Evidence map›Paper›PMID 15569926›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

A critical role for p27kip1 gene dosage in a mouse model of prostate carcinogenesis.

Hui Gao, Xuesong Ouyang, Whitney Banach-Petrosky, Alexander D Borowsky, Yong Lin, Minjung Kim, Hansol Lee, Weichung-Joseph Shih, Robert D Cardiff, Michael M Shen and 1 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 119 citations in OpenAlex.

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  5. Copy Number Loss of 17q22 Is Associated with Enzalutamide Resistance and Poor Prognosis in Metastatic Castration-Resistant Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Observational
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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

11 authors at 3 institutions in 1 country.

Hui GaoCenter for Advanced Biotechnology and Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.
Xuesong Ouyang
Whitney Banach-Petrosky
Alexander D Borowsky
Yong Lin
Minjung Kim
Hansol Lee
Weichung-Joseph Shih
Robert D Cardiff
Michael M Shen
Cory Abate-Shen
University of California, Davis · USRutgers, The State University of New Jersey · USDana-Farber Cancer Institute · US

Funding

Elucidation of cancer pathways and druggable targets using mouse models.U01CA084294 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ABATE-SHEN, CORY · 1999 to 2013
$11.4M
Roles of Nkx3.1 in prostate development and cancerR01CA076501 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ABATE-SHEN, CORY · 1998 to 2007
$2.5M
Growth Factor Signaling in Prostate Development &CancerR01DK060887 · NIDDK · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI SHEN, MICHAEL M. · 2001 to 2004
$1.4M
NCI NIH HHS R01 CA076501NCI NIH HHS R01 CA76501NCI NIH HHS U01 CA084294NCI NIH HHS U01 CA84294NIDDK NIH HHS DK60887NIDDK NIH HHS R01 DK060887
6 · The paper itself

Abstract

In human prostate cancer, the frequent down-regulation of p27(kip1) protein expression is correlated with poor clinical outcome, yet p27(kip1) rarely undergoes mutational inactivation. Here, we investigate the consequences of reducing or eliminating p27(kip1) function for prostate carcinogenesis in the context of a mouse modeling lacking the Nkx3.1 homeobox gene and the Pten tumor suppressor. Unexpectedly, we find that triple mutant mice heterozygous for a p27(kip1) null allele (Nkx3.1(+/- or -/-); Pten(+/-); p27(+/-)) display enhanced prostate carcinogenesis, whereas mice that are homozygous null for p27(kip1) (Nkx3.1(+/- or -/-); Pten(+/-); p27(-/-)) show inhibition of cancer progression. Expression profiling reveals that Cyclin D1 is highly up-regulated in compound p27(kip1) heterozygotes, but is down-regulated in the compound p27(kip1) homozygous mutants. Using RNA interference in prostate cancer cell lines with distinct p27(kip1) gene doses, we show that prostate tumorigenicity depends on levels of p27(kip1) and that the consequences of p27(kip1) gene dosage can be attributed, in part, to altered levels of Cyclin D1. Our findings suggest that p27(kip1) possesses dosage-sensitive positive as well as negative modulatory roles in prostate cancer progression.

Indexed as

Gene DosageAnimalsCell Cycle ProteinsCyclin D1Cyclin-Dependent Kinase Inhibitor p27Disease Models, AnimalDisease ProgressionGene Expression Regulation, NeoplasticGenotypeHomeodomain ProteinsMaleMiceMice, KnockoutMice, Mutant StrainsProstatic NeoplasmsProtein Tyrosine PhosphatasesCdkn1b protein, mouseCell Cycle ProteinsCyclin D1Cyclin-Dependent Kinase Inhibitor p27Homeodomain ProteinsNkx3-1 protein, mouseProtein Tyrosine PhosphatasesPTEN PhosphohydrolasePten protein, mouseTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID15569926
PMCPMC535400
OpenAlexW2125941911

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.