Evidence map›Paper›PMID 15615849›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Evidence for a p27 tumor suppressive function independent of its role regulating cell proliferation in the prostate.

David R Shaffer, Agnes Viale, Ryota Ishiwata, Margaret Leversha, Semra Olgac, Katia Manova, Jaya Satagopan, Howard Scher, Andrew Koff

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Phase II trial of docetaxel with rapid androgen cycling for progressive noncastrate prostate cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2008
    Trial
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  9. SV40 reporter viruses.Journal of virological methods · 2008
    Article
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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

9 authors.

David R ShafferDepartment of Medicine, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA.
Agnes Viale
Ryota Ishiwata
Margaret Leversha
Semra Olgac
Katia Manova
Jaya Satagopan
Howard Scher
Andrew Koff

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
P27KIP1 EXPRESSION, A PROGNOSTIC INDICATOR==BUT WHY?R01CA089563 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI KOFF, ANDREW · 2001 to 2011
$4.2M
REGULATION OF P27 AND ITS ROLE IN G1 PROGRESSIONR01GM052597 · NIGMS · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI KOFF, ANDREW · 1996 to 2003
$1.4M
NCI NIH HHS CA 89563NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA089563NIGMS NIH HHS R01 GM052597
6 · The paper itself

Abstract

Reduced p27 levels correlate with poor prognosis in a wide spectrum of human tumors and can accelerate tumorigenesis in mouse tissues. To determine whether p27 deficiency can accelerate tumorigenesis in tissues with inactive Rb and p53 pathways, we examined the effect of p27 status on prostate tumorigenesis in mice expressing simian virus 40 large T antigen (LT). In p27-deficient mice expressing LT, tumors progressed from high-grade prostatic intraepithelial neoplasia to poorly differentiated carcinoma at a greatly accelerated rate. p27 deficiency could not collaborate with a mutant of LT that fails to inactivate the Rb pathway alone. Furthermore, p27 deficiency does not increase the proliferation index, reduce the apoptotic index, or affect the expression of E2F-dependent genes in cells expressing LT at any stage of the disease. Expression of LT alone leads to maximal proliferation, but p27 deficiency still increases the amount of cyclin A and cyclin-dependent kinase 2-associated kinase activity in tissues. Interestingly, this model recapitulates an important feature of the human disease, specifically a high frequency of allelic loss of chromosome 16q, which is syntenic to mouse chromosome 8. Loss of heterozygosity may accelerate the inactivation of other tumor suppressors, such as E-cadherin, which are located in this interval. These experiments provide direct physiological and causal evidence that p27 has tumor suppressive functions independent of its role regulating cell proliferation.

Indexed as

AnimalsAntigens, Viral, TumorCDC2-CDC28 KinasesCell Cycle ProteinsCell DivisionChromosome AberrationsCyclin ACyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p27Genomic InstabilityMaleMiceProstateProstatic NeoplasmsRetinoblastoma ProteinSimian virus 40Antigens, Viral, TumorCDC2-CDC28 KinasesCdk2 protein, mouseCdkn1b protein, mouseCell Cycle ProteinsCyclin ACyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p27Retinoblastoma ProteinTumor Suppressor Proteins

Identifiers

PMID15615849
PMCPMC539141

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.