Evidence map›Paper›PMID 12045150›Full record

ArticleGenome research2002

A bioinformatics-based strategy identifies c-Myc and Cdc25A as candidates for the Apmt mammary tumor latency modifiers.

Diana Cozma, Luanne Lukes, Jessica Rouse, Ting Hu Qiu, Edison T Liu, Kent W Hunter

Abstract read
In one paragraph

Article in Genome research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Integrated cross-species transcriptional network analysis of metastatic susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  4. Article
  5. Article
  6. CDC 25A gene 263C/T, -350C/T, and -51C/G polymorphisms in breast carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2010
    Article
  7. Lessons in signaling and tumorigenesis from polyomavirus middle T antigen.Microbiology and molecular biology reviews : MMBR · 2009
    Review
  8. Review
  9. Mouse modifier genes in mammary tumorigenesis and metastasis.Journal of mammary gland biology and neoplasia · 2008
    Review
  10. Mammary cancer susceptibility: human genes and rodent models.Mammalian genome : official journal of the International Mammalian Genome Society · 2007
    Review
  11. Is breast cancer prognosis inherited?Breast cancer research : BCR · 2007
    Article
  12. Article
  13. Modifiers of mammary tumor progression and metastasis on mouse chromosomes 7, 9, and 17.Mammalian genome : official journal of the International Mammalian Genome Society · 2005
    Article
  14. Article
  15. Refractory nature of normal human diploid fibroblasts with respect to oncogene-mediated transformation.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  16. 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

6 authors.

Diana CozmaLaboratory of Population Genetics, Medicine Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, Bethesda, MD 20892, USA.
Luanne Lukes
Jessica Rouse
Ting Hu Qiu
Edison T Liu
Kent W Hunter

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epistatically interacting modifier loci (Apmt1 and Apmt2) accelerate the polyoma Middle-T (PyVT)-induced mammary tumor. To identify potential candidate genes loci, a combined bioinformatics and genomics strategy was used. On the basis of the assumption that the loci were functioning in the same or intersecting pathways, a search of the literature databases was performed to identify molecular pathways containing genes from both candidate intervals. Among the genes identified by this method were the cell cycle-associated genes Cdc25A and c-Myc, both of which have been implicated in breast cancer. Genomic sequencing revealed noncoding polymorphism in both genes, in the promoter region of Cdc25A, and in the 3' UTR of c-Myc. Molecular and in vitro analysis showed that the polymorphisms were functionally significant. In vivo analysis was performed by generating compound PyVT/Myc double-transgenic animals to mimic the hypothetical model, and was found to recapitulate the age-of-onset phenotype. These data suggest that c-Myc and Cdc25A are Apmt1 and Apmt2, and suggest that, at least in certain instances, bioinformatics can be utilized to bypass congenic construction and subsequent mapping in conventional QTL studies.

Indexed as

Epistasis, Genetic3T3 CellsAnimalscdc25 PhosphatasesComputational BiologyGenes, mycGenetic MarkersHumansMammary Neoplasms, ExperimentalMiceMice, TransgenicProto-Oncogene Proteins c-mycQuantitative Trait, HeritableCDC25A protein, humanCdc25a protein, mousecdc25 PhosphatasesGenetic MarkersProto-Oncogene Proteins c-myc

Identifiers

PMID12045150
PMCPMC1383737

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Registered trials

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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.