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Postmenopausal Hormone Therapy and Colorectal Cancer Risk by Molecularly Defined Subtypes and Tumor Location.
Labadie, Julia D; Harrison, Tabitha A; Banbury, Barbara; Amtay, Efrat L; Bernd, Sonja; Brenner, Hermann; Buchanan, Daniel D; Campbell, Peter T; Cao, Yin; Chan, Andrew T; Chang-Claude, Jenny; English, Dallas; Figueiredo, Jane C; Gallinger, Steven J; Giles, Graham G; Gunter, Marc J; Hoffmeister, Michael; Hsu, Li; Jenkins, Mark A; Lin, Yi; Milne, Roger L; Moreno, Victor; Murphy, Neil; Ogino, Shuji; Phipps, Amanda I; Sakoda, Lori C; Slattery, Martha L; Southey, Melissa C; Sun, Wei; Thibodeau, Stephen N; Van Guelpen, Bethany; Zaidi, Syed H; Peters, Ulrike; Newcomb, Polly A.
Afiliação
  • Labadie JD; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
  • Harrison TA; Department of Epidemiology, University of Washington, Seattle, WA, USA.
  • Banbury B; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
  • Amtay EL; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
  • Bernd S; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Brenner H; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
  • Buchanan DD; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Campbell PT; Division of Preventive Oncology, German Cancer Research Center (DKFZ) and National Center for Tumor Diseases (NCT), Heidelberg, Germany.
  • Cao Y; Colorectal Oncogenomics Group, Department of Clinical Pathology, The University of Melbourne, Parkville, Victoria, Australia.
  • Chan AT; Behavioral and Epidemiology Research Group, American Cancer Society, Atlanta, GA, USA.
  • Chang-Claude J; Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St Louis, MO, USA.
  • English D; Alvin J. Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine, St Louis, MO, USA.
  • Figueiredo JC; Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St Louis, MO, USA.
  • Gallinger SJ; Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, USA.
  • Giles GG; Clinical and Translational Epidemiology Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.
  • Gunter MJ; Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Hoffmeister M; University Medical Centre Hamburg-Eppendorf, University Cancer Centre Hamburg (UCCH), Hamburg, Germany.
  • Hsu L; Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria, Australia.
  • Jenkins MA; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Victoria, Australia.
  • Lin Y; Department of Medicine, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai, Los Angeles, CA, USA.
  • Milne RL; Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
  • Moreno V; Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada.
  • Murphy N; Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria, Australia.
  • Ogino S; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Victoria, Australia.
  • Phipps AI; Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria, Australia.
  • Sakoda LC; Nutrition and Metabolism Section, International Agency for Research on Cancer, World Health Organization, Lyon, France.
  • Slattery ML; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Southey MC; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
  • Sun W; Department of Biostatistics, University of Washington, Seattle, WA, USA.
  • Thibodeau SN; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Victoria, Australia.
  • Van Guelpen B; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
  • Zaidi SH; Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria, Australia.
  • Peters U; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Victoria, Australia.
  • Newcomb PA; Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria, Australia.
JNCI Cancer Spectr ; 4(5): pkaa042, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32923935
ABSTRACT

Background:

Postmenopausal hormone therapy (HT) is associated with a decreased colorectal cancer (CRC) risk. As CRC is a heterogeneous disease, we evaluated whether the association of HT and CRC differs across etiologically relevant, molecularly defined tumor subtypes and tumor location.

Methods:

We pooled data on tumor subtypes (microsatellite instability status, CpG island methylator phenotype status, BRAF and KRAS mutations, pathway adenoma-carcinoma, alternate, serrated), tumor location (proximal colon, distal colon, rectum), and HT use among 8220 postmenopausal women (3898 CRC cases and 4322 controls) from 8 observational studies. We used multinomial logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CIs) for the association of ever vs never HT use with each tumor subtype compared with controls. Models were adjusted for study, age, body mass index, smoking status, and CRC family history. All statistical tests were 2-sided.

Results:

Among postmenopausal women, ever HT use was associated with a 38% reduction in overall CRC risk (OR =0.62, 95% CI = 0.56 to 0.69). This association was similar according to microsatellite instability, CpG island methylator phenotype and BRAF or KRAS status. However, the association was attenuated for tumors arising through the serrated pathway (OR = 0.81, 95% CI = 0.66 to 1.01) compared with the adenoma-carcinoma pathway (OR = 0.63, 95% CI = 0.55 to 0.73; P het =.04) and alternate pathway (OR = 0.61, 95% CI = 0.51 to 0.72). Additionally, proximal colon tumors had a weaker association (OR = 0.71, 95% CI = 0.62 to 0.80) compared with rectal (OR = 0.54, 95% CI = 0.46 to 0.63) and distal colon (OR = 0.57, 95% CI = 0.49 to 0.66; P het =.01) tumors.

Conclusions:

We observed a strong inverse association between HT use and overall CRC risk, which may predominantly reflect a benefit of HT use for tumors arising through the adenoma-carcinoma and alternate pathways as well as distal colon and rectal tumors.
Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Idioma: Inglês Revista: JNCI Cancer Spectr Ano de publicação: 2020 Tipo de documento: Artigo País de afiliação: Estados Unidos

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Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Idioma: Inglês Revista: JNCI Cancer Spectr Ano de publicação: 2020 Tipo de documento: Artigo País de afiliação: Estados Unidos