Relationship between alcohol metabolism and chemotherapy-induced emetic events in breast cancer patients

Relationship between alcohol metabolism and chemotherapy-induced emetic events in breast cancer... Breast Cancer (2017) 24:702–707 DOI 10.1007/s12282-017-0761-4 ORIGINAL ARTICLE Relationship between alcohol metabolism and chemotherapy- induced emetic events in breast cancer patients 1 1 2 3 • • • • Toshitaka Uomori Yoshiya Horimoto Kaoru Mogushi Joe Matsuoka Mitsue Saito Received: 19 October 2016 / Accepted: 8 February 2017 / Published online: 20 February 2017 The Japanese Breast Cancer Society 2017 Abstract institution. ALDH2 genotypes were analyzed employing Background Chemotherapy-induced nausea and vomiting the smart amplification process in peripheral blood (CINV) can negatively affect quality of life and treatment samples. compliance in breast cancer patients. Habitual alcohol Results The wild type (ALDH2*1/*1), heterozygote consumption reportedly shows an inverse correlation with (ALDH2*1/*2), and mutant homozygote (ALDH2*2/*2) CINV, though the underlying mechanism is unknown. genotypes were found in 53, 44, and 3% of patients, Acetaldehyde dehydrogenase 2 (ALDH2), one of the two respectively. Complete response, i.e., no vomiting without ALDH isozymes, is reportedly the major factor among rescue anti-emetics, was more frequent in patients who several genetic polymorphisms possibly affecting alcohol habitually consumed alcohol than in those who did not metabolism. More than 40% of Japanese have ALDH2 (p = 0.036). This trend remained only in ALDH2 mutations, while almost all Westerners http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Breast Cancer Springer Journals

Relationship between alcohol metabolism and chemotherapy-induced emetic events in breast cancer patients

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Publisher
Springer Japan
Copyright
Copyright © 2017 by The Japanese Breast Cancer Society
Subject
Medicine & Public Health; Surgical Oncology; Oncology; Surgery; Cancer Research
ISSN
1340-6868
eISSN
1880-4233
D.O.I.
10.1007/s12282-017-0761-4
Publisher site
See Article on Publisher Site

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