Evidence map›Paper›PMID 24441040›Full record

ReviewOncogene2015

Alternative splicing in cancer: implications for biology and therapy.

J Chen, W A Weiss

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed
16.8field-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

159 citing papers in PubMed, 309 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Differential Expression ofIranian journal of public health · 2023
    Article
  17. Article
  18. Review
  19. Article
  20. Article

99 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

2 authors at 1 institution in 1 country.

J Chen1] Biomedical Sciences Graduate Program, University of California, San Francisco, CA, USA [2] Department of Neurology, University of California, San Francisco, CA, USA.
W A Weiss1] Department of Neurology, University of California, San Francisco, CA, USA [2] Department of Neurological Surgery and Pediatrics, University of California, San Francisco, CA, USA.
University of California, San Francisco · US

Funding

Vascular endothelial cell integrins in angiogenesisP01CA081403 · NCI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI SEEGER, ROBERT CHARLES · 2000 to 2014
$28.5M
Mouse models to discover new drivers of medulloblastomaR01CA159859 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Michael D. Taylor, WILLIAM A WEISS · 2011 to 2026
$10.4M
The vascular niche in glioma propagation and resistance to therapyU54CA163155 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BISTRUP, ANNETTE · 2011 to 2015
$4.4M
Murine Neuroblastoma Models for Preclinical TherapeuticsR01CA102321 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WEISS, WILLIAM A · 2003 to 2016
$3.4M
Medulloblastoma and MetastasesR01CA148699 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TAYLOR, MICHAEL D., WEISS, WILLIAM A · 2010 to 2014
$2.4M
Optical Measurement of Fast Drug Kinetics in TumorR01CA082104 · NCI · UNIVERSITY OF CALIF-LOS ALAMOS NAT LAB · PI BIGIO, IRVING J · 1999 to 2006
$2.1M
Mycn and MedulloblastomaR01CA133091 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WEISS, WILLIAM A · 2009 to 2013
$1.6M
Genetic network analysis of cancer targetsU01CA176287 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WEISS, WILLIAM A · 2013 to 2016
$1.2M
NCI NIH HHS CA081403NCI NIH HHS CA102321NCI NIH HHS CA133091NCI NIH HHS CA148699NCI NIH HHS CA159859NCI NIH HHS CA163155NCI NIH HHS CA176287NCI NIH HHS CA82104NCI NIH HHS R01 CA102321
6 · The paper itself

Abstract

Alternative splicing has critical roles in normal development and can promote growth and survival in cancer. Aberrant splicing, the production of noncanonical and cancer-specific mRNA transcripts, can lead to loss-of-function in tumor suppressors or activation of oncogenes and cancer pathways. Emerging data suggest that aberrant splicing products and loss of canonically spliced variants correlate with stage and progression in malignancy. Here, we review the splicing landscape of TP53, BARD1 and AR to illuminate roles for alternative splicing in cancer. We also examine the intersection between alternative splicing pathways and novel therapeutic approaches.

Indexed as

Alternative SplicingAnimalsBreast NeoplasmsCell ProliferationDisease ProgressionExonsFemaleHumansMiceNeoplasmsReceptors, AndrogenRNA, MessengerRNA SplicingTumor Suppressor Protein p53Tumor Suppressor ProteinsUbiquitin-Protein LigasesBARD1 protein, humanReceptors, AndrogenRNA, MessengerTP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID24441040
OpenAlexW2042012882

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.