Evidence map›Paper›PMID 40588721›Full record

ArticlePigment cell & melanoma research2025

Prospective Isolation According to Melanin Pigment Content of Melanoma Cells With Heterogeneous Potentials for Disease Propagation.

Clare Fedele, Gamze Kuser-Abali, Ralph Rossi, Peinan Zhao, Jason Li, Malaka Ameratunga, Pacman Szeto, YouFang Zhang, Miles Andrews, Mark Shackleton

Abstract read
In one paragraph

Article in Pigment cell & melanoma research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

10 authors.

Clare FedeleDepartment of Pathology, University of Melbourne, Parkville, Victoria, Australia.ORCID 0000-0003-2392-5754
Gamze Kuser-AbaliSchool of Translational Medicine, Monash University, Prahran, Victoria, Australia.ORCID 0000-0002-4590-0577
Ralph RossiPeter MacCallum Cancer Centre, Melbourne, Victoria, Australia.
Peinan ZhaoSchool of Translational Medicine, Monash University, Prahran, Victoria, Australia.ORCID 0000-0002-9716-3441
Jason LiPeter MacCallum Cancer Centre, Melbourne, Victoria, Australia.
Malaka AmeratungaSchool of Translational Medicine, Monash University, Prahran, Victoria, Australia.ORCID 0000-0002-7171-6781
Pacman SzetoSchool of Translational Medicine, Monash University, Prahran, Victoria, Australia.ORCID 0000-0002-6159-9913
YouFang ZhangSchool of Translational Medicine, Monash University, Prahran, Victoria, Australia.
Miles AndrewsSchool of Translational Medicine, Monash University, Prahran, Victoria, Australia.ORCID 0000-0003-1231-8641
Mark ShackletonSchool of Translational Medicine, Monash University, Prahran, Victoria, Australia.ORCID 0000-0002-7673-4655

Funding

Melanoma Research Alliance (USA)Melanoma Research VictoriaNational Health and Medical Research Council of AustraliaVictorian Cancer Biobank
6 · The paper itself

Abstract

Intra-tumoral heterogeneity poses a major challenge to treating and managing cancer patients. A characteristic feature of melanoma is its composition of cancer cells with typically heterogeneous content of melanin pigment, the production of which is a hallmark of normal melanocytic differentiation but of poorly understood consequence in melanoma cells, as prospective assessment of pigment heterogeneity in melanoma cells has been experimentally challenging. Here, we describe a novel flow cytometric method for high purity separation of viable melanoma cells based on their melanin content, exploiting the light scattering properties of melanin. By fluorescence-activated cell sorting, we show that cells with low-pigment content (LPCs) in melanoma cell lines and patient tumors are usually far more abundant than high-pigment cells (HPCs) and have substantially increased potentials for colony formation in vitro and tumor formation in vivo. In RNAseq analysis, HPCs showed P53 activation and perturbed cell cycling, whereas LPCs displayed upregulation of MYC-associated transcription and activated ribosome biogenesis. In proof-of-concept studies, the latter was targeted by topoisomerase 2 beta targeting with CX-5461, which induced senescent HPC phenotypes and irreversible loss of clonogenic activity. These data indicate an 'inverted pyramid' hierarchical model of melanoma cell propagation wherein abundant LPCs frequently renew their own malignant potential to propagate disease but also infrequently generate HPCs that spontaneously lose this ability in a manner that might be exploited as an anti-melanoma strategy.

Indexed as

Cell SeparationMelaninsMelanomaSkin NeoplasmsAnimalsCell Line, TumorFlow CytometryHumansTumor Suppressor Protein p53MelaninsTumor Suppressor Protein p53melanocytic differentiationpigment heterogeneityribosome biogenesis

Identifiers

PMID40588721
PMCPMC12209049

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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.