Evidence map›Paper›PMID 14647411›Full record

ArticleOncogene2004

Distinct roles for p53, p27Kip1, and p21Cip1 during tumor development.

Jeannette Philipp-Staheli, Kyung-Hoon Kim, Denny Liggitt, Kay E Gurley, Gary Longton, Christopher J Kemp

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
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  9. Article
  10. CDK inhibitors for muscle stem cell differentiation and self-renewal.The journal of physical fitness and sports medicine · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Single-nucleotide polymorphisms in the p53 signaling pathway.Cold Spring Harbor perspectives in biology · 2010
    Review
  16. Article
  17. Article
  18. Article
  19. P21 and p27: roles in carcinogenesis and drug resistance.Expert reviews in molecular medicine · 2008
    Review
  20. 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 at 3 institutions in 2 countries.

Jeannette Philipp-StaheliFred Hutchinson Cancer Research Center, C1-015, 1100 Fairview Ave N, Seattle, WA 90109-1024, USA.
Kyung-Hoon Kim
Denny Liggitt
Kay E Gurley
Gary Longton
Christopher J Kemp
Cape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa · ZAFred Hutch Cancer Center · USUniversity of Washington · US

Funding

Comparative Mouse Genomics CenterU01ES011045 · NIEHS · UNIVERSITY OF WASHINGTON · PI LADIGES, WARREN C. · 2001 to 2006
$7.2M
The Role of Double Strand Breaks in CarcinogenesisR01CA070414 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI KEMP, CHRISTOPHER J · 1996 to 2006
$2.2M
NCI NIH HHS CA70414NIEHS NIH HHS ES011045
6 · The paper itself

Abstract

Mutations in p53 and reduced expression of the Cdk inhibitor p27Kip1 are frequently observed in a wide variety of human cancers, but it is not known whether alterations in these tumor suppressors interact to influence tumor progression. To address this, we measured tumor latency and spectrum in p53 and p27 single and compound mutant mice. p53-/- (null) mice developed T-cell lymphomas and soft-tissue sarcomas, while p27-/- mice developed adenomas of the pituitary and lung, but with much longer latency. The latency for tumor development in p53-/- p27-/- and p53-/- p27+/- compound mutant mice was significantly reduced, by 15-30%, compared to single mutant p53-/- mice. The tumor spectrum in the compound mutants was similar to that of p53-/- mice, and additional tumors of diverse histotypes. In tumors from p53-/- mice, p27 protein levels were reduced to a greater extent than were mRNA levels, indicating that p27 is downregulated in tumors at the transcriptional as well as post-transcriptional levels. In contrast, mice deficient in another Cdk inhibitor p21Cip1, which is also a transcriptional target and effector of p53, showed only a marginal increase in tumor predisposition in response to ENU treatment. Thus, downregulation of p27 is a common feature in p53-/- tumors. Germline deletion of one or both alleles of p27 accelerates tumor development and associated mortality in p53-/- mice, indicating potent synergy between loss of p27 and p53. Although p21 is functionally similar to both p53 and p27, it plays a lesser role in tumor suppression. These results further highlight the highly cooperative nature of p27 and its central role in tumor suppression.

Indexed as

AnimalsBase SequenceCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27CyclinsDNA PrimersImmunohistochemistryMiceMice, Inbred C57BLMice, KnockoutNeoplasms, ExperimentalTumor Suppressor Protein p53Tumor Suppressor ProteinsCdkn1a protein, mouseCdkn1b protein, mouseCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27CyclinsDNA PrimersTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID14647411
OpenAlexW2068026673

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.