Evidence map›Paper›PMID 17626791›Full record

ArticleGenes & development2007

Discovery of an oncogenic activity in p27Kip1 that causes stem cell expansion and a multiple tumor phenotype.

Arnaud Besson, Harry C Hwang, Samantha Cicero, Stacy L Donovan, Mark Gurian-West, Dianna Johnson, Bruce E Clurman, Michael A Dyer, James M Roberts

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing 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

107 citing papers in PubMed, 209 citations in OpenAlex.

  1. Subclonal Complete Loss of CDKN1B as a Common Genomic Alteration in Prostate Cancer: Associations With Race and Prostate Cancer Outcomes.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. The roles of ubiquitination in AML.Annals of hematology · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Regulation of p27Biomolecules · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. p27The Journal of pathology · 2019
    Article
  19. p27 transcriptionally coregulates cJun to drive programs of tumor progression.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Arnaud BessonDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
Harry C Hwang
Samantha Cicero
Stacy L Donovan
Mark Gurian-West
Dianna Johnson
Bruce E Clurman
Michael A Dyer
James M Roberts
Fred Hutch Cancer Center · USSt. Jude Children's Research Hospital · USUniversity of Tennessee Health Science Center · US

Funding

CELL CYCLE REGULATION IN NORMAL AND CANCER CELLSR01CA118043 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI ROBERTS, JAMES M · 2006 to 2010
$2.4M
Pathways in p27-associated hematolymphoid malignancyK08HL073670 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HWANG, HARRY C · 2003 to 2007
$637k
NCI NIH HHS 1R01CA118043NCI NIH HHS R01 CA118043NHLBI NIH HHS 1K08HL073670-01NHLBI NIH HHS K08 HL073670PHS HHS R01084069
6 · The paper itself

Abstract

The cell cycle inhibitor p27Kip1 also has cyclin-cyclin-dependent kinase (CDK)-independent functions. To investigate the significance of these functions in vivo, we generated a knock-in mouse in which four amino acid substitutions in the cdkn1b gene product prevent its interaction with cyclins and CDKs (p27CK-). In striking contrast to complete deletion of the cdkn1b gene, which causes spontaneous tumorigenesis only in the pituitary, the p27CK- protein dominantly caused hyperplastic lesions and tumors in multiple organs, including the lung, retina, pituitary, ovary, adrenals, spleen, and lymphomas. Moreover, the high incidence of spontaneous tumors in the lung and retina was associated with amplification of stem/progenitor cell populations. Therefore, independently of its role as a CDK inhibitor, p27Kip1 promoted stem cell expansion and functioned as a dominant oncogene in vivo. Thus, the p27CK- mouse unveils a dual role for p27 during tumorigenesis: It is a tumor suppressor by virtue of its cyclin-CDK regulatory function, and also an oncogene through a cyclin-CDK-independent function. This may explain why the cdkn1b gene is rarely inactivated in human tumors, and the p27CK- mouse in which the tumor suppressor function is lost but the cyclin-CDK-independent-oncogenic-function is maintained may represent a more faithful model for the widespread role of p27 misregulation in human cancers than the p27 null.

Indexed as

OncogenesAllelesAmino Acid SubstitutionAnimalsBronchiCyclin-Dependent Kinase Inhibitor p27FemaleGene DeletionHumansLung NeoplasmsMaleMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsModels, BiologicalCdkn1b protein, mouseCyclin-Dependent Kinase Inhibitor p27

Identifiers

PMID17626791
PMCPMC1920168
OpenAlexW2098157104

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.