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Article

The BCL-2 family member BOK promotes KRAS-driven lung cancer progression in a p53-dependent manner.

Oncogene - 1 Feb 2022

Meinhardt Anna-Lena, Munkhbaatar Enkhtsetseg, Höckendorf Ulrike, Dietzen Michelle, Dechant Marta, Anton Martina, Jacob Anne, Steiger Katja, Weichert Wilko, Brcic Luka, McGranahan Nicholas, Branca Caterina, Kaufmann Thomas, Dengler Michael A, Jost Philipp J

Abstract excerpt

A variety of cancer entities are driven by KRAS mutations, which remain difficult to target clinically. Survival pathways, such as resistance to cell death, may represent a promising treatment approach in KRAS mutated cancers. Based on the frequently observed genomic deletions of BCL-2-related ovarian killer (BOK) in cancer patients, we explored the function of BOK in a mutant KrasG12D-driven murine model of lung...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 35091677
DOI: 10.1038/s41388-021-02161-1
PMCID: PMC8881215

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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The BCL-2 family member BOK promotes KRAS-driven lung cancer progression in a p53-dependent manner.PMID 35091677Read ↗

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