Evidence map›Paper›PMID 24957944›Full record

ReviewNature reviews. Cancer2014

Targeting RAF kinases for cancer therapy: BRAF-mutated melanoma and beyond.

Matthew Holderfield, Marian M Deuker, Frank McCormick, Martin McMahon

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 445 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
445citing papers in PubMed, 1 pooled it
35.6field-weighted citation impact, top 1% 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

445 citing papers in PubMed, 1 synthesis or guideline pooled it, 817 citations in OpenAlex.

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385 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Matthew Holderfield1] Helen Diller Family Comprehensive Cancer Center and Department of Cell and Molecular Pharmacology, University of California, San Francisco, California 94158, USA. [2].
Marian M Deuker1] Helen Diller Family Comprehensive Cancer Center and Department of Cell and Molecular Pharmacology, University of California, San Francisco, California 94158, USA. [2].
Frank McCormickHelen Diller Family Comprehensive Cancer Center and Department of Cell and Molecular Pharmacology, University of California, San Francisco, California 94158, USA.
Martin McMahonHelen Diller Family Comprehensive Cancer Center and Department of Cell and Molecular Pharmacology, University of California, San Francisco, California 94158, USA.
UCSF Helen Diller Family Comprehensive Cancer Center · US

Funding

RESEARCH TRAINING IN CHEMISTRY AND CHEMICAL BIOLOGYT32GM064337 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CRAIK, CHARLES SCOTT · 2002 to 2021
$7.8M
Studying the initiation, progression and therapy of lung cancer in mouse modelsR01CA131261 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI MARTIN MCMAHON · 2009 to 2026
$5.3M
Targeting Oncogenic NRAS, BRAF plus PI3'-Kinase Signaling for Melanoma TherapyR01CA176839 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI MARTIN MCMAHON · 2013 to 2026
$2.9M
NCI NIH HHS R01 CA131261NCI NIH HHS R01 CA176839NIGMS NIH HHS T32 GM064337
6 · The paper itself

Abstract

The identification of mutationally activated BRAF in many cancers altered our conception of the part played by the RAF family of protein kinases in oncogenesis. In this Review, we describe the development of BRAF inhibitors and the results that have emerged from their analysis in both the laboratory and the clinic. We discuss the spectrum of RAF mutations in human cancer and the complex interplay between the tissue of origin and the response to RAF inhibition. Finally, we enumerate mechanisms of resistance to BRAF inhibition that have been characterized and postulate how strategies of RAF pathway inhibition may be extended in scope to benefit not only the thousands of patients who are diagnosed annually with BRAF-mutated metastatic melanoma but also the larger patient population with malignancies harbouring mutationally activated RAF genes that are ineffectively treated with the current generation of BRAF kinase inhibitors.

Indexed as

AnimalsDrug Resistance, NeoplasmHumansMelanomaMutationProtein Kinase InhibitorsProto-Oncogene Proteins B-rafSkin NeoplasmsProtein Kinase InhibitorsProto-Oncogene Proteins B-raf

Identifiers

PMID24957944
PMCPMC4250230
OpenAlexW1985821753

What OpenQuestion holds

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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.