Evidence map›Paper›PMID 15314168›Full record

ArticleMolecular and cellular biology2004

Cyclin D1 genetic heterozygosity regulates colonic epithelial cell differentiation and tumor number in ApcMin mice.

James Hulit, Chenguang Wang, Zhiping Li, Chris Albanese, Mahadev Rao, Dolores Di Vizio, Salimuddin Shah, Stephen W Byers, Radma Mahmood, Leonard H Augenlicht and 2 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.7field-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

74 citing papers in PubMed, 140 citations in OpenAlex.

  1. Trial
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  6. Review
  7. Modeling Intestinal Stem Cell Function with Organoids.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
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  15. Zyxin promotes colon cancer tumorigenesis in a mitotic phosphorylation-dependent manner and through CDK8-mediated YAP activation.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

James HulitThe Lombardi Comprehensive Cancer Center, Department of Oncology, Georgetown University, Research Building Room E501, 3970 Reservoir Rd., N.W., Box 571468, Washington, DC 20057-1468, USA.
Chenguang Wang
Zhiping Li
Chris Albanese
Mahadev Rao
Dolores Di Vizio
Salimuddin Shah
Stephen W Byers
Radma Mahmood
Leonard H Augenlicht
Robert Russell
Richard G Pestell
Albert Einstein College of Medicine · USGeorgetown University · USYeshiva University · US

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI STEPHEN W BYERS · 1990 to 2026
$71.5M
Initiation and Maintenance In Mammary TumorigenesisR01CA075503 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 1998 to 2011
$4.6M
CYCLIN D1 FUNCTION IN PROSTATE CANCERR01CA086072 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 2001 to 2013
$3.3M
REGULATION OF CYCLIN D1 EXPRESSIONR01CA070896 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 2000 to 2010
$3.2M
Mouse Models of ErbB-2 and Cyclin D1 in Prostate CancerR03AG020337 · NIA · YESHIVA UNIVERSITY · PI ALBANESE, CHRISTOPHER · 2002 to 2002
$84k
NCI NIH HHS P30 CA051008NCI NIH HHS P30 CA51008-13NCI NIH HHS R01 CA070896NCI NIH HHS R01 CA075503NCI NIH HHS R01 CA086072NCI NIH HHS R01CA70896NCI NIH HHS R01CA75503NCI NIH HHS R01CA86071NCI NIH HHS R01CA86072NIA NIH HHS R03AG20337
6 · The paper itself

Abstract

Constitutive beta-catenin/Tcf activity, the primary transforming events in colorectal carcinoma, occurs through induction of the Wnt pathway or APC gene mutations that cause familial adenomatous polyposis. Mice carrying Apc mutations in their germ line (ApcMin) develop intestinal adenomas. Here, the crossing of ApcMin with cyclin D1-/- mice reduced the intestinal tumor number in animals genetically heterozygous or nullizygous for cyclin D1. Decreased tumor number in the duodenum, intestines, and colons of ApcMin/cyclin D1+/- mice correlated with reduced cellular proliferation and increased differentiation. Cyclin D1 deficiency reduced DNA synthesis and induced differentiation of colonic epithelial cells harboring mutant APC but not wild-type APC cells in vivo. In previous studies, the complete loss of cyclin D1 through homozygous genetic deletion conveyed breast tumor resistance. The protection of mice, genetically predisposed to intestinal tumorigenesis, through cyclin D1 heterozygosity suggests that modalities that reduce cyclin D1 abundance could provide chemoprotection.

Indexed as

Adenomatous Polyposis Coli ProteinAnimalsbeta CateninCell DifferentiationColonCyclin D1Cytoskeletal ProteinsEpithelial CellsFemaleGastrointestinal NeoplasmsGenetic Predisposition to DiseaseGenotypeHumansIntestinal MucosaIntestinal PolypsMaleAdenomatous Polyposis Coli Proteinbeta CateninCTNNB1 protein, humanCTNNB1 protein, mouseCyclin D1Cytoskeletal ProteinsReceptors, Cytoplasmic and NuclearTrans-ActivatorsTranscription Factors

Identifiers

PMID15314168
PMCPMC507010
OpenAlexW2135854450

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.