Evidence map›Paper›PMID 11696442›Full record

ArticleThe American journal of pathology2001

GSTP1 CpG island hypermethylation is responsible for the absence of GSTP1 expression in human prostate cancer cells.

X Lin, M Tascilar, W H Lee, W J Vles, B H Lee, R Veeraswamy, K Asgari, D Freije, B van Rees, W R Gage and 6 more

Open access · greenAbstract read
In one paragraph

Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 243 citations in OpenAlex.

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15 more citing papers are in PubMed but not listed here.

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

16 authors at 2 institutions in 1 country.

X LinDepartment of Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
M Tascilar
W H Lee
W J Vles
B H Lee
R Veeraswamy
K Asgari
D Freije
B van Rees
W R Gage
G S Bova
W B Isaacs
J D Brooks
T L DeWeese
A M De Marzo
W G Nelson
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
GSTPI PROMOTOR HYPERMETHYLATION IN HUMAN PROSTATE CANCERR01CA070196 · NCI · JOHNS HOPKINS UNIVERSITY · PI NELSON, WILLIAM GEORGE · 1996 to 2012
$3.9M
NCI NIH HHS CA58236NCI NIH HHS CA70196NCI NIH HHS P50 CA058236NCI NIH HHS R01 CA070196
6 · The paper itself

Abstract

GSTP1 CpG island hypermethylation is the most common somatic genome alteration described for human prostate cancer (PCA); lack of GSTP1 expression is characteristic of human PCA cells in vivo. We report here that loss of GSTP1 function may have been selected during the pathogenesis of human PCA. Using a variety of techniques to detect GSTP1 CpG island DNA hypermethylation in PCA DNA, we found only hypermethylated GSTP1 alleles in each PCA cell in all but two PCA cases studied. In these two cases, CpG island hypermethylation was present at only one of two GSTP1 alleles in PCA DNA. In one of the cases, DNA hypermethylation at one GSTP1 allele and deletion of the other GSTP1 allele were evident. In the other case, an unmethylated GSTP1 allele was detected, accompanied by abundant GSTP1 expression. GSTP1 CpG island DNA hypermethylation was responsible for lack of GSTP1 expression by LNCaP PCA cells: treatment of the cells with 5-azacytidine (5-aza-C), an inhibitor of DNA methyltransferases, reversed the GSTP1 promoter DNA hypermethylation, activated GSTP1 transcription, and restored GSTP1 expression. GSTP1 promoter activity, assessed via transfection of GSTP1 promoter-CAT reporter constructs in LNCaP cells, was inhibited by SssI-catalyzed CpG dinucleotide methylation. Remarkably, although selection for loss of GSTP1 function may be inferred for human PCA, GSTP1 did not act like a tumor suppressor gene, as LNCaP cells expressing GSTP1, either after 5-aza-C treatment or as a consequence of transfection with GSTP1 cDNA, grew well in vitro and in vivo. Perhaps, GSTP1 inactivation may render prostatic cells susceptible to additional genome alterations, caused by electrophilic or oxidant carcinogens, that provide a selective growth advantage.

Indexed as

AllelesBase SequenceBlotting, SouthernCarcinogenicity TestsCell DivisionCpG IslandsDNA, NeoplasmGlutathione S-Transferase piGlutathione TransferaseHumansIsoenzymesMaleMethylationProstatic NeoplasmsReference ValuesTumor Cells, CulturedDNA, NeoplasmGlutathione S-Transferase piGlutathione TransferaseGSTP1 protein, humanIsoenzymes

Identifiers

PMID11696442
PMCPMC1867052
OpenAlexW2004797953

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.