Evidence map›Paper›PMID 25836739›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2015

Expression of the class 1 histone deacetylases HDAC8 and 3 are associated with improved survival of patients with metastatic melanoma.

James S Wilmott, Andrew J Colebatch, Hojabr Kakavand, Ping Shang, Matteo S Carlino, John F Thompson, Georgina V Long, Richard A Scolyer, Peter Hersey

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  4. HDAC/σ1R Dual-Ligand as a Targeted Melanoma Therapeutic.Pharmaceuticals (Basel, Switzerland) · 2025
    Article
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  7. Article
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  13. Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022
    Review
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  15. Article
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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

9 authors at 6 institutions in 1 country.

James S Wilmott1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Discipline of Medicine, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
Andrew J Colebatch1] Molecular Oncology Laboratory, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia [2] Discipline of Medicine, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
Hojabr Kakavand1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Discipline of Medicine, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
Ping ShangMelanoma Institute Australia, Sydney, New South Wales, Australia.
Matteo S Carlino1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Westmead Institute for Cancer Research, The University of Sydney at Westmead Millennium Institute, Westmead, New South Wales, Australia [3] Crown Princess Mary Cancer Centre, Westmead Hospital, Westmead, New South Wales, Australia.
John F Thompson1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Departments of Melanoma and Surgical Oncology, Camperdown, New South Wales, Australia [3] Mater Hospital, North Sydney, Sydney, New South Wales, Australia [4] Discipline of Surgery, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
Georgina V Long1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Discipline of Medicine, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
Richard A Scolyer1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Departments of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia [3] Discipline of Pathology, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
Peter Hersey1] Melanoma Institute Australia, Sydney, New South Wales, Australia [2] Discipline of Medicine, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia [3] Kolling Institute, Royal North Shore Hospital, The University of Sydney, Sydney, New South Wales, Australia.
Melanoma Institute Australia · AUThe University of Sydney · AUCooperative Trials Group for Neuro-Oncology · AUPeter MacCallum Cancer Centre · AURoyal Prince Alfred Hospital · AUWestmead Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prior studies have shown that combinations of histone deacetylase (HDAC) and BRAF inhibitors (BRAFi) have synergistic effects on BRAFi-resistant melanoma through enhanced apoptosis and inhibition of the cAMP-dependent drug resistance pathway. However, little is known about the expression of various HDACs and their associations with BRAF/NRAS mutation status, clinicopathologic characteristics, and patient outcome. The present study extensively profiled HDAC class 1 and their targets/regulators utilizing immunohistochemistry in human melanoma samples from patients with stage IV melanoma, known BRAF/NRAS mutational status, and detailed clinicopatholgical data. HDAC8 was increased in BRAF-mutated melanoma (P=0.016), however, no association between expression of other HDACs and NRAS/BRAF status was identified. There was also a correlation between HDAC1, HDAC8 expression, and phosphorylated NFκb p65 immunoreactivity (P<0.001). Increased cytoplasmic HDAC8 immunoreactivity was independently associated with an improved survival from both diagnosis of primary melanoma and from first detection of stage IV disease to melanoma death on multivariate analysis (HR 0.992, 95% CI 0.987-0.996; P<0.001 and HR 0.993, 95% CI 0.988-0.998; P=0.009, respectively). These results suggest not only that HDAC8 may be a prognostic biomarker in melanoma, but also provide important data regarding the regulation of HDACs in melanoma and a rational basis for targeting them therapeutically.

Indexed as

CytoplasmFemaleHistone Deacetylase 3Histone DeacetylasesHumansMaleMelanomaMutationNF-kappa BPhosphorylationPrognosisProto-Oncogene Proteins B-rafRepressor ProteinsSkin NeoplasmsSurvival RateHDAC8 protein, humanHistone Deacetylase 3Histone DeacetylasesNF-kappa BProto-Oncogene Proteins B-rafRepressor Proteins

Identifiers

PMID25836739
OpenAlexW1985425266

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.