Evidence map›Paper›PMID 38275886›Full record

ArticleCancers2024

The Clinical, Genomic, and Transcriptomic Landscape of BRAF Mutant Cancers.

Suzanne Kazandjian, Emmanuelle Rousselle, Matthew Dankner, David W Cescon, Anna Spreafico, Kim Ma, Petr Kavan, Gerald Batist, April A N Rose

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. GTP biosynthesis is a therapeutic vulnerability in Rac1-mutant melanoma.bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Braf-Mutant Melanomas: Biology and Therapy.Current oncology (Toronto, Ont.) · 2024
    Review
  11. Article
  12. Article
  13. 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

9 authors at 3 institutions in 1 country.

Suzanne KazandjianGerald Bronfman Department of Oncology, McGill University, Montreal, QC H4A 3T2, Canada.ORCID 0000-0001-6875-697X
Emmanuelle RousselleLady Davis Institute, Jewish General Hospital, Montreal, QC H3T 1E2, Canada.
Matthew DanknerLady Davis Institute, Jewish General Hospital, Montreal, QC H3T 1E2, Canada.ORCID 0000-0003-4869-5895
David W CesconDepartment of Medical Oncology and Hematology, Princess Margaret Cancer Center, Toronto, ON M5G 2M9, Canada.ORCID 0000-0002-1080-0998
Anna SpreaficoDepartment of Medical Oncology and Hematology, Princess Margaret Cancer Center, Toronto, ON M5G 2M9, Canada.ORCID 0000-0002-3034-3042
Kim MaGerald Bronfman Department of Oncology, McGill University, Montreal, QC H4A 3T2, Canada.
Petr KavanGerald Bronfman Department of Oncology, McGill University, Montreal, QC H4A 3T2, Canada.
Gerald BatistGerald Bronfman Department of Oncology, McGill University, Montreal, QC H4A 3T2, Canada.
April A N RoseGerald Bronfman Department of Oncology, McGill University, Montreal, QC H4A 3T2, Canada.
Jewish General Hospital · CAMcGill University Health Centre · CAPrincess Margaret Cancer Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBRAF mutations are classified into four molecularly distinct groups, and Class 1 (V600) mutant tumors are treated with targeted therapies. Effective treatment has not been established for Class 2/3 or BRAF Fusions. We investigated whether BRAF mutation class differed according to clinical, genomic, and transcriptomic variables in cancer patients.

methodsUsing the AACR GENIE (v.12) cancer database, the distribution of BRAF mutation class in adult cancer patients was analyzed according to sex, age, primary race, and tumor type. Genomic alteration data and transcriptomic analysis was performed using The Cancer Genome Atlas.

resultsBRAF mutations were identified in 9515 (6.2%) samples among 153,834, with melanoma (31%), CRC (20.7%), and NSCLC (13.9%) being the most frequent cancer types. Class 1 harbored co-mutations outside of the MAPK pathway (TERT, RFN43) vs. Class 2/3 mutations (RAS, NF1). Across all tumor types, Class 2/3 were enriched for alterations in genes involved in UV response and WNT/β-catenin. Pathway analysis revealed enrichment of WNT/β-catenin and Hedgehog signaling in non-V600 mutated CRC. Males had a higher proportion of Class 3 mutations vs. females (17.4% vs. 12.3% q = 0.003). Non-V600 mutations were generally more common in older patients (aged 60+) vs. younger (38% vs. 15%

conclusionsClass 2/3 BRAFs are more present in Black male patients with co-mutations outside of the MAPK pathway, likely requiring additional oncogenic input for tumorigenesis. Improving access to NGS and trial enrollment will help the development of targeted therapies for non-V600 BRAF mutations.

Indexed as

BRAF mutationcolorectal cancerMAPK pathwaymelanomanon-small cell lung cancer

Identifiers

PMID38275886
PMCPMC10814895
OpenAlexW4391023398

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.