Evidence map›Paper›PMID 38183207›Full record

ArticleBriefings in functional genomics2025

Systematic analysis of the transcriptional landscape of melanoma reveals drug-target expression plasticity.

Brad Balderson, Mitchell Fane, Tracey J Harvey, Michael Piper, Aaron Smith, Mikael Bodén

Open access · hybridAbstract read
In one paragraph

Article in Briefings in functional genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. 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

6 authors at 3 institutions in 2 countries.

Brad BaldersonSchool of Chemistry and Molecular Biosciences, University of Queensland, Brisbane, 4072 Queensland, Australia.ORCID 0000-0002-5153-6601
Mitchell FaneFox Chase Cancer Centre, Philadelphia, 19019 Pennsylvania, United States of America.
Tracey J HarveySchool of Biomedical Sciences, University of Queensland, Brisbane, 4072 Queensland, Australia.
Michael PiperSchool of Biomedical Sciences, University of Queensland, Brisbane, 4072 Queensland, Australia.ORCID 0000-0002-6759-2560
Aaron SmithSchool of Biomedical Sciences, Queensland University of Technology, Brisbane, 4072 Queensland, Australia.
Mikael BodénSchool of Chemistry and Molecular Biosciences, University of Queensland, Brisbane, 4072 Queensland, Australia.ORCID 0000-0003-3548-268X
Queensland University of Technology · AUThe University of Queensland · AUFox Chase Cancer Center · US

Funding

The role of MER/PROS1 in promoting stromal induced emergence from metastatic melanoma dormancyR00CA263017 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI FANE, MITCHELL EDWARD · 2023 to 2025
$747k
The role of MER/PROS1 in promoting stromal induced emergence from metastatic melanoma dormancyK99CA263017 · NCI · JOHNS HOPKINS UNIVERSITY · PI FANE, MITCHELL EDWARD · 2022 to 2022
$121k
Australian Government Research Training ProgramNCI NIH HHS K99 CA263017NCI NIH HHS R00 CA263017
6 · The paper itself

Abstract

Metastatic melanoma originates from melanocytes of the skin. Melanoma metastasis results in poor treatment prognosis for patients and is associated with epigenetic and transcriptional changes that reflect the developmental program of melanocyte differentiation from neural crest stem cells. Several studies have explored melanoma transcriptional heterogeneity using microarray, bulk and single-cell RNA-sequencing technologies to derive data-driven models of the transcriptional-state change which occurs during melanoma progression. No study has systematically examined how different models of melanoma progression derived from different data types, technologies and biological conditions compare. Here, we perform a cross-sectional study to identify averaging effects of bulk-based studies that mask and distort apparent melanoma transcriptional heterogeneity; we describe new transcriptionally distinct melanoma cell states, identify differential co-expression of genes between studies and examine the effects of predicted drug susceptibilities of different cell states between studies. Importantly, we observe considerable variability in drug-target gene expression between studies, indicating potential transcriptional plasticity of melanoma to down-regulate these drug targets and thereby circumvent treatment. Overall, observed differences in gene co-expression and predicted drug susceptibility between studies suggest bulk-based transcriptional measurements do not reliably gauge heterogeneity and that melanoma transcriptional plasticity is greater than described when studies are considered in isolation.

Indexed as

Gene Expression Regulation, NeoplasticMelanomaTranscription, GeneticGene Expression ProfilingHumanscancerdrugmelanomametastasisphenotype switchingscRNA-seqtrajectory inference

Identifiers

PMID38183207
PMCPMC11979751
OpenAlexW4390645853

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.