Endogenous sex steroid hormones and risk of liver cancer among US men: Results from the Liver Cancer Pooling Project.

Androgen Liver cancer Male Oestrogen Sex steroid hormone

Journal

JHEP reports : innovation in hepatology
ISSN: 2589-5559
Titre abrégé: JHEP Rep
Pays: Netherlands
ID NLM: 101761237

Informations de publication

Date de publication:
Jul 2023
Historique:
received: 31 10 2022
revised: 28 02 2023
accepted: 03 03 2023
medline: 10 7 2023
pubmed: 10 7 2023
entrez: 10 7 2023
Statut: epublish

Résumé

Incidence rates of liver cancer in most populations are two to three times higher among men than women. The higher rates among men have led to the suggestion that androgens are related to increased risk whereas oestrogens are related to decreased risk. This hypothesis was investigated in the present study via a nested case-control analysis of pre-diagnostic sex steroid hormone levels among men in five US cohorts. Concentrations of sex steroid hormones and sex hormone-binding globulin were quantitated using gas chromatography-mass spectrometry and a competitive electrochemiluminescence immunoassay, respectively. Multivariable conditional logistic regression was used to calculate odds ratios (ORs) and 95% CIs for associations between hormones and liver cancer among 275 men who subsequently developed liver cancer and 768 comparison men. Higher concentrations of total testosterone (OR per one-unit increase in log Higher concentrations of both androgens (testosterone, dihydrotestosterone) and their aromatised oestrogenic metabolites (oestrone, oestradiol) were observed among men who subsequently developed liver cancer compared with men who did not. As DHEA is an adrenal precursor of both androgens and oestrogens, these results may suggest that a lower capacity to convert DHEA to androgens, and their subsequent conversion to oestrogens, confers a lower risk of liver cancer, whereas a greater capacity to convert DHEA confers a greater risk. This study does not fully support the current hormone hypothesis as both androgen and oestrogen levels were associated with increased risk of liver cancer among men. The study also found that higher DHEA levels were associated with lower risk, thus suggesting the hypothesis that greater capacity to convert DHEA could be associated with increased liver cancer risk among men.

Sections du résumé

Background & Aims UNASSIGNED
Incidence rates of liver cancer in most populations are two to three times higher among men than women. The higher rates among men have led to the suggestion that androgens are related to increased risk whereas oestrogens are related to decreased risk. This hypothesis was investigated in the present study via a nested case-control analysis of pre-diagnostic sex steroid hormone levels among men in five US cohorts.
Methods UNASSIGNED
Concentrations of sex steroid hormones and sex hormone-binding globulin were quantitated using gas chromatography-mass spectrometry and a competitive electrochemiluminescence immunoassay, respectively. Multivariable conditional logistic regression was used to calculate odds ratios (ORs) and 95% CIs for associations between hormones and liver cancer among 275 men who subsequently developed liver cancer and 768 comparison men.
Results UNASSIGNED
Higher concentrations of total testosterone (OR per one-unit increase in log
Conclusions UNASSIGNED
Higher concentrations of both androgens (testosterone, dihydrotestosterone) and their aromatised oestrogenic metabolites (oestrone, oestradiol) were observed among men who subsequently developed liver cancer compared with men who did not. As DHEA is an adrenal precursor of both androgens and oestrogens, these results may suggest that a lower capacity to convert DHEA to androgens, and their subsequent conversion to oestrogens, confers a lower risk of liver cancer, whereas a greater capacity to convert DHEA confers a greater risk.
Impact and implications UNASSIGNED
This study does not fully support the current hormone hypothesis as both androgen and oestrogen levels were associated with increased risk of liver cancer among men. The study also found that higher DHEA levels were associated with lower risk, thus suggesting the hypothesis that greater capacity to convert DHEA could be associated with increased liver cancer risk among men.

Identifiants

pubmed: 37425211
doi: 10.1016/j.jhepr.2023.100742
pii: S2589-5559(23)00073-3
pmc: PMC10326694
doi:

Types de publication

Journal Article

Langues

eng

Pagination

100742

Déclaration de conflit d'intérêts

The authors declare no conflicts of interest that pertain to this work. Please refer to the accompanying ICMJE disclosure forms for further details.

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Auteurs

Zeni Wu (Z)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Jessica L Petrick (JL)

Slone Epidemiology Center, Boston University, Boston, MA, USA.

Andrea A Florio (AA)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Chantal Guillemette (C)

Pharmacogenomics Laboratory, Centre Hospitalier Universitaire de Québec-(CHU de Québec) Research Center-Université Laval, Québec, QC, Canada.
Faculty of Pharmacy and Cancer Research Center, Laval University, Québec, QC, Canada.

Laura E Beane Freeman (LE)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Julie E Buring (JE)

Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Department of Epidemiology, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.

Gary Bradwin (G)

Clinical and Epidemiologic Research Laboratory, Department of Laboratory Medicine, Boston Children's Hospital, Boston, MA, USA.

Patrick Caron (P)

Pharmacogenomics Laboratory, Centre Hospitalier Universitaire de Québec-(CHU de Québec) Research Center-Université Laval, Québec, QC, Canada.

Yu Chen (Y)

Department of Population Health, New York University School of Medicine, New York, NY, USA.

A Heather Eliassen (AH)

Department of Epidemiology, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.
Department of Nutrition, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.

Lawrence S Engel (LS)

Department of Epidemiology, University of North Carolina, Chapel Hill, NC, USA.

Neal D Freedman (ND)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

J Michael Gaziano (JM)

Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.

Edward L Giovannuci (EL)

Department of Epidemiology, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.
Department of Nutrition, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.

Jonathan N Hofmann (JN)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Wen-Yi Huang (WY)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Victoria A Kirsh (VA)

Ontario Institute for Cancer Research, Toronto, ON, Canada.
Epidemiology Division, Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada.

Cari M Kitahara (CM)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Jill Koshiol (J)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

I-Min Lee (IM)

Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Department of Epidemiology, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.

Linda M Liao (LM)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Christina C Newton (CC)

Department of Population Science, American Cancer Society, Atlanta, GA, USA.

Julie R Palmer (JR)

Slone Epidemiology Center, Boston University, Boston, MA, USA.

Mark P Purdue (MP)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Thomas E Rohan (TE)

Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York, NY, USA.

Lynn Rosenberg (L)

Slone Epidemiology Center, Boston University, Boston, MA, USA.

Howard D Sesso (HD)

Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Department of Epidemiology, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.

Rashmi Sinha (R)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Meir J Stampfer (MJ)

Department of Epidemiology, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.
Department of Nutrition, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.

Caroline Y Um (CY)

Department of Population Science, American Cancer Society, Atlanta, GA, USA.

Stephen K Van Den Eeden (SK)

Division of Research, Kaiser Permanente Northern California, Oakland, CA, USA.

Kala Visvanathan (K)

Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.

Jean Wactawski-Wende (J)

Department of Epidemiology and Environmental Health, University at Buffalo, Buffalo, NY, USA.

Anne Zeleniuch-Jacquotte (A)

Department of Population Health, New York University School of Medicine, New York, NY, USA.

Xuehong Zhang (X)

Department of Nutrition, T.H. Chan School of Public Health, Harvard University, Boston, MA, USA.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.

Barry I Graubard (BI)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Peter T Campbell (PT)

Albert Einstein College of Medicine, New York, NY, USA.

Katherine A McGlynn (KA)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA.

Classifications MeSH