Evidence map›Paper›PMID 23624841›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Deletion of p21/Cdkn1a confers protective effect against prostate tumorigenesis in transgenic adenocarcinoma of the mouse prostate model.

Anil K Jain, Komal Raina, Rajesh Agarwal

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 38% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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  7. Interception Targets ofCancer prevention research (Philadelphia, Pa.) · 2021
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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

3 authors at 3 institutions in 1 country.

Anil K JainDepartment of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Komal Raina
Rajesh Agarwal
The Medical Center of Aurora · USUniversity of Colorado Cancer Center · USUniversity of Montana · US

Funding

Prostate cancer prevention and treatment by sillibininR01CA102514 · NCI · UNIVERSITY OF COLORADO DENVER · PI AGARWAL, RAJESH · 2003 to 2013
$3.6M
Prostate Cancer Chemoprevention by Inositol Hexaphosphate Efficacy and MechanismR01CA116636 · NCI · UNIVERSITY OF COLORADO DENVER · PI AGARWAL, RAJESH · 2006 to 2010
$1.3M
NCI NIH HHS R01 CA102514NCI NIH HHS R01 CA116636
6 · The paper itself

Abstract

Cyclin-dependent kinase inhibitors (CDKIs) p21(Cip1/Waf1) (p21) and p27(Kip1) (p27) play a determining role in cell cycle progression by regulating CDK activity; however, p21 role in prostate cancer (PCa) is controversial. Whereas p21 upregulation by anticancer agents causes cell cycle arrest in various PCa cell lines, elevated p21 levels have been associated with higher Gleason score, poor survival and increased PCa recurrence. These conflicting findings suggest that more studies are needed to examine p21 role in PCa. Herein, employing genetic approach, transgenic mice harboring p21/Cdkn1a homozygous deletion (p21(-/-)) were crossed with the transgenic adenocarcinoma of the mouse prostate (TRAMP) mice to characterize in vivo consequences of p21 deletion on prostate tumorigenesis. Lower urogenital tract weight of p21(-/-)/TRAMP mice was significantly lower than those of p21(+/-)/TRAMP and TRAMP mice. Histopathology further supported these observations, showing less aggressiveness in prostates of p21(-/-)/TRAMP. Furthermore, a significantly higher incidence of low-grade prostatic intraepithelial lesions (PIN) with a concomitant reduction in adenocarcinoma incidence was observed in p21(-/-)/TRAMP mice compared with TRAMP mice. In addition, whereas TRAMP mice showed the presence of poorly differentiated adenocarcinoma lesions, no such lesions were observed in p21/TRAMP transgenic mice. Specifically, there was a significant reduction in the severity of lesions in both p21(-/-)/TRAMP and p21(+/-)/TRAMP mice compared with TRAMP mice. Together, our data showed that p21 deletion reduces prostate tumorigenesis by slowing-down progression of PIN (pre-malignant) to adenocarcinoma (malignant), suggesting that intact p21 expression is associated with PCa aggressiveness, while its decreased levels may in fact confer protection against prostate tumorigenesis.

Indexed as

AdenocarcinomaAnimalsCarcinogenesisCyclin-Dependent Kinase Inhibitor p21Disease Models, AnimalDisease ProgressionMaleMiceMice, Inbred C57BLMice, TransgenicNeoplasm GradingProstatic NeoplasmsCyclin-Dependent Kinase Inhibitor p21cell cyclep21 knockdownprostate cancerTRAMP

Identifiers

PMID23624841
PMCPMC3680539
OpenAlexW2013068686

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.