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1. Carotenoids, retinol, tocopherols, and prostate cancer risk: pooled analysis of 15 studies 1–3

Author

Key, Timothy J, Appleby, Paul N, Travis, Ruth C, Albanes, Demetrius, Alberg, Anthony J, Barricarte, Aurelio, Black, Amanda, Boeing, Heiner, Bueno-de-Mesquita, H Bas, Chan, June M, Chen, Chu, Cook, Michael B, Donovan, Jenny L, Galan, Pilar, Gilbert, Rebecca, Giles, Graham G, Giovannucci, Edward, Goodman, Gary E, Goodman, Phyllis J, Gunter, Marc J, Hamdy, Freddie C, Heliövaara, Markku, Helzlsouer, Kathy J, Henderson, Brian E, Hercberg, Serge, Hoffman-Bolton, Judy, Hoover, Robert N, Johansson, Mattias, Khaw, Kay-Tee, King, Irena B, Knekt, Paul, Kolonel, Laurence N, Le Marchand, Loic, Männistö, Satu, Martin, Richard M, Meyer, Haakon E, Mondul, Alison M, Moy, Kristin A, Neal, David E, Neuhouser, Marian L, Palli, Domenico, Platz, Elizabeth A, Pouchieu, Camille, Rissanen, Harri, Schenk, Jeannette M, Severi, Gianluca, Stampfer, Meir J, Tjønneland, Anne, Touvier, Mathilde, Trichopoulou, Antonia, Weinstein, Stephanie J, Ziegler, Regina G, Zhou, Cindy Ke, Allen, Naomi E, Biomarkers, Endogenous Hormones Nutritional, and Group, Prostate Cancer Collaborative

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prevention, Urologic Diseases, Nutrition, Prostate Cancer, Cancer, Aging, Clinical Research, Adult, Biomarkers, Carotenoids, Case-Control Studies, Cohort Studies, Cross-Sectional Studies, Humans, Lycopene, Male, Meta-Analysis as Topic, Middle Aged, Neoplasm Grading, Neoplasm Staging, Observational Studies as Topic, Prospective Studies, Prostate, Prostatic Neoplasms, Risk Factors, Vitamin A, alpha-Tocopherol, prostate cancer, carotenoids, retinol, tocopherols, vitamin E, vitamin A, pooled analysis, nested case-control study, biomarkers, Endogenous Hormones Nutritional Biomarkers Prostate Cancer Collaborative Group, Engineering, Medical and Health Sciences, Nutrition & Dietetics, Clinical sciences, Nutrition and dietetics
Abstract

BackgroundIndividual studies have suggested that circulating carotenoids, retinol, or tocopherols may be associated with prostate cancer risk, but the studies have not been large enough to provide precise estimates of associations, particularly by stage and grade of disease.ObjectiveThe objective of this study was to conduct a pooled analysis of the associations of the concentrations of 7 carotenoids, retinol, α-tocopherol, and γ-tocopherol with risk of prostate cancer and to describe whether any associations differ by stage or grade of the disease or other factors.DesignPrincipal investigators of prospective studies provided individual participant data for prostate cancer cases and controls. Risk by study-specific fifths of each biomarker was estimated by using multivariable-adjusted conditional logistic regression in matched case-control sets.ResultsData were available for up to 11,239 cases (including 1654 advanced stage and 1741 aggressive) and 18,541 controls from 15 studies. Lycopene was not associated with overall risk of prostate cancer, but there was statistically significant heterogeneity by stage of disease, and the OR for aggressive disease for the highest compared with the lowest fifth of lycopene was 0.65 (95% CI: 0.46, 0.91; P-trend = 0.032). No other carotenoid was significantly associated with overall risk of prostate cancer or with risk of advanced-stage or aggressive disease. For retinol, the OR for the highest compared with the lowest fifth was 1.13 (95% CI: 1.04, 1.22; P-trend = 0.015). For α-tocopherol, the OR for the highest compared with the lowest fifth was 0.86 (95% CI: 0.78, 0.94; P-trend < 0.001), with significant heterogeneity by stage of disease; the OR for aggressive prostate cancer was 0.74 (95% CI: 0.59, 0.92; P-trend = 0.001). γ-Tocopherol was not associated with risk.ConclusionsOverall prostate cancer risk was positively associated with retinol and inversely associated with α-tocopherol, and risk of aggressive prostate cancer was inversely associated with lycopene and α-tocopherol. Whether these associations reflect causal relations is unclear.

Published
2015

2. Data from The Premenopausal Breast Cancer Collaboration: A Pooling Project of Studies Participating in the National Cancer Institute Cohort Consortium

Author

Nichols, Hazel B., primary, Schoemaker, Minouk J., primary, Wright, Lauren B., primary, McGowan, Craig, primary, Brook, Mark N., primary, McClain, Kathleen M., primary, Jones, Michael E., primary, Adami, Hans-Olov, primary, Agnoli, Claudia, primary, Baglietto, Laura, primary, Bernstein, Leslie, primary, Bertrand, Kimberly A., primary, Blot, William J., primary, Boutron-Ruault, Marie-Christine, primary, Butler, Lesley, primary, Chen, Yu, primary, Doody, Michele M., primary, Dossus, Laure, primary, Eliassen, A. Heather, primary, Giles, Graham G., primary, Gram, Inger T., primary, Hankinson, Susan E., primary, Hoffman-Bolton, Judy, primary, Kaaks, Rudolf, primary, Key, Timothy J., primary, Kirsh, Victoria A., primary, Kitahara, Cari M., primary, Koh, Woon-Puay, primary, Larsson, Susanna C., primary, Lund, Eiliv, primary, Ma, Huiyan, primary, Merritt, Melissa A., primary, Milne, Roger L., primary, Navarro, Carmen, primary, Overvad, Kim, primary, Ozasa, Kotaro, primary, Palmer, Julie R., primary, Peeters, Petra H., primary, Riboli, Elio, primary, Rohan, Thomas E., primary, Sadakane, Atsuko, primary, Sund, Malin, primary, Tamimi, Rulla M., primary, Trichopoulou, Antonia, primary, Vatten, Lars, primary, Visvanathan, Kala, primary, Weiderpass, Elisabete, primary, Willett, Walter C., primary, Wolk, Alicja, primary, Zeleniuch-Jacquotte, Anne, primary, Zheng, Wei, primary, Sandler, Dale P., primary, and Swerdlow, Anthony J., primary

Published
2023
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3. Table S1 from The Premenopausal Breast Cancer Collaboration: A Pooling Project of Studies Participating in the National Cancer Institute Cohort Consortium

Author

Nichols, Hazel B., primary, Schoemaker, Minouk J., primary, Wright, Lauren B., primary, McGowan, Craig, primary, Brook, Mark N., primary, McClain, Kathleen M., primary, Jones, Michael E., primary, Adami, Hans-Olov, primary, Agnoli, Claudia, primary, Baglietto, Laura, primary, Bernstein, Leslie, primary, Bertrand, Kimberly A., primary, Blot, William J., primary, Boutron-Ruault, Marie-Christine, primary, Butler, Lesley, primary, Chen, Yu, primary, Doody, Michele M., primary, Dossus, Laure, primary, Eliassen, A. Heather, primary, Giles, Graham G., primary, Gram, Inger T., primary, Hankinson, Susan E., primary, Hoffman-Bolton, Judy, primary, Kaaks, Rudolf, primary, Key, Timothy J., primary, Kirsh, Victoria A., primary, Kitahara, Cari M., primary, Koh, Woon-Puay, primary, Larsson, Susanna C., primary, Lund, Eiliv, primary, Ma, Huiyan, primary, Merritt, Melissa A., primary, Milne, Roger L., primary, Navarro, Carmen, primary, Overvad, Kim, primary, Ozasa, Kotaro, primary, Palmer, Julie R., primary, Peeters, Petra H., primary, Riboli, Elio, primary, Rohan, Thomas E., primary, Sadakane, Atsuko, primary, Sund, Malin, primary, Tamimi, Rulla M., primary, Trichopoulou, Antonia, primary, Vatten, Lars, primary, Visvanathan, Kala, primary, Weiderpass, Elisabete, primary, Willett, Walter C., primary, Wolk, Alicja, primary, Zeleniuch-Jacquotte, Anne, primary, Zheng, Wei, primary, Sandler, Dale P., primary, and Swerdlow, Anthony J., primary

Published
2023
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5. Carotenoids, retinol, tocopherols, and prostate cancer risk: pooled analysis of 15 studies1-3

Author

Key, Timothy J, Appleby, Paul N, Travis, Ruth C, Albanes, Demetrius, Alberg, Anthony J, Barricarte, Aurelio, Black, Amanda, Boeing, Heiner, Bueno-de-Mesquita, H Bas, Chan, June M, Chen, Chu, Cook, Michael B, Donovan, Jenny L, Galan, Pilar, Gilbert, Rebecca, Giles, Graham G, Giovannucci, Edward, Goodman, Gary E, Goodman, Phyllis J, Gunter, Marc J, Hamdy, Freddie C, Heliövaara, Markku, Helzlsouer, Kathy J, Henderson, Brian E, Hercberg, Serge, Hoffman-Bolton, Judy, Hoover, Robert N, Johansson, Mattias, Khaw, Kay-Tee, King, Irena B, Knekt, Paul, Kolonel, Laurence N, Le Marchand, Loic, Männistö, Satu, Martin, Richard M, Meyer, Haakon E, Mondul, Alison M, Moy, Kristin A, Neal, David E, Neuhouser, Marian L, Palli, Domenico, Platz, Elizabeth A, Pouchieu, Camille, Rissanen, Harri, Schenk, Jeannette M, Severi, Gianluca, Stampfer, Meir J, Tjønneland, Anne, Touvier, Mathilde, Trichopoulou, Antonia, Weinstein, Stephanie J, Ziegler, Regina G, Zhou, Cindy Ke, Allen, Naomi E, and Biomarkers, Nutritional

Published
2015

6. Circulating Carotenoids and Risk of Breast Cancer: Pooled Analysis of Eight Prospective Studies

Author

Eliassen, A. Heather, Hendrickson, Sara J., Brinton, Louise A., Buring, Julie E., Campos, Hannia, Dai, Qi, Dorgan, Joanne F., Franke, Adrian A., Gao, Yu-tang, Goodman, Marc T., Hallmans, Göran, Helzlsouer, Kathy J., Hoffman-Bolton, Judy, Hultén, Kerstin, Sesso, Howard D., Sowell, Anne L., Tamimi, Rulla M., Toniolo, Paolo, Wilkens, Lynne R., Winkvist, Anna, Zeleniuch-Jacquotte, Anne, Zheng, Wei, and Hankinson, Susan E.

Published
2012
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7. Breast Cancer Risk After Recent Childbirth

Author

Nichols, Hazel B., primary, Schoemaker, Minouk J., additional, Cai, Jianwen, additional, Xu, Jiawei, additional, Wright, Lauren B., additional, Brook, Mark N., additional, Jones, Michael E., additional, Adami, Hans-Olov, additional, Baglietto, Laura, additional, Bertrand, Kimberly A., additional, Blot, William J., additional, Boutron-Ruault, Marie-Christine, additional, Dorronsoro, Miren, additional, Dossus, Laure, additional, Eliassen, A. Heather, additional, Giles, Graham G., additional, Gram, Inger T., additional, Hankinson, Susan E., additional, Hoffman-Bolton, Judy, additional, Kaaks, Rudolf, additional, Key, Timothy J., additional, Kitahara, Cari M., additional, Larsson, Susanna C., additional, Linet, Martha, additional, Merritt, Melissa A., additional, Milne, Roger L., additional, Pala, Valeria, additional, Palmer, Julie R., additional, Peeters, Petra H., additional, Riboli, Elio, additional, Sund, Malin, additional, Tamimi, Rulla M., additional, Tjønneland, Anne, additional, Trichopoulou, Antonia, additional, Ursin, Giske, additional, Vatten, Lars, additional, Visvanathan, Kala, additional, Weiderpass, Elisabete, additional, Wolk, Alicja, additional, Zheng, Wei, additional, Weinberg, Clarice R., additional, Swerdlow, Anthony J., additional, and Sandler, Dale P., additional

Published
2018
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8. Association of Variants in Genes Related to the Immune Response and Obesity with Benign Prostatic Hyperplasia in CLUE II

Author

Lopez, David S., Peskoe, Sarah B., Tsilidis, Konstantinos K., Hoffman-Bolton, Judy, Helzlsouer, Kathy J., Isaacs, William B., Smith, Michael W., and Platz, Elizabeth A.

Subjects
Male, benign prostatic hyperplasia, Genotype, urogenital system, Immunity, Prostatic Hyperplasia, Middle Aged, urologic and male genital diseases, Polymerase Chain Reaction, Polymorphism, Single Nucleotide, Article, Odds Ratio, Humans, Obesity, genes, risk, Aged
Abstract

BACKGROUND Chronic inflammation and obesity may contribute to the genesis or progression of benign prostatic hyperplasia (BPH) and BPH-associated lower urinary tract symptoms (LUTS). The influence of variants in genes related to these states on BPH has not been studied extensively. Thus, we evaluated the association of 17 single nucleotide polymorphisms (SNPs) in immune response genes (IL1B, IL6, IL8, IL10, TNF, CRP, TLR4, RNASEL) and genes involved in obesity, including insulin regulation (LEP, ADIPOQ, PPARG, TCF7L2), with BPH. METHODS BPH cases (N=568) and age-frequency matched controls (N=568) were selected from among adult male CLUE II cohort participants who responded in 2000 to a mailed questionnaire. BPH was defined as BPH surgery, use of BPH medications, or symptomatic BPH (American Urological Association Symptom Index Score ≥15). Controls were men who had not had BPH surgery, did not use BPH medications, and whose symptom score was ≤7. Age-adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression. RESULTS None of the candidate SNPs was statistically significantly associated with BPH. However, we could not rule out possible weak associations for CRP rs1205 (1082C>T), ADIPOQ rs1501299 (276C>A), PPARG rs1801282 (-49C>G), and TCF7L2 rs7903146 (47833T>C). After summing risk alleles, men with ≥4 had an increased BPH risk compared with those with ≤1 (OR, 1.78; 95% CI, 1.10-2.89; Ptrend=0.006). CONCLUSION SNPs in genes related to immune response and obesity, especially in combination, may be associated with BPH.

Published
2014

9. Carotenoids, retinol, tocopherols, and prostate cancer risk: pooled analysis of 15 studies

Author

Key, Timothy J, Appleby, Paul N, Travis, Ruth C, Albanes, Demetrius, Alberg, Anthony J, Barricarte, Aurelio, Black, Amanda, Boeing, Heiner, Bueno-de-Mesquita, H Bas, Chan, June M, Chen, Chu, Cook, Michael B, Donovan, Jenny L, Galan, Pilar, Gilbert, Rebecca, Giles, Graham G, Giovannucci, Edward, Goodman, Gary E, Goodman, Phyllis J, Gunter, Marc J, Hamdy, Freddie C, Heliövaara, Markku, Helzlsouer, Kathy J, Henderson, Brian E, Hercberg, Serge, Hoffman-Bolton, Judy, Hoover, Robert N, Johansson, Mattias, Khaw, Kay-Tee, King, Irena B, Knekt, Paul, Kolonel, Laurence N, Le Marchand, Loic, Männistö, Satu, Martin, Richard M, Meyer, Haakon E, Mondul, Alison M, Moy, Kristin A, Neal, David E, Neuhouser, Marian L, Palli, Domenico, Platz, Elizabeth A, Pouchieu, Camille, Rissanen, Harri, Schenk, Jeannette M, Severi, Gianluca, Stampfer, Meir J, Tjønneland, Anne, Touvier, Mathilde, Trichopoulou, Antonia, Weinstein, Stephanie J, Ziegler, Regina G, Zhou, Cindy Ke, Allen, Naomi E, and Endogenous Hormones Nutritional Biomarkers Prostate Cancer Collaborative Group

Subjects
Adult, Male, Urologic Diseases, Aging, alpha-Tocopherol, vitamin E, Medical and Health Sciences, vitamin A, Cohort Studies, Lycopene, Engineering, Meta-Analysis as Topic, nested case-control study, Risk Factors, Clinical Research, Humans, Prospective Studies, Neoplasm Staging, Cancer, Nutrition, Endogenous Hormones Nutritional Biomarkers Prostate Cancer Collaborative Group, Nutrition & Dietetics, Prostate Cancer, Prevention, Prostate, carotenoids, Prostatic Neoplasms, biomarkers, Middle Aged, Observational Studies as Topic, Cross-Sectional Studies, Case-Control Studies, Neoplasm Grading, pooled analysis, tocopherols, retinol
Abstract

BackgroundIndividual studies have suggested that circulating carotenoids, retinol, or tocopherols may be associated with prostate cancer risk, but the studies have not been large enough to provide precise estimates of associations, particularly by stage and grade of disease.ObjectiveThe objective of this study was to conduct a pooled analysis of the associations of the concentrations of 7 carotenoids, retinol, α-tocopherol, and γ-tocopherol with risk of prostate cancer and to describe whether any associations differ by stage or grade of the disease or other factors.DesignPrincipal investigators of prospective studies provided individual participant data for prostate cancer cases and controls. Risk by study-specific fifths of each biomarker was estimated by using multivariable-adjusted conditional logistic regression in matched case-control sets.ResultsData were available for up to 11,239 cases (including 1654 advanced stage and 1741 aggressive) and 18,541 controls from 15 studies. Lycopene was not associated with overall risk of prostate cancer, but there was statistically significant heterogeneity by stage of disease, and the OR for aggressive disease for the highest compared with the lowest fifth of lycopene was 0.65 (95% CI: 0.46, 0.91; P-trend = 0.032). No other carotenoid was significantly associated with overall risk of prostate cancer or with risk of advanced-stage or aggressive disease. For retinol, the OR for the highest compared with the lowest fifth was 1.13 (95% CI: 1.04, 1.22; P-trend = 0.015). For α-tocopherol, the OR for the highest compared with the lowest fifth was 0.86 (95% CI: 0.78, 0.94; P-trend < 0.001), with significant heterogeneity by stage of disease; the OR for aggressive prostate cancer was 0.74 (95% CI: 0.59, 0.92; P-trend = 0.001). γ-Tocopherol was not associated with risk.ConclusionsOverall prostate cancer risk was positively associated with retinol and inversely associated with α-tocopherol, and risk of aggressive prostate cancer was inversely associated with lycopene and α-tocopherol. Whether these associations reflect causal relations is unclear.

Published
2015

10. The Premenopausal Breast Cancer Collaboration: A Pooling Project of Studies Participating in the National Cancer Institute Cohort Consortium

Author

Nichols, Hazel B., primary, Schoemaker, Minouk J., additional, Wright, Lauren B., additional, McGowan, Craig, additional, Brook, Mark N., additional, McClain, Kathleen M., additional, Jones, Michael E., additional, Adami, Hans-Olov, additional, Agnoli, Claudia, additional, Baglietto, Laura, additional, Bernstein, Leslie, additional, Bertrand, Kimberly A., additional, Blot, William J., additional, Boutron-Ruault, Marie-Christine, additional, Butler, Lesley, additional, Chen, Yu, additional, Doody, Michele M., additional, Dossus, Laure, additional, Eliassen, A. Heather, additional, Giles, Graham G., additional, Gram, Inger T., additional, Hankinson, Susan E., additional, Hoffman-Bolton, Judy, additional, Kaaks, Rudolf, additional, Key, Timothy J., additional, Kirsh, Victoria A., additional, Kitahara, Cari M., additional, Koh, Woon-Puay, additional, Larsson, Susanna C., additional, Lund, Eiliv, additional, Ma, Huiyan, additional, Merritt, Melissa A., additional, Milne, Roger L., additional, Navarro, Carmen, additional, Overvad, Kim, additional, Ozasa, Kotaro, additional, Palmer, Julie R., additional, Peeters, Petra H., additional, Riboli, Elio, additional, Rohan, Thomas E., additional, Sadakane, Atsuko, additional, Sund, Malin, additional, Tamimi, Rulla M., additional, Trichopoulou, Antonia, additional, Vatten, Lars, additional, Visvanathan, Kala, additional, Weiderpass, Elisabete, additional, Willett, Walter C., additional, Wolk, Alicja, additional, Zeleniuch-Jacquotte, Anne, additional, Zheng, Wei, additional, Sandler, Dale P., additional, and Swerdlow, Anthony J., additional

Published
2017
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11. A genetic variant nearGATA3implicated in inherited susceptibility and etiology of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS)

Author

Na, Rong, primary, Helfand, Brian T., additional, Chen, Haitao, additional, Conran, Carly A., additional, Crawford, Susan E., additional, Hayward, Simon W., additional, Tammela, Teuvo L.J., additional, Hoffman-Bolton, Judy, additional, Zheng, Siqun L., additional, Walsh, Patrick C., additional, Schleutker, Johanna, additional, Platz, Elizabeth A., additional, Isaacs, William B., additional, and Xu, Jianfeng, additional

Published
2017
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12. Breast Cancer Risk After Recent Childbirth: A Pooled Analysis of 15 Prospective Studies.

Author

Nichols, Hazel B., Schoemaker, Minouk J., Cai, Jianwen, Xu, Jiawei, Wright, Lauren B., Brook, Mark N., Jones, Michael E., Adami, Hans-Olov, Baglietto, Laura, Bertrand, Kimberly A., Blot, William J., Boutron-Ruault, Marie-Christine, Dorronsoro, Miren, Dossus, Laure, Eliassen, A. Heather, Giles, Graham G., Gram, Inger T., Hankinson, Susan E., Hoffman-Bolton, Judy, and Kaaks, Rudolf

Subjects
CHILDBIRTH, BREAST cancer, BREASTFEEDING, PROPORTIONAL hazards models, EPIDERMAL growth factor receptors, BREAST tumor diagnosis, PROTEIN analysis, BREAST tumors, COMPARATIVE studies, DISEASE susceptibility, LABOR (Obstetrics), LONGITUDINAL method, MATERNAL age, RESEARCH methodology, MEDICAL cooperation, RESEARCH, RESEARCH funding, PERIMENOPAUSE, EVALUATION research, PARITY (Obstetrics)
Abstract

Background: Parity is widely recognized as protective for breast cancer, but breast cancer risk may be increased shortly after childbirth. Whether this risk varies with breastfeeding, family history of breast cancer, or specific tumor subtype has rarely been evaluated.Objective: To characterize breast cancer risk in relation to recent childbirth.Design: Pooled analysis of individual-level data from 15 prospective cohort studies.Setting: The international Premenopausal Breast Cancer Collaborative Group.Participants: Women younger than 55 years.Measurements: During 9.6 million person-years of follow-up, 18 826 incident cases of breast cancer were diagnosed. Hazard ratios (HRs) and 95% CIs for breast cancer were calculated using Cox proportional hazards regression.Results: Compared with nulliparous women, parous women had an HR for breast cancer that peaked about 5 years after birth (HR, 1.80 [95% CI, 1.63 to 1.99]) before decreasing to 0.77 (CI, 0.67 to 0.88) after 34 years. The association crossed over from positive to negative about 24 years after birth. The overall pattern was driven by estrogen receptor (ER)-positive breast cancer; no crossover was seen for ER-negative cancer. Increases in breast cancer risk after childbirth were pronounced when combined with a family history of breast cancer and were greater for women who were older at first birth or who had more births. Breastfeeding did not modify overall risk patterns.Limitations: Breast cancer diagnoses during pregnancy were not uniformly distinguishable from early postpartum diagnoses. Data on human epidermal growth factor receptor 2 (HER2) oncogene overexpression were limited.Conclusion: Compared with nulliparous women, parous women have an increased risk for breast cancer for more than 20 years after childbirth. Health care providers should consider recent childbirth a risk factor for breast cancer in young women.Primary Funding Source: The Avon Foundation, the National Institute of Environmental Health Sciences, Breast Cancer Now and the UK National Health Service, and the Institute of Cancer Research. [ABSTRACT FROM AUTHOR]

Published
2019
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