Evidence map›Paper›PMID 22157285›Full record

ReviewCancer journal (Sudbury, Mass.)

The genetics of cancer risk.

Mark M Pomerantz, Matthew L Freedman

Abstract readReview
In one paragraph

Review in Cancer journal (Sudbury, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–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

28 citing papers in PubMed.

  1. Tumor risks and surveillance outcomes inEndocrine oncology (Bristol, England) · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Evolutionary Origins of Metabolic Reprogramming in Cancer.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Knowledge, Attitudes, Willingness to Pay, and Patient Preferences About Genetic Testing and Subsequent Risk Management for Cancer Prevention.Journal of cancer education : the official journal of the American Association for Cancer Education · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. The Genetic Architecture of High Bone Mass.Frontiers in endocrinology · 2020
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  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.

Mark M PomerantzDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Matthew L Freedman

Funding

Fine mapping and characterization of the 8q24 prostate cancer risk locusR01CA129435 · NCI · DANA-FARBER CANCER INST · PI FREEDMAN, MATTHEW L · 2007 to 2009
$1.5M
NCI NIH HHS R01 CA129435
6 · The paper itself

Abstract

One hundred years ago, decades before the discovery of the structure of DNA, debate raged regarding how human traits were passed from one generation to the next. Phenotypes, including risk of disease, had long been recognized as having a familial component. Yet it was difficult to reconcile genetic segregation as described by Mendel with observations exhaustively documented by Karl Pearson and others regarding the normal distribution of human characteristics. In 1918, R. A. Fisher published his landmark article, "The Correlation Between Relatives on the Supposition of Mendelian Inheritance," bridging this divide and demonstrating that multiple alleles, all individually obeying Mendel's laws, account for the phenotypic variation observed in nature.Since that time, geneticists have sought to identify the link between genotype and phenotype. Trait-associated alleles vary in their frequency and degree of penetrance. Some minor alleles may approach a frequency of 50% in the human population, whereas others are present within only a few individuals. The spectrum for penetrance is similarly wide. These characteristics jointly determine the segregation pattern of a given trait, which, in turn, determine the method used to map the trait. Until recently, identification of rare, highly penetrant alleles was most practical. Revolutionary studies in genomics reported over the past decade have made interrogation of most of the spectrum of genetic variation feasible.The following article reviews recent discoveries in the genetic basis of inherited cancer risk and how these discoveries inform cancer biology and patient management. Although this article focuses on prostate cancer, the principles are generic for any cancer and, indeed, for any trait.

Indexed as

Genetic Predisposition to DiseaseHumansNeoplasms

Identifiers

PMID22157285
PMCPMC3934208

What OpenQuestion holds

Textmetadata
LicenceTDM
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.