Evidence map›Paper›PMID 26967246›Full record

ReviewOncotarget2016

The clinical value of aberrant epigenetic changes of DNA damage repair genes in human cancer.

Dan Gao, James G Herman, Mingzhou Guo

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
8.9field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 90 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Higher Levels ofMedical sciences (Basel, Switzerland) · 2026
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  13. Unveiling the vulnerabilities of synthetic lethality in triple-negative breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
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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

3 authors at 3 institutions in 2 countries.

Dan GaoDepartment of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing, China.
James G HermanThe Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.
Mingzhou GuoDepartment of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing, China.
Chinese PLA General Hospital · CNNankai University · CNUPMC Hillman Cancer Center · US

Funding

MIF in progression and treatment of ALDU01AA020821 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 2012 to 2016
$2.1M
Corticostriatal networks and NMDAR mediation of habitual and flexible actionK22AA020303 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI BRIGMAN, JONATHAN L · 2011 to 2013
$486k
NIAAA NIH HHS K22 AA020303NIAAA NIH HHS U01 AA020821
6 · The paper itself

Abstract

The stability and integrity of the human genome are maintained by the DNA damage repair (DDR) system. Unrepaired DNA damage is a major source of potentially mutagenic lesions that drive carcinogenesis. In addition to gene mutation, DNA methylation occurs more frequently in DDR genes in human cancer. Thus, DNA methylation may play more important roles in DNA damage repair genes to drive carcinogenesis. Aberrant methylation patterns in DNA damage repair genes may serve as predictive, diagnostic, prognostic and chemosensitive markers of human cancer. MGMT methylation is a marker for poor prognosis in human glioma, while, MGMT methylation is a sensitive marker of glioma cells to alkylating agents. Aberrant epigenetic changes in DNA damage repair genes may serve as therapeutic targets. Treatment of MLH1-methylated colon cancer cell lines with the demethylating agent 5'-aza-2'-deoxycytidine induces the expression of MLH1 and sensitizes cancer cells to 5-fluorouracil. Synthetic lethality is a more exciting approach in patients with DDR defects. PARP inhibitors are the most effective anticancer reagents in BRCA-deficient cancer cells.

Indexed as

Epigenesis, GeneticAntimetabolites, AntineoplasticAzacitidineBiomarkers, TumorCarcinogenesisCpG IslandsDecitabineDNA DamageDNA MethylationDNA Modification MethylasesDNA RepairDNA Repair EnzymesDrug Resistance, NeoplasmFluorouracilHumansMolecular Targeted TherapyAntimetabolites, AntineoplasticAzacitidineBiomarkers, TumorDecitabineDNA Modification MethylasesDNA Repair EnzymesFluorouracilMGMT protein, humanTumor Suppressor ProteinsDNA damage repairDNA methylationMGMTPARP inhibitorsynthetic lethality

Identifiers

PMID26967246
PMCPMC5095080
OpenAlexW2396936815

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.