Evidence map›Paper›PMID 33112375›Full record

ArticleThe Journal of experimental medicine2021

Sustained androgen receptor signaling is a determinant of melanoma cell growth potential and tumorigenesis.

Min Ma, Soumitra Ghosh, Daniele Tavernari, Atul Katarkar, Andrea Clocchiatti, Luigi Mazzeo, Anastasia Samarkina, Justine Epiney, Yi-Ru Yu, Ping-Chih Ho and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.3field-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

37 citing papers in PubMed, 56 citations in OpenAlex.

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  12. X and Y Differences in Melanoma Survival Between the Sexes.Pigment cell & melanoma research · 2025
    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 7 institutions in 2 countries.

Min MaDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Soumitra GhoshDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Daniele TavernariDepartment of Computational Biology, University of Lausanne, Lausanne, Switzerland.
Atul KatarkarDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Andrea ClocchiattiCutaneous Biology Research Center, Massachusetts General Hospital, Charlestown, MA.
Luigi MazzeoDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Anastasia SamarkinaDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Justine EpineyDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Yi-Ru YuDepartment of Oncology, University of Lausanne, Ludwig Institute for Cancer Research Lausanne, Epalinges, Switzerland.
Ping-Chih HoDepartment of Oncology, University of Lausanne, Ludwig Institute for Cancer Research Lausanne, Epalinges, Switzerland.
Mitchell P LevesqueDepartment of Dermatology, University Hospital Zürich, University of Zürich, Zürich, Switzerland.
Berna C ÖzdemirDepartment of Oncology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Giovanni CirielloDepartment of Computational Biology, University of Lausanne, Lausanne, Switzerland.
Reinhard DummerDepartment of Dermatology, University Hospital Zürich, University of Zürich, Zürich, Switzerland.
G Paolo DottoDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.
University of Lausanne · CHLudwig Cancer Research · CHSIB Swiss Institute of Bioinformatics · CHUniversity of Zurich · CHHarvard University · USMassachusetts General Hospital · USUniversity Hospital of Lausanne · CH

Funding

GROWTH DIFFERENTIATION CONTROL IN PRIMARY KERATINOCYTES.R01AR039190 · NIAMS · YALE UNIVERSITY · PI DOTTO, GIAN-PAOLO · 1988 to 2021
$9.5M
Dermal fibroblast/ATF3 control of skin homeostasisR01AR064786 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DOTTO, GIAN-PAOLO · 2014 to 2018
$1.9M
NIAMS NIH HHS R01 AR039190NIAMS NIH HHS R01 AR064786
6 · The paper itself

Abstract

Melanoma susceptibility differs significantly in male versus female populations. Low levels of androgen receptor (AR) in melanocytes of the two sexes are accompanied by heterogeneous expression at various stages of the disease. Irrespective of expression levels, genetic and pharmacological suppression of AR activity in melanoma cells blunts proliferation and induces senescence, while increased AR expression or activation exert opposite effects. AR down-modulation elicits a shared gene expression signature associated with better patient survival, related to interferon and cytokine signaling and DNA damage/repair. AR loss leads to dsDNA breakage, cytoplasmic leakage, and STING activation, with AR anchoring the DNA repair proteins Ku70/Ku80 to RNA Pol II and preventing RNA Pol II-associated DNA damage. AR down-modulation or pharmacological inhibition suppresses melanomagenesis, with increased intratumoral infiltration of macrophages and, in an immune-competent mouse model, cytotoxic T cells. AR provides an attractive target for improved management of melanoma independent of patient sex.

Indexed as

AnimalsCarcinogenesisCell Line, TumorCell ProliferationDNA DamageDNA RepairDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMaleMelanomaMiceMice, Inbred C57BLMice, Inbred NODMice, SCIDAR protein, humanReceptors, AndrogenRNA Polymerase II

Identifiers

PMID33112375
PMCPMC7596884
OpenAlexW3095941576

What Socratic 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 Socratic graph.