Evidence map›Paper›PMID 18614011›Full record

ArticleCell2008

Growth-inhibitory and tumor- suppressive functions of p53 depend on its repression of CD44 expression.

Samuel Godar, Tan A Ince, George W Bell, David Feldser, Joana Liu Donaher, Jonas Bergh, Anne Liu, Kevin Miu, Randolph S Watnick, Ferenc Reinhardt and 3 more

Abstract read
In one paragraph

Article in Cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 269 papers.

0numbers the graph read from it
0cells of the map it votes in
269citing papers in PubMed
13.9field-weighted citation impact, top 1% 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

269 citing papers in PubMed, 465 citations in OpenAlex.

  1. Article
  2. Article
  3. Endocytic Control of Cell-Autonomous and Non-Cell-Autonomous Functions of p53.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Galectin-9 inhibition of the MIF-CD74/CD44 pathway suppresses chronic arthritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Samuel GodarWhitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.
Tan A Ince
George W Bell
David Feldser
Joana Liu Donaher
Jonas Bergh
Anne Liu
Kevin Miu
Randolph S Watnick
Ferenc Reinhardt
Sandra S McAllister
Tyler Jacks
Robert A Weinberg
Whitehead Institute for Biomedical Research · USMassachusetts Institute of Technology · USBoston Children's Hospital · USSophiahemmet Hospital · SE

Funding

Use of Organotypic and Mammary Gland Models to Investigate the Outcomes of ClonalP01CA080111 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI DILLON, DEBORAH · 1999 to 2018
$36.0M
Variation in Receptor Tyrosine Kinases and Breast Cancer RiskP50CA089393 · NCI · DANA-FARBER CANCER INSTITUTE · PI HARRIS, LYNDSAY NORINE · 2000 to 2009
$28.8M
Development of Tumor Specific Transcript PanelsK08CA092013 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI INCE, TAN A · 2001 to 2006
$697k
NCI NIH HHS CA089393NCI NIH HHS CA092013NCI NIH HHS K08 CA092013NCI NIH HHS P01 CA080111NCI NIH HHS P50 CA089393
6 · The paper itself

Abstract

The p53 tumor suppressor is a key mediator of cellular responses to various stresses. Here, we show that under conditions of basal physiologic and cell-culture stress, p53 inhibits expression of the CD44 cell-surface molecule via binding to a noncanonical p53-binding sequence in the CD44 promoter. This interaction enables an untransformed cell to respond to stress-induced, p53-dependent cytostatic and apoptotic signals that would otherwise be blocked by the actions of CD44. In the absence of p53 function, the resulting derepressed CD44 expression is essential for the growth and tumor-initiating ability of highly tumorigenic mammary epithelial cells. In both tumorigenic and nontumorigenic cells, CD44's expression is positively regulated by p63, a paralogue of p53. Our data indicate that CD44 is a key tumor-promoting agent in transformed tumor cells lacking p53 function. They also suggest that the derepression of CD44 resulting from inactivation of p53 can potentially aid the survival of immortalized, premalignant cells.

Indexed as

AnimalsCell LineCell Line, TumorEpithelial CellsGene Expression Regulation, NeoplasticHumansHyaluronan ReceptorsMembrane ProteinsMiceTumor Suppressor Protein p53CD44 protein, humanCKAP4 protein, humanHyaluronan ReceptorsMembrane ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID18614011
PMCPMC3222460
OpenAlexW2167291962

What OpenQuestion holds

Textmetadata
LicenceTDM
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.