Article

Identification of targetable vulnerabilities of PLK1-overexpressing cancers by synthetic dosage lethality

2024-07-22

Abstract excerpt

<h4>Summary</h4> Tumor heterogeneity poses a significant challenge in combating treatment resistance. Despite Polo-like kinase 1 (PLK1) being universally overexpressed in cancers and contributing to chromosomal instability (CIN), direct PLK1 inhibition hasn’t yielded clinical progress. To address this, we utilized the synthetic dosage lethality (SDL) approach, targeting PLK1’s genetic interactions for selective k...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 0fcb9a1f-e788-5e51-bdde-392ef42edb89
DOI: 10.1101/2024.07.18.603978

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Identification of targetable vulnerabilities of PLK1-overexpressing cancers by synthetic dosage lethalityDOI 10.1101/2024.07.18.603978Read

Identification of targetable vulnerabilities of PLK1-overexpressing cancers by synthetic dosage lethalitySemantic proximity Read

The CINs of Polo-Like Kinase 1 in CancerSemantic proximity Read

Therapeutic relevance of the protein phosphatase 2A in cancer.Semantic proximity Read

Pharmacogenomic discovery of genetically targeted cancer therapies optimized against clinical outcomesSemantic proximity Read

Polo-like Kinase 1 Inhibition as a Therapeutic Approach to Selectively Target BRCA1-Deficient Cancer Cells by Synthetic Lethality InductionSemantic proximity Read

CRISPR-enabled genetic screens identify synthetic lethal targets across frequently altered cancer driversSemantic proximity Read

A Synthetic Dosage Lethal Genetic Interaction Between CKS1B and PLK1 Is Conserved in Yeast and Human Cancer CellsSemantic proximity Read

Uncovering cancer vulnerabilities by machine learning prediction of synthetic lethality.Semantic proximity Read

Synthetic Lethality in Cancer Therapeutics: The Next GenerationSemantic proximity Read

Topoisomerase 1 Inhibition in MYC-Driven Cancer Promotes Aberrant R-Loop Accumulation to Induce Synthetic LethalitySemantic proximity Read

A synthetic lethal dependency on casein kinase 2 in response to replication-perturbing therapeutics in RB1-deficient cancer cellsSemantic proximity Read

Genome-based cancer therapeutics: targets, kinase drug resistance and future strategies for precision oncologySemantic proximity Read