Evidence map›Paper›PMID 20627871›Full record

Trial reportCarcinogenesis2010

Genetic variations in regulator of G-protein signaling genes as susceptibility loci for second primary tumor/recurrence in head and neck squamous cell carcinoma.

Jianming Wang, Scott M Lippman, J Jack Lee, Hushan Yang, Fadlo R Khuri, Edward Kim, Jie Lin, David W Chang, Reuben Lotan, Waun K Hong and 1 more

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
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

11 authors at 3 institutions in 1 country.

Jianming WangDepartment of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.
Scott M Lippman
J Jack Lee
Hushan Yang
Fadlo R Khuri
Edward Kim
Jie Lin
David W Chang
Reuben Lotan
Waun K Hong
Xifeng Wu
Molecular Oncology (United States) · USThe University of Texas MD Anderson Cancer Center · USEmory University · US

Funding

Targeting the p53 pathway for reversal of oral premalignancyP50CA097007 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MYERS, JEFFREY NICHOLAS · 2002 to 2012
$26.1M
TRANSLATIONAL STUDY OF RETINOID REVERSAL OR ORAL CARCINOGENESISP01CA052051 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI HITTLEMAN, WALTER N · 1991 to 2002
$4.2M
NCI NIH HHS CA52051NCI NIH HHS CA97007NCI NIH HHS P01 CA052051NCI NIH HHS P50 CA097007
6 · The paper itself

Abstract

Curatively treated patients with early-stage head and neck squamous cell carcinoma (HNSCC) are at high risks for second primary tumor (SPT) and recurrence. The regulator of G-protein signaling (RGS) is important in essential signaling transduction and cellular activities. We hypothesize that genetic variations of RGS may modulate the risk of SPT/recurrence in patients with early-stage HNSCC. In a nested case-control study, we evaluated 98 single-nucleotide polymorphisms (SNPs) in 17 RGS genes for the risk of SPT/recurrence among 450 HNSCC patients. Eight SNPs showed significant associations with the risk of SPT/recurrence, with the most significant one of rs2179653, which is located in the 5'-flanking region of RGS2 gene. Under a recessive genetic model, the homozygous variant genotype of this SNP was associated with 2.95-fold [95% confidence interval (CI): 1.52-5.74] increased risk of SPT/recurrence. This association remained significant after the adjustment for multiple comparisons. Cumulative effects analysis revealed that the risk increased significantly with the increasing numbers of unfavorable genotypes. Compared with subjects carrying 0-2 unfavorable genotypes, the hazard ratios (95% CIs) for those carrying 3 or 4+ were 1.73 (1.10-2.70) and 3.05 (1.92-4.83), respectively. Furthermore, survival tree analysis revealed potential higher order gene-gene interactions and indicated different outcomes based on distinct genotype profiles. Genetic variations of RGS genes may modulate the susceptibility to SPT/recurrence in early-stage HNSCC patients individually and cumulatively. Our results stressed the importance of taking a polygenic approach to evaluate the cumulative and interaction effects of genetic variations in the prediction of cancer risk and prognosis.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAgedCarcinoma, Squamous CellGene DosageGenetic VariationHead and Neck NeoplasmsHumansMiddle AgedMultivariate AnalysisNeoplasm Recurrence, LocalNeoplasms, Second PrimaryRGS ProteinsRGS13 protein, humanRGS2 protein, humanRGS Proteins

Identifiers

PMID20627871
PMCPMC2950933
OpenAlexW2104903477

What OpenQuestion holds

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Registered trials

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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.