Evidence map›Paper›PMID 28947418›Full record

ArticleCancer research2017

KIT Suppresses BRAF

James V Neiswender, Robert L Kortum, Caitlin Bourque, Melissa Kasheta, Leonard I Zon, Deborah K Morrison, Craig J Ceol

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Metrnl in mitigating radiation enteritisActa pharmaceutica Sinica. B · 2026
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  12. MEK1/2 as a Therapeutic Target in Sickle Cell Disease.International journal of blood research and disorders · 2019
    Article
  13. BRAFV600E and KIT immunoexpression in early-stage melanoma.Anais brasileiros de dermatologia · 2019
    Article
  14. Article
  15. Review
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

7 authors at 4 institutions in 1 country.

James V NeiswenderProgram in Molecular Medicine, Department of Molecular, Cell, and Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts.
Robert L KortumLaboratory of Cell and Developmental Signaling, National Cancer Institute at Frederick, Frederick, Maryland.
Caitlin BourqueHoward Hughes Medical Institute, Stem Cell Program and Division of Hematology/Oncology, Boston Children's Hospital, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts.
Melissa KashetaProgram in Molecular Medicine, Department of Molecular, Cell, and Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts.
Leonard I ZonHoward Hughes Medical Institute, Stem Cell Program and Division of Hematology/Oncology, Boston Children's Hospital, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts.
Deborah K MorrisonLaboratory of Cell and Developmental Signaling, National Cancer Institute at Frederick, Frederick, Maryland.
Craig J CeolProgram in Molecular Medicine, Department of Molecular, Cell, and Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts. Craig.Ceol@umassmed.edu.
University of Massachusetts Chan Medical School · USDana-Farber Cancer Institute · USFrederick National Laboratory for Cancer Research · USUniformed Services University of the Health Sciences · US

Funding

Regulation of Ras-Dependent Signal Transduction PathwaysZIABC010329 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MORRISON, DEBORAH · 2009 to 2025
$16.1M
Use of comparative genomics to identify novel regulators of melanoma progressionR01AR063850 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CEOL, CRAIG JOSEPH · 2013 to 2017
$1.8M
Identifying Events and Genetic Regulators of Melanoma ProgressionR00AR056899 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CEOL, CRAIG JOSEPH · 2010 to 2012
$725k
NIAMS NIH HHS R00 AR056899NIAMS NIH HHS R01 AR063850
6 · The paper itself

Abstract

The receptor tyrosine kinase KIT promotes survival and migration of melanocytes during development, and excessive KIT activity hyperactivates the RAS/MAPK pathway and can drive formation of melanomas, most notably of rare melanomas that occur on volar and mucosal surfaces of the skin. The much larger fraction of melanomas that occur on sun-exposed skin is driven primarily by BRAF- or NRAS-activating mutations, but these melanomas exhibit a surprising loss of KIT expression, which raises the question of whether loss of KIT in these tumors facilitates tumorigenesis. To address this question, we introduced a

Indexed as

MutationAnimalsAnimals, Genetically ModifiedBlotting, WesternCell Line, TumorGene Expression Regulation, NeoplasticHEK293 CellsHumansIn Situ HybridizationMAP Kinase Signaling SystemMelanomaProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-kitras ProteinsTumor Suppressor Protein p53ZebrafishProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-kitras ProteinsTumor Suppressor Protein p53

Identifiers

PMID28947418
PMCPMC5679278
OpenAlexW2760117061

What OpenQuestion holds

Textmetadata
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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.