Evidence map›Paper›PMID 16848908›Full record

ArticleMolecular cancer2006

Methylation mediated silencing of TMS1/ASC gene in prostate cancer.

Partha M Das, Kavitha Ramachandran, Jane Vanwert, Larry Ferdinand, Gopal Gopisetty, Isildinha M Reis, Rakesh Singal

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.2field-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

57 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
  2. Review
  3. Journal of medicine and life · 2024
    Article
  4. Review
  5. Article
  6. Epigenetic (De)regulation in Prostate Cancer.Cancer treatment and research · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Dual Role of Inflammasome Adaptor ASC in Cancer.Frontiers in cell and developmental biology · 2020
    Review
  17. Article
  18. Article
  19. Review
  20. 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

7 authors at 2 institutions in 1 country.

Partha M DasSylvester Comprehensive Cancer Center, University of Miami, Miami, FL 33136, USA. pdmanas30@yahoo.com
Kavitha Ramachandran
Jane Vanwert
Larry Ferdinand
Gopal Gopisetty
Isildinha M Reis
Rakesh Singal
University of Miami · USSylvester Comprehensive Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTranscriptional silencing associated with aberrant promoter methylation has been established as an alternate pathway for the development of cancer by inactivating tumor suppressor genes. TMS1 (Target of Methylation induced Silencing), also known as ASC (Apoptosis Speck like protein containing a CARD) is a tumor suppressor gene which encodes for a CARD (caspase recruitment domain) containing regulatory protein and has been shown to promote apoptosis directly and by activation of downstream caspases. This study describes the methylation induced silencing of TMS1/ASC gene in prostate cancer cell lines. We also examined the prevalence of TMS1/ASC gene methylation in prostate cancer tissue samples in an effort to correlate race and clinico-pathological features with TMS1/ASC gene methylation.

resultsLoss of TMS1/ASC gene expression associated with complete methylation of the promoter region was observed in LNCaP cells. Gene expression was restored by a demethylating agent, 5-aza-2'deoxycytidine, but not by a histone deacetylase inhibitor, Trichostatin A. Chromatin Immunoprecipitation (ChIP) assay showed enrichment of MBD3 (methyl binding domain protein 3) to a higher degree than commonly associated MBDs and MeCP2. We evaluated the methylation pattern in 66 prostate cancer and 34 benign prostatic hyperplasia tissue samples. TMS1/ASC gene methylation was more prevalent in prostate cancer cases than controls in White patients (OR 7.6, p 0.002) while no difference between the cases and controls was seen in Black patients (OR 1.1, p 0.91).

conclusionOur study demonstrates that methylation-mediated silencing of TMS1/ASC is a frequent event in prostate cancer, thus identifying a new potential diagnostic and prognostic marker for the treatment of the disease. Racial differences in TMS1/ASC methylation patterns implicate the probable role of molecular markers in determining in susceptibility to prostate cancer in different ethnic groups.

Indexed as

DNA MethylationGene SilencingAgedAged, 80 and overAzacitidineCARD Signaling Adaptor ProteinsCell Line, TumorChromatin ImmunoprecipitationCpG IslandsCytoskeletal ProteinsDecitabineDNA Modification MethylasesDNA, NeoplasmEnzyme InhibitorsGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsAzacitidineCARD Signaling Adaptor ProteinsCytoskeletal ProteinsDecitabineDNA Modification MethylasesDNA, NeoplasmEnzyme InhibitorsHistone Deacetylase InhibitorsHydroxamic AcidsPYCARD protein, humantrichostatin A

Identifiers

PMID16848908
PMCPMC1543653
OpenAlexW2133478283

What OpenQuestion holds

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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.