ArticleSmall GTPases2011
Mechanism of RAF isoform switching induced by oncogenic RAS in melanoma.
Article in Small GTPases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Correlation of somatic mutations and clinical outcome in melanoma patients treated with Carboplatin, Paclitaxel, and sorafenib.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Trial
- P40 and TTF-1 double-expressing non-small cell lung cancer with EML4-ALK and PIK3CA gene mutations: A case report and review of the literature.Oncology letters · 2023Article
- Phenotype Switching and the Melanoma Microenvironment; Impact on Immunotherapy and Drug Resistance.International journal of molecular sciences · 2023Review
- Resistance mechanisms in BRAFFrontiers in oncology · 2022Review
- Simultaneous blocking of the pan-RAF and S100B pathways as a synergistic therapeutic strategy against malignant melanoma.Journal of cellular and molecular medicine · 2021Article
- Cyclic adenosine monophosphate (cAMP) signaling in melanocyte pigmentation and melanomagenesis.Pigment cell & melanoma research · 2021Review
- Isoform- and Paralog-Switching in IR-Signaling: When Diabetes Opens the Gates to Cancer.Biomolecules · 2020Review
- Exon-4 Mutations in KRAS Affect MEK/ERK and PI3K/AKT Signaling in Human Multiple Myeloma Cell Lines.Cancers · 2020Article
- MicroRNA-23a-3p Inhibits Mucosal Melanoma Growth and Progression through Targeting Adenylate Cyclase 1 and Attenuating cAMP and MAPK Pathways.Theranostics · 2019Article
- EPAC-RAP1 Axis-Mediated Switch in the Response of Primary and Metastatic Melanoma to Cyclic AMP.Molecular cancer research : MCR · 2017Article
- RAF proteins exert both specific and compensatory functions during tumour progression of NRAS-driven melanoma.Nature communications · 2017Article
- Article
- Investigation of cAMP microdomains as a path to novel cancer diagnostics.Biochimica et biophysica acta · 2014Review
- Ras-mutant cancer cells display B-Raf binding to Ras that activates extracellular signal-regulated kinase and is inhibited by protein kinase A phosphorylation.The Journal of biological chemistry · 2013Article
- NRAS mutant melanoma: biological behavior and future strategies for therapeutic management.Oncogene · 2013Review
- PDE8A runs interference to limit PKA inhibition of Raf-1.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRAF and RAS are often mutated in cutaneous melanoma and both mutations stimulate the MAPK pathway. However the biological consequences of BRAF and NRAS mutations are different because when RAS is mutated in melanoma, cells use CRAF rather than BRAF to activate MEK/ERK. The mechanism of this BRAF to CRAF isoform switching in response to oncogenic RAS has recently been described. Activation of the MAPK pathway, which results from a mutation of NRAS, induces phosphorylation of BRAF on serine 151 by ERK which prevents its binding to NRAS. To circumvent this negative feedback inhibition of BRAF, melanoma cells containing a mutation of RAS use CRAF to activate MEK/ERK. However, because the cAMP pathway in melanocytes constitutively inhibits CRAF, RAF isoform switching in melanoma is accompanied by an inhibition of the cAMP pathway. This inhibition is due to an increase in phosphodiesterase activity, which degrades cAMP thereby preventing inhibition of CRAF by PKA. These data highlight the importance of CRAF downstream of oncogenic Ras in tumor development.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.