Evidence map›Paper›PMID 15322517›Full record

ReviewOncogene2004

The search for low-penetrance cancer susceptibility alleles.

Richard S Houlston, Julian Peto

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 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

55 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. PLCE1 rs2274223 A>G polymorphism and cancer risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Gene polymorphisms and risk of head and neck squamous cell carcinoma: a systematic review.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The OncoArray Consortium: A Network for Understanding the Genetic Architecture of Common Cancers.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Colitis-associated colon cancer: Is it in your genes?World journal of gastroenterology · 2015
    Review
  18. Genetic susceptibility to cervical cancer: role of common polymorphisms in apoptosis-related genes.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Review
  19. 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

2 authors.

Richard S HoulstonSection of Cancer Genetics, Institute of Cancer Research, Sutton, Surrey, SM2 5NG, UK. richard.houlston@icr.ac.uk
Julian Peto

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Much of the familial aggregation of common cancer results from inherited susceptibility, but highly penetrant mutations in known genes cannot account for most of the excess. Some of the unexplained familial risk is presumably due to high-penetrance mutations in as yet unidentified genes, but polygenic mechanisms are likely to account for a greater proportion, particularly in breast cancer. This inference, coupled with technological developments, has led to a renaissance in association studies. Most such studies have evaluated small numbers of single-nucleotide polymorphisms (SNPs) in a few candidate genes, but reliable high-density oligonucleotide arrays and other novel techniques will allow genome-wide allelic association studies to be conducted. High-density genome-wide SNP analysis will include targets identified by structural considerations, as well as the growing list of candidate genes. In the longer term, high-throughput re-sequencing will be required to identify the rare pathogenic variants that may constitute the majority of low-penetrance alleles. The detection of low-penetrance cancer susceptibility genes will then be restricted mainly by the availability of large numbers of well-characterized cases and controls. Cancer patients with affected relatives are considerably more informative than unselected cases for such studies.

Indexed as

FamilyGenetic LinkageGenetic Predisposition to DiseaseHumansNeoplasmsPolymorphism, GeneticPolymorphism, Single NucleotideRisk Factors

Identifiers

PMID15322517

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.