Evidence map›Paper›PMID 20007775›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Alterations of the Notch pathway in lung cancer.

Britta Westhoff, Ivan N Colaluca, Giovanni D'Ario, Maddalena Donzelli, Daniela Tosoni, Sara Volorio, Giuseppe Pelosi, Lorenzo Spaggiari, Giovanni Mazzarol, Giuseppe Viale and 2 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
236citing papers in PubMed, 2 pooled it
10.8field-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

236 citing papers in PubMed, 2 syntheses or guidelines pooled it, 393 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. NOTCH pathway inactivation promotes bladder cancer progression.The Journal of clinical investigation · 2015
    Trial
  4. Review
  5. Endocytic Control of Cell-Autonomous and Non-Cell-Autonomous Functions of p53.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. The CRL7Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  11. Decoding the NRF2-NOTCH Crosstalk in Lung Cancer-An Update.Antioxidants (Basel, Switzerland) · 2025
    Review
  12. Article
  13. Review
  14. Article
  15. Hippo/YAP signaling's multifaceted crosstalk in cancer.Frontiers in cell and developmental biology · 2025
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

176 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

12 authors at 3 institutions in 1 country.

Britta WesthoffIFOM, Fondazione Istituto FIRC di Oncologia Molecolare, Milan, Italy.
Ivan N Colaluca
Giovanni D'Ario
Maddalena Donzelli
Daniela Tosoni
Sara Volorio
Giuseppe Pelosi
Lorenzo Spaggiari
Giovanni Mazzarol
Giuseppe Viale
Salvatore Pece
Pier Paolo Di Fiore
FIRC Institute of Molecular Oncology · ITEuropean Institute of Oncology · ITUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Notch signaling regulates cell specification and homeostasis of stem cell compartments, and it is counteracted by the cell fate determinant Numb. Both Numb and Notch have been implicated in human tumors. Here, we show that Notch signaling is altered in approximately one third of non-small-cell lung carcinomas (NSCLCs), which are the leading cause of cancer-related deaths: in approximately 30% of NSCLCs, loss of Numb expression leads to increased Notch activity, while in a smaller fraction of cases (around 10%), gain-of-function mutations of the NOTCH-1 gene are present. Activation of Notch correlates with poor clinical outcomes in NSCLC patients without TP53 mutations. Finally, primary epithelial cell cultures, derived from NSCLC harboring constitutive activation of the Notch pathway, are selectively killed by inhibitors of Notch (gamma-secretase inhibitors), showing that the proliferative advantage of these tumors is dependent upon Notch signaling. Our results show that the deregulation of the Notch pathway is a relatively frequent event in NSCLCs and suggest that it might represent a possible target for molecular therapies in these tumors.

Indexed as

AgedBase SequenceBasic Helix-Loop-Helix ProteinsCarcinoma, Non-Small-Cell LungDNA Mutational AnalysisDNA, NeoplasmFemaleGene ExpressionHomeodomain ProteinsHumansLung NeoplasmsMaleMembrane ProteinsMiddle AgedMutationNerve Tissue ProteinsBasic Helix-Loop-Helix ProteinsDNA, NeoplasmHES1 protein, humanHomeodomain ProteinsMembrane ProteinsNerve Tissue ProteinsNOTCH1 protein, humanNUMB protein, humanReceptor, Notch1Receptors, NotchRNA, MessengerRNA, NeoplasmTranscription Factor HES-1

Identifiers

PMID20007775
PMCPMC2799768
OpenAlexW2146949185

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.