Evidence map›Paper›PMID 18758480›Full record

ReviewOncogene2008

Notch tumor suppressor function.

G P Dotto

Open access · greenAbstract readReview
In one paragraph

Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed, 2 pooled it
8.4field-weighted citation impact, top 2% 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

151 citing papers in PubMed, 2 syntheses or guidelines pooled it, 238 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. p73α1, a p73 C-terminal isoform, regulates tumor suppression and the inflammatory response via Notch1.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Molecular Mechanisms of Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2022
    Review
  13. Review
  14. Review
  15. Article
  16. The two-hit theory hits 50.Molecular biology of the cell · 2021
    Article
  17. Review
  18. Identification of HPV16-p16Epigenetics · 2021
    Article
  19. Review
  20. Article

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

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

1 author at 1 institution in 1 country.

G P DottoDepartment of Biochemistry, Lausanne University, Epalinges, Switzerland. gian-paolo.dotto@unil.ch
University of Lausanne · CH

Funding

VIRAL SMALL RNPS--ROLES IN CELL TRANSFORMATIONP01CA016038 · NCI · YALE UNIVERSITY · PI DIMAIO, DANIEL C. · 1985 to 2020
$25.6M
GROWTH DIFFERENTIATION CONTROL IN PRIMARY KERATINOCYTES.R01AR039190 · NIAMS · YALE UNIVERSITY · PI DOTTO, GIAN-PAOLO · 1988 to 2021
$9.5M
KINASES AND EPITHELIAL DIFFERENTIATION CONTROLR01CA073796 · NCI · UNIVERSITY OF LAUSANNE · PI DOTTO, GIAN-PAOLO · 1998 to 2006
$2.0M
Calcineurin signaling in the keratinocyte UVB responseR01AR054856 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DOTTO, GIAN-PAOLO · 2007 to 2011
$1.8M
NCI NIH HHS P01 CA016038NCI NIH HHS R01 CA073796NIAMS NIH HHS AR054856NIAMS NIH HHS AR39190NIAMS NIH HHS R01 AR039190NIAMS NIH HHS R01 AR054856
6 · The paper itself

Abstract

Cancer development results from deregulated control of stem cell populations and alterations in their surrounding environment. Notch signaling is an important form of direct cell-cell communication involved in cell fate determination, stem cell potential and lineage commitment. The biological function of this pathway is critically context dependent. Here we review the pro-differentiation role and tumor suppressing function of this pathway, as revealed by loss-of-function in keratinocytes and skin, downstream of p53 and in cross-connection with other determinants of stem cell potential and/or tumor formation, such as p63 and Rho/CDC42 effectors. The possibility that Notch signaling elicits a duality of signals, involved in growth/differentiation control and cell survival will be discussed, in the context of novel approaches for cancer therapy.

Indexed as

AnimalsApoptosisCell DifferentiationCell Transformation, NeoplasticDNA DamageFemaleGenes, Tumor SuppressorHumansKeratinocytesMiceNeoplasmsOncogene Proteins, ViralReceptor, Notch1Receptors, NotchSignal TransductionSpecies SpecificityNOTCH1 protein, humanNotch1 protein, mouseOncogene Proteins, ViralReceptor, Notch1Receptors, NotchTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID18758480
PMCPMC2747622
OpenAlexW2142622865

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.