Synthetic lethality in ATM-deficient RAD50-mutant tumors underlies outlier response to cancer therapy Academic Article uri icon

Overview

MeSH Major

  • Ataxia Telangiectasia Mutated Proteins
  • DNA Repair Enzymes
  • DNA-Binding Proteins
  • Mutation
  • Neoplasms

abstract

  • Strategies to effect deep and lasting responses to cancer therapy in patients with metastatic disease have remained difficult to attain, especially in early-phase clinical trials. Here, we present an in-depth genomic and functional genetic analysis identifying RAD50 hypomorphism as a contributing factor to a curative response to systemic combination therapy in a patient with recurrent, metastatic small-cell cancer.

publication date

  • January 2014

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC4155059

Digital Object Identifier (DOI)

  • 10.1158/2159-8290.CD-14-0380

PubMed ID

  • 24934408

Additional Document Info

start page

  • 1014

end page

  • 21

volume

  • 4

number

  • 9