Evidence map›Paper›PMID 28984291›Full record

ReviewNature reviews. Cancer2017

New perspectives for targeting RAF kinase in human cancer.

Zoi Karoulia, Evripidis Gavathiotis, Poulikos I Poulikakos

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
229citing papers in PubMed, 2 pooled it
15.9field-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

229 citing papers in PubMed, 2 syntheses or guidelines pooled it, 398 citations in OpenAlex.

  1. Pooled it
  2. Network indirect comparison of 3 BRAF + MEK inhibitors for the treatment of advanced BRAF mutated melanoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Pooled it
  3. Response to Anti-EGFR Therapy in Patients with BRAF non-V600-Mutant Metastatic Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Trial
  4. Article
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  11. Review
  12. Expression Analysis ofIranian journal of medical sciences · 2026
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Up-regulation of NGEF via the BRAFBiochemistry and biophysics reports · 2025
    Article
  19. Article
  20. Article

169 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

3 authors at 2 institutions in 1 country.

Zoi KarouliaDepartment of Oncological Sciences and Department of Dermatology, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.
Evripidis GavathiotisDepartment of Biochemistry, Department of Medicine, Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Poulikos I PoulikakosDepartment of Oncological Sciences and Department of Dermatology, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.
Icahn School of Medicine at Mount Sinai · USAlbert Einstein College of Medicine · US

Funding

Small Molecule Activators of Pro-apoptotic BAX for Cancer TherapyR01CA178394 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI GAVATHIOTIS, EVRIPIDIS · 2014 to 2024
$3.7M
Mechanism-based strategies to target oncogenic BRAF signalingR01CA204314 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI POULIKAKOS, POULIKOS I · 2017 to 2021
$2.1M
NCI NIH HHS R01 CA178394NCI NIH HHS R01 CA204314
6 · The paper itself

Abstract

The discovery that a subset of human tumours is dependent on mutationally deregulated BRAF kinase intensified the development of RAF inhibitors to be used as potential therapeutics. The US Food and Drug Administration (FDA)-approved second-generation RAF inhibitors vemurafenib and dabrafenib have elicited remarkable responses and improved survival of patients with BRAF-V600E/K melanoma, but their effectiveness is limited by resistance. Beyond melanoma, current clinical RAF inhibitors show modest efficacy when used for colorectal and thyroid BRAF-V600E tumours or for tumours harbouring BRAF alterations other than the V600 mutation. Accumulated experimental and clinical evidence indicates that the complex biochemical mechanisms of RAF kinase signalling account both for the effectiveness of RAF inhibitors and for the various mechanisms of tumour resistance to them. Recently, a number of next-generation RAF inhibitors, with diverse structural and biochemical properties, have entered preclinical and clinical development. In this Review, we discuss the current understanding of RAF kinase regulation, mechanisms of inhibitor action and related clinical resistance to these drugs. The recent elucidation of critical structural and biochemical aspects of RAF inhibitor action, combined with the availability of a number of structurally diverse RAF inhibitors currently in preclinical and clinical development, will enable the design of more effective RAF inhibitors and RAF-inhibitor-based therapeutic strategies, tailored to different clinical contexts.

Indexed as

HumansNeoplasmsProtein Kinase Inhibitorsraf KinasesProtein Kinase Inhibitorsraf Kinases

Identifiers

PMID28984291
PMCPMC6000833
OpenAlexW2762842128

What OpenQuestion holds

Textmetadata
LicenceTDM
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.