Evidence map›Paper›PMID 24858661›Full record

ArticleMelanoma research2014

Resistance surveillance in a BRAF mutant melanoma patient on long-term BRAF-inhibitor treatment.

Gabriel Mak, Hendrik-Tobias Arkenau, Melvin Chin

Open access · hybridAbstract readCase Reports
In one paragraph

Article in Melanoma research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 37% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Gabriel MakaMedical Professorial Unit, Prince of Wales Hospital and University of New South Wales, Randwick, New South Wales, Australia bSarah Cannon Research UK and University College London, London, UK.
Hendrik-Tobias Arkenau
Melvin Chin
Prince of Wales Hospital · AUSarah Cannon Research Institute · GBUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treatment responses of BRAF mutant melanoma to BRAF inhibitors are often limited by the development of resistance. This case report describes the use of multiplatform molecular profiling in sequential surgical samples of a treatment-resistant tumour site subjected to ongoing treatment with dabrafenib in a patient with metastatic cutaneous BRAF mutant melanoma. Next-generation sequencing showed the presence of the V600E, fibroblast growth factor receptor 2 (FGFR2), phosphatase and tensin homologue (PTEN) and p53 gene mutations. With a continuous presence of the BRAF V600E, FGFR2 and PTEN mutations and appearances of new mutations in the PTEN gene at R137H and T321fs and p53 R273C genes during ongoing treatment, this case report indicates intratumoural clonal evolution as a resistance mechanism. Two new mutations, the G542E exon 12 mutation variant of the FGFR2 gene and the R273C mutation variant of the p53 gene, are reported for the first time in BRAF mutant melanoma.

Indexed as

MutationAdultDrug Administration ScheduleDrug Resistance, NeoplasmHumansImidazolesIn Situ HybridizationMaleMelanomaOximesProtein Kinase InhibitorsProto-Oncogene Proteins B-rafSkin NeoplasmsYoung AdultBRAF protein, humandabrafenibImidazolesOximesProtein Kinase InhibitorsProto-Oncogene Proteins B-raf

Identifiers

PMID24858661
PMCPMC4086757
OpenAlexW2008976980

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.