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

Global Phosphoproteomics Reveal CDK Suppression as a Vulnerability to KRas Addiction in Pancreatic Cancer

20 Apr 2021

Abstract excerpt

Abstract Purpose: Among human cancers that harbor mutant (mt) KRas, some, but not all, are dependent on mt KRas. However, little is known about what drives KRas dependency. Experimental Design: Global phosphoproteomics, screening of a chemical library of FDA drugs, and genome-wide CRISPR/Cas9 viability database analysis were used to identify vulnerabilities of KRas dependency. Results: Global phosphoproteomics...

Read the complete abstract on PubMed

Topics

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

Share to Cancer Genomics and Diagnostics
Share to Cancer-related Molecular Pathways
Share to Pancreatic and Hepatic Oncology Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 33879459
DOI: 10.1158/1078-0432.ccr-20-4781

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Global Phosphoproteomics Reveal CDK Suppression as a Vulnerability to KRas Addiction in Pancreatic CancerPMID 33879459Read ↗

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

The KRAS-regulated kinome identifies WEE1 and ERK coinhibition as a potential therapeutic strategy in KRAS-mutant pancreatic cancer.Semantic proximity Read ↗

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

Developing SHP2-based combination therapy for KRAS-amplified cancer.Semantic proximity Read ↗

Simultaneous targeting of KRAS and CDK4 synergistically induces durable growth arrest in pancreatic cancer cells.Semantic proximity Read ↗

Survival of pancreatic cancer cells lacking KRAS functionSemantic proximity Read ↗

An allele-agnostic mutant-KRAS inhibitor suppresses tumor maintenance signals and reprograms tumor immunity in pancreatic cancer.Semantic proximity Read ↗

Pharmacologically targeting KRAS <sup>G12D</sup> in PDAC models: tumor cell intrinsic and extrinsic impactSemantic proximity Read ↗

Genome-wide CRISPR screens identify PKMYT1 as a therapeutic target in pancreatic ductal adenocarcinomaSemantic proximity Read ↗

A window trial in metastatic pancreatic ductal adenocarcinoma reveals resistance mechanisms to targeting the KRAS-MEK pathwaySemantic proximity Read ↗

A Genome-scale CRISPR Screen Identifies the ERBB and mTOR Signaling Networks as Key Determinants of Response to PI3K Inhibition in Pancreatic CancerSemantic proximity Read ↗

Determining the ERK-regulated phosphoproteome driving KRAS-mutant cancer.Semantic proximity Read ↗

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