Evidence map›Paper›PMID 19155292›Full record

ReviewCancer research2009

Emerging paradigms in cancer genetics: some important findings from high-density single nucleotide polymorphism array studies.

Manny D Bacolod, Gunter S Schemmann, Sarah F Giardina, Philip Paty, Daniel A Notterman, Francis Barany

Abstract readReview
In one paragraph

Review in Cancer research, 2009. 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
5.8field-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

28 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. Genetic diversity, inbreeding and cancer.Proceedings. Biological sciences · 2018
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Performance of the Genomic Evaluators of Metastatic Prostate Cancer (GEMCaP) tumor biomarker for identifying recurrent disease in African American patients.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2014
    Article
  10. Article
  11. Review
  12. Epigenetic modifications in cancer.Clinical genetics · 2012
    Review
  13. Article
  14. Article
  15. Review
  16. Pathogenesis and consequences of uniparental disomy in cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 3 institutions in 1 country.

Manny D BacolodDepartment of Microbiology, Weill Medical College of Cornell University, New York, NY 10021, USA. barany@med.cornell.edu
Gunter S Schemmann
Sarah F Giardina
Philip Paty
Daniel A Notterman
Francis Barany
Cornell University · USPrinceton University · USMemorial Sloan Kettering Cancer Center · US

Funding

NEW METHODS FOR CANCER DETECTIONP01CA065930 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI BARANY, FRANCIS · 1997 to 2007
$14.1M
Scientific and Technical Computing CoreP2CHD047879 · NICHD · PRINCETON UNIVERSITY · PI SALGANIK, MATTHEW J. · 2014 to 2018
$2.0M
NCI NIH HHS P01 CA065930NCI NIH HHS P01-CA65930
6 · The paper itself

Abstract

High-density single nucleotide polymorphism (SNP) mapping arrays have identified chromosomal features whose importance to cancer predisposition and progression is not yet clearly defined. Of interest is that the genomes of normal somatic cells (reflecting the combined parental germ-line contributions) often contain long homozygous stretches. These chromosomal segments may be explained by the common ancestry of the individual's parents and thus may also be called autozygous. Several studies link consanguinity to higher rates of cancer, suggesting that autozygosity (a genomic consequence of consanguinity) may be a factor in cancer predisposition. SNP array analysis has also identified chromosomal regions of somatic uniparental disomy (UPD) in cancer genomes. These are chromosomal segments characterized by loss of heterozygosity (LOH) and a normal copy number (two) but which are not autozygous in the germ-line or normal somatic cell genome. In this review, we will also discuss a model [cancer gene activity model (CGAM)] that may explain how autozygosity influences cancer predisposition. CGAM can also explain how the occurrence of certain chromosomal aberrations (copy number gain, LOH, and somatic UPDs) during carcinogenesis may be dependent on the germ-line genotypes of important cancer-related genes (oncogenes and tumor suppressors) found in those chromosomal regions.

Indexed as

Polymorphism, Single NucleotideGenetic Predisposition to DiseaseHumansNeoplasms

Identifiers

PMID19155292
PMCPMC4378658
OpenAlexW2122550449

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.