Evidence map›Paper›PMID 22248731›Full record

ReviewBiochemical pharmacology2012

Regulation of chemoresistance via alternative messenger RNA splicing.

Scott T Eblen

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Aberrant splicing and drug resistance in AML.Journal of hematology & oncology · 2016
    Review
  6. Article
  7. Serine-arginine protein kinase 1 is associated with hepatocellular carcinoma progression and poor patient survival.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
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.

Scott T EblenDepartment of Cell and Molecular Pharmacology, Medical University of South Carolina, Charleston, 29425, USA. eblen@musc.edu
Medical University of South Carolina · US

Funding

Regulation of Ovarian Cancer Multidrug Resistance by MAP KinasesR01CA131200 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI EBLEN, SCOTT T · 2009 to 2013
$1.5M
NCI NIH HHS 1R01CA131200NCI NIH HHS R01 CA131200
6 · The paper itself

Abstract

The acquisition of resistance to chemotherapy is a significant problem in the treatment of cancer, greatly increasing patient morbidity and mortality. Tumors are often sensitive to chemotherapy upon initial treatment, but repeated treatments can select for those cells that were able to survive initial therapy and have acquired cellular mechanisms to enhance their resistance to subsequent chemotherapy treatment. Many cellular mechanisms of drug resistance have been identified, most of which result from changes in gene and protein expression. While changes at the transcriptional level have been duly noted, it is primarily the post-transcriptional processing of pre-mRNA into mature mRNA that regulates the composition of the proteome and it is the proteome that actually regulates the cell's response to chemotherapeutic insult, inducing cell survival or death. During pre-mRNA processing, intronic non-protein-coding sequences are removed and protein-coding exons are spliced to form a continuous template for protein translation. Alternative splicing involves the differential inclusion or exclusion of exonic sequences into the mature transcript, generating different mRNA templates for protein production. This regulatory mechanism enables the potential to produce many different protein isoforms from the same gene. In this review I will explain the mechanism of alternative pre-mRNA splicing and look at some specific examples of how splicing factors, splicing factor kinases and alternative splicing of specific pre-mRNAs from genes have been shown to contribute to acquisition of the drug resistant phenotype.

Indexed as

Alternative SplicingCyclin D1Drug Resistance, NeoplasmHumansNeoplasmsProtein Serine-Threonine KinasesReceptors, AndrogenRNA-Binding ProteinsRNA PrecursorsRNA Splicing FactorsSpliceosomesSTAT2 Transcription FactorCCND1 protein, humanCyclin D1Protein Serine-Threonine KinasesRBM17 protein, humanReceptors, AndrogenRNA-Binding ProteinsRNA PrecursorsRNA Splicing FactorsSRPK1 protein, humanSTAT2 Transcription Factor

Identifiers

PMID22248731
PMCPMC3299811
OpenAlexW2015014748

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.