Evidence map›Paper›PMID 29202482›Full record

ArticleThe Journal of clinical investigation2018

Ligand-activated BMP signaling inhibits cell differentiation and death to promote melanoma.

Arvind M Venkatesan, Rajesh Vyas, Alec K Gramann, Karen Dresser, Sharvari Gujja, Sanchita Bhatnagar, Sagar Chhangawala, Camilla Borges Ferreira Gomes, Hualin Simon Xi, Christine G Lian and 5 more

Open access · bronzeAbstract readVideo-Audio Media
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.7field-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

38 citing papers in PubMed, 71 citations in OpenAlex.

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  10. Review
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  12. BMP signaling in cancer stemness and differentiation.Cell regeneration (London, England) · 2023
    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 5 institutions in 3 countries.

Arvind M VenkatesanProgram in Molecular Medicine.
Rajesh VyasProgram in Molecular Medicine.
Alec K GramannProgram in Molecular Medicine.
Karen DresserDepartment of Pathology, and.
Sharvari GujjaProgram in Molecular Medicine.
Sanchita BhatnagarProgram in Molecular Medicine.
Sagar ChhangawalaDepartments of Surgery and Medicine, Weill Cornell Medical College, New York, New York, USA.
Camilla Borges Ferreira GomesProgram in Dermatopathology, Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Hualin Simon XiProgram in Molecular Medicine.
Christine G LianProgram in Dermatopathology, Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Yariv HouvrasDepartments of Surgery and Medicine, Weill Cornell Medical College, New York, New York, USA.
Yvonne J K EdwardsProgram in Molecular Medicine.
April DengDepartment of Pathology, and.
Michael GreenProgram in Molecular Medicine.
Craig J CeolProgram in Molecular Medicine.
Institute of Molecular and Cell Biology · RUInstitute of Molecular Medicine · INBrigham and Women's Hospital · USCornell University · USHoward Hughes Medical Institute · US

Funding

Use of comparative genomics to identify novel regulators of melanoma progressionR01AR063850 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CEOL, CRAIG JOSEPH · 2013 to 2017
$1.8M
NIAMS NIH HHS R01 AR063850
6 · The paper itself

Abstract

Oncogenomic studies indicate that copy number variation (CNV) alters genes involved in tumor progression; however, identification of specific driver genes affected by CNV has been difficult, as these rearrangements are often contained in large chromosomal intervals among several bystander genes. Here, we addressed this problem and identified a CNV-targeted oncogene by performing comparative oncogenomics of human and zebrafish melanomas. We determined that the gene encoding growth differentiation factor 6 (GDF6), which is the ligand for the BMP family, is recurrently amplified and transcriptionally upregulated in melanoma. GDF6-induced BMP signaling maintained a trunk neural crest gene signature in melanomas. Additionally, GDF6 repressed the melanocyte differentiation gene MITF and the proapoptotic factor SOX9, thereby preventing differentiation, inhibiting cell death, and promoting tumor growth. GDF6 was specifically expressed in melanomas but not melanocytes. Moreover, GDF6 expression levels in melanomas were inversely correlated with patient survival. Our study has identified a fundamental role for GDF6 and BMP signaling in governing an embryonic cell gene signature to promote melanoma progression, thus providing potential opportunities for targeted therapy to treat GDF6-positive cancers.

Indexed as

Cell DifferentiationSignal TransductionAnimalsBone Morphogenetic ProteinsCell Line, TumorFemaleGrowth Differentiation Factor 6HEK293 CellsHumansLigandsMelanomaMiceMice, Inbred BALB CMice, NudeMicrophthalmia-Associated Transcription FactorNeoplasm ProteinsBone Morphogenetic ProteinsGDF6 protein, humanGrowth Differentiation Factor 6LigandsMicrophthalmia-Associated Transcription FactorMITF protein, humanNeoplasm ProteinsCancerDevelopmentOncology

Identifiers

PMID29202482
PMCPMC5749509
OpenAlexW2773070885

What OpenQuestion holds

Textmetadata
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.