作者: Xiao Chen , Rutaganda Theobard , Jianying Zhang , Xiaofeng Dai
DOI: 10.1042/BSR20192546
关键词:
摘要: RAD50 is commonly depleted in basal-like breast cancer with concomitant absence of INPP4B and several tumor suppressors such as BRCA1 TP53. Our previous study revealed that interact an interaction associated survival at the transcriptional, translational genomic levels. In present study, we explored single nucleotide polymorphisms (SNPs) these two genes have synergistic effects on to decipher mechanisms driving their interactions genetic level. The Cox's proportional hazards model was used test whether SNPs are interactively survival, following expression quantitative trait loci (eQTL) analysis functional investigations. disease-associating blocks, each encompassing five non-linkage disequilibrium linked RAD50, respectively. Concomitant presence any rare homozygote from block synergistically prognostic poor survival. Such synergy mediated via bypassing pathways controlling cell proliferation DNA damage repair, which represented by RAD50. provided evidence between deepened our understandings orchestrated machinery governing progression.