Search

Your search keyword '"Titus-Ernstoff, L."' showing total 188 results
Start Over Author "Titus-Ernstoff, L." Search Limiters Full Text

Refine your results

188 results on '"Titus-Ernstoff, L."'

1. Validating genetic risk associations for ovarian cancer through the international Ovarian Cancer Association Consortium.

Author

Pearce, CL, Near, AM, Van Den Berg, DJ, Ramus, SJ, Gentry-Maharaj, A, Menon, U, Gayther, SA, Anderson, AR, Edlund, CK, Wu, AH, Chen, X, Beesley, J, Webb, PM, Holt, SK, Chen, C, Doherty, JA, Rossing, MA, Whittemore, AS, McGuire, V, DiCioccio, RA, Goodman, MT, Lurie, G, Carney, ME, Wilkens, LR, Ness, RB, Moysich, KB, Edwards, R, Jennison, E, Kjaer, SK, Hogdall, E, Hogdall, CK, Goode, EL, Sellers, TA, Vierkant, RA, Cunningham, JM, Schildkraut, JM, Berchuck, A, Moorman, PG, Iversen, ES, Cramer, DW, Terry, KL, Vitonis, AF, Titus-Ernstoff, L, Song, H, Pharoah, PDP, Spurdle, AB, Anton-Culver, H, Ziogas, A, Brewster, W, Galitovskiy, V, Chenevix-Trench, G, Australian Cancer Study, and Australian Ovarian Cancer Study Group

Subjects
Australian Cancer Study, Australian Ovarian Cancer Study Group, Humans, Ovarian Neoplasms, Neoplasm Invasiveness, Genetic Predisposition to Disease, DNA Ligases, DNA-Binding Proteins, Risk Factors, Case-Control Studies, Cohort Studies, Genotype, Heterozygote, Homozygote, Polymorphism, Single Nucleotide, Adult, Aged, Middle Aged, Female, Cytochrome P-450 CYP3A, DNA Ligase ATP, ovarian cancer, genetic susceptibility, oestrogen metabolism, CYP3A4, pooled-analyses, Polymorphism, Single Nucleotide, Ovarian Cancer, Genetics, Clinical Research, Cancer, Rare Diseases, 2.1 Biological and endogenous factors, Oncology & Carcinogenesis, Oncology and Carcinogenesis, Public Health and Health Services
Abstract

The search for genetic variants associated with ovarian cancer risk has focused on pathways including sex steroid hormones, DNA repair, and cell cycle control. The Ovarian Cancer Association Consortium (OCAC) identified 10 single-nucleotide polymorphisms (SNPs) in genes in these pathways, which had been genotyped by Consortium members and a pooled analysis of these data was conducted. Three of the 10 SNPs showed evidence of an association with ovarian cancer at P< or =0.10 in a log-additive model: rs2740574 in CYP3A4 (P=0.011), rs1805386 in LIG4 (P=0.007), and rs3218536 in XRCC2 (P=0.095). Additional genotyping in other OCAC studies was undertaken and only the variant in CYP3A4, rs2740574, continued to show an association in the replication data among homozygous carriers: OR(homozygous(hom))=2.50 (95% CI 0.54-11.57, P=0.24) with 1406 cases and 2827 controls. Overall, in the combined data the odds ratio was 2.81 among carriers of two copies of the minor allele (95% CI 1.20-6.56, P=0.017, p(het) across studies=0.42) with 1969 cases and 3491 controls. There was no association among heterozygous carriers. CYP3A4 encodes a key enzyme in oestrogen metabolism and our finding between rs2740574 and risk of ovarian cancer suggests that this pathway may be involved in ovarian carcinogenesis. Additional follow-up is warranted.

Published
2009

5. Ovarian cancer and smoking: individual participant meta-analysis including 28,114 women with ovarian cancer from 51 epidemiological studies

Author

Gaitskell, K, Hermon, C, Moser, K, Reeves, G, Peto, R, Brinton, L, Marchbanks, P, Negri, E, Ness, R, Peeters, PHM, Vessey, M, Calle, EE, Gapstur, SM, Patel, AV, Dal Maso, L, Talamini, R, Chetrit, A, Hirsh-Yechezkel, G, Lubin, F, Sadetzki, S, Banks, E, Beral, V, Bull, D, Callaghan, K, Crossley, B, Goodill, A, Green, J, Key, T, Sitas, F, Collins, R, Doll, R, Gonzalez, A, Lee, N, Ory, HW, Peterson, HB, Wingo, PA, Martin, N, Pardthaisong, T, Silpisornkosol, S, Theetranont, C, Boosiri, B, Chutivongse, S, Jimakorn, P, Virutamasen, P, Wongsrichanalai, C, Tjonneland, A, Titus-Ernstoff, L, Byers, T, Rohan, T, Mosgaard, BJ, Yeates, D, Freudenheim, JL, Chang-Claude, J, Kaaks, R, Anderson, KE, Folsom, A, Robien, K, Hampton, J, Newcomb, PA, Rossing, MA, Thomas, DB, Weiss, NS, Riboli, E, Clavel-Chapelon, F, Cramer, D, Hankinson, SE, Tworoger, SS, Franceschi, S, La Vecchia, C, Adami, HO, Magnusson, C, Riman, T, Weiderpass, Elisabete, Wolk, A, Schouten, LJ, van den Brandt, PA, Chantarakul, N, Koetsawang, S, Rachawat, D, Palli, D, Black, A, Brinton, LA, Freedman, DM, Hartge, P, Hsing, AW, Lacey, JV, Hoover, RN, Schairer, C, Urban, M, Graff-Iversen, Sidsel, Selmer, Randi, Bain, CJ, Green, AC, Purdie, DM, Siskind, V, Webb, PM, Moysich, K, McCann, SE, Hannaford, P, Kay, C, Binns, CW, Lee, AH, Zhang, M, Ness, RB, Nasca, P, Coogan, PF, Palmer, JR, Rosenberg, L, Kelsey, J, Paffenbarger, R, Whittemore, A, Katsouyanni, K, Trichopoulou, A, Trichopoulos, D, Tzonou, A, Dabancens, A, Martinez, L, Molina, R, Salas, O, Goodman, MT, Lurie, G, Carney, ME, Wilkens, LR, Hartman, L, Manjer, J, Olsson, H, Grisso, JA, Morgan, M, Wheeler, JE, Bunker, CH, Edwards, RP, Modugno, F, Casagrande, J, Pike, MC, Ross, RK, Wu, AH, Miller, AB, Kumle, Merethe, Gram, Inger Torhild, Lund, Eiliv, McGowan, L, Shu, XO, Zheng, W, Farley, TMM, Holck, S, Meirik, O, Risch, HA, E. E. Calle, S. M. Gapstur, A. V. Patel, L. Dal Maso, R. Talamini, A. Chetrit, G. Hirsh Yechezkel, F. Lubin, S. Sadetzki, E. Bank, V. Beral, D. Bull, K. Callaghan, B. Crossley, K. Gaitskell, A. Goodill, J. Green, C. Hermon, T. Key, K. Moser, G. Reeve, F. Sita, R. Collin, R. Doll, R. Peto, C. A. Gonzalez, N. Lee, P. Marchbank, H. W. Ory, H. B. Peterson, P. A. Wingo, N. Martin, T. Pardthaisong, S. Silpisornkosol, C. Theetranont, B. Boosiri, S. Chutivongse, P. Jimakorn, P. Virutamasen, C. Wongsrichanalai, A. Tjonneland, L. Titus Ernstoff, T. Byer, T. Rohan, B. J. Mosgaard, M. Vessey, D. Yeate, J. L. Freudenheim, J. Chang Claude, R. Kaak, K. E. Anderson, A. Folsom, K. Robien, J. Hampton, P. A. Newcomb, M. A. Rossing, D. B. Thoma, N. S. Wei, E. Riboli, F. Clavel Chapelon, D. Cramer, S. E. Hankinson, S. S. Tworoger, S. Franceschi, C. La Vecchia, E. Negri, H. O. Adami, C. Magnusson, T. Riman, E. Weiderpa, A. Wolk, L. J. Schouten, P. A. van den Brandt, N. Chantarakul, S. Koetsawang, D. Rachawat, D. Palli, A. Black, L. A. Brinton, D. M. Freedman, P. Hartge, A. W. Hsing, J. Lacey, R. N. Hoover, C. Schairer, M. Urban, S. Graff Iversen, R. Selmer, C. J. Bain, A. C. Green, D. M. Purdie, V. Siskind, P. M. Webb, K. Moysich, S. E. Mccann, P. Hannaford, C. Kay, C. W. Binn, A. H. Lee, M. Zhang, R. B. Ne, P. Nasca, P. F. Coogan, J. R. Palmer, L. Rosenberg, J. Kelsey, R. Paffenbarger, A. Whittemore, K. Katsouyanni, A. Trichopoulou, D. Trichopoulo, A. Tzonou, A. Dabancen, L. Martinez, R. Molina, O. Sala, M. T. Goodman, G. Lurie, M. E. Carney, L. R. Wilken, L. Hartman, J. Manjer, H. Olsson, J. A. Grisso, M. Morgan, J. E. Wheeler, C. H. Bunker, R. P. Edward, F. Modugno, P. H. M. Peeter, J. Casagrande, M. C. Pike, R. K. Ro, A. H. Wu, A. B. Miller, M. Kumle, I. T. Gram, E. Lund, L. Mcgowan, X. O. Shu, W. Zheng, T. M. M. Farley, S. Holck, O. Meirik, H. A. Risch, Epidemiologie, RS: CAPHRI School for Public Health and Primary Care, and RS: GROW - School for Oncology and Reproduction

Subjects
hormonal factor, Oncology, body-mass index, Comorbidity, anthropometric measurement, Body Mass Index, 0302 clinical medicine, Epidemiology, Cancer Type - Ovarian Cancer, 030212 general & internal medicine, epithelial ovarian, Prospective cohort study, oral contraceptives, Ovarian Neoplasms, Incidence (epidemiology), Incidence, Smoking, Articles, Middle Aged, Adenocarcinoma, Mucinous, 3. Good health, Causality, Europe, risk-factor, Serous fluid, 030220 oncology & carcinogenesis, Meta-analysis, Adenocarcinoma, Female, Risk, Adult, medicine.medical_specialty, prospective cohort, Etiology - Exogenous Factors in the Origin and Cause of Cancer, Risk Assessment, methods, 03 medical and health sciences, Internal medicine, oral-contraceptive use, medicine, cancer, Humans, Women, tobacco smoking, therapy, cigarette-smoking, VDP::Medical disciplines: 700::Clinical medical disciplines: 750::Oncology: 762, business.industry, Research, medicine.disease, VDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Onkologi: 762, Relative risk, North America, Other, United-State, business, Ovarian cancer, Meta-Analysis
Abstract

BACKGROUND: Smoking has been linked to mucinous ovarian cancer, but its effects on other ovarian cancer subtypes and on overall ovarian cancer risk are unclear, and the findings from most studies with relevant data are unpublished. To assess these associations, we review the published and unpublished evidence. METHODS: Eligible epidemiological studies were identified by electronic searches, review articles, and discussions with colleagues. Individual participant data for 28,114 women with and 94,942 without ovarian cancer from 51 epidemiological studies were analysed centrally, yielding adjusted relative risks (RRs) of ovarian cancer in smokers compared with never smokers. FINDINGS: After exclusion of studies with hospital controls, in which smoking could have affected recruitment, overall ovarian cancer incidence was only slightly increased in current smokers compared with women who had never smoked (RR 1·06, 95% CI 1·01-1·11, p=0·01). Of 17,641 epithelial cancers with specified histology, 2314 (13%) were mucinous, 2360 (13%) endometrioid, 969 (5%) clear-cell, and 9086 (52%) serous. Smoking-related risks varied substantially across these subtypes (p(heterogeneity)

Published
2016

6. Ovarian cancer and smoking: individual participant meta-analysis including 28 114 women with ovarian cancer from 51 epidemiological studies

Author

Beral, V. Gaitskell, K. Hermon, C. Moser, K. Reeves, G. and Peto, R. Brinton, L. Marchbanks, P. Negri, E. Ness, R. Peeters, P. H. M. Vessey, M. Calle, E. E. Gapstur, S. M. Patel, A. V. Dal Maso, L. Talamini, R. Chetrit, A. and Hirsh-Yechezkel, G. Lubin, F. Sadetzki, S. Banks, E. and Bull, D. Callaghan, K. Crossley, B. Goodill, A. Green, J. Key, T. Sitas, F. Collins, R. Doll, R. Gonzalez, A. Lee, N. Ory, H. W. Peterson, H. B. Wingo, P. A. and Martin, N. Pardthaisong, T. Silpisornkosol, S. Theetranont, C. Boosiri, B. Chutivongse, S. Jimakorn, P. Virutamasen, P. Wongsrichanalai, C. Tjonneland, A. Titus-Ernstoff, L. and Byers, T. Rohan, T. Mosgaard, B. J. Yeates, D. and Freudenheim, J. L. Chang-Claude, J. Kaaks, R. Anderson, K. E. Folsom, A. Robien, K. Hampton, J. Newcomb, P. A. and Rossing, M. A. Thomas, D. B. Weiss, N. S. Riboli, E. and Clavel-Chapelon, F. Cramer, D. Hankinson, S. E. Tworoger, S. S. Franceschi, S. La Vecchia, C. Adami, H. O. Magnusson, C. Riman, T. Weiderpass, E. Wolk, A. Schouten, L. J. and van den Brandt, P. A. Chantarakul, N. Koetsawang, S. and Rachawat, D. Palli, D. Black, A. Freedman, D. M. Hartge, P. Hsing, A. W. Lacey, Jr., J. V. Hoover, R. N. and Schairer, C. Urban, M. Graff-Iversen, S. Selmer, R. and Bain, C. J. Green, A. C. Purdie, D. M. Siskind, V. Webb, P. M. Moysich, K. McCann, S. E. Hannaford, P. Kay, C. and Binns, C. W. Lee, A. H. Zhang, M. Nasca, P. Coogan, P. F. Palmer, J. R. Rosenberg, L. Kelsey, J. and Paffenbarger, R. Whittemore, A. Katsouyanni, K. and Trichopoulou, A. Trichopoulos, D. Tzonou, A. Dabancens, A. and Martinez, L. Molina, R. Salas, O. Goodman, M. T. and Lurie, G. Carney, M. E. Wilkens, L. R. Hartman, L. and Manjer, J. Olsson, H. Grisso, J. A. Morgan, M. Wheeler, J. E. Bunker, C. H. Edwards, R. P. Modugno, F. and Casagrande, J. Pike, M. C. Ross, R. K. Wu, A. H. Miller, A. B. Kumle, M. Gram, I. T. Lund, E. McGowan, L. and Shu, X. O. Zheng, W. Farley, T. M. M. Holck, S. Meirik, O. Risch, H. A. Collaborative Grp Epidemiological Natl Israeli Study Ovarian Canc Nurses Hlth Study

Abstract

Background Smoking has been linked to mucinous ovarian cancer, but its effects on other ovarian cancer subtypes and on overall ovarian cancer risk are unclear, and the findings from most studies with relevant data are unpublished. To assess these associations, we review the published and unpublished evidence. Methods Eligible epidemiological studies were identified by electronic searches, review articles, and discussions with colleagues. Individual participant data for 28 114 women with and 94 942 without ovarian cancer from 51 epidemiological studies were analysed centrally, yielding adjusted relative risks (RRs) of ovarian cancer in smokers compared with never smokers. Findings After exclusion of studies with hospital controls, in which smoking could have affected recruitment, overall ovarian cancer incidence was only slightly increased in current smokers compared with women who had never smoked (RR 1.06, 95% CI 1.01-1.11, p=0.01). Of 17 641 epithelial cancers with specified histology, 2314 (13%) were mucinous, 2360 (13%) endometrioid, 969 (5%) clear-cell, and 9086 (52%) serous. Smoking-related risks varied substantially across these subtypes (p(heterogeneity)

Published
2012

7. Ovarian Cancer and Body Size: Individual Participant Meta-Analysis Including 25,157 Women with Ovarian Cancer from 47 Epidemiological Studies

Author

Beral, V. Hermon, C. Peto, R. Reeves, G. Brinton, L. and Marchbanks, P. Negri, E. Ness, R. Peeters, P. H. M. and Vessey, M. Calle, E. E. Gapstur, S. M. Patel, A. V. Dal Maso, L. Talamini, R. Chetrit, A. Hirsh-Yechezkel, G. and Lubin, F. Sadetzki, S. Allen, N. Bull, D. Callaghan, K. and Crossley, B. Gaitskell, K. Goodill, A. Green, J. and Key, T. Moser, K. Collins, R. Doll, R. Gonzalez, C. A. and Lee, N. Ory, H. W. Peterson, H. B. Wingo, P. A. and Martin, N. Pardthaisong, T. Silpisornkosol, S. Theetranont, C. Boosiri, B. Chutivongse, S. Jimakorn, P. Virutamasen, P. Wongsrichanalai, C. Tjonneland, A. Titus-Ernstoff, L. and Byers, T. Rohan, T. Mosgaard, B. J. Yeates, D. and Freudenheim, J. L. Chang-Claude, J. Kaaks, R. Anderson, K. E. Folsom, A. Robien, K. Rossing, M. A. Thomas, D. B. and Weiss, N. S. Riboli, E. Clavel-Chapelon, F. Cramer, D. and Hankinson, S. E. Tworoger, S. S. Franceschi, S. La Vecchia, C. Magnusson, C. Riman, T. Weiderpass, E. Wolk, A. Schouten, L. J. van den Brandt, P. A. Chantarakul, N. and Koetsawang, S. Rachawat, D. Palli, D. Black, A. de Gonzalez, A. Berrington Freedman, D. M. Hartge, P. Hsing, A. W. Lacey, Jr., J. V. Hoover, R. N. Schairer, C. and Graff-Iversen, S. Selmer, R. Bain, C. J. Green, A. C. and Purdie, D. M. Siskind, V. Webb, P. M. McCann, S. E. and Hannaford, P. Kay, C. Binns, C. W. Lee, A. H. Zhang, M. and Ness, R. B. Nasca, P. Coogan, P. F. Palmer, J. R. and Rosenberg, L. Kelsey, J. Paffenbarger, R. Whittemore, A. and Katsouyanni, K. Trichopoulou, A. Trichopoulos, D. Tzonou, A. and Dabancens, A. Martinez, L. Molina, R. Salas, O. and Goodman, M. T. Lurie, G. Carney, M. E. Wilkens, L. R. and Hartman, L. Manjer, J. Olsson, H. Grisso, J. A. Morgan, M. Wheeler, J. E. Casagrande, J. Pike, M. C. Ross, R. K. and Wu, A. H. Miller, A. B. Kumle, M. Lund, E. McGowan, L. Shu, X. O. Zheng, W. Farley, T. M. M. Holck, S. and Meirik, O. Risch, H. A. Collaborative Grp Epidemiol Studie

Abstract

Background: Only about half the studies that have collected information on the relevance of women’s height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships. Methods and Findings: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p

Published
2012

8. Birth size and breast cancer risk: re-analysis of individual participant data from 32 studies

Author

Silva, IS, De Stavola, B, McCormack, V, Leon, D, Macintyre, S, Hodgson, ME, Newman, B, Sorensen, TIA, Olsen, LW, Baker, JL, Baron, JA, Newcomb, PA, Titus-Ernstoff, L, Egan, KM, Trentham-Dietz, A, Carbone, PP, Melleemkjaer, L, Sorensen, HT, Sandhu, MS, Bingham, S, Khaw, KT, Hilakivi-Clarke, L, Eriksson, J, Osmond, C, Lahmann, PH, Berglund, G, Kuh, D, Hardy, R, Mishra, G, Troisi, R, Palmer, J, Hatch, EE, Innes, K, Michels, KM, Park, SK, Brinton, LA, Garcia-Closas, M, Lissowska, J, Lissner, L, Hulthen, L, Sanderson, M, Malone, K, Daling, J, Stanford, J, Zheng, W, Shu, XO, Vatten, LJ, Nilsen, TIL, Ekbom, A, Kaijser, M, Cnattingius, S, Cade, JE, Burley, VJ, Greenwood, DC, Koupil, I, Freudenheim, JL, Nie, J, Liff, JM, and Christensen, D

Abstract

BACKGROUND: Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS: Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effects did not appear to be confounded or mediated by established breast cancer risk factors and were not modified by age or menopausal status. The cumulative incidence of breast cancer per 100 women by age 80 y in the study populations was estimated to be 10.0, 10.0, 10.4, and 11.5 in those who were, respectively, in the bottom, second, third, and top fourths of the birth length distribution. CONCLUSIONS: This pooled analysis of individual participant data is consistent with birth size, and in particular birth length, being an independent correlate of breast cancer risk in adulthood

Published
2008

9. Ovarian cancer and oral contraceptives: collaborative reanalysis of data from 45 epidemiological studies including 23 257 women with ovarian cancer and 87 303 controls

Author

Beral, V. Doll, R. Hermon, C. Peto, R. Reeves, G. and Brinton, L. Green, A. C. Marchbanks, P. Negri, E. Ness, R. Peeters, P. Vessey, M. Calle, E. E. Rodriguez, C. and Dal Maso, L. Talamini, R. Cramer, D. Hankinson, S. E. and Tworoger, S. S. Chetrit, A. Hirsh-Yechezkel, G. Lubin, F. and Sadetzki, S. Appleby, P. Banks, E. de Gonzalez, A. Berrington Bull, D. Crossley, B. Goodil, A. Green, I. and Green, J. Key, T. Collins, R. Gonzalez, C. A. Lee, N. Ory, H. W. Peterson, H. B. Wingo, P. A. Martin, N. and Pardthaisong, T. Silpisornkosol, S. Theetranont, C. and Boosiri, B. Chutivongse, S. Jimakorn, P. Virutamasen, P. and Wongsrichanalai, C. Titus-Ernstoff, L. Mosgaard, M. J. and Yeates, D. Chang-Claude, J. Rossing, M. A. Thomas, D. and Weiss, N. Franceschi, S. La Vecchia, C. Adami, H. O. and Magnusson, C. Riman, T. Weiderpass, E. Wolk, A. Brinton, L. A. Freedman, D. M. Hartge, P. Lacey, J. M. Hoover, R. and Schouten, L. J. van den Brandt, P. A. Chantarakul, N. and Koetsawang, S. Rachawat, D. Graff-Iversen, S. Selmer, R. and Bain, C. J. Green, A. C. Purdie, D. M. Siskind, V. Webb, P. M. McCann, S. E. Hannaford, P. Kay, C. Binns, C. W. and Lee, A. H. Zhang, M. Nasca, P. Coogan, P. F. Kelsey, J. Paffenbarger, R. Whittemore, A. Katsouyanni, K. and Trichopoulou, A. Trichopoulos, D. Tzonou, A. Dabancens, A. and Martinez, L. Molina, R. Salas, O. Goodman, M. T. and Laurie, G. Carney, M. E. Wilkens, L. R. Bladstrom, A. and Olsson, H. Ness, R. B. Grisso, J. A. Morgan, M. Wheeler, J. E. Peeters, P. Casagrande, J. Pike, M. C. Ross, R. K. and Wu, A. H. Kumle, M. Lund, E. McGowan, L. Shu, X. O. and Zheng, W. Farley, T. M. M. Holck, S. Meirik, O. and Risch, H. A. Collaborative Grp Epidemiological

Abstract

Background Oral contraceptives were introduced almost 50 years ago, and over 100 million women currently use them. Oral contraceptives can reduce the risk of ovarian cancer, but the eventual public-health effects of this reduction will depend on how long the protection lasts after use ceases. We aimed to assess these effects. Methods Individual data for 23 257 women with ovarian cancer (cases) and 87 303 without ovarian cancer (controls) from 45 epidemiological studies in 21 countries were checked and analysed centrally. The relative risk of ovarian cancer in relation to oral contraceptive use was estimated, stratifying by study, age, parity, and hysterectomy. Findings Overall 7308 (31%) cases and 32 717 (37%) controls had ever used oral contraceptives, for average durations among users of 4 . 4 and 5 . 0 years, respectively. The median year of cancer diagnosis was 1993, when cases were aged an average of 56 years. The longer that women had used oral contraceptives, the greater the reduction in ovarian cancer risk (p

Published
2008

10. Ovarian Cancer and Body Size : Individual Participant Meta-Analysis Including 25,157 Women with Ovarian Cancer from 47 Epidemiological Studies

Author

Beral, V., Hermon, C., Peto, R., Reeves, G., Brinton, L., Marchbanks, P., Negri, E., Ness, R., Peeters, P. H. M., Vessey, M., Calle, E. E., Gapstur, S. M., Patel, A. V., Dal Maso, L., Talamini, R., Chetrit, A., Hirsh-Yechezkel, G., Lubin, F., Sadetzki, S., Allen, N., Bull, D., Callaghan, K., Crossley, B., Gaitskell, K., Goodill, A., Green, J., Key, T., Moser, K., Collins, R., Doll, R., Gonzalez, C. A., Lee, N., Ory, H. W., Peterson, H. B., Wingo, P. A., Martin, N., Pardthaisong, T., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Tjonneland, A., Titus-Ernstoff, L., Byers, T., Rohan, T., Mosgaard, B. J., Yeates, D., Freudenheim, J. L., Chang-Claude, J., Kaaks, R., Anderson, K. E., Folsom, A., Robien, K., Rossing, M. A., Thomas, D. B., Weiss, N. S., Riboli, E., Clavel-Chapelon, F., Cramer, D., Hankinson, S. E., Tworoger, S. S., Franceschi, S., La Vecchia, C., Magnusson, C., Riman, T., Weiderpass, E., Wolk, A., Schouten, L. J., van den Brandt, P. A., Chantarakul, N., Koetsawang, S., Rachawat, D., Palli, D., Black, A., de Gonzalez, A. Berrington, Freedman, D. M., Hartge, P., Hsing, A. W., Lacey, J. V., Jr., Hoover, R. N., Schairer, C., Graff-Iversen, S., Selmer, R., Bain, C. J., Green, A. C., Purdie, D. M., Siskind, V., Webb, P. M., McCann, S. E., Hannaford, P., Kay, C., Binns, C. W., Lee, A. H., Zhang, M., Ness, R. B., Nasca, P., Coogan, P. F., Palmer, J. R., Rosenberg, L., Kelsey, J., Paffenbarger, R., Whittemore, A., Katsouyanni, K., Trichopoulou, A., Trichopoulos, D., Tzonou, A., Dabancens, A., Martinez, L., Molina, R., Salas, O., Goodman, M. T., Lurie, G., Carney, M. E., Wilkens, L. R., Hartman, L., Manjer, J., Olsson, H., Grisso, J. A., Morgan, M., Wheeler, J. E., Casagrande, J., Pike, M. C., Ross, R. K., Wu, A. H., Miller, A. B., Kumle, M., Lund, E., McGowan, L., Shu, X. O., Zheng, W., Farley, T. M. M., Holck, S., Meirik, O., Risch, H. A., Beral, V., Hermon, C., Peto, R., Reeves, G., Brinton, L., Marchbanks, P., Negri, E., Ness, R., Peeters, P. H. M., Vessey, M., Calle, E. E., Gapstur, S. M., Patel, A. V., Dal Maso, L., Talamini, R., Chetrit, A., Hirsh-Yechezkel, G., Lubin, F., Sadetzki, S., Allen, N., Bull, D., Callaghan, K., Crossley, B., Gaitskell, K., Goodill, A., Green, J., Key, T., Moser, K., Collins, R., Doll, R., Gonzalez, C. A., Lee, N., Ory, H. W., Peterson, H. B., Wingo, P. A., Martin, N., Pardthaisong, T., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Tjonneland, A., Titus-Ernstoff, L., Byers, T., Rohan, T., Mosgaard, B. J., Yeates, D., Freudenheim, J. L., Chang-Claude, J., Kaaks, R., Anderson, K. E., Folsom, A., Robien, K., Rossing, M. A., Thomas, D. B., Weiss, N. S., Riboli, E., Clavel-Chapelon, F., Cramer, D., Hankinson, S. E., Tworoger, S. S., Franceschi, S., La Vecchia, C., Magnusson, C., Riman, T., Weiderpass, E., Wolk, A., Schouten, L. J., van den Brandt, P. A., Chantarakul, N., Koetsawang, S., Rachawat, D., Palli, D., Black, A., de Gonzalez, A. Berrington, Freedman, D. M., Hartge, P., Hsing, A. W., Lacey, J. V., Jr., Hoover, R. N., Schairer, C., Graff-Iversen, S., Selmer, R., Bain, C. J., Green, A. C., Purdie, D. M., Siskind, V., Webb, P. M., McCann, S. E., Hannaford, P., Kay, C., Binns, C. W., Lee, A. H., Zhang, M., Ness, R. B., Nasca, P., Coogan, P. F., Palmer, J. R., Rosenberg, L., Kelsey, J., Paffenbarger, R., Whittemore, A., Katsouyanni, K., Trichopoulou, A., Trichopoulos, D., Tzonou, A., Dabancens, A., Martinez, L., Molina, R., Salas, O., Goodman, M. T., Lurie, G., Carney, M. E., Wilkens, L. R., Hartman, L., Manjer, J., Olsson, H., Grisso, J. A., Morgan, M., Wheeler, J. E., Casagrande, J., Pike, M. C., Ross, R. K., Wu, A. H., Miller, A. B., Kumle, M., Lund, E., McGowan, L., Shu, X. O., Zheng, W., Farley, T. M. M., Holck, S., Meirik, O., and Risch, H. A.

Abstract

Background: Only about half the studies that have collected information on the relevance of women's height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships. Methods and Findings: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p<0.001); this relationship did not vary significantly by women's age, year of birth, education, age at menarche, parity, menopausal status, smoking, alcohol consumption, having had a hysterectomy, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy. For body mass index, there was significant heterogeneity (p<0.001) in the findings between ever-users and never-users of menopausal hormone therapy, but not by the 11 other factors listed above. The relative risk for ovarian cancer per 5 kg/m(2) increase in body mass index was 1.10 (95% CI, 1.07-1.13; p<0.001) in never-users and 0.95 (95% CI, 0.92-0.99; p = 0.02) in ever-users of hormone therapy. Conclusions: Ovarian cancer is associated with height and, among never-users of hormone therapy, with body mass index. In high-income countries, both height and body mass index have been increasing in birth cohorts now developing the disease. If all other relevant factors had remained constant, then these increases in height and weight would be associated with

Published
2012
Full Text
View/download PDF

11. Validating genetic risk associations for ovarian cancer through the international Ovarian Cancer Association Consortium

Author

Pearce, C L, Near, A M, Van Den Berg, D J, Ramus, S J, Gentry-Maharaj, A, Menon, U, Gayther, S A, Anderson, A R, Edlund, C K, Wu, A H, Chen, X, Beesley, J, Webb, P M, Holt, S K, Chen, C, Doherty, J A, Rossing, M A, Whittemore, A S, McGuire, V, DiCioccio, R A, Goodman, M T, Lurie, G, Carney, M E, Wilkens, L R, Ness, R B, Moysich, K B, Edwards, R, Jennison, E, Kjær, Susanne Krüger, Hogdall, E, Hogdall, C K, Goode, E L, Sellers, T A, Vierkant, R A, Cunningham, J M, Cunningham, J C, Schildkraut, J M, Berchuck, A, Moorman, P G, Iversen, E S, Cramer, D W, Terry, K L, Vitonis, A F, Titus-Ernstoff, L, Song, H, Pharoah, P D P, Spurdle, A B, Anton-Culver, H, Ziogas, A, Brewster, W, Pearce, C L, Near, A M, Van Den Berg, D J, Ramus, S J, Gentry-Maharaj, A, Menon, U, Gayther, S A, Anderson, A R, Edlund, C K, Wu, A H, Chen, X, Beesley, J, Webb, P M, Holt, S K, Chen, C, Doherty, J A, Rossing, M A, Whittemore, A S, McGuire, V, DiCioccio, R A, Goodman, M T, Lurie, G, Carney, M E, Wilkens, L R, Ness, R B, Moysich, K B, Edwards, R, Jennison, E, Kjær, Susanne Krüger, Hogdall, E, Hogdall, C K, Goode, E L, Sellers, T A, Vierkant, R A, Cunningham, J M, Cunningham, J C, Schildkraut, J M, Berchuck, A, Moorman, P G, Iversen, E S, Cramer, D W, Terry, K L, Vitonis, A F, Titus-Ernstoff, L, Song, H, Pharoah, P D P, Spurdle, A B, Anton-Culver, H, Ziogas, A, and Brewster, W

Abstract

Udgivelsesdato: 2009-Jan-27, The search for genetic variants associated with ovarian cancer risk has focused on pathways including sex steroid hormones, DNA repair, and cell cycle control. The Ovarian Cancer Association Consortium (OCAC) identified 10 single-nucleotide polymorphisms (SNPs) in genes in these pathways, which had been genotyped by Consortium members and a pooled analysis of these data was conducted. Three of the 10 SNPs showed evidence of an association with ovarian cancer at P< or =0.10 in a log-additive model: rs2740574 in CYP3A4 (P=0.011), rs1805386 in LIG4 (P=0.007), and rs3218536 in XRCC2 (P=0.095). Additional genotyping in other OCAC studies was undertaken and only the variant in CYP3A4, rs2740574, continued to show an association in the replication data among homozygous carriers: OR(homozygous(hom))=2.50 (95% CI 0.54-11.57, P=0.24) with 1406 cases and 2827 controls. Overall, in the combined data the odds ratio was 2.81 among carriers of two copies of the minor allele (95% CI 1.20-6.56, P=0.017, p(het) across studies=0.42) with 1969 cases and 3491 controls. There was no association among heterozygous carriers. CYP3A4 encodes a key enzyme in oestrogen metabolism and our finding between rs2740574 and risk of ovarian cancer suggests that this pathway may be involved in ovarian carcinogenesis. Additional follow-up is warranted.

Published
2009

12. Validating genetic risk associations for ovarian cancer through the international Ovarian Cancer Association Consortium.

Author

Chenevix-Trench G., Gard G., Nevell D., Young B., Nattress K., Beale P., Beith J., Carter J., Dalrymple C., Hamilton A., Houghton R., Russell P., Crandon A., Cummings M., Horwood K., Obermair A., Wyld D., Nicklin J., Perrin L., Ward B., Papadimos D., Davy M., Hall C., Dodd T., Healy T., Pittman K., Henderson D., Miller J., Pierdes J., Jayde V., Blomfield P., Challis D., McIntosh R., Parker A., Brown B., Rome R., Allen D., Grant P., Hyde S., Laurie R., Robbie M., Traficante N., Fereday S., Bowes L., Phillips K., Rischin D., Waring P., Loughrey M., O'Callaghan N., Murray B., Haviv I., Billson V., Galloway S., Pyman J., Quinn M., Hammond I., McCartney A., Leung Y., Jobling T., Tran H., Pearce C.L., Near A.M., Van Den Berg D.J., Ramus S.J., Gentry-Maharaj A., Menon U., Gayther S.A., Anderson A.R., Edlund C.K., Wu A.H., Chen X., Beesley J., Webb P., Holt S.K., Chen C., Doherty J.A., Rossing M.A., Whittemore A.S., McGuire V., DiCioccio R.A., Goodman M.T., Lurie G., Carney M.E., Wilkens L.R., Ness R.B., Moysich K.B., Edwards R., Jennison E., Kjaer S.K., Hogdall E., Hogdall C.K., Goode E.L., Sellers T.A., Vierkant R.A., Cunningham J.C., Schildkraut J.M., Berchuck A., Moorman P.G., Iversen E.S., Cramer D.W., Terry K.L., Vitonis A.F., Titus-Ernstoff L., Song H., Pharoah P.D.P., Spurdle A.B., Anton-Culver H., Ziogas A., Brewster W., Galitovskiy V., Gertig D., Vanden Bergh T., Camaris C., Crouch R., Edwards L., Hacker N., Marsden D., Robertson G., DeFazio A., Hung J., Chiew Y.E., Stenlake A., Sullivan H., Brand A., Jaworski R., Harnett P., Wain G., Green A., Moore S., Harrap K., Sadkowsky T., Purdie D., Whiteman D., Alexander B., Ashover P., Brown S., Corrish T., Green L., Jackman L., Martin K., Ranieri B., White J., Mamers P., Healy D., Maniolitas T., McNealage J., Rogers P., Susil B., Veitch A., Constable J., Ping Tong S., Robinson I., Simpson I., Schmidt T., Shirley H., Viduka S., Bilic S., Glavinas L., Zeps N., Mellon A., Robertson R., Proietto A., Braye S., Otton G., Bonaventura T., Stewart J., Friedlander M., Maidens J., Bell D., Baron-Hay S., Ferrier A., Chenevix-Trench G., Gard G., Nevell D., Young B., Nattress K., Beale P., Beith J., Carter J., Dalrymple C., Hamilton A., Houghton R., Russell P., Crandon A., Cummings M., Horwood K., Obermair A., Wyld D., Nicklin J., Perrin L., Ward B., Papadimos D., Davy M., Hall C., Dodd T., Healy T., Pittman K., Henderson D., Miller J., Pierdes J., Jayde V., Blomfield P., Challis D., McIntosh R., Parker A., Brown B., Rome R., Allen D., Grant P., Hyde S., Laurie R., Robbie M., Traficante N., Fereday S., Bowes L., Phillips K., Rischin D., Waring P., Loughrey M., O'Callaghan N., Murray B., Haviv I., Billson V., Galloway S., Pyman J., Quinn M., Hammond I., McCartney A., Leung Y., Jobling T., Tran H., Pearce C.L., Near A.M., Van Den Berg D.J., Ramus S.J., Gentry-Maharaj A., Menon U., Gayther S.A., Anderson A.R., Edlund C.K., Wu A.H., Chen X., Beesley J., Webb P., Holt S.K., Chen C., Doherty J.A., Rossing M.A., Whittemore A.S., McGuire V., DiCioccio R.A., Goodman M.T., Lurie G., Carney M.E., Wilkens L.R., Ness R.B., Moysich K.B., Edwards R., Jennison E., Kjaer S.K., Hogdall E., Hogdall C.K., Goode E.L., Sellers T.A., Vierkant R.A., Cunningham J.C., Schildkraut J.M., Berchuck A., Moorman P.G., Iversen E.S., Cramer D.W., Terry K.L., Vitonis A.F., Titus-Ernstoff L., Song H., Pharoah P.D.P., Spurdle A.B., Anton-Culver H., Ziogas A., Brewster W., Galitovskiy V., Gertig D., Vanden Bergh T., Camaris C., Crouch R., Edwards L., Hacker N., Marsden D., Robertson G., DeFazio A., Hung J., Chiew Y.E., Stenlake A., Sullivan H., Brand A., Jaworski R., Harnett P., Wain G., Green A., Moore S., Harrap K., Sadkowsky T., Purdie D., Whiteman D., Alexander B., Ashover P., Brown S., Corrish T., Green L., Jackman L., Martin K., Ranieri B., White J., Mamers P., Healy D., Maniolitas T., McNealage J., Rogers P., Susil B., Veitch A., Constable J., Ping Tong S., Robinson I., Simpson I., Schmidt T., Shirley H., Viduka S., Bilic S., Glavinas L., Zeps N., Mellon A., Robertson R., Proietto A., Braye S., Otton G., Bonaventura T., Stewart J., Friedlander M., Maidens J., Bell D., Baron-Hay S., and Ferrier A.

Abstract

The search for genetic variants associated with ovarian cancer risk has focused on pathways including sex steroid hormones, DNA repair, and cell cycle control. The Ovarian Cancer Association Consortium (OCAC) identified 10 single-nucleotide polymorphisms (SNPs) in genes in these pathways, which had been genotyped by Consortium members and a pooled analysis of these data was conducted. Three of the 10 SNPs showed evidence of an association with ovarian cancer at P<=0.10 in a log-additive model: rs2740574 in CYP3A4 (P=0.011), rs1805386 in LIG4 (P=0.007), and rs3218536 in XRCC2 (P=0.095). Additional genotyping in other OCAC studies was undertaken and only the variant in CYP3A4, rs2740574, continued to show an association in the replication data among homozygous carriers: ORhomozygous(hom)=2.50 (95% CI 0.54-11.57, P=0.24) with 1406 cases and 2827 controls. Overall, in the combined data the odds ratio was 2.81 among carriers of two copies of the minor allele (95% CI 1.20-6.56, P=0.017, phet across studies=0.42) with 1969 cases and 3491 controls. There was no association among heterozygous carriers. CYP3A4 encodes a key enzyme in oestrogen metabolism and our finding between rs2740574 and risk of ovarian cancer suggests that this pathway may be involved in ovarian carcinogenesis. Additional follow-up is warranted. © 2009 Cancer Research UK.

Published
2009

13. Influence of movie smoking exposure and team sports participation on established smoking

Author

Adachi-Mejia, AM, Primack, BA, Beach, ML, Titus-Ernstoff, L, Longacre, MR, Weiss, JE, Dalton, MA, Adachi-Mejia, AM, Primack, BA, Beach, ML, Titus-Ernstoff, L, Longacre, MR, Weiss, JE, and Dalton, MA

Abstract

Objective: To examine the joint effects of movie smoking exposure and team sports participation on established smoking. Design: Longitudinal study. Setting: School- and telephone-based surveys in New Hampshire and Vermont between September 1999 through November 1999 and February 2006 through February 2007. Participants: A total of 2048 youths aged 16 to 21 years at follow-up. Main Exposures: Baseline movie smoking exposure categorized in quartiles assessed when respondents were aged 9 to 14 years and team sports participation assessed when respondents were aged 16 to 21 years. Main Outcome Measure: Established smoking (having smoked ≥100 cigarettes in one's lifetime) at follow-up. Results: At follow-up, 353 respondents (17.2%) were established smokers. Exposure to the highest quartile of movie smoking compared with the lowest increased the likelihood of established smoking (odds ratio=1.63; 95% confidence interval, 1.03-2.57), and team sports nonparticipants compared with participants were twice as likely to be established smokers (odds ratio=2.01; 95% confidence interval, 1.47-2.74). The joint effects of movie smoking exposure and team sports participation revealed that at each quartile of movie smoking exposure, the odds of established smoking were greater for team sports nonparticipants than for participants. We saw a dose-response relationship of movie smoking exposure for established smoking only among team sports participants. Conclusions: Team sports participation clearly plays a protective role against established smoking, even in the face of exposure to movie smoking. However, movie smoking exposure increases the risk of established smoking among both team sports participants and nonparticipants. Parents, teachers, coaches, and clinicians should be aware that encouraging team sports participation in tandem with minimizing early exposure to movie smoking may offer the greatest likelihood of preventing youth smoking. ©2009 American Medical Association. All ri

Published
2009

16. Sun exposure and melanoma risk at different latitudes: a pooled analysis of 5700 cases and 7216 controls

Author

Chang, Y.-m., primary, Barrett, J. H., additional, Bishop, D. T., additional, Armstrong, B. K., additional, Bataille, V., additional, Bergman, W., additional, Berwick, M., additional, Bracci, P. M., additional, Elwood, J. M., additional, Ernstoff, M. S., additional, Gallagher, R. P., additional, Green, A. C., additional, Gruis, N. A., additional, Holly, E. A., additional, Ingvar, C., additional, Kanetsky, P. A., additional, Karagas, M. R., additional, Lee, T. K., additional, Le Marchand, L., additional, Mackie, R. M., additional, Olsson, H., additional, Osterlind, A., additional, Rebbeck, T. R., additional, Sasieni, P., additional, Siskind, V., additional, Swerdlow, A. J., additional, Titus-Ernstoff, L., additional, Zens, M. S., additional, and Newton-Bishop, J. A., additional

Published
2009
Full Text
View/download PDF

22. Age at Natural Menopause in Women Exposed to Diethylstilbestrol in Utero

Author

Hatch, E, primary, Troisi, R, additional, Wise, L, additional, Hyer, M, additional, Palmer, J, additional, Titus-Ernstoff, L, additional, Strohsnitter, W, additional, Kaufmann, R, additional, Adam, E, additional, Noller, K, additional, Herbst, A, additional, Robboy, S, additional, Hartge, P, additional, and Hoover, R, additional

Published
2006
Full Text
View/download PDF

24. Mortality in women given diethylstilbestrol during pregnancy

Author

Titus-Ernstoff, L, primary, Troisi, R, additional, Hatch, E E, additional, Palmer, J R, additional, Wise, L A, additional, Ricker, W, additional, Hyer, M, additional, Kaufman, R, additional, Noller, K, additional, Strohsnitter, W, additional, Herbst, A L, additional, Hartge, P, additional, and Hoover, R N, additional

Published
2006
Full Text
View/download PDF

29. Birth weight and breast cancer risk

Author

Troisi, R, primary, Hatch, E E, additional, Titus-Ernstoff, L, additional, Palmer, J R, additional, Hyer, M, additional, Strohsnitter, W C, additional, Robboy, S J, additional, Kaufman, R, additional, Herbst, A, additional, Adam, E, additional, and Hoover, R N, additional

Published
2006
Full Text
View/download PDF

34. Cancer Risk in Men Exposed In Utero to Diethylstilbestrol

Author

Strohsnitter, W. C., primary, Noller, K. L., additional, Hoover, R. N., additional, Robboy, S. J., additional, Palmer, J. R., additional, Titus-Ernstoff, L., additional, Kaufman, R. H., additional, Adam, E., additional, Herbst, A. L., additional, and Hatch, E. E., additional

Published
2001
Full Text
View/download PDF

37. Age at Any Full-term Pregnancy and Breast Cancer Risk

Author

Chie, W.-C., primary, Hsieh, C.-c., additional, Newcomb, P. A., additional, Longnecker, M. P, additional, Mittendorf, R., additional, Greenberg, E. R., additional, Clapp, R. W., additional, Burke, K. P., additional, Titus-Ernstoff, L., additional, Trentham-Dietz, A., additional, and MacMahon, B., additional

Published
2000
Full Text
View/download PDF

43. Metabolic disorders and breast cancer risk (United States).

Author

Baron, John, Weiderpass, Elisabete, Newcomb, Polly, Stampfer, Meir, Titus-Ernstoff, Linda, Egan, Kathleen, Greenberg, E., Baron, J A, Weiderpass, E, Newcomb, P A, Stampfer, M, Titus-Ernstoff, L, Egan, K M, and Greenberg, E R

Abstract

Objective: To clarify the hormonal context of breast cancer etiology we used data from a large, population-based case-control study to investigate the relationship between breast cancer risk and a history of diabetes mellitus, disorders associated with estrogen stimulation (uterine fibroids, endometriosis, gallstones), and disorders associated with androgen stimulation (acne, hirsutism, and polycystic ovaries).Methods: Breast cancer patients between 50 and 75 years old were identified from state-wide tumor registries in Wisconsin, Massachusetts, and New Hampshire; controls were randomly selected from drivers' license lists (age less than 65) or Medicare enrollment files (age 65-74). Information on reproductive history, medical history, and personal habits was obtained by telephone interview. A total of 5659 cases and 5928 controls were interviewed and provided suitable data.Results: There was no overall association between breast cancer risk and reported history of diabetes mellitus, endometriosis, uterine fibroids, gallstones, or cholecystectomy. However, the disorders with androgenic associations all conferred an increased risk: the overall odds ratio (OR) for a history of acne was 1.4 (95% CI 1.0-1.9), that for hirsutism was 1.2 (95% CI 0.81-1.8), and that for polycystic ovaries 1.6 (95% CI 0.8-3.2). Diabetes mellitus diagnosed before age 35 conferred an odds ratio of 0.52 (95% 0.25-1.1), while diabetes diagnosed at a later age was associated with an increased risk (OR = 1.2, 95% CI 1.0-1.4).Conclusions: Androgen-related phenomena are likely to be important in the etiology of breast cancer. [ABSTRACT FROM AUTHOR]

Published
2001
Full Text
View/download PDF

45. Weight change and risk of postmenopausal breast cancer (United States).

Author

Trentham-Dietz, Amy, Newcomb, Polly, Egan, Kathleen, Titus-Ernstoff, Linda, Baron, John, Storer, Barry, Stampfer, Meir, Willett, Walter, Trentham-Dietz, A, Newcomb, P A, Egan, K M, Titus-Ernstoff, L, Baron, J A, Storer, B E, Stampfer, M, and Willett, W C

Subjects
OBESITY complications, BREAST tumors, COMPARATIVE studies, RESEARCH methodology, MEDICAL cooperation, RESEARCH, RESEARCH evaluation, RESEARCH funding, STATURE, WEIGHT loss, WEIGHT gain, LOGISTIC regression analysis, EVALUATION research, BODY mass index, DISEASE incidence, POSTMENOPAUSE, ODDS ratio
Abstract

Objective: Although many studies have shown that higher weight increases the risk of postmenopausal breast cancer, some aspects of this association are unclear. In order to examine the risk associated with different patterns of weight change, we analyzed data from a large case-control study of postmenopausal breast cancer.Methods: Participants included women aged 50 79 years (n = 5031) who are newly diagnosed with invasive breast cancer in Massachusetts, New Hampshire, and Wisconsin. Similarly-aged population controls (n = 5255) were selected at random from driver's license files and Medicare beneficiary lists. Height, weight, and information on other breast cancer risk factors were ascertained by structured telephone interviews from 1992 to 1995, and logistic regression was used to estimate multivariable-adjusted odds ratios (OR) and 95% confidence intervals (CI).Results: Women in the top quintile groups for height at age 20, recent weight, and recent body mass index had significantly increased risks of breast cancer. Among women who reached their highest adult weight at younger ages (<45 years), increasing weight loss since that age was associated with a reduced risk of postmenopausal breast cancer (OR 0.90, CI 0.84 0.98, per 5 kg). However, weight loss among women whose highest weight occurred after age 45 was not associated with risk (OR 1.00, CI 0.95 1.05, per 5 kg). Weight gain since the lowest adult weight increased risk by 8% for each 5 kg of gain (OR 1.08, CI 1.06-1. 11). Temporary weight cycling (weight loss followed by weight gain) was not associated with increased risk.Conclusions: Weight gain clearly increased risk of postmenopausal breast cancer. These data lend further support to efforts aimed at helping women avoid weight gain as they age. [ABSTRACT FROM AUTHOR]

Published
2000
Full Text
View/download PDF

46. Left-handedness in relation to breast cancer risk in postmenopausal women.

Author

Titus-Ernstoff, Linda, Newcomb, Polly A., Egan, Kathleen M., Baron, John A., Greenberg, E. Robert, Trichopoulos, Dimitrios, Willett, Walter C., Stampfer, Meir J., Titus-Ernstoff, L, Newcomb, P A, Egan, K M, Baron, J A, Greenberg, E R, Trichopoulos, D, Willett, W C, and Stampfer, M J

Published
2000

47. The relation of breast size to breast cancer risk in postmenopausal women (United States).

Author

Egan, Kathleen, Newcomb, Polly, Titus-Ernstoff, Linda, Trentham-Dietz, Amy, Baron, John, Willett, Walter, Stampfer, Meir, Trichopoulos, Dimitrios, Egan, K M, Newcomb, P A, Titus-Ernstoff, L, Trentham-Dietz, A, Baron, J A, Willett, W C, Stampfer, M J, and Trichopoulos, D

Abstract

Objective: Breast size has been hypothesized to predict a woman's risk of breast cancer although studies in the main have not supported an association. In a large, population-based case-control study we examined whether breast size might emerge as a significant risk factor among very lean women in whom breast size might be a truer reflection of the volume of gland mass at risk for malignant change.Methods: The data derive from a population-based case-control study of women aged 50 to 79 years conducted in several New England states and Wisconsin. Incident cases of invasive breast cancer (n = 2015) were identified through state tumor registries and controls (n = 2556) were selected at random within age strata from population lists. Telephone interviews were conducted to obtain information on known and suspected risk factors which included bra dimensions (cup and back size) prior to a first birth, or at the age of 20 for nulliparous women.Results: We observed a significant positive association for cup size which was limited to women who were the most lean as young adults based on chest circumference. Among those reporting a chest size under 34 inches multivariate-adjusted relative risks were 1.34 (95% CI: 1.04 to 1.74) for cup size B, and 1.76 (95% CI: 1.04 to 3.01) for cup size C and larger, compared to a cup size smaller than B, and the trend for increasing cup size was statistically significant (P = 0.005). There was no relation with breast size among women reporting an average or larger back circumference (34 inches or larger).Conclusion: Breast size before a pregnancy is a positive predictor of postmenopausal breast cancer, but this association is limited to those who were especially lean as young women. [ABSTRACT FROM AUTHOR]

Published
1999
Full Text
View/download PDF

48. The accuracy of skin self-examination for atypical nevi.

Author

Titus-Ernstoff, Linda, Thörn, Magnus, Tosteson, Tor D., Brahme, Eva Månsson, Yuen, Jonathan, Baron, John A., Adami, Hans-Olov, Titus-Ernstoff, L, Thörn, M, Tosteson, T D, Brahme, E M, Yuen, J, Baron, J A, and Adami, H O

Published
1996

50. Telomere Length and Genetic Variation in Telomere Maintenance Genes in Relation to Ovarian Cancer Risk

Author

Terry, Kathryn Lynne, Tworoger, Shelley Slate, Vitonis, A. F., Wong, Jason, Titus-Ernstoff, L., De Vivo, Immaculata, and Cramer, Daniel William

Subjects
telomeres, ovarian cancer, polymorphisms, TERT
Abstract

Background Telomeres protect chromosomal ends, shorten with cellular division, and signal cellular senescence but unchecked telomere attrition can lead to telomere dysfunction, upregulation of telomerase, and carcinogenesis. Shorter telomeres in peripheral blood leukocytes (PBLs) have been associated with elevated cancer risk. Further, genetic variants in and around the TERT gene have been implicated in carcinogenesis. Methods We measured relative telomere length (RTL) in PBLs of 911 cases and 948 controls from the New England Case Control Study, a population-based study of ovarian cancer. In addition, we assessed germline genetic variation in five telomere maintenance genes among 2112 cases and 2456 controls from the New England Case Control Study and the Nurses’ Health Study, a prospective cohort study. Odds ratios and 95% confidence intervals were estimated using logistic regression. Results Overall, we observed no differences in telomere length between cases and controls. Compared to women with RTL in the longest tertile, women with RTL in the shortest tertile had no increase in risk (OR=1.01, 95% CI: 0.80, 1.28). However, several SNPs in the TERT gene, including RS2736122, RS4246742, RS4975605, RS10069690, RS2736100, RS2853676, RS7726159, were significantly associated with ovarian cancer risk. We observed a significant gene-level association between TERT and ovarian cancer risk (p=0.00008). Conclusion Our observations suggest genetic variation in the TERT gene may influence ovarian cancer risk, but the association between average telomere length in PBLs and ovarian cancer remains unclear. Impact The role of telomeres in ovarian carcinogenesis remains unsettled and warrants further investigation.

Published
2012
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results