Literature DB >> 35512400

Genome-Wide Interaction Analysis of Genetic Variants With Menopausal Hormone Therapy for Colorectal Cancer Risk.

Yu Tian1,2, Andre E Kim3, Stephanie A Bien4, Yi Lin4, Conghui Qu4, Tabitha A Harrison4, Robert Carreras-Torres5,6,7, Virginia Díez-Obrero5,6,7, Niki Dimou8, David A Drew9,10, Akihisa Hidaka4, Jeroen R Huyghe4, Kristina M Jordahl4,11, John Morrison3, Neil Murphy8, Mireia Obón-Santacana5,6,7, Cornelia M Ulrich12,13, Jennifer Ose12,13, Anita R Peoples12,13, Edward A Ruiz-Narvaez14, Anna Shcherbina15, Mariana C Stern16, Yu-Ru Su4,17, Franzel J B van Duijnhoven18, Volker Arndt19, James W Baurley20,21, Sonja I Berndt22, D Timothy Bishop23, Hermann Brenner19,24,25, Daniel D Buchanan26,27,28, Andrew T Chan9,10,29,30,31,32, Jane C Figueiredo33,34, Steven Gallinger35, Stephen B Gruber16, Sophia Harlid36, Michael Hoffmeister19, Mark A Jenkins37, Amit D Joshi31, Temitope O Keku38, Susanna C Larsson39, Loic Le Marchand40, Li Li41, Graham G Giles37,42,43, Roger L Milne37,42,43, Hongmei Nan44,45, Rami Nassir46, Shuji Ogino30,31,47,48, Arif Budiarto20, Elizabeth A Platz49, John D Potter4,50, Ross L Prentice4,51, Gad Rennert52,53,54, Lori C Sakoda4,55, Robert E Schoen56, Martha L Slattery57, Stephen N Thibodeau58, Bethany Van Guelpen36,59, Kala Visvanathan49, Emily White4,11, Alicja Wolk39, Michael O Woods60, Anna H Wu34, Peter T Campbell61, Graham Casey62, David V Conti16, Marc J Gunter8, Anshul Kundaje63,64, Juan Pablo Lewinger3, Victor Moreno5,6,7,65, Polly A Newcomb4,11, Bens Pardamean20, Duncan C Thomas16, Konstantinos K Tsilidis66,67, Ulrike Peters4,11, W James Gauderman16, Li Hsu4,51, Jenny Chang-Claude1,68.   

Abstract

BACKGROUND: The use of menopausal hormone therapy (MHT) may interact with genetic variants to influence colorectal cancer (CRC) risk.
METHODS: We conducted a genome-wide, gene-environment interaction between single nucleotide polymorphisms and the use of any MHT, estrogen only, and combined estrogen-progestogen therapy with CRC risk, among 28 486 postmenopausal women (11 519 CRC patients and 16 967 participants without CRC) from 38 studies, using logistic regression, 2-step method, and 2- or 3-degree-of-freedom joint test. A set-based score test was applied for rare genetic variants.
RESULTS: The use of any MHT, estrogen only and estrogen-progestogen were associated with a reduced CRC risk (odds ratio [OR] = 0.71, 95% confidence interval [CI] = 0.64 to 0.78; OR = 0.65, 95% CI = 0.53 to 0.79; and OR = 0.73, 95% CI = 0.59 to 0.90, respectively). The 2-step method identified a statistically significant interaction between a GRIN2B variant rs117868593 and MHT use, whereby MHT-associated CRC risk was statistically significantly reduced in women with the GG genotype (OR = 0.68, 95% CI = 0.64 to 0.72) but not within strata of GC or CC genotypes. A statistically significant interaction between a DCBLD1 intronic variant at 6q22.1 (rs10782186) and MHT use was identified by the 2-degree-of-freedom joint test. The MHT-associated CRC risk was reduced with increasing number of rs10782186-C alleles, showing odds ratios of 0.78 (95% CI = 0.70 to 0.87) for TT, 0.68 (95% CI = 0.63 to 0.73) for TC, and 0.66 (95% CI = 0.60 to 0.74) for CC genotypes. In addition, 5 genes in rare variant analysis showed suggestive interactions with MHT (2-sided P < 1.2 × 10-4).
CONCLUSION: Genetic variants that modify the association between MHT and CRC risk were identified, offering new insights into pathways of CRC carcinogenesis and potential mechanisms involved.
© The Author(s) 2022. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.

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Year:  2022        PMID: 35512400      PMCID: PMC9360460          DOI: 10.1093/jnci/djac094

Source DB:  PubMed          Journal:  J Natl Cancer Inst        ISSN: 0027-8874            Impact factor:   11.816


  48 in total

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