MicroRNAs in endometrial cancers from black and white patients.


Journal Article

OBJECTIVE: Previous studies have identified differences in gene mutations among endometrial cancers from whites and blacks suggesting that differences in tumor biology may explain racial disparities in patient outcome. Micro RNAs (miRNAs) have emerged as regulators of transcript expression and their aberrant expression has been discovered in many diseases, including endometrial cancer. We performed quantitative polymerase chain reaction-based analysis in a set of endometrial cancers to identify whether there are racial differences in miRNA expression. STUDY DESIGN: Tumor cells from 50 stage-I endometrioid endometrial cancer specimens from 41 white and 9 black patients were prepared by laser microdissection and miRNA extracts were analyzed using TaqMan (Life Technologies, Carlsbad, CA) low-density arrays. Statistically significant, differentially expressed miRNAs between blacks and whites were identified using multidimensional scaling, Wilcoxon testing, and analysis of variance. RESULTS: There were no global differences in miRNA expression between endometrial cancers from 41 white and 9 black patients. To minimize potential bias introduced by unbalanced sample size, we performed a subset analysis with stage- and histology-matched specimens from 9 whites and 9 blacks that identified 18 differentially abundant miRNAs (>2-fold at P < .005). Quantitative polymerase chain reaction validated miRNA-337-3p in an independent set of endometrial cancer specimens from 23 white and 24 black women. There were no racial differences in hsa-miR-337-3p expression in normal endometrium. CONCLUSION: These data indicate that hsa-mir-337-3p is more frequently down-regulated in endometrial cancers from whites compared to blacks. Future studies are focused on determining the phenotypic impact of miR-337-3p and whether its differential expression is associated with clinical outcome.

Full Text

Duke Authors

Cited Authors

  • Maxwell, GL; Shoji, Y; Darcy, K; Litzi, T; Berchuck, A; Hamilton, CA; Conrads, TP; Risinger, JI

Published Date

  • February 2015

Published In

Volume / Issue

  • 212 / 2

Start / End Page

  • 191.e1 - 191.10

PubMed ID

  • 25174797

Pubmed Central ID

  • 25174797

Electronic International Standard Serial Number (EISSN)

  • 1097-6868

Digital Object Identifier (DOI)

  • 10.1016/j.ajog.2014.08.028


  • eng

Conference Location

  • United States