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

Enterocyte-like differentiation defines metabolic gene signatures of CMS3 colorectal cancers and provides therapeutic vulnerability.

Nature communications - 2 Jan 2025

Torang Arezo, Kirov Aleksandar B, Lammers Veerle, Cameron Kate, Wouters Valérie M, Jackstadt Rene F, Lannagan Tamsin R M, de Jong Joan H, Koster Jan, Sansom Owen, Medema Jan Paul

Abstract excerpt

Colorectal cancer (CRC) is stratified into four consensus molecular subtypes (CMS1-4). CMS3 represents the metabolic subtype, but its wiring remains largely undefined. To identify the underlying tumorigenesis of CMS3, organoids derived from 16 genetically engineered mouse models are analyzed. Upon in vitro Cre-recombinase activation, transformation is established and transcriptional profiling reveals that...

Read the complete abstract on PubMed

Topics

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

Share to Carcinogenesis
Share to Cell Proliferation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Colorectal Neoplasms

Share to Enterocytes

Share to Gene Expression Regulation, Neoplastic

Share to Organoids

Share to Proto-Oncogene Proteins p21(ras)

Share to Pyrimidines

Source

Open in PubMed Open full text

Identifiers

PMID: 39747069
DOI: 10.1038/s41467-024-55574-3
PMCID: PMC11696116

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Enterocyte-like differentiation defines metabolic gene signatures of CMS3 colorectal cancers and provides therapeutic vulnerability.PMID 39747069Read ↗

Multi-omics, organoid-based modeling reveals an SRC/mTOR-dependent fetal-like stem cell trajectory in colorectal cancerSemantic proximity Read ↗

Colorectal Cancer: Pathogenesis and Targeted TherapySemantic proximity Read ↗

Elucidating the Reprograming of Colorectal Cancer Metabolism Using Genome-Scale Metabolic ModelingSemantic proximity Read ↗

EGFR controls transcriptional and metabolic rewiring in KRASG12D colorectal cancer.Semantic proximity Read ↗

Genetic editing of colonic organoids provides a molecularly distinct and orthotopic preclinical model of serrated carcinogenesis.Semantic proximity Read ↗

Metabolic Studies in Organoids: Current Applications, Opportunities and ChallengesSemantic proximity Read ↗

Oncogenic KRAS creates an aspartate metabolism signature in colorectal cancer cells.Semantic proximity Read ↗

Strategies to target energy metabolism in consensus molecular subtype 3 along with Kirsten rat sarcoma viral oncogene homolog mutations for colorectal cancer therapy.Semantic proximity Read ↗

A Colorectal Tumor Organoid Library Demonstrates Progressive Loss of Niche Factor Requirements during Tumorigenesis.Semantic proximity Read ↗

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

FOXO1 links KRAS G12D and G12V alleles to glutamine and nitrogen metabolism in colorectal cancer.Semantic proximity Read ↗

Characterizing heterogeneity along EMT and metabolic axes in colorectal cancer reveals underlying consensus molecular subtype-specific trendsSemantic proximity Read ↗

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