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54. Circulating Sex Hormone Levels and Risk of Esophageal Adenocarcinoma in a Prospective Study in Men

Author

Xie, Shao-Hua, Ness-Jensen, Eivind, Rabbani, Sirus, Langseth, Hilde, Gislefoss, Randi Elin, Mattsson, Fredrik, and Lagergren, Jesper

Abstract

OBJECTIVES: Sex hormones have been hypothesized to explain the strong male predominance in esophageal adenocarcinoma, but evidence is needed. This study examined how circulating sex hormone levels influence future risk of esophageal adenocarcinoma. METHODS: This case-control study was nested in a prospective Norwegian cohort (Janus Serum Bank Cohort), including 244 male patients with esophageal adenocarcinoma and 244 male age-matched control participants. Associations between prediagnostic circulating levels of 12 sex hormones and risk of esophageal adenocarcinoma were assessed using conditional logistic regression. In addition, a random-effect meta-analysis combined these data with a similar prospective study for 5 sex hormones. RESULTS: Decreased odds ratios (ORs) of esophageal adenocarcinoma were found comparing the highest with lowest quartiles of testosterone (OR = 0.44, 95% confidence interval [CI] 0.22–0.88), testosterone:estradiol ratio (OR = 0.37, 95% CI 0.19–0.72), and luteinizing hormone (OR = 0.50, 95% CI 0.30–0.98), after adjustment for tobacco smoking and physical activity. These associations were attenuated after further adjustment for body mass index (OR = 0.56, 95% CI 0.27–1.13 for testosterone; OR = 0.46, 95% CI 0.23–0.91 for testosterone:estradiol ratio; OR = 0.55, 95% CI 0.29–1.08 for luteinizing hormone). No associations were observed for sex hormone–binding globulin, dehydroepiandrosterone sulfate, follicle-stimulating hormone, prolactin, 17-OH progesterone, progesterone, androstenedione, or free testosterone index. The meta-analysis showed an inverse association between testosterone levels and risk of esophageal adenocarcinoma (pooled OR for the highest vs lowest quartile = 0.60, 95% CI 0.38–0.97), whereas no associations were identified for androstenedione, sex hormone–binding globulin, estradiol, or testosterone:estradiol ratio. DISCUSSION: Higher circulating testosterone levels may decrease the risk of esophageal adenocarcinoma in men.

Published
2019

55. Prediagnostic serum organochlorine concentrations and metastatic prostate cancer: a nested case-control study in the Norwegian Janus Serum Bank cohort

Author

Koutros, Stella, Langseth, Hilde, Grimsrud, Tom K., Barr, Dana Boyd, Vermeulen, Roel, Portengen, Lutzen, Wacholder, Sholom, Freeman, Laura E. Beane, Blair, Aaron, Hayes, Richard B., Rothman, Nathaniel, and Engel, Lawrence S.

Subjects
Insecticides -- Health aspects -- Research, Polychlorinated biphenyls -- Health aspects -- Research, Prostate cancer -- Development and progression -- Research, Cancer metastasis -- Research, Environmental issues, Health
Abstract

BACKGROUND: Organochlorine (OC) insecticides and polychlorinated biphenyls (PCBs) have been shown to have estrogenic, antiestrogenic, or antiandrogenic properties; as a result, the impact of exposure to these compounds and risk of hormonal cancers, such as prostate cancer, is a concern. OBJECTIVES: We conducted a nested case--control study, using prospectively collected serum, to estimate associations between OC exposures and metastatic prostate cancer in a population-based cohort from Norway. METHODS: Sera from 150 cases and 314 controls matched on date of blood draw, age at blood draw, and region was used to determine concentrations of 11 OC pesticide metabolites and 34 PCB congeners. Odds ratios (ORs) and 95% confidence intervals (95% CIs) for quartiles of lipid-corrected metabolite levels were calculated using conditional logistic regression. RESULTS: Metastatic prostate cancer was two times as likely among men with serum concentrations of oxychlordane in the highest quartile compared with those in the lowest quartile (OR = 2.03; 95% CI: 1.03, 4.03; p-trend 0.05). Elevated but nonsignificant ORs were estimated for the highest versus lowest quartile of heptachlor epoxide, HCB, and mirex, although these exposures were correlated with oxychlordane. Findings for specific PCB congeners showed a significant inverse association between natural log-transformed lipid-adjusted PCB 44 and metastatic prostate cancer (OR = 0.74; 95% CI: 0.56, 0.97; p-trend = 0.02). CONCLUSIONS: Our study highlights the importance of estimating associations with specific OC chemicals and suggests a possible role of OC insecticides and PCBs in the etiology of metastatic prostate cancer. http://dx.doi.org/10.1289/ehp.1408245, Introduction Organochlorines (OCs) are a diverse group of persistent synthetic compounds that have been used as pesticides (mostly insecticides) and for various industrial and commercial applications. OC insecticides were widely [...]

Published
2015
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59. Prediagnostic blood levels of organochlorines and risk of non‐Hodgkin lymphoma in three prospective cohorts in China and Singapore

Author

Bassig, Bryan A., primary, Shu, Xiao‐Ou, additional, Sjödin, Andreas, additional, Koh, Woon‐Puay, additional, Gao, Yu‐Tang, additional, Adams‐Haduch, Jennifer, additional, Davis, Mark, additional, Wang, Renwei, additional, Xiang, Yong‐Bing, additional, Engel, Lawrence S., additional, Purdue, Mark P., additional, Ji, Bu‐Tian, additional, Yang, Gong, additional, Jones, Richard S., additional, Langseth, Hilde, additional, Hosgood, H. Dean, additional, Grimsrud, Tom K., additional, Seow, Wei Jie, additional, Wong, Jason Y.Y., additional, Hu, Wei, additional, Chen, Dazhe, additional, Zheng, Wei, additional, Yuan, Jian‐Min, additional, Lan, Qing, additional, and Rothman, Nathaniel, additional

Published
2019
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60. Recommended Definitions of Aggressive Prostate Cancer for Etiologic Epidemiologic Research.

Author

Hurwitz, Lauren M, Agalliu, Ilir, Albanes, Demetrius, Barry, Kathryn Hughes, Berndt, Sonja I, Cai, Qiuyin, Chen, Chu, Cheng, Iona, Genkinger, Jeanine M, Giles, Graham G, Huang, Jiaqi, Joshu, Corinne E, Key, Tim J, Knutsen, Synnove, Koutros, Stella, Langseth, Hilde, Li, Sherly X, MacInnis, Robert J, Markt, Sarah C, and Penney, Kathryn L

Subjects
PROSTATE cancer, CANCER diagnosis, PROSTATE-specific antigen, ETIOLOGY of cancer, GLEASON grading system, RESEARCH, PREDICTIVE tests, RESEARCH methodology, PROSTATE, EVALUATION research, TUMOR classification, COMPARATIVE studies, RESEARCH funding, PROSTATE tumors, TUMOR grading
Abstract

Background: In the era of widespread prostate-specific antigen testing, it is important to focus etiologic research on the outcome of aggressive prostate cancer, but studies have defined this outcome differently. We aimed to develop an evidence-based consensus definition of aggressive prostate cancer using clinical features at diagnosis for etiologic epidemiologic research.Methods: Among prostate cancer cases diagnosed in 2007 in the National Cancer Institute's Surveillance, Epidemiology, and End Results-18 database with follow-up through 2017, we compared the performance of categorizations of aggressive prostate cancer in discriminating fatal prostate cancer within 10 years of diagnosis, placing the most emphasis on sensitivity and positive predictive value (PPV).Results: In our case population (n = 55 900), 3073 men died of prostate cancer within 10 years. Among 12 definitions that included TNM staging and Gleason score, sensitivities ranged from 0.64 to 0.89 and PPVs ranged from 0.09 to 0.23. We propose defining aggressive prostate cancer as diagnosis of category T4 or N1 or M1 or Gleason score of 8 or greater prostate cancer, because this definition had one of the higher PPVs (0.23, 95% confidence interval = 0.22 to 0.24) and reasonable sensitivity (0.66, 95% confidence interval = 0.64 to 0.67) for prostate cancer death within 10 years. Results were similar across sensitivity analyses.Conclusions: We recommend that etiologic epidemiologic studies of prostate cancer report results for this definition of aggressive prostate cancer. We also recommend that studies separately report results for advanced category (T4 or N1 or M1), high-grade (Gleason score ≥8), and fatal prostate cancer. Use of this comprehensive set of endpoints will facilitate comparison of results from different studies and help elucidate prostate cancer etiology. [ABSTRACT FROM AUTHOR]

Published
2021
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61. Circulating isoflavone and lignan concentrations and prostate cancer risk : a meta-analysis of individual participant data from seven prospective studies including 2,828 cases and 5,593 controls

Author

Perez-Cornago, Aurora, Appleby, Paul N., Boeing, Heiner, Gil, Leire, Kyro, Cecilie, Ricceri, Fulvio, Murphy, Neil, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Khaw, Kay-Tee, Luben, Robert N., Gislefoss, Randi E., Langseth, Hilde, Drake, Isabel, Sonestedt, Emily, Wallström, Peter, Stattin, Pär, Johansson, Anders, Landberg, Rikard, Nilsson, Lena Maria, Ozasa, Kotaro, Tamakoshi, Akiko, Mikami, Kazuya, Kubo, Tatsuhiko, Sawada, Norie, Tsugane, Shoichiro, Key, Timothy J., Allen, Naomi E., Travis, Ruth C., Perez-Cornago, Aurora, Appleby, Paul N., Boeing, Heiner, Gil, Leire, Kyro, Cecilie, Ricceri, Fulvio, Murphy, Neil, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Khaw, Kay-Tee, Luben, Robert N., Gislefoss, Randi E., Langseth, Hilde, Drake, Isabel, Sonestedt, Emily, Wallström, Peter, Stattin, Pär, Johansson, Anders, Landberg, Rikard, Nilsson, Lena Maria, Ozasa, Kotaro, Tamakoshi, Akiko, Mikami, Kazuya, Kubo, Tatsuhiko, Sawada, Norie, Tsugane, Shoichiro, Key, Timothy J., Allen, Naomi E., and Travis, Ruth C.

Abstract

Phytoestrogens may influence prostate cancer development. This study aimed to examine the association between prediagnostic circulating concentrations of isoflavones (genistein, daidzein, equol) and lignans (enterolactone and enterodiol) and the risk of prostate cancer. Individual participant data were available from seven prospective studies (two studies from Japan with 241 cases and 503 controls and five studies from Europe with 2,828 cases and 5,593 controls). Because of the large difference in circulating isoflavone concentrations between Japan and Europe, analyses of the associations of isoflavone concentrations and prostate cancer risk were evaluated separately. Prostate cancer risk by study-specific fourths of circulating concentrations of each phytoestrogen was estimated using multivariable-adjusted conditional logistic regression. In men from Japan, those with high compared to low circulating equol concentrations had a lower risk of prostate cancer (multivariable-adjusted OR for upper quartile [Q4] vs. Q1 = 0.61, 95% confidence interval [CI] = 0.39-0.97), although there was no significant trend (OR per 75 percentile increase = 0.69, 95 CI = 0.46-1.05, p(trend) = 0.085); Genistein and daidzein concentrations were not significantly associated with risk (ORs for Q4 vs. Q1 = 0.70, 0.45-1.10 and 0.71, 0.45-1.12, respectively). In men from Europe, circulating concentrations of genistein, daidzein and equol were not associated with risk. Circulating lignan concentrations were not associated with the risk of prostate cancer, overall or by disease aggressiveness or time to diagnosis. There was no strong evidence that prediagnostic circulating concentrations of isoflavones or lignans are associated with prostate cancer risk, although further research is warranted in populations where isoflavone intakes are high.

Published
2018
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62. Prediagnostic circulating levels of sex hormones and survival in esophageal adenocarcinoma.

Author

Xie, Shao‐Hua, Ness‐Jensen, Eivind, Langseth, Hilde, Gislefoss, Randi E., Mattsson, Fredrik, and Lagergren, Jesper

Subjects
SEX hormones, SURGICAL excision, BODY mass index, ADENOCARCINOMA
Abstract

Sex hormonal differences may contribute to the strong male predominance in esophageal adenocarcinoma (EAC), but whether sex hormone levels influence survival in EAC is unstudied. Our study aimed to assess associations between prediagnostic sex hormone levels and survival in EAC. In a population‐based cohort study, 244 male EAC patients from the Janus Serum Bank Cohort in Norway were followed up through 2018. Associations between prediagnostic serum levels of 12 sex hormone measures and disease‐specific mortality were assessed using multivariable Cox regression, providing hazard ratios (HR) with 95% confidence intervals (CI) adjusted for age, calendar year, body mass index, tobacco smoking, physical activity and surgical resection. Higher levels of sex hormone‐binding globulin (SHBG) indicated decreased disease‐specific mortality (HR 0.68, 95% CI 0.44‐1.07, highest vs lowest tertile). In stratified analyses by surgery, such associations remained in nonoperated patients (HR 0.58, 95% CI 0.35‐0.96, highest vs lowest tertile), but not in operated patients. Higher levels of follicle‐stimulating hormone (FSH) were associated with increased disease‐specific mortality in an exposure‐response pattern; HRs for the middle and highest tertiles vs the lowest tertile were 1.35 (95% CI 0.89‐2.05) and 1.61 (95% CI 1.06‐2.43), respectively. No clear associations were observed with serum levels of dehydroepiandrosterone sulfate, luteinizing hormone, prolactin, testosterone, 17‐OH‐progesterone, progesterone, estradiol, androstenedione, testosterone:estradiol ratio or free testosterone index. These findings suggest that higher endogenous levels of SHBG and lower levels of FSH may increase the survival in EAC. The other 10 examined sex hormone measures may not influence the survival. What's new? Esophageal adenocarcinoma (EAC) occurs more frequently in men than women. Whether this pattern is linked to differences in sex hormone levels and whether such differences impact EAC survival remain unclear. In this study of male EAC patients in Norway, analyses of prediagnostic sex hormone measures uncovered associations between reduced disease‐specific mortality and increased sex hormone‐binding globulin and decreased follicle‐stimulating hormone levels. The associations were detected only in patients who had not undergone surgery. Ten other sex hormone measures also analyzed had no influence on survival. Additional investigation is needed to better understand relationships between sex hormone levels and EAC survival. [ABSTRACT FROM AUTHOR]

Published
2021
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63. Prediagnostic serum sCD27 and sCD30 in serial samples and risks of non‐Hodgkin lymphoma subtypes.

Author

Purdue, Mark P., Lan, Qing, Langseth, Hilde, Grimsrud, Tom K., Hildesheim, Allan, and Rothman, Nathaniel

Subjects
CHRONIC lymphocytic leukemia, BIOMARKERS, IMMUNE serums, SERUM
Abstract

Elevated prediagnostic serum levels of the immune activation markers sCD27 and sCD30 have been associated with non‐Hodgkin lymphoma (NHL). However, the use of a single sample per participant in these studies has limited etiologic inferences. We report findings, overall and by NHL subtype, from a case–control analysis (422 cases, 434 controls) within the Janus Serum Bank with two samples per subject collected on average 5 years apart. Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) was associated with elevated sCD27 in the later, but not earlier, prediagnostic sample (odds ratio [OR] 4.2, 95% confidence interval [CI] 1.5–11.6 and 1.7, 0.7–4.7 per log increase, respectively) in analyses adjusting for both analytes, while follicular lymphoma (FL) was associated with elevated sCD30 in both the later and earlier samples (OR 2.9, 95% CI 1.4–4.4 and 2.3, 1.2–4.4, respectively). CLL/SLL cases were significantly more likely than controls to have higher sCD27 in the later vs. earlier sample (OR 1.4, 95% CI 1.1–1.9 per standard deviation increase); no such difference in sCD30 was apparent for FL. In a joint analysis, NHL cases were more likely than controls to have below‐median sCD27 in the earlier sample and above‐median sCD27 in the later sample (OR 1.5, 95% CI 1.0–2.3). For sCD30, the association between sCD30 and FL was confined to subjects with above‐median analyte levels in both samples (OR 2.5, 95% CI 1.1–5.9). Our findings are compatible with elevated sCD27 representing a disease‐induced effect and sCD30 representing a marker of increased FL susceptibility. What's new? Elevated pre‐diagnostic serum levels of sCD27 and sCD30 are associated with an increased risk of non‐Hodgkin lymphoma (NHL). However, the use of a single sample per subject in past studies has limited etiologic inferences. Here, analyses of banked samples collected five years apart from NHL patients and controls show that sCD27 elevation is present only in later samples in NHL cases. By contrast, sCD30 levels were increased in early and late samples, specifically in association with follicular lymphoma. The findings suggest that increases in sCD27 are due to disease‐induced effects, whereas sCD30 is a potential marker of follicular lymphoma susceptibility. [ABSTRACT FROM AUTHOR]

Published
2020
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65. Prediagnostic blood levels of organochlorines and risk of non‐Hodgkin lymphoma in three prospective cohorts in China and Singapore.

Author

Bassig, Bryan A., Shu, Xiao‐Ou, Sjödin, Andreas, Koh, Woon‐Puay, Gao, Yu‐Tang, Adams‐Haduch, Jennifer, Davis, Mark, Wang, Renwei, Xiang, Yong‐Bing, Engel, Lawrence S., Purdue, Mark P., Ji, Bu‐Tian, Yang, Gong, Jones, Richard S., Langseth, Hilde, Hosgood, H. Dean, Grimsrud, Tom K., Seow, Wei Jie, Wong, Jason Y.Y., and Hu, Wei

Subjects
PERSISTENT pollutants, BLOOD collection, ENVIRONMENTAL exposure, LYMPHOMAS, BLOOD, OSTEOCHONDROSIS
Abstract

Specific organochlorines (OCs) have been associated with non‐Hodgkin lymphoma (NHL) with varying degrees of evidence. These associations have not been evaluated in Asia, where the high exposure and historical environmental contamination of certain OC pesticides (e.g., dichlorodiphenyltrichloroethane [DDT], hexachlorocyclohexane [HCH]) are different from Western populations. We evaluated NHL risk and prediagnostic blood levels of OC pesticides/metabolites and polychlorinated biphenyl congeners in a case–control study of 167 NHL cases and 167 controls nested within three prospective cohorts in Shanghai and Singapore. Conditional logistic regression was used to analyze lipid‐adjusted OC levels and NHL risk. Median levels of p,p′‐dichlorodiphenyldichloroethylene (p,p′‐DDE), the primary DDT metabolite, and β‐HCH were up to 12 and 65 times higher, respectively, in samples from the Asian cohorts compared to several cohorts in the United States and Norway. An increased risk of NHL was observed among those with higher β‐HCH levels both overall (3rd vs. 1st tertile OR = 1.8, 95%CI = 1.0–3.2; ptrend = 0.049) and after excluding cases diagnosed within 2 years of blood collection (3rd vs. 1st tertile OR = 2.0, 95%CI = 1.1–3.9; ptrend = 0.03), and the association was highly consistent across the three cohorts. No significant associations were observed for other OCs, including p,p′‐DDE. Our findings provide support for an association between β‐HCH blood levels and NHL risk. This is a concern because substantial quantities of persistent, toxic residues of HCH are present in the environment worldwide. Although there is some evidence that DDT is associated with NHL, our findings for p,p′‐DDE do not support an association. What's new? Organochlorines (OC) are environmentally persistent organic pollutants that have been associated with cancer risk. Here the authors conducted a prospective study of blood OC levels and risk of non‐Hodgkin lymphoma (NHL) in Asia, where high exposures and historical environmental contamination of certain OC pesticides have been reported. They find an association between risk of NHL and higher levels of β‐hexachlorocyclohexane, median levels of which were up to 65‐times higher in the Asian samples than in samples from several Western populations. These results add to the weight of evidence that environmental exposure to HCH is carcinogenic. [ABSTRACT FROM AUTHOR]

Published
2020
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66. Circulating isoflavone and lignan concentrations and prostate cancer risk: a meta-analysis of individual participant data from seven prospective studies including 2,828 cases and 5,593 controls

Author

Perez-Cornago, Aurora, primary, Appleby, Paul N., additional, Boeing, Heiner, additional, Gil, Leire, additional, Kyrø, Cecilie, additional, Ricceri, Fulvio, additional, Murphy, Neil, additional, Trichopoulou, Antonia, additional, Tsilidis, Konstantinos K., additional, Khaw, Kay-Tee, additional, Luben, Robert N., additional, Gislefoss, Randi E, additional, Langseth, Hilde, additional, Drake, Isabel, additional, Sonestedt, Emily, additional, Wallström, Peter, additional, Stattin, Pär, additional, Johansson, Anders, additional, Landberg, Rikard, additional, Nilsson, Lena Maria, additional, Ozasa, Kotaro, additional, Tamakoshi, Akiko, additional, Mikami, Kazuya, additional, Kubo, Tatsuhiko, additional, Sawada, Norie, additional, Tsugane, Shoichiro, additional, Key, Timothy J., additional, Allen, Naomi E., additional, and Travis, Ruth C., additional

Published
2018
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73. A high-resolution map of the human small non-coding transcriptome

Author

Fehlmann, Tobias, primary, Backes, Christina, additional, Alles, Julia, additional, Fischer, Ulrike, additional, Hart, Martin, additional, Kern, Fabian, additional, Langseth, Hilde, additional, Rounge, Trine, additional, Umu, Sinan Ugur, additional, Kahraman, Mustafa, additional, Laufer, Thomas, additional, Haas, Jan, additional, Staehler, Cord, additional, Ludwig, Nicole, additional, Hübenthal, Matthias, additional, Meder, Benjamin, additional, Franke, Andre, additional, Lenhof, Hans-Peter, additional, Meese, Eckart, additional, and Keller, Andreas, additional

Published
2017
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74. A comprehensive profile of circulating RNAs in human serum

Author

Umu, Sinan Uğur, primary, Langseth, Hilde, additional, Bucher-Johannessen, Cecilie, additional, Fromm, Bastian, additional, Keller, Andreas, additional, Meese, Eckart, additional, Lauritzen, Marianne, additional, Leithaug, Magnus, additional, Lyle, Robert, additional, and Rounge, Trine B., additional

Published
2017
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76. Cohort Profile Update: The Janus Serum Bank Cohort in Norway

Author

Hjerkind, Kirsti Vik, primary, Gislefoss, Randi E., additional, Tretli, Steinar, additional, Nystad, Wenche, additional, Bjørge, Tone, additional, Engeland, Anders, additional, Meyer, Haakon E., additional, Holvik, Kristin, additional, Ursin, Giske, additional, and Langseth, Hilde, additional

Published
2017
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78. Longitudinal biobanks-based study on the joint effects of infections, nutrition and hormones on risk of prostate cancer.

Author

Lumme, Sonja, Tenkanen, Leena, Langseth, Hilde, Gislefoss, Randi, Hakama, Matti, Stattin, Pär, Hallmans, Göran, Adlercreutz, Herman, Saikku, Pekka, Stenman, Ulf-Håkan, Tuohimaa, Pentti, Luostarinen, Tapio, Dillner, Joakim, Lumme, Sonja, Tenkanen, Leena, Langseth, Hilde, Gislefoss, Randi, Hakama, Matti, Stattin, Pär, Hallmans, Göran, Adlercreutz, Herman, Saikku, Pekka, Stenman, Ulf-Håkan, Tuohimaa, Pentti, Luostarinen, Tapio, and Dillner, Joakim

Abstract

Background To evaluate the individual and combined effects of enterolactone, vitamin D, free testosterone, Chlamydia trachomatis and HPV-18 on the risk of prostate cancer in a large population-based biochemical material that combined three Nordic serum sample banks. Material and methods A joint cohort of 209 000 healthy men was followed using cancer registry linkages. From this cohort altogether 699 incident cases of prostate cancer were identified. Four controls were selected by incidence density sampling and matching for country, age and date of the blood sampling. Complete data for all investigated exposures was available for 483 eligible cases and 1055 eligible controls. Multivariate regression analyses were performed to investigate the solitary and combined effects. Results The solitary effects were small. Significantly increased risk [rate ratio 1.6 (95% CI 1.0-2.5)] was found in those seronegative for C. trachomatis infection. The joint effect in risk levels of enterolactone and vitamin D was antagonistic [observed rate ratio (RR) 1.4 (1.0-2.1), expected RR 2.0 (1.0-4.1)] as well as that of HPV-18 and C. trachomatis [observed RR 1.9 (0.8-4.5), expected RR 9.9 (1.1-87.0)]. Conclusion A large follow-up study combining data from several previously investigated exposures to investigate joint effects found no evidence that exposure to two risk factors would increase the risk of prostate cancer from that expected on basis of exposure to one risk factor. If anything, the results were consistent with antagonistic interactions.

Published
2016
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79. Pre-diagnostic serum levels of EGFR and ErbB2 and genetic glioma risk variants : a nested case-control study

Author

Späth, Florentin, Andersson, Ulrika, Dahlin, Anna M., Langseth, Hilde, Hovig, Eivind, Johannesen, Tom Borge, Grankvist, Kjell, Björkblom, Benny, Wibom, Carl, Melin, Beatrice, Späth, Florentin, Andersson, Ulrika, Dahlin, Anna M., Langseth, Hilde, Hovig, Eivind, Johannesen, Tom Borge, Grankvist, Kjell, Björkblom, Benny, Wibom, Carl, and Melin, Beatrice

Abstract

Genetic variants have been associated with the risk of developing glioma, but functional mechanisms on disease phenotypic traits remain to be investigated. One phenotypic trait of glioblastoma is the mutation and amplification of the epidermal growth factor receptor (EGFR) gene. We investigated associations between pre-diagnostic serum protein concentrations of EGFR and ErbB2, both members of the EGFR family, and future risk of glioma. Further, we studied if EGFR glioma risk variants were associated with EGFR and ErbB2 serum levels. We assessed the associations between genetic glioma risk variants and serum concentrations of EGFR and ErbB2, as measured in pre-diagnostic cohort serum samples of 593 glioma patients and 590 matched cancer-free controls. High serum EGFR and ErbB2 levels were associated with risk of developing glioblastoma (P = 0.008; OR = 1.58, 95 % CI = 1.13-2.22 and P = 0.017, OR = 1.63, 95 % CI = 1.09-2.44, respectively). High serum ErbB2 concentration was also associated with glioma risk overall (P = 0.049; OR = 1.39, 95 % CI = 1.00-1.93). Glioma risk variants were not associated with high serum protein abundance. In contrast, the EGFR risk variant rs4947986 (T) was correlated with decreased EGFR serum levels (study cohort P = 0.024 and controls P = 0.009). To our knowledge, this is the first study showing an association of EGFR and ErbB2 serum levels with glioma more than a decade before diagnosis, indicating that EGFR and ErbB2 serum proteins are important in early gliomagenesis. However, we did not find evidence that glioma risk variants were associated with high pre-diagnostic serum concentrations of EGFR and ErbB2.

Published
2016
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80. Metabolomic screening of pre-diagnostic serum samples identifies association between alpha- and gamma-tocopherols and glioblastoma risk

Author

Björkblom, Benny, Wibom, Carl, Jonsson, Pär, Mörén, Lina, Andersson, Ulrika, Johannesen, Tom Borge, langseth, Hilde, Antti, Henrik, Melin, Beatrice, Björkblom, Benny, Wibom, Carl, Jonsson, Pär, Mörén, Lina, Andersson, Ulrika, Johannesen, Tom Borge, langseth, Hilde, Antti, Henrik, and Melin, Beatrice

Abstract

Glioblastoma is associated with poor prognosis with a median survival of one year. High doses of ionizing radiation is the only established exogenous risk factor. To explore new potential biological risk factors for glioblastoma, we investigated alterations in metabolite concentrations in pre-diagnosed serum samples from glioblastoma patients diagnosed up to 22 years after sample collection, and undiseased controls. The study points out a latent biomarker for future glioblastoma consisting of nine metabolites (gamma-tocopherol, alpha-tocopherol, erythritol, erythronic acid, myo-inositol, cystine, 2-keto-L-gluconic acid, hypoxanthine and xanthine) involved in antioxidant metabolism. We detected significantly higher serum concentrations of alpha-tocopherol (p=0.0018) and gamma-tocopherol (p=0.0009) in future glioblastoma cases. Compared to their matched controls, the cases showed a significant average fold increase of alpha- and gamma-tocopherol levels: 1.2 for alpha-T (p=0.018) and 1.6 for gamma-T (p=0.003). These tocopherol levels were associated with a glioblastoma odds ratio of 1.7 (alpha-T, 95% CI: 1.0-3.0) and 2.1 (gamma-T, 95% CI: 1.2-3.8). Our exploratory metabolomics study detected elevated serum levels of a panel of molecules with antioxidant properties as well as oxidative stress generated compounds. Additional studies are necessary to confirm the association between the observed serum metabolite pattern and future glioblastoma development.

Published
2016
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81. Serum biomarkers of polyomavirus infection and risk of lung cancer in never smokers

Author

Malhotra, Jyoti, primary, Waterboer, Tim, additional, Pawlita, Michael, additional, Michel, Angelika, additional, Cai, Qiuyin, additional, Zheng, Wei, additional, Gao, Yu-Tang, additional, Lan, Qing, additional, Rothman, Nathaniel, additional, Langseth, Hilde, additional, Grimsrud, Tom K, additional, Yuan, Jian-Min, additional, Koh, Woon-Puay, additional, Wang, Renwei, additional, Arslan, Alan A, additional, Zeleniuch-Jacquotte, Anne, additional, and Boffetta, Paolo, additional

Published
2016
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83. Abstract 4290: Serum biomarkers of polyomavirus infection and risk of lung cancer in never smokers

Author

Malhotra, Jyoti, primary, Waterboer, Tim, additional, Pawlita, Michael, additional, Michel, Angelika, additional, Cai, Qiuyin, additional, Zheng, Wei, additional, Lan, Qing, additional, Rothman, Nathaniel, additional, Langseth, Hilde, additional, Grimsrud, Tom K., additional, Yuan, Jian-Min, additional, Koh, Woon-Puay, additional, Arslan, Alan A., additional, Zeleniuch-Jacquotte, Anne, additional, and Boffetta, Paolo, additional

Published
2016
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88. Longitudinal biobanks-based study on the joint effects of infections, nutrition and hormones on risk of prostate cancer

Author

Lumme, Sonja, primary, Tenkanen, Leena, additional, Langseth, Hilde, additional, Gislefoss, Randi, additional, Hakama, Matti, additional, Stattin, Pär, additional, Hallmans, Göran, additional, Adlercreutz, Herman, additional, Saikku, Pekka, additional, Stenman, Ulf-Håkan, additional, Tuohimaa, Pentti, additional, Luostarinen, Tapio, additional, and Dillner, Joakim, additional

Published
2016
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89. Investigation of Established Genetic Risk Variants for Glioma in Prediagnostic Samples from a Population-Based Nested Case-Control Study

Author

Wibom, Carl, Späth, Florentin, Dahlin, Anna M., Langseth, Hilde, Hovig, Eivind, Rajaraman, Preetha, Johannesen, Tom Borge, Andersson, Ulrika, Melin, Beatrice, Wibom, Carl, Späth, Florentin, Dahlin, Anna M., Langseth, Hilde, Hovig, Eivind, Rajaraman, Preetha, Johannesen, Tom Borge, Andersson, Ulrika, and Melin, Beatrice

Abstract

Background: Although glioma etiology is poorly understood in general, growing evidence indicates a genetic component. Four large genome-wide association studies (GWAS) have linked common genetic variants with an increased glioma risk. However, to date, these studies are based largely on a case-control design, where cases have been recruited at the time of or after diagnosis. They may therefore suffer from a degree of survival bias, introduced when rapidly fatal cases are not included. Methods: To confirm glioma risk variants in a prospective setting, we have analyzed 11 previously identified risk variants in a set of prediagnostic serum samples with 598 cases and 595 matched controls. Serum samples were acquired from The Janus Serum Bank, a Norwegian population-based biobank reserved for cancer research. Results: We confirmed the association with glioma risk for variants within five genomic regions: 8q24.21 (CCDC26), 9p21.3 (CDKN2B-AS1), 11q23.3 (PHLDB1), 17p13.1 (TP53), and 20q13.33 (RTEL1). However, previously identified risk variants within the 7p11.2 (EGFR) region were not confirmed by this study. Conclusions: Our results indicate that the risk variants that were confirmed by this study are truly associated with glioma risk and may, consequently, affect gliomagenesis. Though the lack of positive confirmation of EGFR risk variants may be attributable to relatively limited statistical power, it nevertheless raises the question whether they truly are risk variants or markers for glioma prognosis. Impact: Our findings indicate the need for further studies to clarify the role of glioma risk loci with respect to prolonged survival versus etiology.

Published
2015
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90. Prediagnostic Serum Organochlorine Concentrations and Metastatic Prostate Cancer: A Nested Case-Control Study in the Norwegian Janus Serum Bank Cohort

Author

dIRAS RA-I&I RA, Infection & Immunity, Risk Assessment, LS IRAS EEPI GRA (Gezh.risico-analyse), Sub IRAS EEPI Algemeen, Koutros, Stella, Langseth, Hilde, Grimsrud, Tom K, Barr, Dana Boyd, Vermeulen, Roel, Portengen, Lützen, Wacholder, Sholom, Freeman, Laura E Beane, Blair, Aaron, Hayes, Richard B, Rothman, Nathaniel, Engel, Lawrence S, dIRAS RA-I&I RA, Infection & Immunity, Risk Assessment, LS IRAS EEPI GRA (Gezh.risico-analyse), Sub IRAS EEPI Algemeen, Koutros, Stella, Langseth, Hilde, Grimsrud, Tom K, Barr, Dana Boyd, Vermeulen, Roel, Portengen, Lützen, Wacholder, Sholom, Freeman, Laura E Beane, Blair, Aaron, Hayes, Richard B, Rothman, Nathaniel, and Engel, Lawrence S

Published
2015

91. Subsite-Specific Dietary Risk Factors for Colorectal Cancer: A Review of Cohort Studies

Author

Hjartåker, Anette, Aagnes, Bjarte, Robsahm, Trude Eid, Langseth, Hilde, Bray, Freddie, and Larsen, Inger Kristin

Subjects
Article Subject, food and beverages
Abstract

Objective. A shift in the total incidence from left- to right-sided colon cancer has been reported and raises the question as to whether lifestyle risk factors are responsible for the changing subsite distribution of colon cancer. The present study provides a review of the subsite-specific risk estimates for the dietary components presently regarded as convincing or probable risk factors for colorectal cancer: red meat, processed meat, fiber, garlic, milk, calcium, and alcohol. Methods. Studies were identified by searching PubMed through October 8, 2012 and by reviewing reference lists. Thirty-two prospective cohort studies are included, and the estimates are compared by sex for each risk factor. Results. For alcohol, there seems to be a stronger association with rectal cancer than with colon cancer, and for meat a somewhat stronger association with distal colon and rectal cancer, relative to proximal colon cancer. For fiber, milk, and calcium, there were only minor differences in relative risk across subsites. No statement could be given regarding garlic. Overall, many of the subsite-specific risk estimates were nonsignificant, irrespective of exposure. Conclusion. For some dietary components the associations with risk of cancer of the rectum and distal colon appear stronger than for proximal colon, but not for all.

Published
2013
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92. A high-resolution map of the human small non-coding transcriptome.

Author

Fehlmann, Tobias, Backes, Christina, Alles, Julia, Fischer, Ulrike, Hart, Martin, Kern, Fabian, Langseth, Hilde, Rounge, Trine, Umu, Sinan Ugur, and Kahraman, Mustafa

Subjects
NON-coding RNA, RNA sequencing, TRANSCRIPTOMES, NUCLEOTIDE sequencing, MICRORNA
Abstract

MOTIVATION: Although the amount of small non-coding RNA-sequencing data is continuously increasing, it is still unclear to which extent small RNAs are represented in the human genome. RESULTS: In this study we analyzed 303 billion sequencing reads from nearly 25 000 datasets to answer this question. We determined that 0.8% of the human genome are reliably covered by 874 123 regions with an average length of 31 nt. On the basis of these regions, we found that among the known small non-coding RNA classes, microRNAs were the most prevalent. In subsequent steps, we characterized variations of miRNAs and performed a staged validation of 11 877 candidate miRNAs. Of these, many were actually expressed and significantly dysregulated in lung cancer. Selected candidates were finally validated by northern blots. Although isolated miRNAs could still be present in the human genome, our presented set likely contains the largest fraction of human miRNAs. [ABSTRACT FROM AUTHOR]

Published
2018
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96. Survival of women with cancers of breast and genital organs in Europe 1999–2007: Results of the EUROCARE-5 study

Author

Sant, Milena, primary, Chirlaque Lopez, Maria Dolores, additional, Agresti, Roberto, additional, Sánchez Pérez, Maria José, additional, Holleczek, Bernd, additional, Bielska-Lasota, Magdalena, additional, Dimitrova, Nadya, additional, Innos, Kaire, additional, Katalinic, Alexander, additional, Langseth, Hilde, additional, Larrañaga, Nerea, additional, Rossi, Silvia, additional, Siesling, Sabine, additional, Minicozzi, Pamela, additional, Hackl, M., additional, Zielonke, N., additional, Oberaigner, W., additional, Van Eycken, E., additional, Henau, K., additional, Valerianova, Z., additional, Dimitrova, N., additional, Sekerija, M., additional, Zvolský, M., additional, Dušek, L., additional, Storm, H., additional, Engholm, G., additional, Mägi, M., additional, Aareleid, T., additional, Malila, N., additional, Seppä, K., additional, Velten, M., additional, Troussard, X., additional, Bouvier, V., additional, Launoy, G., additional, Guizard, A.V., additional, Faivre, J., additional, Bouvier, A.M., additional, Arveux, P., additional, Maynadié, M., additional, Woronoff, A.S., additional, Robaszkiewicz, M., additional, Baldi, I., additional, Monnereau, A., additional, Tretarre, B., additional, Bossard, N., additional, Belot, A., additional, Colonna, M., additional, Molinié, F., additional, Bara, S., additional, Schvartz, C., additional, Lapôtre-Ledoux, B., additional, Grosclaude, P., additional, Meyer, M., additional, Stabenow, R., additional, Luttmann, S., additional, Eberle, A., additional, Brenner, H., additional, Nennecke, A., additional, Engel, J., additional, Schubert-Fritschle, G., additional, Kieschke, J., additional, Heidrich, J., additional, Holleczek, B., additional, Katalinic, A., additional, Jónasson, J.G., additional, Tryggvadóttir, L., additional, Comber, H., additional, Mazzoleni, G., additional, Bulatko, A., additional, Buzzoni, C., additional, Giacomin, A., additional, Sutera Sardo, A., additional, Mancuso, P., additional, Ferretti, S., additional, Crocetti, E., additional, Caldarella, A., additional, Gatta, G., additional, Sant, M., additional, Amash, H., additional, Amati, C., additional, Baili, P., additional, Berrino, F., additional, Bonfarnuzzo, S., additional, Botta, L., additional, Di Salvo, F., additional, Foschi, R., additional, Margutti, C., additional, Meneghini, E., additional, Minicozzi, P., additional, Trama, A., additional, Serraino, D., additional, Dal Maso, L., additional, De Angelis, R., additional, Caldora, M., additional, Capocaccia, R., additional, Carrani, E., additional, Francisci, S., additional, Mallone, S., additional, Pierannunzio, D., additional, Roazzi, P., additional, Rossi, S., additional, Santaquilani, M., additional, Tavilla, A., additional, Pannozzo, F., additional, Busco, S., additional, Bonelli, L., additional, Vercelli, M., additional, Gennaro, V., additional, Ricci, P., additional, Autelitano, M., additional, Randi, G., additional, Ponz De Leon, M., additional, Marchesi, C., additional, Cirilli, C., additional, Fusco, M., additional, Vitale, M.F., additional, Usala, M., additional, Traina, A., additional, Staiti, R., additional, Vitale, F., additional, Ravazzolo, B., additional, Michiara, M., additional, Tumino, R., additional, Giorgi Rossi, P., additional, Di Felice, E., additional, Falcini, F., additional, Iannelli, A., additional, Sechi, O., additional, Cesaraccio, R., additional, Piffer, S., additional, Madeddu, A., additional, Tisano, F., additional, Maspero, S., additional, Fanetti, A.C., additional, Zanetti, R., additional, Rosso, S., additional, Candela, P., additional, Scuderi, T., additional, Stracci, F., additional, Bianconi, F., additional, Tagliabue, G., additional, Contiero, P., additional, Dei Tos, A.P., additional, Guzzinati, S., additional, Pildava, S., additional, Smailyte, G., additional, Calleja, N., additional, Agius, D., additional, Johannesen, T.B., additional, Rachtan, J., additional, Gózdz, S., additional, Mezyk, R., additional, Blaszczyk, J., additional, Bebenek, M., additional, Bielska-Lasota, M., additional, Forjaz de Lacerda, G., additional, Bento, M.J., additional, Castro, C., additional, Miranda, A., additional, Mayer-da-Silva, A., additional, Nicula, F., additional, Coza, D., additional, Safaei Diba, C., additional, Primic-Zakelj, M., additional, Almar, E., additional, Ramírez, C., additional, Errezola, M., additional, Bidaurrazaga, J., additional, Torrella-Ramos, A., additional, Díaz García, J.M., additional, Jimenez-Chillaron, R., additional, Marcos-Gragera, R., additional, Izquierdo Font, A., additional, Sanchez, M.J., additional, Chang, D.Y.L., additional, Navarro, C., additional, Chirlaque, M.D., additional, Moreno-Iribas, C., additional, Ardanaz, E., additional, Galceran, J., additional, Carulla, M., additional, Lambe, M., additional, Khan, S., additional, Mousavi, M., additional, Bouchardy, C., additional, Usel, M., additional, Ess, S.M., additional, Frick, H., additional, Lorez, M., additional, Herrmann, C., additional, Bordoni, A., additional, Spitale, A., additional, Konzelmann, I., additional, Visser, O., additional, Lemmens, V., additional, Coleman, M., additional, Allemani, C., additional, Rachet, B., additional, Verne, J., additional, Easey, N., additional, Lawrence, G., additional, Moran, T., additional, Rashbass, J., additional, Roche, M., additional, Wilkinson, J., additional, Gavin, A., additional, Donnelly, C., additional, Brewster, D.H., additional, Huws, D.W., additional, White, C., additional, and Otter, R., additional

Published
2015
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