Evidence map›Paper›PMID 19214578›Full record

ReviewHuman genetics2009

Gene polymorphisms, apoptotic capacity and cancer risk.

Evgeny N Imyanitov

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Observational
  4. Article
  5. Apoptotic capacity and risk of squamous cell carcinoma of the head and neck.European journal of cancer (Oxford, England : 1990) · 2017
    Article
  6. Article
  7. Article
  8. Article
  9. Genetic determinants of neuronal vulnerability to apoptosis.Cellular and molecular life sciences : CMLS · 2013
    Review
  10. Article
  11. Caspases and cancer.Cell death and differentiation · 2011
    Review
  12. Article
  13. Article
  14. Technologies in the Whole-Genome Age: MALDI-TOF-Based Genotyping.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2009
    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

1 author at 1 institution in 1 country.

Evgeny N ImyanitovN. N. Petrov Institute of Oncology, St. Petersburg, Russia. evgeny@imyanitov.spb.ru
Institute of Oncology NN Petrov · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Programmed cell death has been implicated in various aspects of cancer development. Apoptotic capacity is a subject of significant interindividual variations, which are largely attributed to hereditary traits. Single nucleotide polymorphisms (SNPs) located within cell death genes may influence cancer risk in various ways. Low activity of apoptosis may favor cancer development because of the failure to eliminate cellular clones carrying DNA damage and propensity to inflammation, but may also protect against malignancy due to preservation of antitumor immune cells. Phenotyping studies assessing cell death rate in cancer patients versus healthy controls are limited in number and produced controversial results. TP53 R72P polymorphism is the only SNP whose functional impact on apoptotic response has been replicated in independent investigations. Intriguingly, meta-analysis of TP53 genotyping studies has provided evidence for the association between apoptosis-deficient TP53 genotype and tumor susceptibility. Systematic analysis of cancer-predisposing relevance of other apoptotic gene SNPs remains to be done.

Indexed as

Polymorphism, GeneticApoptosisCase-Control StudiesDNA DamageGenes, p53GenotypeHumansNeoplasmsPolymorphism, Single NucleotideRisk Factors

Identifiers

PMID19214578
OpenAlexW2095028604

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.