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Pan‐cancer clinical and molecular analysis of racial disparities
Author(s) -
Lara Olivia D.,
Wang Ying,
Asare Amma,
Xu Tao,
Chiu HuaSheng,
Liu Yuexin,
Hu Wei,
Sumazin Pavel,
Uppal Shitanshu,
Zhang Lin,
RauhHain J. Alejandro,
Sood Anil K.
Publication year - 2020
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/cncr.32598
Subject(s) - medicine , cancer , breast cancer , epigenetics , oncology , prostate cancer , dna methylation , thyroid cancer , hazard ratio , kidney cancer , bioinformatics , genetics , gene , biology , gene expression , confidence interval
Background Racial disparities in cancer outcomes are increasingly recognized, but comprehensive analyses, including molecular studies, are limited. The objective of the current study was to perform a pan‐cancer clinical and epigenetic molecular analysis of outcomes in African American (AA) and European American (EA) patients. Methods Cross‐platform analyses using cancer databases (the Surveillance, Epidemiology, and End Results program database and the National Cancer Data Base) and a molecular database (The Cancer Genome Ancestry Atlas) were performed to evaluate clinical and epigenetic molecular differences between AA and EA patients based on genetic ancestry. Results In the primary pan‐cancer survival analysis using the Surveillance, Epidemiology, and End Results database (2,045,839 patients; 87.5% EA and 12.5% AA), AA patients had higher mortality rates for 28 of 42 cancer types analyzed (hazard ratio, >1.0). AAs continued to have higher mortality in 13 cancer types after adjustment for socioeconomic variables using the National Cancer Database (5,150,023 patients; 11.6% AA and 88.4% EA). Then, molecular features of 5,283 tumors were analyzed in patients who had genetic ancestry data available (87.2% EA and 12.8% AA). Genes were identified with altered DNA methylation along with increased microRNA expression levels unique to AA patients that are associated with cancer drug resistance. Increased miRNAs ( miR‐15a , miR‐17 , miR‐130‐3p , miR‐181a ) were noted in common among AAs with breast, kidney, thyroid, or prostate carcinomas. Conclusions The current results identified epigenetic features in AA patients who have cancer that may contribute to higher mortality rates compared with EA patients who have cancer. Therefore, a focus on molecular signatures unique to AAs may identify actionable molecular abnormalities.