Evidence map›Paper›PMID 25627962›Full record

ArticleJournal of translational medicine2015

Activating PIK3CA mutations coexist with BRAF or NRAS mutations in a limited fraction of melanomas.

Antonella Manca, Amelia Lissia, Mariaelena Capone, Paolo A Ascierto, Gerardo Botti, Corrado Caracò, Ignazio Stanganelli, Maria Colombino, MariaCristina Sini, Antonio Cossu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  12. Autophagy: In the cROSshairs of cancer.Biochemical pharmacology · 2017
    Review
  13. Melanoma Brain Metastasis: Mechanisms, Models, and Medicine.International journal of molecular sciences · 2016
    Review
  14. Article
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

11 authors at 3 institutions in 1 country.

Antonella Manca
Amelia Lissia
Mariaelena Capone
Paolo A Ascierto
Gerardo Botti
Corrado Caracò
Ignazio Stanganelli
Maria Colombino
MariaCristina Sini
Antonio Cossu
Giuseppe PalmieriInstitute of Biomolecular Chemistry, National Research Council (CNR), Traversa La Crucca 3 - Baldinca Li Punti, Sassari, 07100, Italy. gpalmieri@yahoo.com.
Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · ITNational Research Council · ITIstituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundActivated PI3K-AKT pathway may contribute to decrease sensitivity to inhibitors of key pathogenetic effectors (mutated BRAF, active NRAS or MEK) in melanoma. Functional alterations are deeply involved in PI3K-AKT activation, with a minimal role reported for mutations in PIK3CA, the catalytic subunit of the PI3K gene. We here assessed the prevalence of the coexistence of BRAF/NRAS and PIK3CA mutations in a series of melanoma samples.

methodsA total of 245 tumor specimens (212 primary melanomas and 33 melanoma cell lines) was screened for mutations in BRAF, NRAS, and PIK3CA genes by automated direct sequencing.

resultsOverall, 110 (44.9%) samples carried mutations in BRAF, 26 (10.6%) in NRAS, and 24 (9.8%) in PIK3CA. All identified PIK3CA mutations have been reported to induce PI3K activation; those detected in cultured melanomas were investigated for their interference with the antiproliferative activity of the BRAF-mutant inhibitor vemurafenib. A reduced suppression in cell growth was observed in treated cells carrying both BRAF and PIK3CA mutations as compared with those presenting a mutated BRAF only. Among the analysed melanomas, 12/245 (4.9%) samples presented the coexistence of PIK3CA and BRAF/NRAS mutations.

conclusionsOur study further suggests that PIK3CA mutations account for a small fraction of PI3K pathway activation and have a limited impact in interfering with the BRAF/NRAS-driven growth in melanoma.

Indexed as

AdultAgedAged, 80 and overCell Line, TumorClass I Phosphatidylinositol 3-KinasesFemaleGTP PhosphohydrolasesHumansMaleMelanomaMembrane ProteinsMiddle AgedPhosphatidylinositol 3-KinasesProto-Oncogene Proteins B-rafYoung AdultClass I Phosphatidylinositol 3-KinasesGTP PhosphohydrolasesMembrane ProteinsNRAS protein, humanPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene Proteins B-raf

Identifiers

PMID25627962
PMCPMC4312444
OpenAlexW2124863040

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Registered trials

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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.