Evidence map›Paper›PMID 31342168›Full record

ArticleJournal of cancer research and clinical oncology2019

Heterozygous loss of keratinocyte TRIM16 expression increases melanocytic cell lesions and lymph node metastasis.

Selina K Sutton, Belamy B Cheung, Hassina Massudi, Owen Tan, Jessica Koach, Chelsea Mayoh, Daniel R Carter, Glenn M Marshall

Open access · hybridAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Selina K SuttonChildren's Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, UNSW Sydney, Kensington, NSW, Australia.
Belamy B CheungChildren's Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, UNSW Sydney, Kensington, NSW, Australia. bcheung@ccia.unsw.edu.au.ORCID http://orcid.org/0000-0001-8784-860X
Hassina MassudiChildren's Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, UNSW Sydney, Kensington, NSW, Australia.
Owen TanChildren's Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, UNSW Sydney, Kensington, NSW, Australia.
Jessica KoachChildren's Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, UNSW Sydney, Kensington, NSW, Australia.
Chelsea MayohChildren's Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, UNSW Sydney, Kensington, NSW, Australia.
Daniel R CarterChildren's Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, UNSW Sydney, Kensington, NSW, Australia.
Glenn M MarshallChildren's Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, UNSW Sydney, Kensington, NSW, Australia. g.marshall@unsw.edu.au.
UNSW Sydney · AUUniversity of Technology Sydney · AU

Funding

Cancer Council NSW PG-11-06Cancer Institute NSW 10/TPG/1-13the National Health and Medical Research Council Australia APP1016699
6 · The paper itself

Abstract

purposeThe tripartite motif (TRIM)16 acts as a tumour suppressor in both squamous cell carcinoma (SCC) and melanoma. TRIM16 is known to be secreted by keratinocytes, but no studies have been reported yet to assess the relationship between TRIM16 keratinocyte expression and melanoma development.

methodsTo study the role of TRIM16 in skin cancer development, we developed a keratinocyte TRIM16-specific knockout mouse model, and used the classical two-stage skin carcinogenesis challenge method, to assess the loss of keratinocyte TRIM16 on both papilloma, SCC and melanoma development in the skin after topical carcinogen treatment.

resultsHeterozygous, but not homozygous, TRIM16 knockout mice exhibited an accelerated development of skin papillomas and melanomas, larger melanoma lesions and an increased potential for lymph node metastasis.

conclusionThis study provides the first evidence that keratinocyte loss of the putative melanoma tumour suppressor protein, TRIM16, enhances melanomagenesis. Our data also suggest that TRIM16 expression in keratinocytes is involved in cross talk between keratinocytes and melanocytes, and has a role in melanoma tumorigenesis.

Indexed as

AnimalsCarcinoma, Squamous CellCarrier ProteinsCells, CulturedCell Transformation, NeoplasticGene Expression Regulation, NeoplasticKeratinocytesLoss of HeterozygosityLymphatic MetastasisLymph NodesMelanocytesMelanomaMiceMice, KnockoutSkinSkin NeoplasmsCarrier ProteinsTrim16 protein, mouseTripartite Motif ProteinsUbiquitin-Protein LigasesCarcinogenesisKeratinocyteMelanomaMetastasisMigrationTRIM16

Identifiers

PMID31342168
PMCPMC6708510
OpenAlexW2962839521

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.