Evidence map›Paper›PMID 30254212›Full record

ArticleOncogene2019

BRAF fusions identified in melanomas have variable treatment responses and phenotypes.

Jacqueline A Turner, Judson G T Bemis, Stacey M Bagby, Anna Capasso, Betelehem W Yacob, Tugs-Saikhan Chimed, Robert Van Gulick, Hannah Lee, Richard Tobin, John J Tentler and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. Gene fusions in melanocytic lesions: an updated comprehensive review.Journal of pathology and translational medicine · 2026
    Article
  3. Article
  4. Oncogenic gene fusions in cancer: from biology to therapy.Signal transduction and targeted therapy · 2025
    Review
  5. Review
  6. TargetingBiotechnologia · 2025
    Article
  7. Braf-Mutant Melanomas: Biology and Therapy.Current oncology (Toronto, Ont.) · 2024
    Review
  8. Amelanotic Melanoma-Biochemical and Molecular Induction Pathways.International journal of molecular sciences · 2024
    Review
  9. Tumor-Agnostic Genomic and Clinical Analysis of BRAF Fusions Identifies Actionable Targets.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Unraveling the Wide Spectrum of Melanoma Biomarkers.Diagnostics (Basel, Switzerland) · 2021
    Review
  19. Article
  20. 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

14 authors at 1 institution in 1 country.

Jacqueline A TurnerDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Judson G T BemisDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Stacey M BagbyDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Anna CapassoDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Betelehem W YacobDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Tugs-Saikhan ChimedDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Robert Van GulickDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Hannah LeeDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Richard TobinDivision Surgical Oncology, Department of Surgery, University of Colorado Denver, Aurora, CO, USA.
John J TentlerDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Todd PittsDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Martin McCarterDivision Surgical Oncology, Department of Surgery, University of Colorado Denver, Aurora, CO, USA.
William A RobinsonDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA.
Kasey L CoutsDivision of Medical Oncology, Department of Medicine, University of Colorado Denver, Aurora, CO, USA. kasey.couts@ucdenver.edu.
University of Colorado Denver · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Colorado Clinical and Translational Sciences InstituteUL1TR001082 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2013 to 2017
$48.0M
PREDOCTORAL TRAINING PROGRAM IN PHARMACOLOGYT32GM007635 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 1985 to 2023
$6.1M
NIGMS NIH HHS T32 GM007635NIH HHS P30CA046934NIH HHS UL1 TR001082
6 · The paper itself

Abstract

Oncogenic BRAF fusions have emerged as an alternate mechanism for BRAF activation in melanomas and other cancers. A number of BRAF fusions with different 5' gene partners and BRAF exon breakpoints have been described, but the effects of different partners and breakpoints on cancer phenotypes and treatment responses has not been well characterized. Targeted RNA sequencing was used to screen 60 melanoma patient-derived xenograft (PDX) models for BRAF fusions. We identified three unique BRAF fusions, including a novel SEPT3-BRAF fusion, occurring in four tumors (4/60, 6.7%), all of which were "pan-negative" (lacking other common mutations) (4/18, 22.2%). The BRAF fusion PDX models showed variable growth rates and responses to MAPK inhibitors in vivo. Overexpression of BRAF fusions identified in our study, as well as other BRAF fusions previously identified in melanomas, resulted in a high degree of variability in 2D proliferation and 3D invasion between the different fusions. While exogenously expressed BRAF fusions all responded to MAPK inhibition in vitro, we observed potential differences in signaling and feedback mechanisms. In summary, BRAF fusions are actionable therapeutic targets, however there are significant differences in phenotypes, treatment responses, and signaling which may be clinically relevant.

Indexed as

Cell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMelanomaMutationNeoplasm InvasivenessOncogene Proteins, FusionProtein Kinase InhibitorsProto-Oncogene Proteins B-rafSeptinsSequence Analysis, RNASignal TransductionXenograft Model Antitumor AssaysBRAF protein, humanOncogene Proteins, FusionProtein Kinase InhibitorsProto-Oncogene Proteins B-rafseptin 3Septins

Identifiers

PMID30254212
OpenAlexW2894448865

What OpenQuestion holds

Textmetadata
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.