Evidence map›Paper›PMID 14528285›Full record

ReviewOncogene2003

Notch signaling as a therapeutic target in cancer: a new approach to the development of cell fate modifying agents.

Brian J Nickoloff, Barbara A Osborne, Lucio Miele

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing 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

121 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. HtrA1 suppresses the growth of pancreatic cancer cells by modulating Notch-1 expression.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

61 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

3 authors.

Brian J NickoloffDepartment of Pathology, Loyola University, Chicago, USA.
Barbara A Osborne
Lucio Miele

Funding

SLC and dendritic cells in antitumor immunity &therapyP01CA059327 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHANG, ALFRED E · 1992 to 2005
$8.2M
NOTCH-1 IN REGULATION OF APOPTOSIS IN TUMOR CELLSR01CA084065 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MIELE, LUCIO · 2000 to 2004
$1.2M
MOLECULAR ANALYSIS OF APOPTOSIS IN T CELLSR01AG016690 · NIA · UNIVERSITY OF MASSACHUSETTS AMHERST · PI OSBORNE, BARBARA A · 1998 to 2002
$823k
NCI NIH HHS P01 CA59327NCI NIH HHS R01 CA84065-01NIA NIH HHS R01 AG 16690
6 · The paper itself

Abstract

Notch signaling controls cell fate decisions including during development and stem cell renewal and differentiation in many postnatal tissues. Increasing evidence suggests that the Notch signaling network is frequently deregulated in human malignancies and that genetic or pharmacological manipulation of Notch signaling is a novel potential strategy for the treatment of human neoplasms. This review article summarizes the most recent preclinical and clinical evidence linking Notch signaling to cancer, delineates questions that remain unanswered and explores potential biopharmacological strategies to manipulate Notch signaling in vivo.

Indexed as

AnimalsHumansMammalsMelanomaMembrane ProteinsModels, BiologicalNeoplasmsProto-Oncogene ProteinsReceptors, Cell SurfaceReceptors, NotchSignal TransductionMembrane ProteinsProto-Oncogene ProteinsReceptors, Cell SurfaceReceptors, Notch

Identifiers

PMID14528285

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.