Evidence map›Paper›PMID 24336324›Full record

ReviewOncogene2014

Hallmarks of alternative splicing in cancer.

S Oltean, D O Bates

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 413 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
413citing papers in PubMed, 3 pooled it
14.4field-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

413 citing papers in PubMed, 3 syntheses or guidelines pooled it, 696 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Alternative splicing and cancer: a systematic review.Signal transduction and targeted therapy · 2021
    Pooled it
  4. Protein-Ratio Rheostats: Integrating Stoichiometry, Abundance, and Binding Affinity in Cellular Function.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
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353 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.

S OlteanSchool of Physiology and Pharmacology, University of Bristol, Bristol, UK.
D O BatesDivision of Pre-clinical Oncology, School of Clinical Sciences, University of Nottingham, Queen's Medical Center, Nottingham, UK.
University of Bristol · GB

Funding

Biotechnology and Biological Sciences Research Council BB/J007293/1British Heart Foundation PG08/022/21636
6 · The paper itself

Abstract

The immense majority of genes are alternatively spliced and there are many isoforms specifically associated with cancer progression and metastasis. The splicing pattern of specific isoforms of numerous genes is altered as cells move through the oncogenic process of gaining proliferative capacity, acquiring angiogenic, invasive, antiapoptotic and survival properties, becoming free from growth factor dependence and growth suppression, altering their metabolism to cope with hypoxia, enabling them to acquire mechanisms of immune escape, and as they move through the epithelial-mesenchymal and mesenchymal-epithelial transitions and metastasis. Each of the 'hallmarks of cancer' is associated with a switch in splicing, towards a more aggressive invasive cancer phenotype. The choice of isoforms is regulated by several factors (signaling molecules, kinases, splicing factors) currently being identified systematically by a number of high-throughput, independent and unbiased methodologies. Splicing factors are de-regulated in cancer, and in some cases are themselves oncogenes or pseudo-oncogenes and can contribute to positive feedback loops driving cancer progression. Tumour progression may therefore be associated with a coordinated splicing control, meaning that there is the potential for a relatively small number of splice factors or their regulators to drive multiple oncogenic processes. The understanding of how splicing contributes to the various phenotypic traits acquired by tumours as they progress and metastasise, and in particular how alternative splicing is coordinated, can and is leading to the development of a new class of anticancer therapeutics-the alternative-splicing inhibitors.

Indexed as

Alternative SplicingAntineoplastic AgentsDisease ProgressionEpithelial-Mesenchymal TransitionHumansNeoplasm MetastasisNeoplasmsOncogene ProteinsProtein IsoformsSignal TransductionAntineoplastic AgentsOncogene ProteinsProtein Isoforms

Identifiers

PMID24336324
OpenAlexW2009258895

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.