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Article

A synthetic lethal screen identifies ATR-inhibition as a novel therapeutic approach for POLD1-deficient cancers.

Oncotarget - 9 Feb 2016

Hocke Sandra, Guo Yang, Job Albert, Orth Michael, Ziesch Andreas, Lauber Kirsten, De Toni Enrico N, Gress Thomas M, Herbst Andreas, Göke Burkhard, Gallmeier Eike

Abstract excerpt

The phosphoinositide 3-kinase-related kinase ATR represents a central checkpoint regulator and mediator of DNA-repair. Its inhibition selectively eliminates certain subsets of cancer cells in various tumor types, but the underlying genetic determinants remain enigmatic. Here, we applied a synthetic lethal screen directed against 288 DNA-repair genes using the well-defined ATR knock-in model of DLD1 colorectal...

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Share to Ataxia Telangiectasia Mutated Proteins
Share to DNA Polymerase III

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA Repair Enzymes

Share to Fluorometry

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Source

Open in PubMed Open full text

Identifiers

PMID: 26755646
DOI: 10.18632/oncotarget.6857
PMCID: PMC4872770

Genes

ATR
POLD1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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