Evidence map›Paper›PMID 23444219›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013

Clinical correlates of promoter hypermethylation of four target genes in head and neck cancer: a cooperative group correlative study.

Jong-Lyel Roh, Xin Victoria Wang, Judith Manola, David Sidransky, Arlene A Forastiere, Wayne M Koch

Open access · bronzeAbstract readMulticenter Study
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 3 pooled it
3.1field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 3 syntheses or guidelines pooled it, 28 citations in OpenAlex.

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  13. Prognostic factors in oral and oropharyngeal cancer based on ultrastructural analysis and DNA methylation of the tumor and surgical margin.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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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 5 institutions in 2 countries.

Jong-Lyel RohDepartments of Otolaryngology-Head, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA.
Xin Victoria Wang
Judith Manola
David Sidransky
Arlene A Forastiere
Wayne M Koch
Ulsan College · KRAsan Medical Center · KRDana-Farber Cancer Institute · USJohns Hopkins University · USUniversity of Ulsan · KR

Funding

ECOG OPERATIONS OFFICE (IBCSG)U10CA021115 · NCI · UNIVERSITY OF WISCONSIN MADISON · PI COMIS, ROBERT L · 1985 to 2013
$132.6M
ECOG Specimen BankingU24CA114737 · NCI · FRONTIER SCI &TECHNOLOGY RSCH FDN, INC · PI COMIS, ROBERT L · 2005 to 2014
$9.3M
GENETIC ALTERATIONS AS DIAGNOSTIC AND PROGNOSTIC BIOMARKR01DE013152 · NIDCR · JOHNS HOPKINS UNIVERSITY · PI KOCH, WAYNE M · 1999 to 2013
$5.0M
NCI NIH HHS U10 CA021115NCI NIH HHS U24 CA114737NIDCR NIH HHS R01 DE013152NIDCR NIH HHS R01 DE013152-11
6 · The paper itself

Abstract

purposePromoter hypermethylation is a well-documented mechanism for tumor-specific alteration of suppressor gene activity in human malignancy including head and neck cancer (HNC). The abrogation of specific suppressor gene activity may influence tumor behavior and clinical outcome. In this study we examined methylation of DCC, KIF1A, EDNRB, and p16(INK4a) in a large cohort of HNC patients from Eastern Cooperative Group (ECOG) 4393/Radiation Therapy Oncology Group (RTOG) 9614 to identify clinical correlates of methylation of these genes. EXPERIMENTAL

designMethylation was assessed by quantitative methylation-specific PCR in DNA from tumor specimens and was considered as a continuous and a binary variable. Clinical data including demographics, stage, risk factor exposure, treatment, and outcome were collected by ECOG and RTOG. Methylation status was also correlated with mutation of TP53 (previously reported) and human papilloma virus status.

resultsMethylation results were available for 368 cases, 353 of which also have p53 mutation status. At least one methylation event was present in all tumors. In multivariate analysis of the entire cohort, methylation of p16 was associated with decreased survival (HR = 1.008; P = 0.045). However, in tumors with disruptive TP53 mutation (poor prognostic group), the additional presence of methylation of p16 was protective (P = 0.019 considering p16 methylation as a continuous variable).

conclusionMethylation of tumor-related genes contributes to the biological behavior of HNC and influences overall survival in conjunction with other known prognostic molecular events.

Indexed as

DNA MethylationPromoter Regions, GeneticAgedCarcinoma, Squamous CellCyclin-Dependent Kinase Inhibitor p16DCC ReceptorFemaleGene Expression Regulation, NeoplasticHead and Neck NeoplasmsHumansKaplan-Meier EstimateKinesinsLinear ModelsMaleMiddle AgedMultivariate AnalysisCyclin-Dependent Kinase Inhibitor p16DCC protein, humanDCC ReceptorKIF1A protein, humanKinesinsReceptor, Endothelin BReceptors, Cell SurfaceTP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID23444219
PMCPMC3642232
OpenAlexW2021319851

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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.