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

Systematic analysis of BRAF(V600E) melanomas reveals a role for JNK/c-Jun pathway in adaptive resistance to drug-induced apoptosis.

Molecular systems biology - 26 Mar 2015

Fallahi-Sichani Mohammad, Moerke Nathan J, Niepel Mario, Zhang Tinghu, Gray Nathanael S, Sorger Peter K

Abstract excerpt

Drugs that inhibit RAF/MEK signaling, such as vemurafenib, elicit profound but often temporary anti-tumor responses in patients with BRAF(V) (600E) melanoma. Adaptive responses to RAF/MEK inhibition occur on a timescale of hours to days, involve homeostatic responses that reactivate MAP kinase signaling and compensatory mitogenic pathways, and attenuate the anti-tumor effects of RAF/MEK inhibitors. We profile...

Read the complete abstract on PubMed

Topics

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

Share to Cell Survival
Share to Drug Synergism

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Indoles

Share to MAP Kinase Signaling System

Share to Melanoma

Share to Proto-Oncogene Proteins B-raf

Share to Sulfonamides

Share to Vemurafenib

Source

Open in PubMed Open full text

Identifiers

PMID: 25814555
DOI: 10.15252/msb.20145877
PMCID: PMC4380931

Genes

BRAF

Variants

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.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Systematic analysis of BRAF(V600E) melanomas reveals a role for JNK/c-Jun pathway in adaptive resistance to drug-induced apoptosis.PMID 25814555Read ↗

Adaptive resistance of melanoma cells to RAF inhibition via reversible induction of a slowly dividing de-differentiated state.Semantic proximity Read ↗

Exploiting Drug Addiction Mechanisms to Select against MAPKi-Resistant MelanomaSemantic proximity Read ↗

Signaling and transcriptional dynamics underlying early adaptation to oncogenic BRAF inhibitionSemantic proximity Read ↗

Sporadic ERK pulses drive non-genetic resistance in drug-adapted BRAF <sup>V600E</sup> melanoma cellsSemantic proximity Read ↗

Adaptive resistance to <scp>RAF</scp> inhibitors in melanomaSemantic proximity Read ↗

Parallel In Vivo Assessment of Drug Phenotypes at Various Time Points during Systemic BRAF Inhibition Reveals Tumor Adaptation and Altered Treatment Vulnerabilities.Semantic proximity Read ↗

Molecular pathways: adaptive kinome reprogramming in response to targeted inhibition of the BRAF-MEK-ERK pathway in cancer.Semantic proximity Read ↗

Systems biology analysis of mitogen activated protein kinase inhibitor resistance in malignant melanomaSemantic proximity Read ↗

Mechanistic model of MAPK signaling reveals how allostery and rewiring contribute to drug resistance.Semantic proximity Read ↗

Rapidly induced drug adaptation mediates escape from BRAF inhibition in single melanoma cellsSemantic proximity Read ↗

Multiple cancer types rapidly escape from multiple MAPK inhibitors to generate mutagenesis-prone subpopulationsSemantic proximity Read ↗

Systems biology analysis of mitogen activated protein kinase inhibitor resistance in malignant melanomaSemantic proximity Read ↗

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