancy, Risk Factors, Smoking adverse effects, Cytochrome P-450 CYP1A1 genetics, Glutathione Transferase genetics, Leukemia etiology, Leukemia genetics, Prenatal Exposure Delayed Effects
- Abstract
Metabolic polymorphisms may influence the risk of childhood leukaemia related to maternal tobacco, coffee or alcohol consumption. The data were extracted from a case-control study including 280 cases of acute leukaemia and 288 controls. Blood sampling was obtained for a representative subset of 219 cases and 105 controls. Gene-environment interactions were estimated using both case-control and case-only analyses. The polymorphisms of CYP1A1, GSTM1, GSTP1, GSTT1 and NQO1 were not associated with the risk of leukaemia. The slow EPHX1 allele was negatively associated with childhood leukaemia while an inverse non-significant association was observed with the fast EPHX1 allele. Maternal smoking during pregnancy was not related to leukaemia, but an interaction was observed in the case-only analysis with CYP1A1*2A variant allele (odds ratio (OR) 2.2 [1.0-4.9]) and with GSTM1 deletion (OR 2.3 [1.2-4.4]). Conversely, coffee drinking interacted negatively with NQO1 polymorphism in the case-only analysis (OR 0.6 [0.3-1.2] and 0.4 [0.1-1.0] for light and heavy coffee consumptions, respectively). This study suggests that maternal smoking may be a risk factor for leukaemia in children who carry CYP1A1 or GSTM1 genotypes, which might increase reactive metabolites of polycyclic aromatic hydrocarbons.
- Published
- 2005
- Full Text
- View/download PDF
19. Maternal coffee and alcohol consumption during pregnancy, parental smoking and risk of childhood acute leukaemia.
- Author
-
Menegaux F, Steffen C, Bellec S, Baruchel A, Lescoeur B, Leverger G, Nelken B, Philippe N, Sommelet D, Hémon D, and Clavel J
- Subjects
- Adolescent, Case-Control Studies, Child, Child, Preschool, Female, Humans, Infant, Male, Mothers, Pregnancy, Risk Factors, Socioeconomic Factors, Alcohol Drinking adverse effects, Coffee adverse effects, Leukemia epidemiology, Leukemia etiology, Maternal Exposure adverse effects, Tobacco Smoke Pollution adverse effects
- Abstract
Introduction: We investigated the role of maternal alcohol and coffee drinking and parental smoking on the risk of childhood acute leukemia in a multicenter case-control study., Methods: The study included 280 incident cases and 288 hospitalized controls, frequency matched with the cases by age, gender and center. Data collection was completed by face-to-face standardized interviews of the case and control mothers., Results: An association with maternal alcohol consumption during pregnancy was observed with acute lymphoid leukemia (ALL) (OR=2.0 [1.4-3.0]) and acute non-lymphoid leukemia (ANLL) (OR=2.6 [1.2-5.8]). Maternal coffee consumption during pregnancy was associated with childhood acute leukemia, ORs increasing in ALL with coffee consumption (OR=1.1 [0.7-1.8], OR=2.4 [1.3-4.7] and OR=3.1 [1.0-9.5], respectively, for < or =3, 4-8 and >8 cups/day). No association with maternal smoking during pregnancy or parental smoking before or after the index child's birth was observed., Discussion: Our results suggest an association with maternal alcohol and coffee drinking during pregnancy and call for further investigations. Besides, the present study does not support the hypothesis of an increase in the risk of childhood leukemia related to parental smoking.
- Published
- 2005
- Full Text
- View/download PDF
20. Nonchromosomal birth defects and risk of childhood acute leukemia: An assessment in 15 000 leukemia cases and 46 000 controls from the Childhood Cancer and Leukemia International Consortium
- Author
-
Lupo, Philip J, Chambers, Tiffany M, Mueller, Beth A, Clavel, Jacqueline, Dockerty, John D, Doody, David R, Erdmann, Friederike, Ezzat, Sameera, Filippini, Tommaso, Hansen, Johnni, Heck, Julia E, Infante‐Rivard, Claire, Kang, Alice Y, Magnani, Corrado, Malagoli, Carlotta, Marcotte, Erin L, Metayer, Catherine, Bailey, Helen D, Mora, Ana M, Ntzani, Evangelia, Petridou, Eleni Th, Pombo‐de‐Oliveira, Maria S, Rashed, Wafaa M, Roman, Eve, Schüz, Joachim, Wesseling, Catharina, Spector, Logan G, and Scheurer, Michael E
- Subjects
Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Rare Diseases ,Clinical Research ,Cancer ,Pediatric ,Hematology ,Pediatric Cancer ,Childhood Leukemia ,Pediatric Research Initiative ,2.1 Biological and endogenous factors ,Aetiology ,Child ,Humans ,Infant ,Risk Factors ,Leukemia ,Myeloid ,Acute ,Birth Weight ,Logistic Models ,Case-Control Studies ,Surveys and Questionnaires ,acute lymphoblastic leukemia ,acute myeloid leukemia ,birth defects ,childhood leukemia ,epidemiology ,Oncology & Carcinogenesis ,Oncology and carcinogenesis - Abstract
Although recent studies have demonstrated associations between nonchromosomal birth defects and several pediatric cancers, less is known about their role on childhood leukemia susceptibility. Using data from the Childhood Cancer and Leukemia International Consortium, we evaluated associations between nonchromosomal birth defects and childhood leukemia. Pooling consortium data from 18 questionnaire-based and three registry-based case-control studies across 13 countries, we used multivariable logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between a spectrum of birth defects and leukemia. Our analyses included acute lymphoblastic leukemia (ALL, n = 13 115) and acute myeloid leukemia (AML, n = 2120) cases, along with 46 172 controls. We used the false discovery rate to account for multiple comparisons. In the questionnaire-based studies, the prevalence of birth defects was 5% among cases vs 4% in controls, whereas, in the registry-based studies, the prevalence was 11% among cases vs 7% in controls. In pooled adjusted analyses, there were several notable associations, including (1) digestive system defects and ALL (OR = 2.70, 95% CI: 1.46-4.98); (2) congenital anomalies of the heart and circulatory system and AML (OR = 2.86, 95% CI: 1.81-4.52) and (3) nervous system defects and AML (OR = 4.23, 95% CI: 1.50-11.89). Effect sizes were generally larger in registry-based studies. Overall, our results could point to novel genetic and environmental factors associated with birth defects that could also increase leukemia susceptibility. Additionally, differences between questionnaire- and registry-based studies point to the importance of complementary sources of birth defect phenotype data when exploring these associations.
- Published
- 2024
21. Caesarean delivery and risk of childhood leukaemia: a pooled analysis from the Childhood Leukemia International Consortium (CLIC)
- Author
-
Marcotte, Erin L, Thomopoulos, Thomas P, Infante-Rivard, Claire, Clavel, Jacqueline, Petridou, Eleni Th, Schüz, Joachim, Ezzat, Sameera, Dockerty, John D, Metayer, Catherine, Magnani, Corrado, Scheurer, Michael E, Mueller, Beth A, Mora, Ana M, Wesseling, Catharina, Skalkidou, Alkistis, Rashed, Wafaa M, Francis, Stephen S, Ajrouche, Roula, Erdmann, Friederike, Orsi, Laurent, and Spector, Logan G
- Subjects
Reproductive Medicine ,Biomedical and Clinical Sciences ,Pediatric Cancer ,Rare Diseases ,Childhood Leukemia ,Cancer ,Hematology ,Pediatric ,2.1 Biological and endogenous factors ,Adolescent ,Canada ,Cesarean Section ,Child ,Child ,Preschool ,Costa Rica ,Egypt ,Female ,France ,Germany ,Greece ,Humans ,Infant ,Infant ,Newborn ,Italy ,Leukemia ,Myeloid ,Acute ,New Zealand ,Precursor Cell Lymphoblastic Leukemia-Lymphoma ,Pregnancy ,Risk Factors ,United States ,Cardiorespiratory Medicine and Haematology ,Clinical Sciences ,Cardiovascular medicine and haematology - Abstract
BackgroundResults from case-control studies have shown an increased risk of acute lymphoblastic leukaemia (ALL) in young children born by caesarean delivery, and prelabour caesarean delivery in particular; however, an association of method of delivery with childhood leukaemia subtypes has yet to be established. We therefore did a pooled analysis of data to investigate the association between childhood leukaemia and caesarean delivery.MethodsWe pooled data from 13 case-control studies from the Childhood Leukemia International Consortium done in nine countries (Canada, Costa Rica, Egypt, France, Germany, Greece, Italy, New Zealand, and the USA) for births from 1970-2013. We analysed caesarean delivery overall and by indications that probably resulted in prelabour caesarean delivery or emergency caesarean delivery. We used multivariable logistic regression models, adjusted for child's birthweight, sex, age, ethnic origin, parental education, maternal age, and study, to estimate odds ratios (ORs) and 95% CIs for the risk of ALL and acute myeloid leukaemia (AML) in children aged 0-14 years at diagnosis.FindingsThe studies provided data for 8780 ALL cases, 1332 AML cases, and 23 459 controls, of which the birth delivery method was known for 8655 (99%) ALL cases, 1292 (97%) AML cases, and 23 351 (>99%) controls. Indications for caesarean delivery were available in four studies (there were caesarean deliveries for 1061 of 4313 ALL cases, 138 of 664 AML cases, and 1401 of 5884 controls). The OR for all indications of caesarean delivery and ALL was 1·06 (95% CI 0·99-1·13), and was significant for prelabour caesarean delivery and ALL (1·23 [1·04-1·47]; p=0·018). Emergency caesarean delivery was not associated with ALL (OR 1·02 [95% CI 0·81-1·30]). AML was not associated with caesarean delivery (all indications OR 0·99 [95% CI 0·84-1·17]; prelabour caesarean delivery 0·83 [0·54-1·26]; and emergency caesarean delivery 1·05 [0·63-1·77]).InterpretationOur results suggest an increased risk of childhood ALL after prelabour caesarean delivery. If this association is causal, maladaptive immune activation due to an absence of stress response before birth in children born by prelabour caesarean delivery could be considered as a potential mechanism.FundingNational Cancer Institute.
- Published
- 2016
22. Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
- Author
-
Sampson, Joshua N, Wheeler, William A, Yeager, Meredith, Panagiotou, Orestis, Wang, Zhaoming, Berndt, Sonja I, Lan, Qing, Abnet, Christian C, Amundadottir, Laufey T, Figueroa, Jonine D, Landi, Maria Teresa, Mirabello, Lisa, Savage, Sharon A, Taylor, Philip R, De Vivo, Immaculata, McGlynn, Katherine A, Purdue, Mark P, Rajaraman, Preetha, Adami, Hans-Olov, Ahlbom, Anders, Albanes, Demetrius, Amary, Maria Fernanda, An, She-Juan, Andersson, Ulrika, Andriole, Gerald, Andrulis, Irene L, Angelucci, Emanuele, Ansell, Stephen M, Arici, Cecilia, Armstrong, Bruce K, Arslan, Alan A, Austin, Melissa A, Baris, Dalsu, Barkauskas, Donald A, Bassig, Bryan A, Becker, Nikolaus, Benavente, Yolanda, Benhamou, Simone, Berg, Christine, Van Den Berg, David, Bernstein, Leslie, Bertrand, Kimberly A, Birmann, Brenda M, Black, Amanda, Boeing, Heiner, Boffetta, Paolo, Boutron-Ruault, Marie-Christine, Bracci, Paige M, Brinton, Louise, Brooks-Wilson, Angela R, Bueno-de-Mesquita, H Bas, Burdett, Laurie, Buring, Julie, Butler, Mary Ann, Cai, Qiuyin, Cancel-Tassin, Geraldine, Canzian, Federico, Carrato, Alfredo, Carreon, Tania, Carta, Angela, Chan, John KC, Chang, Ellen T, Chang, Gee-Chen, Chang, I-Shou, Chang, Jiang, Chang-Claude, Jenny, Chen, Chien-Jen, Chen, Chih-Yi, Chen, Chu, Chen, Chung-Hsing, Chen, Constance, Chen, Hongyan, Chen, Kexin, Chen, Kuan-Yu, Chen, Kun-Chieh, Chen, Ying, Chen, Ying-Hsiang, Chen, Yi-Song, Chen, Yuh-Min, Chien, Li-Hsin, Chirlaque, María-Dolores, Choi, Jin Eun, Choi, Yi Young, Chow, Wong-Ho, Chung, Charles C, Clavel, Jacqueline, Clavel-Chapelon, Françoise, Cocco, Pierluigi, Colt, Joanne S, Comperat, Eva, Conde, Lucia, Connors, Joseph M, Conti, David, Cortessis, Victoria K, Cotterchio, Michelle, Cozen, Wendy, Crouch, Simon, Crous-Bou, Marta, Cussenot, Olivier, and Davis, Faith G
- Subjects
Tobacco ,Clinical Research ,Urologic Diseases ,Lung ,Genetics ,Rare Diseases ,Lung Cancer ,Human Genome ,Hematology ,Cancer ,Tobacco Smoke and Health ,Prevention ,Lymphoma ,Adult ,Aged ,Asian People ,Bone Neoplasms ,Female ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Humans ,Kidney Neoplasms ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Lung Neoplasms ,Lymphoma ,Large B-Cell ,Diffuse ,Male ,Middle Aged ,Neoplasms ,Osteosarcoma ,Polymorphism ,Single Nucleotide ,Smoking ,Testicular Neoplasms ,Tissue Array Analysis ,Urinary Bladder Neoplasms ,White People ,Oncology and Carcinogenesis ,Oncology & Carcinogenesis - Abstract
BackgroundStudies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.MethodsBetween 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.ResultsGWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.ConclusionOur results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
- Published
- 2015
23. Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for Thirteen Cancer Types.
- Author
-
Sampson, Joshua N, Wheeler, William A, Yeager, Meredith, Panagiotou, Orestis, Wang, Zhaoming, Berndt, Sonja I, Lan, Qing, Abnet, Christian C, Amundadottir, Laufey T, Figueroa, Jonine D, Landi, Maria Teresa, Mirabello, Lisa, Savage, Sharon A, Taylor, Philip R, De Vivo, Immaculata, McGlynn, Katherine A, Purdue, Mark P, Rajaraman, Preetha, Adami, Hans-Olov, Ahlbom, Anders, Albanes, Demetrius, Amary, Maria Fernanda, An, She-Juan, Andersson, Ulrika, Andriole, Gerald, Andrulis, Irene L, Angelucci, Emanuele, Ansell, Stephen M, Arici, Cecilia, Armstrong, Bruce K, Arslan, Alan A, Austin, Melissa A, Baris, Dalsu, Barkauskas, Donald A, Bassig, Bryan A, Becker, Nikolaus, Benavente, Yolanda, Benhamou, Simone, Berg, Christine, Van Den Berg, David, Bernstein, Leslie, Bertrand, Kimberly A, Birmann, Brenda M, Black, Amanda, Boeing, Heiner, Boffetta, Paolo, Boutron-Ruault, Marie-Christine, Bracci, Paige M, Brinton, Louise, Brooks-Wilson, Angela R, Bueno-de-Mesquita, H Bas, Burdett, Laurie, Buring, Julie, Butler, Mary Ann, Cai, Qiuyin, Cancel-Tassin, Geraldine, Canzian, Federico, Carrato, Alfredo, Carreon, Tania, Carta, Angela, Chan, John KC, Chang, Ellen T, Chang, Gee-Chen, Chang, I-Shou, Chang, Jiang, Chang-Claude, Jenny, Chen, Chien-Jen, Chen, Chih-Yi, Chen, Chu, Chen, Chung-Hsing, Chen, Constance, Chen, Hongyan, Chen, Kexin, Chen, Kuan-Yu, Chen, Kun-Chieh, Chen, Ying, Chen, Ying-Hsiang, Chen, Yi-Song, Chen, Yuh-Min, Chien, Li-Hsin, Chirlaque, María-Dolores, Choi, Jin Eun, Choi, Yi Young, Chow, Wong-Ho, Chung, Charles C, Clavel, Jacqueline, Clavel-Chapelon, Françoise, Cocco, Pierluigi, Colt, Joanne S, Comperat, Eva, Conde, Lucia, Connors, Joseph M, Conti, David, Cortessis, Victoria K, Cotterchio, Michelle, Cozen, Wendy, Crouch, Simon, Crous-Bou, Marta, Cussenot, Olivier, and Davis, Faith G
- Subjects
Humans ,Neoplasms ,Osteosarcoma ,Bone Neoplasms ,Testicular Neoplasms ,Lung Neoplasms ,Kidney Neoplasms ,Genetic Predisposition to Disease ,Tissue Array Analysis ,Smoking ,Polymorphism ,Single Nucleotide ,Adult ,Aged ,Middle Aged ,Asian Continental Ancestry Group ,European Continental Ancestry Group ,Female ,Male ,Urinary Bladder Neoplasms ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Lymphoma ,Large B-Cell ,Diffuse ,Genome-Wide Association Study ,Polymorphism ,Single Nucleotide ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Lymphoma ,Large B-Cell ,Diffuse ,Oncology And Carcinogenesis ,Oncology & Carcinogenesis ,Oncology and Carcinogenesis - Abstract
BackgroundStudies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.MethodsBetween 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.ResultsGWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.ConclusionOur results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
- Published
- 2015
24. Genome-wide association study identifies multiple risk loci for chronic lymphocytic leukemia
- Author
-
Berndt, Sonja I, Skibola, Christine F, Joseph, Vijai, Camp, Nicola J, Nieters, Alexandra, Wang, Zhaoming, Cozen, Wendy, Monnereau, Alain, Wang, Sophia S, Kelly, Rachel S, Lan, Qing, Teras, Lauren R, Chatterjee, Nilanjan, Chung, Charles C, Yeager, Meredith, Brooks-Wilson, Angela R, Hartge, Patricia, Purdue, Mark P, Birmann, Brenda M, Armstrong, Bruce K, Cocco, Pierluigi, Zhang, Yawei, Severi, Gianluca, Zeleniuch-Jacquotte, Anne, Lawrence, Charles, Burdette, Laurie, Yuenger, Jeffrey, Hutchinson, Amy, Jacobs, Kevin B, Call, Timothy G, Shanafelt, Tait D, Novak, Anne J, Kay, Neil E, Liebow, Mark, Wang, Alice H, Smedby, Karin E, Adami, Hans-Olov, Melbye, Mads, Glimelius, Bengt, Chang, Ellen T, Glenn, Martha, Curtin, Karen, Cannon-Albright, Lisa A, Jones, Brandt, Diver, W Ryan, Link, Brian K, Weiner, George J, Conde, Lucia, Bracci, Paige M, Riby, Jacques, Holly, Elizabeth A, Smith, Martyn T, Jackson, Rebecca D, Tinker, Lesley F, Benavente, Yolanda, Becker, Nikolaus, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, McKay, James, Staines, Anthony, Rabe, Kari G, Achenbach, Sara J, Vachon, Celine M, Goldin, Lynn R, Strom, Sara S, Lanasa, Mark C, Spector, Logan G, Leis, Jose F, Cunningham, Julie M, Weinberg, J Brice, Morrison, Vicki A, Caporaso, Neil E, Norman, Aaron D, Linet, Martha S, De Roos, Anneclaire J, Morton, Lindsay M, Severson, Richard K, Riboli, Elio, Vineis, Paolo, Kaaks, Rudolph, Trichopoulos, Dimitrios, Masala, Giovanna, Weiderpass, Elisabete, Chirlaque, María-Dolores, Vermeulen, Roel CH, Travis, Ruth C, Giles, Graham G, Albanes, Demetrius, Virtamo, Jarmo, Weinstein, Stephanie, Clavel, Jacqueline, Zheng, Tongzhang, Holford, Theodore R, Offit, Kenneth, Zelenetz, Andrew, Klein, Robert J, Spinelli, John J, and Bertrand, Kimberly A
- Subjects
Cancer ,Case-Control Studies ,Chromosomes ,Human ,Pair 2 ,Genetic Loci ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Humans ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Linkage Disequilibrium ,Polymorphism ,Single Nucleotide ,Recombination ,Genetic ,Risk ,Biological Sciences ,Medical and Health Sciences ,Developmental Biology - Abstract
Genome-wide association studies (GWAS) have previously identified 13 loci associated with risk of chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL). To identify additional CLL susceptibility loci, we conducted the largest meta-analysis for CLL thus far, including four GWAS with a total of 3,100 individuals with CLL (cases) and 7,667 controls. In the meta-analysis, we identified ten independent associated SNPs in nine new loci at 10q23.31 (ACTA2 or FAS (ACTA2/FAS), P=1.22×10(-14)), 18q21.33 (BCL2, P=7.76×10(-11)), 11p15.5 (C11orf21, P=2.15×10(-10)), 4q25 (LEF1, P=4.24×10(-10)), 2q33.1 (CASP10 or CASP8 (CASP10/CASP8), P=2.50×10(-9)), 9p21.3 (CDKN2B-AS1, P=1.27×10(-8)), 18q21.32 (PMAIP1, P=2.51×10(-8)), 15q15.1 (BMF, P=2.71×10(-10)) and 2p22.2 (QPCT, P=1.68×10(-8)), as well as an independent signal at an established locus (2q13, ACOXL, P=2.08×10(-18)). We also found evidence for two additional promising loci below genome-wide significance at 8q22.3 (ODF1, P=5.40×10(-8)) and 5p15.33 (TERT, P=1.92×10(-7)). Although further studies are required, the proximity of several of these loci to genes involved in apoptosis suggests a plausible underlying biological mechanism.
- Published
- 2013
25. Household Exposure to Pesticides and Risk of Childhood Hematopoietic Malignancies: The ESCALE Study (SFCE)
- Author
-
Leverger, Guy, Baruchel, André, Nelken, Brigitte, Robert, Alain, Hémon, Denis, and Clavel, Jacqueline
- Published
- 2007
26. Family Cancer History and Risk of Childhood Acute Leukemia (France)
- Author
-
Perrillat, Florence, Clavel, Jacqueline, Jaussent, Isabelle, Baruchel, André, Leverger, Guy, Nelken, Brigitte, Philippe, Noël, Schaison, Gérard, Sommelet, Danièle, Vilmer, Etienne, Bonaïti-Pellié, Catherine, and Hémon, Denis
- Published
- 2001
27. Maternal consumption of coffee and tea during pregnancy and risk of childhood ALL: a pooled analysis from the childhood Leukemia International Consortium
- Author
-
Milne, Elizabeth, Greenop, Kathryn R., Petridou, Eleni, Bailey, Helen D., Orsi, Laurent, Kang, Alice Y., Baka, Margarita, Bonaventure, Audrey, Kourti, Maria, Metayer, Catherine, and Clavel, Jacqueline
- Published
- 2018
- Full Text
- View/download PDF
28. Maternal Supplementation with Folic Acid and Other Vitamins and Risk of Leukemia in Offspring: A Childhood Leukemia International Consortium Study
- Author
-
Metayer, Catherine, Milne, Elizabeth, Dockerty, John D., Clavel, Jacqueline, Pombo-de-Oliveira, Maria S., Wesseling, Catharina, Spector, Logan G., Schüz, Joachim, Petridou, Eleni, Ezzat, Sameera, Armstrong, Bruce K., Rudant, Jérémie, Koifman, Sergio, Kaatsch, Peter, Moschovi, Maria, Rashed, Wafaa M., Selvin, Steve, McCauley, Kathryn, Hung, Rayjean J., Kang, Alice Y., and Infante-Rivard, Claire
- Published
- 2014
29. Parental occupational paint exposure and risk of childhood leukemia in the offspring: findings from the Childhood Leukemia International Consortium
- Author
-
Bailey, Helen D., Fritschi, Lin, Metayer, Catherine, Infante-Rivard, Claire, Magnani, Corrado, Petridou, Eleni, Roman, Eve, Spector, Logan G., Kaatsch, Peter, Clavel, Jacqueline, Milne, Elizabeth, Dockerty, John D., Glass, Deborah C., Lightfoot, Tracy, Miligi, Lucia, Rudant, Jérémie, Baka, Margarita, Rondelli, Roberto, Amigou, Alicia, Simpson, Jill, Kang, Alice Y., Moschovi, Maria, and Schüz, Joachim
- Published
- 2014
30. Maternal reproductive history, fertility treatments and folic acid supplementation in the risk of childhood acute leukemia: the ESTELLE Study
- Author
-
Ajrouche, Roula, Rudant, Jérémie, Orsi, Laurent, Petit, Arnaud, Baruchel, André, Nelken, Brigitte, Pasquet, Marlène, Michel, Gérard, Bergeron, Christophe, Ducassou, Stéphane, Gandemer, Virginie, Lutz, Patrick, Saumet, Laure, Rialland, Xavier, Hémon, Denis, and Clavel, Jacqueline
- Published
- 2014
31. Folic acid supplementation, MTHFR and MTRR polymorphisms, and the risk of childhood leukemia: the ESCALE study (SFCE)
- Author
-
Amigou, Alicia, Rudant, Jérémie, Orsi, Laurent, Goujon-Bellec, Stéphanie, Leverger, Guy, Baruchel, André, Bertrand, Yves, Nelken, Brigitte, Plat, Geneviève, Michel, Gérard, Haouy, Stéphanie, Chastagner, Pascal, Ducassou, Stéphane, Rialland, Xavier, Hémon, Denis, and Clavel, Jacqueline
- Published
- 2012
32. Maternal smoking during pregnancy, genetic polymorphisms of metabolic enzymes, and childhood acute leukemia: the ESCALE Study (SFCE)
- Author
-
Bonaventure, Audrey, Goujon-Bellec, Stéphanie, Rudant, Jérémie, Orsi, Laurent, Leverger, Guy, Baruchel, André, Bertrand, Yves, Nelken, Brigitte, Pasquet, Marlène, Michel, Gérard, Sirvent, Nicolas, Bordigoni, Pierre, Ducassou, Stéphane, Rialland, Xavier, Zelenika, Diana, Hémon, Denis, and Clavel, Jacqueline
- Published
- 2012
33. Childhood Hematopoietic Malignancies and Parental Use of Tobacco and Alcohol: The ESCALE Study (SFCE)
- Author
-
Rudant, Jérémie, Menegaux, Florence, Leverger, Guy, Baruchel, André, Lambilliotte, Anne, Bertrand, Yves, Patte, Catherine, Pacquement, Hélène, Vérité, Cécile, Robert, Alain, Michel, Gérard, Margueritte, Geneviève, Gandemer, Virginie, Hémon, Denis, and Clavel, Jacqueline
- Published
- 2008
- Full Text
- View/download PDF
34. Infant feeding practices and childhood acute leukemia: Findings from the Childhood Cancer & Leukemia International Consortium.
- Author
-
Schraw, Jeremy M., Bailey, Helen D., Bonaventure, Audrey, Mora, Ana M., Roman, Eve, Mueller, Beth A., Clavel, Jacqueline, Petridou, Eleni T., Karalexi, Maria, Ntzani, Evangelia, Ezzat, Sameera, Rashed, Wafaa M., Marcotte, Erin L., Spector, Logan G., Metayer, Catherine, Kang, Alice Y., Magnani, Corrado, Miligi, Lucia, Dockerty, John D., and Mejίa‐Aranguré, Juan Manuel
- Subjects
CHILDHOOD cancer ,ACUTE leukemia ,CONSORTIA ,LEUKEMIA ,LYMPHOBLASTIC leukemia ,ANKYLOGLOSSIA - Abstract
Increasing evidence suggests that breastfeeding may protect from childhood acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). However, most studies have limited their analyses to any breastfeeding, and only a few data have examined exclusive breastfeeding, or other exposures such as formula milk. We performed pooled analyses and individual participant data metaanalyses of data from 16 studies (N = 17 189 controls; N = 10 782 ALL and N = 1690 AML cases) from the Childhood Leukemia International Consortium (CLIC) to characterize the associations of breastfeeding duration with ALL and AML, as well as exclusive breastfeeding duration and age at introduction to formula with ALL. In unconditional multivariable logistic regression analyses of pooled data, we observed decreased odds of ALL among children breastfed 4 to 6 months (0.88, 95% CI 0.81‐0.96) or 7 to 12 months (OR 0.85, 0.79‐0.92). We observed a similar inverse association between breastfeeding ≥4 months and AML (0.82, 95% CI 0.71‐0.95). Odds of ALL were reduced among children exclusively breastfed 4 to 6 months (OR 0.73, 95% CI 0.63‐0.85) or 7 to 12 months (OR 0.70, 95% CI 0.53‐0.92). Random effects metaanalyses produced similar estimates, and findings were unchanged in sensitivity analyses adjusted for race/ethnicity or mode of delivery, restricted to children diagnosed ≥1 year of age or diagnosed with B‐ALL. Our pooled analyses indicate that longer breastfeeding is associated with decreased odds of ALL and AML. Few risk factors for ALL and AML have been described, therefore our findings highlight the need to promote breastfeeding for leukemia prevention. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
35. Potential impacts of radon, terrestrial gamma and cosmic rays on childhood leukemia in France: a quantitative risk assessment
- Author
-
Laurent, Olivier, Ancelet, Sophie, Richardson, David B., Hémon, Denis, Ielsch, Géraldine, Demoury, Claire, Clavel, Jacqueline, and Laurier, Dominique
- Published
- 2013
- Full Text
- View/download PDF
36. Occupational Exposure to Solvents and Hairy Cell Leukaemia
- Author
-
Clavel, Jacqueline, Mandereau, Laurence, Conso, Françoise, Limasset, Jean-Claude, Pourmir, Isabelle, Flandrin, Georges, and Hemon, Denis
- Published
- 1998
37. Leukaemia near La Hague Nuclear Plant
- Author
-
Clavel, Jacqueline, Hémon, Denis, Law, Graham, Roman, Eve, Wakeford, Richard, Barton, Carol, Ryder, Hilary, Hesse-Honegger, Cornelia, and Viel, Jean-François
- Published
- 1997
38. Farming, pesticide use and hairy-cell leukemia
- Author
-
Clavel, Jacqueline, Hémon, Denis, Mandereau, Laurence, Delemotte, Bernard, Séverin, Fernand, and Flandrin, Georges
- Published
- 1996
39. Seasonal variations in childhood leukaemia incidence in France, 1990-2014.
- Author
-
Bamouni, Sophie, Hémon, Denis, Faure, Laure, Clavel, Jacqueline, and Goujon, Stéphanie
- Subjects
LEUKEMIA ,ACUTE leukemia ,CHILDHOOD cancer ,POISSON regression ,DIAGNOSIS ,SEASONAL variations of diseases - Abstract
Background: Several studies have addressed the potential seasonality of childhood acute leukaemia (AL) without conclusive results. Using data from the National Registry of Childhood Cancers over 1990-2014 in mainland France, we investigated the seasonal variations in childhood AL taken together, and lymphoblastic (ALL) and myeloid (AML) leukaemia separately.Methods: Assuming constant variations over 1990-2014, we used a Poisson regression model to evaluate variations in standardized incidence ratios (SIRs) by month of birth or diagnosis. A scan method for temporal cluster detection was used to identify windows of several consecutive months with high or low SIR. The yearly reproducibility of the observed monthly variations was then evaluated.Results: We included 11,528 AL, of which 9493 ALL and 1,843 AML. No seasonal variation was detected for ALL. With a clear seasonal pattern, differences in AML incidence rates were evidenced between January-April and May-December birth periods (SIR = 0.85, 95% CI 0.77-0.94 and SIR = 1.07, 95% CI 1.01-1.14, respectively). AML incidence variations by month of diagnosis were less clear-cut.Conclusion: Based on a large number of cases from a high-quality registry, we did not evidence any seasonality in ALL incidence rates but evidenced seasonal variations in AML incidence rates by month of birth. [ABSTRACT FROM AUTHOR]- Published
- 2021
- Full Text
- View/download PDF
40. Detection of clusters of a rare disease over a large territory: performance of cluster detection methods
- Author
-
Demoury Claire, Goujon-Bellec Stéphanie, Guyot-Goubin Aurélie, Hémon Denis, and Clavel Jacqueline
- Subjects
Power ,Cluster detection ,Rare disease ,Leukemia ,Large scale ,Spatial scan methods ,Computer applications to medicine. Medical informatics ,R858-859.7 - Abstract
Abstract Background For many years, the detection of clusters has been of great public health interest. Several detection methods have been developed, the most famous of which is the circular scan method. The present study, which was conducted in the context of a rare disease distributed over a large territory (7675 cases registered over 17 years and located in 1895 units), aimed to evaluate the performance of several of the methods in realistic hot-spot cluster situations. Methods All the methods considered aim to identify the most likely cluster area, i.e. the zone that maximizes the likelihood ratio function, among a set of cluster candidates. The circular and elliptic scan methods were developed to detect regularly shaped clusters. Four other methods that focus on irregularly shaped clusters were also considered (the flexible scan method, the genetic algorithm method, and the double connected and maximum linkage spatial scan methods). The power of the methods was evaluated via Monte Carlo simulations under 27 alternative scenarios that corresponded to three cluster population sizes (20, 45 and 115 expected cases), three cluster shapes (linear, U-shaped and compact) and three relative risk values (1.5, 2.0 and 3.0). Results Three situations emerged from this power study. All the methods failed to detect the smallest clusters with a relative risk lower than 3.0. The power to detect the largest cluster with relative risk of 1.5 was markedly better for all methods, but, at most, half of the true cluster was captured. For other clusters, either large or with the highest relative risk, the standard elliptic scan method appeared to be the best method to detect linear clusters, while the flexible scan method localized the U-shaped clusters more precisely than other methods. Large compact clusters were detected well by all methods, with better results for the circular and elliptic scan methods. Conclusions The elliptic scan method and flexible scan method seemed the most able to detect clusters of a rare disease in a large territory. However, the probability of detecting small clusters with relative risk lower than 3.0 remained low with all the methods tested.
- Published
- 2011
- Full Text
- View/download PDF
41. Worldwide comparison of survival from childhood leukaemia for 1995-2009, by subtype, age, and sex (CONCORD-2): a population-based study of individual data for 89 828 children from 198 registries in 53 countries
- Author
-
Bonaventure, Audrey, Harewood, Rhea, Stiller, Charles A., Gatta, Gemma, Clavel, Jacqueline, Stefan, Daniela C., Carreira, Helena, Spika, Devon, Marcos-Gragera, Rafael, Peris-Bonet, Rafael, Piñeros, Marion, Sant, Milena, Kuehni, Claudia E., Murphy, Michael F. G., Coleman, Michel P., Allemani, Claudia, Concord, Working Group, and Health Technology & Services Research
- Subjects
Leukemia ,Leucèmia ,Leukemia in children ,Leucèmia en els infants - Abstract
Global inequalities in access to health care are reflected in differences in cancer survival. The CONCORD programme was designed to assess worldwide differences and trends in population-based cancer survival. In this population-based study, we aimed to estimate survival inequalities globally for several subtypes of childhood leukaemia. Methods Cancer registries participating in CONCORD were asked to submit tumour registrations for all children aged 0–14 years who were diagnosed with leukaemia between Jan 1, 1995, and Dec 31, 2009, and followed up until Dec 31, 2009. Haematological malignancies were defined by morphology codes in the International Classification of Diseases for Oncology, third revision. We excluded data from registries from which the data were judged to be less reliable, or included only lymphomas, and data from countries in which data for fewer than ten children were available for analysis. We also excluded records because of a missing date of birth, diagnosis, or last known vital status. We estimated 5-year net survival (ie, the probability of surviving at least 5 years after diagnosis, after controlling for deaths from other causes [background mortality]) for children by calendar period of diagnosis (1995–99, 2000–04, and 2005–09), sex, and age at diagnosis (
- Published
- 2017
42. The International Childhood Cancer Cohort Consortium (I4C): A research platform of prospective cohorts for studying the aetiology of childhood cancers.
- Author
-
Tikellis, Gabriella, Dwyer, Terence, Paltiel, Ora, Phillips, Gary S., Lemeshow, Stanley, Golding, Jean, Northstone, Kate, Boyd, Andy, Olsen, Sjurdur, Ghantous, Akram, Herceg, Zdenko, Ward, Mary H., Håberg, Siri E., Magnus, Per, Olsen, Jørn, Ström, Marin, Mahabir, Somdat, Jones, Rena R., Ponsonby, Anne‐Louise, and Clavel, Jacqueline
- Subjects
CHILDHOOD cancer ,ETIOLOGY of diseases ,ENVIRONMENTAL exposure ,LEUKEMIA ,CANCER-related mortality ,AGE factors in disease ,COMPARATIVE studies ,DATABASES ,LONGITUDINAL method ,RESEARCH methodology ,MEDICAL cooperation ,RESEARCH ,RESEARCH funding ,TUMORS ,EVALUATION research ,LIFESTYLES ,HEALTH & social status ,ODDS ratio - Abstract
Background: Childhood cancer is a rare but leading cause of morbidity and mortality. Established risk factors, accounting for <10% of incidence, have been identified primarily from case-control studies. However, recall, selection and other potential biases impact interpretations particularly, for modest associations. A consortium of pregnancy and birth cohorts (I4C) was established to utilise prospective, pre-diagnostic exposure assessments and biological samples.Methods: Eligibility criteria, follow-up methods and identification of paediatric cancer cases are described for cohorts currently participating or planning future participation. Also described are exposure assessments, harmonisation methods, biological samples potentially available for I4C research, the role of the I4C data and biospecimen coordinating centres and statistical approaches used in the pooled analyses.Results: Currently, six cohorts recruited over six decades (1950s-2000s) contribute data on 388 120 mother-child pairs. Nine new cohorts from seven countries are anticipated to contribute data on 627 500 additional projected mother-child pairs within 5 years. Harmonised data currently includes over 20 "core" variables, with notable variability in mother/child characteristics within and across cohorts, reflecting in part, secular changes in pregnancy and birth characteristics over the decades.Conclusions: The I4C is the first cohort consortium to have published findings on paediatric cancer using harmonised variables across six pregnancy/birth cohorts. Projected increases in sample size, expanding sources of exposure data (eg, linkages to environmental and administrative databases), incorporation of biological measures to clarify exposures and underlying molecular mechanisms and forthcoming joint efforts to complement case-control studies offer the potential for breakthroughs in paediatric cancer aetiologic research. [ABSTRACT FROM AUTHOR]- Published
- 2018
- Full Text
- View/download PDF
43. Parental occupational pesticide exposure and the risk of childhood leukemia in the offspring: Findings from the Childhood Leukemia International Consortium
- Author
-
Bailey, Helen D, Fritschi, Lin, Infante-Rivard, Claire, Glass, Deborah C, Miligi, Lucia, Dockerty, John D, Lightfoot, Tracy, Clavel, Jacqueline, Roman, Eve, Spector, Logan G, Kaatsch, Peter, Metayer, Catherine, Magnani, Corrado, Milne, Elizabeth, Polychronopoulou, Sophia, Simpson, Jill, Rudant, Jérémie, Sidi, Vasiliki, Rondelli, Roberto, Orsi, Laurent, Kang, Alice, Petridou, Eleni, and Schüz, Joachim
- Subjects
Male ,Leukemia ,Adolescent ,Infant, Newborn ,Infant ,International Agencies ,Prognosis ,Article ,Meta-Analysis as Topic ,Maternal Exposure ,Pregnancy ,Risk Factors ,Case-Control Studies ,Child, Preschool ,Occupational Exposure ,Prenatal Exposure Delayed Effects ,Paternal Exposure ,Humans ,Female ,Pesticides ,Child ,Pregnancy Complications, Neoplastic ,Follow-Up Studies - Abstract
Maternal occupational pesticide exposure during pregnancy and/or paternal occupational pesticide exposure around conception have been suggested to increase risk of leukemia in the offspring. With a view to providing insight in this area we pooled individual level data from 13 case-control studies participating in the Childhood Leukemia International Consortium (CLIC). Occupational data were harmonized to a compatible format. Pooled individual analyses were undertaken using unconditional logistic regression. Using exposure data from mothers of 8,236 cases, and 14,850 controls, and from fathers of 8,169 cases and 14,201 controls the odds ratio (OR) for maternal exposure during pregnancy and the risk of acute lymphoblastic leukemia (ALL) was 1.01 (95% confidence interval (CI) 0.78, 1.30) and for paternal exposure around conception 1.20 (95% 1.06, 1.38). For acute myeloid leukemia (AML), the OR for maternal exposure during pregnancy was 1.94 (CI 1.19, 3.18) and for paternal exposure around conception 0.91 (CI 0.66, 1.24.) based on data from 1,329 case and 12,141 control mothers, and 1,231 case and 11,383 control fathers. Our finding of a significantly increased risk of AML in the offspring with maternal exposure to pesticides during pregnancy is consistent with previous reports. We also found a slight increase in risk of ALL with paternal exposure around conception which appeared to be more evident in children diagnosed at the age of five years or more and those with T cell ALL which raises interesting questions on possible mechanisms.
- Published
- 2014
44. [Epidemiology of childhood cancers]
- Author
-
Clavel, Jacqueline, Epidémiologie environnementale des cancers, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Secretariat, U754
- Subjects
Epstein-Barr Virus Infections ,Leukemia ,Neoplasms, Radiation-Induced ,Adolescent ,Incidence ,Burkitt Lymphoma ,Hodgkin Disease ,Risk Factors ,[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie ,Child, Preschool ,Neoplasms ,hemic and lymphatic diseases ,Humans ,Genetic Predisposition to Disease ,[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie ,France ,Child ,Environmental Pollution ,Immunosuppressive Agents - Abstract
National audience; In industrial countries, 1 child out of 500 develops a cancer before the age of 15 years, and before the age of 6 years for almost half of them. In France, incidence rates were stable over the 15 last years with around 1500 cases each year. A very small fraction of cases is attributable to known risk factors, including heritable cancers or cancers in children with heritable predisposing diseases, cancers induced by high doses of ionizing radiation of medical or accidental origin, by chemotherapeutic or immunosuppressive drugs. Responsibility of Epstein Barr virus in a fraction of Hodgkin's and Burkitt's lymphomas is also established, even though little is still known on the cofactors involved in industrial countries. Other virus could cause leukaemia, as suggested by localized increases in incidence in various conditions of population mixing. Conversely, there is some evidence that early common infections could be protective toward leukaemia risk, probably through their contribution to the maturation of the immune system. Several agents are suspected to induce chemical cancers, particularly pesticides, which are consistently reported in childhood leukaemia and brain tumours. It is more and more likely that genetic factors may modulate risk induced of environmental factors.
- Published
- 2007
45. Residential Proximity to Heavy-Traffic Roads, Benzene Exposure, and Childhood Leukemia--The GEOCAP Study, 2002-2007.
- Author
-
Houot, Jennifer, Marquant, Fabienne, Goujon, Stéphanie, Faure, Laure, Honoré, Cécile, Roth, Marie-Hélène, Hémon, Denis, and Clavel, Jacqueline
- Subjects
LEUKEMIA risk factors ,CONFIDENCE intervals ,HOUSING ,LYMPHOBLASTIC leukemia ,RESEARCH funding ,TRANSPORTATION ,ENVIRONMENTAL exposure ,ACUTE myeloid leukemia ,CASE-control method ,DATA analysis software ,BENZENE derivatives ,DESCRIPTIVE statistics ,ODDS ratio ,CHILDREN - Abstract
Childhood leukemia may be associated with traffic-related environmental exposure to benzene, and additional data are needed. The Géolocalisation des Cancers Pédiatriques (GEOCAP) Study, a nationwide French case-control study, was designed to avoid selection bias due to differential participation and misclassification. The study compared the 2,760 childhood leukemia cases diagnosed in France between 2002 and 2007 (including 2,275 cases of acute lymphoblastic leukemia (ALL) and 418 cases of acute myeloblastic leukemia (AML)) with 30,000 contemporaneous child population controls. The residence addresses were precisely geocoded, and 3 indicators of residential proximity to traffic were considered. Estimates of benzene concentrations were also available for the Île-de-France region (including Paris). A 300-m increase in major road length within 150 m of the geocoded address was significantly associated with AML (odds ratio = 1.2, 95%confidence interval: 1.0, 1.4) but not with ALL (odds ratio = 1.0, 95% confidence interval: 0.9, 1.1), and the association was reinforced in the Île-de-France region when this indicator was combined with benzene estimates. These results, which were free from any participation bias and based on objectively determined indices of exposure, showed an increased incidence of AML associated with heavy-traffic road density near a child's home. The results support a role for traffic-related benzene exposure in the etiology of childhood AML. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
46. Childhood Acute Leukemia, Early Common Infections, and Allergy: The ESCALE Study.
- Author
-
Rudant, Jérémie, Orsi, Laurent, Menegaux, Florence, Petit, Arnaud, Baruchel, André, Bertrand, Yves, Lambilliotte, Anne, Robert, Alain, Michel, Gérard, Margueritte, Geneviève, Tandonnet, Julie, Mechinaud, Françoise, Bordigoni, Pierre, Hémon, Denis, and Clavel, Jacqueline
- Subjects
ALLERGIES ,ANALYSIS of variance ,ANIMALS ,ASTHMA ,BIRTH order ,BREASTFEEDING ,CHILD care ,COMMUNICABLE diseases ,COMPARATIVE studies ,CONFIDENCE intervals ,STATISTICAL correlation ,REPORTING of diseases ,EPIDEMIOLOGY ,IMMUNE system ,LYMPHOBLASTIC leukemia ,QUESTIONNAIRES ,REGRESSION analysis ,DATA analysis ,ACUTE myeloid leukemia ,CASE-control method ,CHILDREN ,LEUKEMIA etiology - Abstract
This study investigated the role of factors considered related to early stimulation of the immune system in the etiology of childhood acute leukemia. The national registry-based case-control study ESCALE was carried out in France in 2003–2004. Population controls were frequency matched to cases on age and gender. Data were obtained from structured telephone questionnaires administered to mothers. Odds ratios were estimated using unconditional regression models adjusted for potential confounders. Included were 634 acute lymphoblastic leukemia cases, 86 acute myeloblastic leukemia cases, and 1,494 controls aged ≥1 year. Negative associations were observed between acute lymphoblastic leukemia and birth order (P for trend < 0.0001), attendance at a day-care center before age 1 year (odds ratio (OR) = 0.8, 95% confidence interval (CI): 0.6, 1.1), prolonged breastfeeding (OR = 0.7, 95% CI: 0.5, 1.0), repeated early common infections (OR = 0.7, 95% CI: 0.6, 0.9), regular contact with farm animals (OR = 0.6, 95% CI: 0.5, 0.8), frequent farm visits in early life (OR = 0.4, 95% CI: 0.3, 0.6), and history of asthma (OR = 0.7, 95% CI: 0.4, 1.0) or eczema (OR = 0.7, 95% CI: 0.6, 0.9). Results support the hypothesis that repeated early infections and asthma may play a role against childhood acute leukemia. [ABSTRACT FROM PUBLISHER]
- Published
- 2010
- Full Text
- View/download PDF
47. CHILDHOOD LEUKEMIA INCIDENCE AND EXPOSURE TO INDOOR RADON, TERRESTRIAL AND COSMIC GAMMA RADIATION.
- Author
-
Evrard, Anne-Sophie, Hémon, Denis, Billon, Solenne, Laurier, Dominique, Jougla, Eric, Tirmarche, Margot, and Clavel, Jacqueline
- Subjects
GAMMA rays ,IONIZING radiation ,RADON ,ACUTE myeloid leukemia ,LEUKEMIA in children ,COSMIC rays ,CANCER ,RADON measures ,LYMPHOMAS - Abstract
The article focuses on the evaluation of the ecological association between terrestrial and cosmic gamma radiation, indoor radon and acute leukemia among children in France. The cases of acute leukemia were recorded by the French National Registry of Childhood Leukemia and Lymphoma. Results of the study showed a retrained ecological association between childhood Acute Myelogenous Leukemia incidence and indoor radon. A case control study of residentially exposed children will have to make up of a large number of cases and controls with individual radon measurements and substantial contrasts in exposure.
- Published
- 2006
- Full Text
- View/download PDF
48. Worldwide comparison of survival from childhood leukaemia for 1995–2009, by subtype, age, and sex (CONCORD-2): a population-based study of individual data for 89 828 children from 198 registries in 53 countries
- Author
-
Bonaventure, Audrey, Harewood, Rhea, Stiller, Charles A, Gatta, Gemma, Clavel, Jacqueline, Stefan, Daniela C, Carreira, Helena, Spika, Devon, Marcos-Gragera, Rafael, Peris-Bonet, Rafael, Piã±eros, Marion, Sant, Milena, Kuehni, Claudia E, Murphy, Michael F. G, Coleman, Michel P, Allemani, Claudia, Bouzbid, S., Hamdi-Chérif, M., Zaidi, Z., Bah, E., Swaminathan, R., Nortje, S. H., El Mistiri, M. M., Bayo, S., Malle, B., Manraj, S. S., Sewpaul-Sungkur, R., Fabowale, Null, Ogunbiyi, O. J., Bradshaw, D., Somdyala, N. I. M., Stefan, D. C., Abdel-Rahman, M., Jaidane, L., Mokni, M., Kumcher, I., Moreno, F., Gonzã¡lez, M. S., Laura, E. A., Espinola, S. B., Calabrano, G. H., Carballo Quintero, B., Fita, R., Garcilazo, D. A., Giacciani, P. L., Diumenjo, M. C., Laspada, W. D., Green, M. A., Lanza, M. F., Ibaã±ez, S. G., Lima, C. A., de Oliveira, E. Lobo, Daniel, C., Scandiuzzi, C., De Souza, P. C. F., Melo, C. D., Del Pino, K., Laporte, C., Curado, M. P., de Oliveira, J. C., Veneziano, C. L. A., Veneziano, D. B., Alexandre, T. S., Verdugo, A. S., Azevedo e. Silva, G., Galaz, J. C., Moya, J. A., Herrmann, D. A., Vargas, S., Herrera, V. M., Uribe, C. J., Bravo, L. E., Arias-Ortiz, N. E., Jurado, D. M., Yã©pez, M. C., Galã¡n, Y. H., Torres, P., MartÃnez-Reyes, F., Pérez-Meza, M. L., Jaramillo, L., Quinto, R., Cueva, P., Yã©pez, J. G., Torres-Cintrón, C. R., Tortolero-Luna, G., Alonso, R., Barrios, E., Nikiforuk, C., Shack, L., Coldman, A. J., Woods, R. R., Noonan, G., Turner, D., Kumar, E., Zhang, B., Mccrate, F. R., Ryan, S., Hannah, H., Dewar, R. A. D., Macintyre, M., Lalany, A., Ruta, M., Marrett, L., Nishri, D. E., Mcclure, C., Vriends, K. A., Bertrand, C., Louchini, R., Robb, K. I., Stuart-Panko, H., Demers, S., Wright, S., George, J. T., Shen, X., Brockhouse, J. T., O'Brien, D. K., Ward, K. C., Almon, L., Bates, J., Rycroft, R., Mueller, L., Phillips, C., Brown, H., Cromartie, B., Schwartz, A. G., Vigneau, F., Mackinnon, J. A., Wohler, B., Bayakly, A. R., Clarke, C. A., Glaser, S. L., West, D., Green, M. D., Hernandez, B. Y., Johnson, C. J., Jozwik, D., Charlton, M. E., Lynch, C. F., Huang, B., Tucker, T. C., Deapen, D., Liu, L., Hsieh, M. C., X. C., Wu, Stern, K., Gershman, S. T., Knowlton, R. C., Alverson, J., Copeland, G. E., Rogers, D. B., Lemons, D., Williamson, L. L., Hood, M., Hosain, G. M., Rees, J. R., Pawlish, K. S., Stroup, A., Key, C., Wiggins, C., Kahn, A. R., Schymura, M. J., Leung, G., Rao, C., Giljahn, L., Warther, B., Pate, A., Patil, M., Schubert, S. S., Rubertone, J. J., Slack, S. J., Fulton, J. P., Rousseau, D. L., Janes, T. A., Schwartz, S. M., Bolick, S. W., Hurley, D. M., Richards, J., Whiteside, M. A., Nogueira, L. M., Herget, K., Sweeney, C., Martin, J., Wang, S., Harrelson, D. G., Cheteri, MB Keitheri, Farley, S., Hudson, A. G., Borchers, R., Stephenson, L., Espinoza, J. R., Weir, H. K., Edwards, B. K., Wang, N., Yang, L., Chen, J. S., Song, G. H., X. P., Gu, Zhang, P., H. M., Ge, Zhao, D. L., Zhang, J. H., Zhu, F. D., Tang, J. G., Shen, Y., Wang, J., Q. L., Li, Yang, X. P., Dong, J., Li, W., Cheng, L. P., Chen, J. G., Huang, Q. H., Huang, S. Q., Guo, G. P., Wei, K., Chen, W. Q., Zeng, H., Demetriou, A. V., Pavlou, P., Mang, W. K., Ngan, K. C., Kataki, A. C., Krishnatreya, M., Jayalekshmi, P. A., Sebastian, P., Sapkota, S. D., Verma, Y., Nandakumar, A., Suzanna, E., Keinan-Boker, L., Silverman, B. G., Ito, H., Nakagawa, H., Hattori, M., Kaizaki, Y., Sugiyama, H., Utada, M., Katayama, K., Narimatsu, H., Kanemura, S., Koike, T., Miyashiro, I., Yoshii, M., Oki, I., Shibata, A., Matsuda, T., Nimri, O., Ab Manan, A., Pathy, N. Bhoo, Chimedsuren, O., Tuvshingerel, S., Al Khater, A. H. M., Al-Eid, H., Jung, K. W., Won, Y. J., Chiang, C. J., Lai, M. S., Suwanrungruang, K., Wiangnon, S., Daoprasert, K., Pongnikorn, D., Geater, S. L., Sriplung, H., Eser, S., Yakut, C. I., Hackl, M., Mã¼hlbã¶ck, H., Oberaigner, W., Zborovskaya, A. A., Aleinikova, O. V., Henau, K., Van Eycken, L., Dimitrova, N., Valerianova, Z., Å ekerija, M., Zvolskã½, M., Engholm, G., Storm, H., Innos, K., Mã¤gi, M., Malila, N., Seppã¤, K., Jã©gu, J., Velten, M., Cornet, E., Troussard, X., Bouvier, A. M., Faivre, J., Guizard, A. V., Bouvier, V., Launoy, G., Arveux, P., Maynadiã©, M., Mounier, M., Fournier, E., Woronoff, A. S., Daoulas, M., Clavel, J., Le Guyader-Peyrou, S., Monnereau, A., Trã©tarre, B., Colonna, M., Cowppli-Bony, A., Moliniã©, F., Bara, S., Degrã©, D., Ganry, O., Lapôtre-Ledoux, B., Grosclaude, P., Estãve, J., Bray, F., Piã±eros, M., Sassi, F., Stabenow, R., Eberle, A., Erb, C., Nennecke, A., Kieschke, J., Sirri, E., Kajueter, H., Emrich, K., Zeissig, S. R., Holleczek, B., Eisemann, N., Katalinic, A., Brenner, H., Asquez, R. A., Kumar, V., Ã'lafsdóttir, E. J., Tryggvadã³ttir, L., Comber, H., Walsh, P. M., Sundseth, H., Devigili, E., Mazzoleni, G., Giacomin, A., Bella, F., Castaing, M., Sutera, A., Gola, G., Ferretti, S., Serraino, D., Zucchetto, A., Lillini, R., Vercelli, M., Busco, S., Pannozzo, F., Vitarelli, S., Ricci, P., Pascucci, C., Autelitano, M., Cirilli, C., Federico, M., Fusco, M., Vitale, M. F., Usala, M., Cusimano, R., Mazzucco, Walter, Michiara, M., Sgargi, P., Maule, M. M., Sacerdote, C., Tumino, R., Di Felice, E., Vicentini, M., Falcini, F., Cremone, L., Budroni, M., Cesaraccio, R., Contrino, M. L., Tisano, F., Fanetti, A. C., Maspero, S., Candela, G., Scuderi, T., Gentilini, M. A., Piffer, S., Rosso, S., Sacchetto, L., Caldarella, A., La Rosa, F., Stracci, F., Contiero, P., Tagliabue, G., Dei Tos, A. P., Zorzi, M., Zanetti, R., Baili, P., Berrino, F., Gatta, G., Sant, M., Capocaccia, R., De Angelis, R., Liepina, E., Maurina, A., Smailyte, G., Agius, D., Calleja, N., Siesling, S., Visser, O., Larã¸nningen, S., Mã¸ller, B., Dyzmann-Sroka, A., Trojanowski, M., Gã³zdz, S., Mezyk, R., Gradalska-Lampart, M., Radziszewska, A. U., Didkowska, J. A., Wojciechowska, U., Blaszczyk, J., Kepska, K., Bielska-Lasota, M., Kwiatkowska, K., Forjaz, G., Rego, R. A., Bastos, J., Silva, M. A., Antunes, L., Bento, M. J., Mayer-da-Silva, A., Miranda, A., Coza, D., Todescu, A. I., Valkov, M. Y., Adamcik, J., Safaei Diba, C., Primic-Žakelj, M., Žagar, T., Stare, J., Almar, E., Mateos, A., Quirã³s, J. R., Bidaurrazaga, J., Larraã±aga, N., DÃaz GarcÃa, J. M., Marcos, A. I., Marcos-Gragera, R., Vilardell Gil, M. L., Molina, E., Sã¡nchez, M. J., Sureda, P. Franch, Montserrat, M. Ramos, Chirlaque, M. D., Navarro, C., Ardanaz, E. E., Moreno-Iribas, C. C., Fernández-Delgado, R., Peris-Bonet, R., Galceran, J., Khan, S., Lambe, M., Camey, B., Bouchardy, C., Usel, M., Ess, S. M., Herrmann, C., Bulliard, J. L., Maspoli-Conconi, M., Frick, H., Kuehni, C. E., Schindler, M., Bordoni, A., Spitale, A., Chiolero, A., Konzelmann, I., Dehler, S. I., Matthes, K. L., Rashbass, J., Stiller, C. A., Fitzpatrick, D., Gavin, A., Bannon, F., Black, R. J., Brewster, D. H., Huws, D. W., White, C., Finan, P., Allemani, C., Bonaventure, A., Carreira, H., Coleman, M. P., Di Carlo, V., Harewood, R., Liu, K., Matz, M., Montel, L., Nikå¡ic, M., Rachet, B., Sanz, N., Spika, D., Stephens, R., Peake, M., Murphy, M. F. G., Chalker, E., Newman, L., Baker, D., Soeberg, M. J., Aitken, J., Scott, C., Stokes, B. C., Venn, A., Farrugia, H., Giles, G. G., Threlfall, T., Currow, D., You, H., Hendrix, J., Lewis, C., Latorre, M. R. D. O., Tanaka, L. F., Bonaventure, A., Harewood, R., Stiller, C., Gatta, G., Clavel, J., Stefan, D., Carreira, H., Spika, D., Marcos-gragera, R., Peris-bonet, R., Piñeros, M., Sant, M., Kuehni, C., Murphy, M., Coleman, M., Allemani, C., Bouzbid, S., Hamdi-chérif, M., Zaidi, Z., Bah, E., Swaminathan, R., Nortje, S., El Mistiri, M., Bayo, S., Malle, B., Manraj, S., Sewpaul-sungkur, R., Fabowale, A., Ogunbiyi, O., Bradshaw, D., Somdyala, N., Abdel-rahman, M., Jaidane, L., Mokni, M., Kumcher, I., Moreno, F., González, M., Laura, E., Espinola, S., Calabrano, G., Carballo Quintero, B., Fita, R., Garcilazo, D., Giacciani, P., Diumenjo, M., Laspada, W., Green, M., Lanza, M., Ibañez, S., Lima, C., Lobo De Oliveira, E., Daniel, C., Scandiuzzi, C., De Souza, P., Melo, C., Del Pino, K., Laporte, C., Curado, M., De Oliveira, J., Veneziano, C., Veneziano, D., Latorre, M., Tanaka, L., Azevedo E. Silva, G., Galaz, J., Moya, J., Herrmann, D., Vargas, S., Herrera, V., Uribe, C., Bravo, L., Arias-ortiz, N., Jurado, D., Yépez, M., Galán, Y., Torres, P., Martínez-reyes, F., Pérez-meza, M., Jaramillo, L., Quinto, R., Cueva, P., Yépez, J., Torres-cintrón, C., Tortolero-luna, G., Alonso, R., Barrios, E., Nikiforuk, C., Shack, L., Coldman, A., Woods, R., Noonan, G., Turner, D., Kumar, E., Zhang, B., Mccrate, F., Ryan, S., Hannah, H., Dewar, R., Macintyre, M., Lalany, A., Ruta, M., Marrett, L., Nishri, D., Mcclure, C., Vriends, K., Bertrand, C., Louchini, R., Robb, K., Stuart-panko, H., Demers, S., Wright, S., George, J., Shen, X., Brockhouse, J., O'Brien, D., Ward, K., Almon, L., Bates, J., Rycroft, R., Mueller, L., Phillips, C., Brown, H., Cromartie, B., Schwartz, A., Vigneau, F., Mackinnon, J., Wohler, B., Bayakly, A., Clarke, C., Glaser, S., West, D., Hernandez, B., Johnson, C., Jozwik, D., Charlton, M., Lynch, C., Huang, B., Tucker, T., Deapen, D., Liu, L., Hsieh, M., Xc, W., Stern, K., Gershman, S., Knowlton, R., Alverson, J., Copeland, G., Rogers, D., Lemons, D., Williamson, L., Hood, M., Hosain, G., Rees, J., Pawlish, K., Stroup, A., Key, C., Wiggins, C., Kahn, A., Schymura, M., Leung, G., Rao, C., Giljahn, L., Warther, B., Pate, A., Patil, M., Schubert, S., Rubertone, J., Slack, S., Fulton, J., Rousseau, D., Janes, Ta:, S., Sm, Bolick, S., Hurley, D., Richards, J., Whiteside, M., Nogueira, L., Herget, K., Sweeney, C., Martin, J., Wang, S., Harrelson, D., Keitheri Cheteri, M., Farley, S., Hudson, A., Borchers, R., Stephenson, L., Espinoza, J., Weir, H., Edwards, B., Wang, N., Yang, L., Chen, J., Song, G., Xp, G., Zhang, P., Hm, G., Zhao, D., Zhang, J., Zhu, F., Tang, J., Shen, Y., Wang, J., Ql, L., Yang, X., Dong, J., Li, W., Cheng, L., Huang, Q., Huang, S., Guo, G., Wei, K., Chen, W., Zeng, H., Demetriou, A., Pavlou, P., Mang, W., Ngan, K., Kataki, A., Krishnatreya, M., Jayalekshmi, P., Sebastian, P., Sapkota, S., Verma, Y., Nandakumar, A., Suzanna, E., Keinan-boker, L., Silverman, B., Ito, H., Nakagawa, H., Hattori, M., Kaizaki, Y., Sugiyama, H., Utada, M., Katayama, K., Narimatsu, H., Kanemura, S., Koike, T., Miyashiro, I., Yoshii, M., Oki, I., Shibata, A., Matsuda, T., Nimri, O., Ab Manan, A., Bhoo-pathy, N., Tuvshingerel, S., Chimedsuren, O., Al Khater, A., Al-eid, H., Jung, K., Won, Y., Chiang, C., Lai, M., Suwanrungruang, K., Wiangnon, S., Daoprasert, K., Pongnikorn, D., Geater, S., Sriplung, H., Eser, S., Yakut, C., Hackl, M., Mühlböck, H., Oberaigner, W., Zborovskaya, A., Aleinikova, O., Henau, K., Van Eycken, L., Dimitrova, N., Valerianova, Z., Šekerija, M., Zvolský, M., Engholm, G., Storm, H., Innos, K., Mägi, M., Malila, N., Seppä, K., Jégu, J., Velten, M., Cornet, E., Troussard, X., Bouvier, A., Faivre, J., Guizard, A., Bouvier, V., Launoy, G., Arveux, P., Maynadié, M., Mounier, M., Fournier, E., Woronoff, A., Daoulas, M., Le Guyader-peyrou, S., Monnereau, A., Trétarre, B., Colonna, M., Cowppli-bony, A., Molinié, F., Bara, S., Degré, D., Ganry, O., Lapôtre-ledoux, B., Grosclaude, P., Estève, J., Bray, F., Sassi, F., Stabenow, R., Eberle, A., Erb, C., Nennecke, A., Kieschke, J., Sirri, E., Kajueter, H., Emrich, K., Zeissig, S., Holleczek, B., Eisemann, N., Katalinic, A., Brenner, H., Asquez, R., Kumar, V., Ólafsdóttir, E., Tryggvadóttir, L., Comber, H., Walsh, P., Sundseth, H., Devigili, E., Mazzoleni, G., Giacomin, A., Bella, F., Castaing, M., Sutera, A., Gola, G., Ferretti, S., Serraino, D., Zucchetto, A., Lillini, R., Vercelli, M., Busco, S., Pannozzo, F., Vitarelli, S., Ricci, P., Pascucci, C., Autelitano, M., Cirilli, C., Federico, M., Fusco, M., Vitale, M., Usala, M., Cusimano, R., Mazzucco, W., Michiara, M., Sgargi, P., Maule, M., Sacerdote, C., Tumino, R., Di Felice, E., Vicentini, M., Falcini, F., Cremone, L., Budroni, M., Cesaraccio, R., Contrino, M., Tisano, F., Fanetti, A., Maspero, S., Candela, G., Scuderi, T., Gentilini, M., Piffer, S., Rosso, S., Sacchetto, L., Caldarella, A., La Rosa, F., Stracci, F., Contiero, P., Tagliabue, G., Dei Tos, A., Zorzi, M., Zanetti, R., Baili, P., Berrino, F., Capocaccia, R., De Angelis, R., Liepina, E., Maurina, A., Smailyte, G., Agius, D., Calleja, N., Siesling, S., Visser, O., Larønningen, S., Møller, B., Dyzmann-sroka, A., Trojanowski, M., Góźdż, S., Mężyk, R., Grądalska-lampart, M., Radziszewska, A., Didkowska, J., Wojciechowska, U., Błaszczyk, J., Kępska, K., Bielska-lasota, M., Kwiatkowska, K., Forjaz, G., Rego, R., Bastos, J., Silva, M., Antunes, L., Bento, M., Mayer-da-silva, A., Miranda, A., Coza, D., Todescu, A., Valkov, M., Adamcik, J., Safaei Diba, C., Primic-žakelj, M., Žagar, T., Stare, J., Almar, E., Mateos, A., Quirós, J., Bidaurrazaga, J., Larrañaga, N., Díaz García, J., Marcos, A., Vilardell Gil, M., Molina, E., Sánchez, M., Franch Sureda, P., Ramos Montserrat, M., Chirlaque, M., Navarro, C., Ardanaz, E., Moreno-iribas, C., Fernández-delgado, R., Galceran, J., Khan, S., Lambe, M., Camey, B., Bouchardy, C., Usel, M., Ess, S., Herrmann, C., Bulliard, J., Maspoli-conconi, M., Frick, H., Schindler, M., Bordoni, A., Spitale, A., Chiolero, A., Konzelmann, I., Dehler, S., Matthes, K., Rashbass, J., Fitzpatrick, D., Gavin, A., Bannon, F., Black, R., Brewster, D., Huws, D., White, C., Finan, P., Di Carlo, V., Liu, K., Matz, M., Montel, L., Nikšić, M., Rachet, B., Sanz, N., Stephens, R., Peake, M., Chalker, E., Newman, L., Baker, D., Soeberg, M., Aitken, J., Scott, C., Stokes, B., Venn, A., Farrugia, H., Giles, G., Threlfall, T., Currow, D., You, H., Hendrix, J., and Lewis, C.
- Subjects
childhood leukaemia ,Cancer registrie ,leukemia ,cancer ,childhood cancer ,Socio-culturale ,Hematology ,Settore MED/42 - Igiene Generale E Applicata ,Hematology, childhood leukaemia, cancer survival ,cancer survival - Abstract
BACKGROUND: Global inequalities in access to health care are reflected in differences in cancer survival. The CONCORD programme was designed to assess worldwide differences and trends in population-based cancer survival. In this population-based study, we aimed to estimate survival inequalities globally for several subtypes of childhood leukaemia. METHODS: Cancer registries participating in CONCORD were asked to submit tumour registrations for all children aged 0-14 years who were diagnosed with leukaemia between Jan 1, 1995, and Dec 31, 2009, and followed up until Dec 31, 2009. Haematological malignancies were defined by morphology codes in the International Classification of Diseases for Oncology, third revision. We excluded data from registries from which the data were judged to be less reliable, or included only lymphomas, and data from countries in which data for fewer than ten children were available for analysis. We also excluded records because of a missing date of birth, diagnosis, or last known vital status. We estimated 5-year net survival (ie, the probability of surviving at least 5 years after diagnosis, after controlling for deaths from other causes [background mortality]) for children by calendar period of diagnosis (1995-99, 2000-04, and 2005-09), sex, and age at diagnosis (
49. Parental occupational exposure to combustion products, metals, silica and asbestos and risk of childhood leukaemia: Findings from the Childhood Cancer and Leukaemia International Consortium (CLIC).
- Author
-
Onyije, Felix M., Olsson, Ann, Erdmann, Friederike, Magnani, Corrado, Petridou, Eleni, Clavel, Jacqueline, Miligi, Lucia, Bonaventure, Audrey, Ferrante, Daniela, Piro, Sara, Peters, Susan, Vermeulen, Roel, Kromhout, Hans, and Schüz, Joachim
- Subjects
- *
ASBESTOS , *OCCUPATIONAL exposure , *CHILDHOOD cancer , *COMBUSTION products , *DIESEL motor exhaust gas , *LEUKEMIA - Abstract
Parental occupational exposures around conception (father) or during pregnancy (mother) have been hypothesized as potential predisposing factors for childhood leukaemia. We investigated parental exposure to several known occupational carcinogens and childhood leukaemia risk. We conducted a pooled analysis using case-control data from four European countries (3362 childhood leukemia cases and 6268 controls). Parental occupational exposures to polycyclic aromatic hydrocarbons (PAH), diesel engine exhaust (DEE), chromium, nickel, crystalline silica, and asbestos were assessed by a general population job-exposure matrix. We estimated odd ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression models for all childhood leukaemia combined, by leukaemia type (ALL and AML) and by ALL subtype (B-lineage and T-lineage). We found an association between high paternal occupational exposure to crystalline silica and childhood ALL (OR 2.20, CI 1.60–3.01) with increasing trend from no exposure to high exposure (P = <0.001), and also for AML (OR 2.03, CI 1.04–3.97; P for trend = 0.008). ORs were similar for B- and T-lineage ALL. For ALL, ORs were also slightly elevated with wide confidence intervals for high paternal occupational exposure to chromium (OR 1.23, CI 0.77–1.96), and DEE (OR 1.21, CI 0.82–1.77). No associations were observed for paternal exposures to nickel, PAH and asbestos. For maternal occupational exposure we found several slightly elevated odds ratios but mostly with very wide confidence intervals due to low numbers of exposed mothers. This is a first study suggesting an association between fathers' occupational exposure to crystalline silica and an increased risk of childhood leukaemia in their offspring. As this association was driven by certain occupations (field crop farmers and miners) where other potentially relevant exposures like pesticides and radon may also occur, more research is needed to confirm our findings of an association with crystalline silica, and if so, mechanistic studies to understand the pathways. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
50. Two high-risk susceptibility loci at 6p25.3 and 14q32.13 for Waldenström macroglobulinemia
- Author
-
Laurie Burdette, Lindsay M. Morton, Neil E. Caporaso, Sonja I. Berndt, Paolo Vineis, Stephen J. Chanock, Stephen M. Ansell, Elisabete Weiderpass, James McKay, Charles C. Chung, Nisha Pradhan, James R. Cerhan, Peter Kraft, Alexandra Nieters, Lauren R. Teras, Lenka Foretova, Paul Brennan, Lesley F. Tinker, Susan L. Slager, Nilanjan Chatterjee, Jianqing Zhang, Caroline Besson, Mark P. Purdue, Zhaoming Wang, Shengchao Alfred Li, Bengt Glimelius, Paige M. Bracci, Qing Lan, Mervin M. Fansler, Jacqueline Clavel, Hans-Olov Adami, Ruth C. Travis, Karin E. Smedby, Christine F. Skibola, Silvia de Sanjosé, Edward Giovannucci, Akinyemi I. Ojesina, Huihuang Yan, Richard K. Severson, Jonathan N. Hofmann, Paolo Boffetta, Lynn R. Goldin, Yawei Zhang, Belynda Hicks, Bryan A. Bassig, Charles E. Lawrence, Andrew L. Feldman, Nathaniel Rothman, Jacques Riby, Yolanda Benavente, Nikolaus Becker, Geffen Kleinstern, Marc Maynadié, Meredith Yeager, Henrik Hjalgrim, Rebecca D. Jackson, Joseph Vijai, Tongzhang Zheng, Roel Vermeulen, Amy K. Hutchinson, Brenda M. Birmann, Bin Zhu, Kenneth Offit, Brian K. Link, Alex Smith, Anthony Staines, Christine Mayr, Federico Canzian, Lucia Conde, Rebecca Montalvan, Elizabeth E. Brown, Wendy Cozen, Anne J. Novak, Claire M. Vajdic, Ju-Hyun Park, W. Ryan Diver, Mary L. McMaster, Mads Melbye, Ann Maria, Kari E. North, Alain Monnereau, McMaster, Mary L., Berndt, Sonja I., Zhang, Jianqing, Slager, Susan L., Li, Shengchao Alfred, Vajdic, Claire M., Smedby, Karin E., Yan, Huihuang, Birmann, Brenda M., Brown, Elizabeth E., Smith, Alex, Kleinstern, Geffen, Fansler, Mervin M., Mayr, Christine, Zhu, Bin, Chung, Charles C., Park, Ju-Hyun, Burdette, Laurie, Hicks, Belynda D., Hutchinson, Amy, Teras, Lauren R., Adami, Hans-Olov, Bracci, Paige M., McKay, Jame, Monnereau, Alain, Link, Brian K., Vermeulen, Roel C. H., Ansell, Stephen M., Maria, Ann, Diver, W. Ryan, Melbye, Mad, Ojesina, Akinyemi I., Kraft, Peter, Boffetta, Paolo, Clavel, Jacqueline, Giovannucci, Edward, Besson, Caroline M., Canzian, Federico, Travis, Ruth C., Vineis, Paolo, Weiderpass, Elisabete, Montalvan, Rebecca, Wang, Zhaoming, Yeager, Meredith, Becker, Nikolau, Benavente, Yolanda, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, Nieters, Alexandra, de Sanjose, Silvia, Staines, Anthony, Conde, Lucia, Riby, Jacque, Glimelius, Bengt, Hjalgrim, Henrik, Pradhan, Nisha, Feldman, Andrew L., Novak, Anne J., Lawrence, Charle, Bassig, Bryan A., Lan, Qing, Zheng, Tongzhang, North, Kari E., Tinker, Lesley F., Cozen, Wendy, Severson, Richard K., Hofmann, Jonathan N., Zhang, Yawei, Jackson, Rebecca D., Morton, Lindsay M., Purdue, Mark P., Chatterjee, Nilanjan, Offit, Kenneth, Cerhan, James R., Chanock, Stephen J., Rothman, Nathaniel, Vijai, Joseph, Goldin, Lynn R., Skibola, Christine F., Caporaso, Neil E., National Cancer Institute [Bethesda] (NCI-NIH), National Institutes of Health [Bethesda] (NIH), International Agency for Cancer Research (IACR), Equipe 7 : EPICEA - Epidémiologie des cancers de l'enfant et de l'adolescent (CRESS - U1153), Université Paris Descartes - Paris 5 (UPD5)-Centre de Recherche Épidémiologie et Statistique Sorbonne Paris Cité (CRESS (U1153 / UMR_A_1125 / UMR_S_1153)), Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Recherche Agronomique (INRA)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Recherche Agronomique (INRA), Department of Internal Medicine [Iowa City], Carver College of Medicine [Iowa City], University of Iowa [Iowa City]-University of Iowa [Iowa City], Mayo Clinic [Rochester], Icahn School of Medicine at Mount Sinai [New York] (MSSM), The Tisch Cancer Institute, Centre de Recherche Épidémiologie et Statistique Sorbonne Paris Cité (CRESS (U1153 / UMR_A_1125 / UMR_S_1153)), Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Recherche Agronomique (INRA), Centre de recherche en épidémiologie et santé des populations (CESP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany, Catalan Institute of Oncology (ICO-IDIBELL), Centre International de Recherche contre le Cancer - International Agency for Research on Cancer (CIRC - IARC), Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Masaryk Memorial Cancer Institute, Masaryk Memorial Cancer Institute (RECAMO), Registre des hématopathies malignes de Côte d'Or (RHEMCO), Centre d'épidémiologie des populations (CEP), Université de Bourgogne (UB)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Université de Bourgogne (UB)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Université de Bourgogne (UB), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Carolina Center for Genome Sciences, University of North Carolina [Chapel Hill] (UNC), University of North Carolina System (UNC)-University of North Carolina System (UNC), Fred Hutchinson Cancer Research Center [Seattle] (FHCRC), Keck School of Medicine [Los Angeles], University of Southern California (USC), Wayne State University [Detroit], Yale School of Public Health (YSPH), Ohio State University [Columbus] (OSU), Johns Hopkins Bloomberg School of Public Health [Baltimore], Johns Hopkins University (JHU), Memorial Sloane Kettering Cancer Center [New York], Emory University [Atlanta, GA], Department of Medical and Clinical Genetics, Institut National de la Recherche Agronomique (INRA)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Recherche Agronomique (INRA)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Recherche Agronomique (INRA)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Paul Brousse-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Université de Bourgogne (UB)-Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc (CRLCC - CGFL)-Université de Bourgogne (UB)-Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc (CRLCC - CGFL)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), One Health Chemisch, dIRAS RA-2, Sub Atmospheric physics and chemistry, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Recherche Agronomique (INRA)-Université Paris Descartes - Paris 5 (UPD5)-Université Sorbonne Paris Cité (USPC)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Recherche Agronomique (INRA)-Université Sorbonne Paris Cité (USPC), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de la Recherche Agronomique (INRA)-Université Paris Descartes - Paris 5 (UPD5)-Université Sorbonne Paris Cité (USPC), and Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)
- Subjects
Genotyping Techniques ,Inheritance Patterns ,Genome-wide association study ,enhanced green fluorescent protein ,Lymphoplasmacytic Lymphoma ,0302 clinical medicine ,Genes, Reporter ,genetics ,B-cell lymphoma ,lcsh:Science ,Malalties del sistema limfàtic ,1184 Genetics, developmental biology, physiology ,Waldenstrom macroglobulinemia ,Leucèmia ,chromosome 14 ,reporter gene ,3. Good health ,030220 oncology & carcinogenesis ,Science & Technology - Other Topics ,Chromosomes, Human, Pair 6 ,NON-HODGKIN-LYMPHOMA ,GERMINAL CENTER B ,Human ,Science ,Green Fluorescent Protein ,General Biochemistry, Genetics and Molecular Biology ,Article ,03 medical and health sciences ,Physics and Astronomy (all) ,LYMPHOPLASMACYTIC LYMPHOMA/WALDENSTROM MACROGLOBULINEMIA ,Genetic predisposition ,inheritance ,Humans ,Family ,GENOME-WIDE ASSOCIATION ,reproducibility ,Inheritance Pattern ,Cancer och onkologi ,Science & Technology ,Biochemistry, Genetics and Molecular Biology (all) ,VDP::Medical disciplines: 700::Clinical medical disciplines: 750::Oncology: 762 ,CHRONIC LYMPHOCYTIC-LEUKEMIA ,nutritional and metabolic diseases ,Molecular Sequence Annotation ,medicine.disease ,Chromosomes Human Pair 6 ,Lymphoma ,030104 developmental biology ,Cancer and Oncology ,Immunology ,molecular genetics ,lcsh:Q ,HIGH-RESOLUTION ,0301 basic medicine ,General Physics and Astronomy ,Genome-wide association studies ,HEK293 Cell ,immune system diseases ,single nucleotide polymorphism ,Risk Factors ,Chromosomes Human Pair 14 ,hemic and lymphatic diseases ,Lymphatic diseases ,EXPRESSION PATTERNS ,FAMILIAL AGGREGATION ,Multidisciplinary ,Leukemia ,Chemistry (all) ,MicroRNA ,Waldenstroem macroglobulinemia ,Multidisciplinary Sciences ,HEK293 cell line ,miRNAs ,Waldenstrom Macroglobulinemia ,Green Fluorescent Proteins ,Reproducibility of Result ,[SDV.CAN]Life Sciences [q-bio]/Cancer ,Biology ,Malignancy ,Polymorphism, Single Nucleotide ,Chromosomes ,Cancer epidemiology ,MD Multidisciplinary ,medicine ,chromosome 6 ,Genetic Predisposition to Disease ,RAL GTPASES ,Cell Proliferation ,Chromosomes, Human, Pair 14 ,Base Sequence ,Risk Factor ,B-CELL LYMPHOMA ,Reproducibility of Results ,nucleotide sequence ,General Chemistry ,Heritability ,VDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Onkologi: 762 ,MicroRNAs ,HEK293 Cells ,Genotyping Technique ,genetic predisposition ,metabolism - Abstract
Waldenström macroglobulinemia (WM)/lymphoplasmacytic lymphoma (LPL) is a rare, chronic B-cell lymphoma with high heritability. We conduct a two-stage genome-wide association study of WM/LPL in 530 unrelated cases and 4362 controls of European ancestry and identify two high-risk loci associated with WM/LPL at 6p25.3 (rs116446171, near EXOC2 and IRF4; OR = 21.14, 95% CI: 14.40–31.03, P = 1.36 × 10−54) and 14q32.13 (rs117410836, near TCL1; OR = 4.90, 95% CI: 3.45–6.96, P = 8.75 × 10−19). Both risk alleles are observed at a low frequency among controls (~2–3%) and occur in excess in affected cases within families. In silico data suggest that rs116446171 may have functional importance, and in functional studies, we demonstrate increased reporter transcription and proliferation in cells transduced with the 6p25.3 risk allele. Although further studies are needed to fully elucidate underlying biological mechanisms, together these loci explain 4% of the familial risk and provide insights into genetic susceptibility to this malignancy., Waldenström macroglobulinemia (WM)/lymphoplasmacytic lymphoma (LPL) is a non-Hodgkin-type B cell lymphoma. Here, the authors identify two risk loci for WM/LPL in a two-stage GWAS involving a family-oversampling approach and provide evidence for a functional role of the non-coding SNP rs116446171.
- Published
- 2018
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.