Back to search

Article

FAK loss reduces BRAFV600E-induced ERK phosphorylation to promote intestinal stemness and cecal tumor formation

2024-01-05

Abstract excerpt

<title>Abstract</title> <p> <italic>BRAF</italic> <sup>V600E</sup> mutation is a driver mutation in the serrated pathway to colorectal cancers. BRAF <sup>V600E</sup> drives tumorigenesis through constitutive downstream extracellular signal-regulated kinase (ERK) activation, but high-intensity ERK activation can also trigger tumor suppression. Whether and how oncogenic ERK signaling can be intrinsically adjus...

Topics

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

Identifiers and source

Literature Corpus work
e154303d-6e70-51eb-8612-c9589b8c4dd0
DOI
10.21203/rs.3.rs-2531119/v2
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
FAK loss reduces BRAFV600E-induced ERK phosphorylation to promote intestinal stemness and cecal tumor formationDOI 10.21203/rs.3.rs-2531119/v2
Similar but different: distinct roles for KRAS and BRAF oncogenes in colorectal cancer development and therapy resistance.Semantic proximity
The proprotein convertase furin is a pro-oncogenic driver in KRAS and BRAF driven colorectal cancer.Semantic proximity
Focal Adhesion Kinase Is Required for Intestinal Regeneration and Tumorigenesis Downstream of Wnt/c-Myc SignalingSemantic proximity
Cell type-dependent differential activation of ERK by oncogenic KRAS in colon cancer and intestinal epitheliumSemantic proximity
Dynamic transitioning between MAPK-driven and WNT-driven cell states drives intestinal cancer and shapes therapy response.Semantic proximity
Furin sustains tumor-promoting signals in KRAS- and BRAF-mutated colorectal cancer by engaging the TGF-β1-COX-2 axis in a reciprocal regulatory network.Semantic proximity
Cell type-dependent differential activation of ERK by oncogenic KRAS in colon cancer and intestinal epitheliumSemantic proximity
A genetic progression model of Braf(V600E)-induced intestinal tumorigenesis reveals targets for therapeutic intervention.Semantic proximity
Intestinal LKB1 loss drives a pre-malignant program along the serrated cancer pathwaySemantic proximity
MEK inhibitors activate Wnt signalling and induce stem cell plasticity in colorectal cancerSemantic proximity
Constitutive activation of mitogen-activated protein kinase kinase (MEK1) in ileal enterocytes leads to dysplasia and a predisposition to cancer.Semantic proximity
Acquired resistance to BRAF inhibitory treatments requires tumor tissue remodeling and reveals targetable vulnerabilities in colorectal cancerSemantic proximity
Select a neighboring publication to make it the new centre.