Evidence map›Paper›PMID 15322521›Full record

ReviewOncogene2004

Genetic susceptibility to tobacco-related cancer.

Xifeng Wu, Hua Zhao, Rebecca Suk, David C Christiani

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 6 pooled it
5.2field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 6 syntheses or guidelines pooled it, 156 citations in OpenAlex.

  1. Pooled it
  2. Xeroderma pigmentosum complementation group D (XPD) gene polymorphisms contribute to bladder cancer risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Smoking and selected DNA repair gene polymorphisms in controls: systematic review and meta-analysis.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2010
    Pooled it
  6. Pooled it
  7. Trial
  8. Review
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  12. Inherited Rare, Deleterious Variants in ATM Increase Lung Adenocarcinoma Risk.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2020
    Article
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  18. Review
  19. Inflammatory Gene Polymorphisms in Lung Cancer Susceptibility.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2018
    Article
  20. 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

4 authors at 2 institutions in 1 country.

Xifeng WuDepartment of Epidemiology, MD Anderson Cancer Center, Houston, TX 77030, USA. xwu@mdanderson.org
Hua Zhao
Rebecca Suk
David C Christiani
Harvard University · USThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although cigarette smoking is the dominant risk factor for several epithelial cancers, only a small fraction of individuals with tobacco exposure develop cancer. The underlying hypothesis is that genetic factors may render certain smokers more susceptible to cancer than others. Genetic alterations in critical regulatory pathways may predispose cells to carcinogenesis. These pathways include regulation of xenobiotic metabolism; control of genomic stability, including DNA repair mechanisms, cell-cycle checkpoints, apoptosis and telomere length; and control of microenvironmental factors, such as matrix metalloproteinases, inflammation and growth factors. In addition, epigenetic events, such as promoter hypermethylation and loss of imprinting, are also involved in carcinogenesis. In this review, we will summarize recent advances in genetic susceptibility to tobacco-related cancer. Emphasizing on risk assessment, we will describe how genetic variations in the above-mentioned genetic pathways modify the tobacco-related cancer risk. In addition, we will discuss how genetic variations may assist in predicting clinical outcome, such as the natural history of cancer and treatment response. The measurements of genetic susceptibility by both genotypic and phenotypic assays are covered in the text. Finally, we present a number of current concerns that need to be addressed as the exciting field of molecular cancer epidemiology advances rapidly.

Indexed as

Cytochrome P-450 Enzyme SystemDNA DamageDNA RepairGenetic Predisposition to DiseaseHumansNeoplasmsNicotianaPolymorphism, GeneticRisk AssessmentSmokingCytochrome P-450 Enzyme System

Identifiers

PMID15322521
OpenAlexW1973231662

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.