Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Determination of synthetic lethal interactions in KRAS oncogene-dependent cancer cells reveals novel therapeutic targeting strategies.

Cell research - 1 Aug 2012

Steckel Michael, Molina-Arcas Miriam, Weigelt Britta, Marani Michaela, Warne Patricia H, Kuznetsov Hanna, Kelly Gavin, Saunders Becky, Howell Michael, Downward Julian, Hancock David C

Abstract excerpt

Oncogenic mutations in RAS genes are very common in human cancer, resulting in cells with well-characterized selective advantages, but also less well-understood vulnerabilities. We have carried out a large-scale loss-of-function screen to identify genes that are required by KRAS-transformed colon cancer cells, but not by derivatives lacking this oncogene. Top-scoring genes were then tested in a larger panel of...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Boronic Acids
Share to Bortezomib

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA Topoisomerases, Type I

Share to GATA2 Transcription Factor

Share to Gemcitabine

Share to Proteasome Inhibitors

Share to Pyrazines

Share to Topoisomerase I Inhibitors

Source

Open in PubMed Open full text

Identifiers

PMID: 22613949
DOI: 10.1038/cr.2012.82
PMCID: PMC3411175

Genes

KRAS
CDC6
GATA2

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.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Determination of synthetic lethal interactions in KRAS oncogene-dependent cancer cells reveals novel therapeutic targeting strategies.PMID 22613949Read ↗

A Landscape of Therapeutic Cooperativity in KRAS Mutant Cancers Reveals Principles for Controlling Tumor Evolution.Semantic proximity Read ↗

Synthetic Lethal Vulnerabilities in KRAS-Mutant Cancers.Semantic proximity Read ↗

Changes in the Transcriptome and Synthetic Lethal Dependencies Following <i>KRAS</i> Mutant Expression Reveal Profound Tissue-SpecificitySemantic proximity Read ↗

Targeting Distinct Cell Cycle Nodes Overcomes KRAS/RAS Inhibitor ResistanceSemantic proximity Read ↗

KRAS inhibitors: resistance drivers and combinatorial strategies.Semantic proximity Read ↗

Small-molecule inhibition of MAP2K4 is synergistic with RAS inhibitors in KRAS-mutant cancers.Semantic proximity Read ↗

Combinatorial strategies to target RAS-driven cancers.Semantic proximity Read ↗

Interleukin-1β as target to induce synthetic lethality in KRAS mutant biliary tract cancer.Semantic proximity Read ↗

MAP kinase and autophagy pathways cooperate to maintain RAS mutant cancer cell survivalSemantic proximity Read ↗

Addicted to proteostasis: How KRAS-driven cancers acquire resistance to clinical KRAS inhibitors.Semantic proximity Read ↗

Identifying chemogenetic interactions from CRISPR knockout screens with drugZSemantic proximity Read ↗

USP39 Deubiquitinase Is Essential for KRAS Oncogene-driven Cancer.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.