Targeting oncogene-induced DNA repair pathway switches (A09)

点击翻译按钮获取中文摘要

Reinhardt has identified a cell state transition in KRAS-driven non-small cell lung cancer cells that features a critical change in DNA damage repair competence accompanied with increased mutational burden and altered cancer drug sensitivities. He will unravel the molecular role of proteins of the ubiquilin family that mediate this transition, identify the gene regulatory elements that trigger ubiquilin overexpression and dissect the mechanism and additional targets of the ubiquilins using proteomics. In addition to these mechanistic studies, he will determine thera-peutic vulnerabilities in vitro and in mouse models.