Evidence map›Paper›PMID 18667590›Full record

ArticleMolecular cancer research : MCR2008

Stage-specific alterations of DNA methyltransferase expression, DNA hypermethylation, and DNA hypomethylation during prostate cancer progression in the transgenic adenocarcinoma of mouse prostate model.

Shannon R Morey Kinney, Dominic J Smiraglia, Smitha R James, Michael T Moser, Barbara A Foster, Adam R Karpf

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 73 citations in OpenAlex.

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  15. p16 hypermethylation: a biomarker for increased esophageal cancer susceptibility in high incidence region of North East India.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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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

6 authors at 2 institutions in 1 country.

Shannon R Morey KinneyDepartment of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.
Dominic J Smiraglia
Smitha R James
Michael T Moser
Barbara A Foster
Adam R Karpf
Roswell Park Comprehensive Cancer Center · USCancer Genetics (United States) · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
DRUG DEVELOPMENT AND CANCER TREATMENTST32CA009072 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI JOHNSON, CANDACE S · 1985 to 2014
$2.3M
CpG island methylation discovery in prostate cancerR21CA121216 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI SMIRAGLIA, DOMINIC JAMES · 2006 to 2007
$337k
Green tea-mediated inhibition of aberrant DNA hypermethylation in prostate cancerR21CA128062 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI KARPF, ADAM R · 2006 to 2007
$294k
NCI NIH HHS CA16056NCI NIH HHS NIH 5T32CA009072NCI NIH HHS NIH R21 CA128062NCI NIH HHS P30 CA016056NCI NIH HHS R21 CA121216NCI NIH HHS R21 CA128062NCI NIH HHS T32 CA009072
6 · The paper itself

Abstract

We analyzed DNA methyltransferase (Dnmt) protein expression and DNA methylation patterns during four progressive stages of prostate cancer in the transgenic adenocarcinoma of mouse prostate (TRAMP) model, including prostatic intraepithelial neoplasia, well-differentiated tumors, early poorly differentiated tumors, and late poorly differentiated tumors. Dnmt1, Dnmt3a, and Dnmt3b protein expression were increased in all stages; however, after normalization to cyclin A to account for cell cycle regulation, Dnmt proteins remained overexpressed in prostatic intraepithelial neoplasia and well-differentiated tumors, but not in poorly differentiated tumors. Restriction landmark genomic scanning analysis of locus-specific methylation revealed a high incidence of hypermethylation only in poorly differentiated (early and late) tumors. Several genes identified by restriction landmark genomic scanning showed hypermethylation of downstream regions correlating with mRNA overexpression, including p16INK4a, p19ARF, and Cacna1a. Parallel gene expression and DNA methylation analyses suggests that gene overexpression precedes downstream hypermethylation during prostate tumor progression. In contrast to gene hypermethylation, genomic DNA hypomethylation, including hypomethylation of repetitive elements and loss of genomic 5-methyldeoxycytidine, occurred in both early and late stages of prostate cancer. DNA hypermethylation and DNA hypomethylation did not correlate in TRAMP, and Dnmt protein expression did not correlate with either variable, with the exception of a borderline significant association between Dnmt1 expression and DNA hypermethylation. In summary, our data reveal the relative timing of and relationship between key alterations of the DNA methylation pathway occurring during prostate tumor progression in an in vivo model system.

Indexed as

Disease Models, AnimalDNA MethylationAdenocarcinomaAnimalsCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeCyclin-Dependent Kinase Inhibitor p16Disease ProgressionDNA (Cytosine-5-)-MethyltransferasesGene Expression Regulation, NeoplasticGenomeMaleMiceMice, Inbred C57BLMice, TransgenicCalcium Channels, N-TypeCalcium Channels, P-TypeCalcium Channels, Q-TypeCdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16DNA (Cytosine-5-)-Methyltransferases

Identifiers

PMID18667590
PMCPMC2835734
OpenAlexW2141835013

What OpenQuestion holds

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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.