Evidence map›Paper›PMID 32913556›Full record

ArticleOncotarget2020

Molecular profiling of melanoma brain metastases compared to primary cutaneous melanoma and to extracranial metastases.

Gino K In, Kelsey Poorman, Michelle Saul, Steven O'Day, Jeffrey M Farma, Anthony J Olszanski, Michael S Gordon, Jacob S Thomas, Burton Eisenberg, Lawrence Flaherty and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-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

25 citing papers in PubMed, 34 citations in OpenAlex.

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  19. Emerging Studies of Melanoma Brain Metastasis.Current oncology reports · 2022
    Review
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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

15 authors at 9 institutions in 1 country.

Gino K InUSC Norris Comprehensive Cancer Center, Los Angeles, CA, USA.
Kelsey PoormanCaris Life Sciences, Phoenix, AZ, USA.
Michelle SaulCaris Life Sciences, Phoenix, AZ, USA.
Steven O'DayJohn Wayne Cancer Institute, Santa Monica, CA, USA.
Jeffrey M FarmaFox Chase Cancer Center, Philadelphia, PA, USA.
Anthony J OlszanskiFox Chase Cancer Center, Philadelphia, PA, USA.
Michael S GordonHonorHealth Medical Group, Scottsdale, AZ, USA.
Jacob S ThomasUSC Norris Comprehensive Cancer Center, Los Angeles, CA, USA.
Burton EisenbergHoag Family Cancer Institute, Newport Beach, CA, USA.
Lawrence FlahertyKarmanos Cancer Institute, Detroit, MI, USA.
Amy WeiseKarmanos Cancer Institute, Detroit, MI, USA.
Steven DaveluyKarmanos Cancer Institute, Detroit, MI, USA.
Geoffrey GibneyGeorgetown Lombardi Comprehensive Cancer Center, Washington, DC, USA.
Michael B AtkinsGeorgetown Lombardi Comprehensive Cancer Center, Washington, DC, USA.
Ari VanderwaldeUniversity of Tennessee Health Science Center, West Cancer Center, Germantown, TN, USA.
The Barbara Ann Karmanos Cancer Institute · USCaris Life Sciences (United States) · USFox Chase Cancer Center · USGeorgetown Lombardi Comprehensive Cancer CenterUSC Norris Comprehensive Cancer Center · USHoag Memorial Hospital Presbyterian · USHonorHealth · USSaint John's Health Center · USUniversity of Tennessee Health Science Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBrain metastases are a significant cause of mortality and morbidity for patients with melanoma. We hypothesize that the development of brain metastases may be explained by molecular heterogeneity between primary cutaneous melanoma (PCM) or extracranial (ECM) and brain (MBM) melanoma metastases. MATERIALS AND

methodsWe compared next-generation sequencing, tumor mutational burden (TMB), and immunohistochemical staining for PD-L1 expression, among 132 MBM, 745 PCM, and 1190 ECM.

resultsThe most common genetic alterations among MBM included: BRAF (52.4%), NRAS (26.6%), CDKN2A (23.3%), NF1 (18.9%), TP53 (18%), ARID2 (13.8%), SETD2 (11.9%), and PBRM1 (7.5%). Four genes were found with higher frequency among MBM compared to PCM or ECM: BRAF (52.4% v 40.4% v 40.9%), SETD2 (11.9% v 1.9% v 3.9%), PBRM1 (7.5% v 1.6% v 2.6%), and DICER1 (4.4% v 0.6% v 0.4%). MBM showed higher TMB (

conclusionsOur findings suggest a unique molecular profile for MBM, including higher rates of BRAF mutations, higher TMB and higher PD-L1 expression, and also implicate chromatin remodeling in the pathogenesis of MBM.

Indexed as

BRAFbrain metastasesmelanomaPD-L1TMB

Identifiers

PMID32913556
PMCPMC7443369
OpenAlexW3070032407

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.