Quantitative assessment of the influence of EPHX1 gene polymorphisms and cancer risk: a meta-analysis with 94,213 subjects

Yang, Xiaoqin; Wang, Yubing; Wang, Guiping

doi:10.1186/preaccept-1877117814129047

Cited by 1 publication

(1 citation statement)

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“…Several polymorphisms have been associated with an increase in lung cancer risk in genes involved in the metabolism of tobacco [45], as well as in genes involved in other pathways such as DNA repair [46]. Comprehensive meta-analyses have been done of specific SNPs [47, 48], as well as a recent review of the existing literature on SNPs in lung cancer [49]. In some of these studies, an association with higher lung cancer risk was found in H/L [50, 51].…”

Section: Hispanics/latinos and Lung Cancermentioning

confidence: 99%

Lung Cancer Mutations and Use of Targeted Agents in Hispanics

Cress¹,

Chiappori²,

Santiago³

et al. 2015

RRCT

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Hispanic/Latinos (H/L) are expected to grow to over 24% of the USA population by 2050 and lung cancer is the number one cause of cancer death among H/L men. Due to the information that is becoming available via genetic testing, lung cancer molecular profiling is allowing for increasing application of personalized lung cancer therapies. However, to benefit the most people, development of these therapies and genetic tests must include research on as many racial and ethnic groups as possible. The purpose of this review is to bring attention to the fact that the mutations driving lung cancer in H/Ls differ in frequency and nature relative to the non-Hispanic White (WNH) majority that dominate current databases and participate in clinical trials that test new therapies. Clinical trials using new agents targeting genetic alterations (driver mutations) in lung cancer have demonstrated significant improvements in patient outcomes (for example, gefitinib, erlotinib or crizotinib for lung adenocarcinomas harboring EGFR mutations or EML4-ALK fusions, respectively). The nature and frequencies of some lung cancer driver mutations have been shown to be considerably different among racial and ethnic groups. This is particularly true for H/Ls. For example, several reports suggest a dramatic shift in the mutation pattern from predominantly KRAS in a WNH population to predominantly EGFR in multiple H/L populations. However, these studies are limited, and the effects of racial and ethnic differences on the incidence of mutations in lung cancer remain incompletely understood. This review serves as a call to address this problem.

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