Evidence map›Paper›PMID 17219200›Full record

ArticleJournal of cancer research and clinical oncology2007

MYH mutations are rare in prostate cancer.

Eyun-Jung Shin, Edward Chappell, Vaijayanti Pethe, Karen Hersey, Theodore van der Kwast, Neil Fleshner, Bharati Bapat

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Contribution ofFrontiers in oncology · 2018
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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

7 authors at 4 institutions in 1 country.

Eyun-Jung ShinSamuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, ON, Canada.
Edward Chappell
Vaijayanti Pethe
Karen Hersey
Theodore van der Kwast
Neil Fleshner
Bharati Bapat
Mount Sinai Hospital · CAUniversity Health Network · CAUniversity of Toronto · CALunenfeld-Tanenbaum Research Institute · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeOxidative stress is considered a risk factor for prostate cancer development and is associated with the production of reactive oxygen species (ROS). The base excision repair gene MYH protects against ROS-mediated damage to DNA. Inherited MYH mutations predispose to colorectal adenomas and cancer. A compromised base-excision repair function due to defective MYH may contribute to prostate carcinogenesis. Here, we examine the genetic contribution of MYH to prostate cancer risk.

methodsPatients diagnosed with high-grade prostatic intraepithelial neoplasia (HGPIN) alone (n = 45), prostate cancer alone (n = 123) or both (n = 82) were screened for the two most common mutations in the MYH gene using PCR-based RFLP analysis. A single patient with an inherited MYH mutation as well as a subset of 26 patients presenting with a family history of colorectal cancer were screened for additional MYH mutations by direct sequencing of the entire coding region.

resultsBiallelic germline mutations in MYH were not detected among prostate cancer patients. Only a single patient was a heterozygous carrier for the Y165C missense mutation. Allelic deletion or somatic mutation of the remaining MYH allele was not identified in this patient's tumor DNA. Two patients harbored V22M polymorphism and three patients were carriers of Q324H polymorphism.

conclusionsMYH mutations are unlikely to contribute to prostate cancer risk.

Indexed as

MutationAdultAgedAged, 80 and overColorectal NeoplasmsDNA GlycosylasesHumansMaleMiddle AgedPolymerase Chain ReactionPolymorphism, Restriction Fragment LengthProstatic NeoplasmsDNA GlycosylasesmutY adenine glycosylase

Identifiers

PMID17219200
PMCPMC12160883
OpenAlexW2000867100

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.