Evidence map›Paper›PMID 34812550›Full record

ReviewCancer science2022

Aberrant RNA splicing and therapeutic opportunities in cancers.

Hirofumi Yamauchi, Kazuki Nishimura, Akihide Yoshimi

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 28 citations in OpenAlex.

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  12. Analysis of the Upregulated Expression Mechanism of Apoptotic Chromatin Condensation Inducer 1 in Hepatocellular Carcinoma Based on Bioinformatics.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
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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 at 1 institution in 1 country.

Hirofumi YamauchiCancer RNA Research Unit, National Cancer Center Research Institute, Tokyo, Japan.ORCID https://orcid.org/0000-0003-0730-6646
Kazuki NishimuraCancer RNA Research Unit, National Cancer Center Research Institute, Tokyo, Japan.ORCID https://orcid.org/0000-0002-2878-7664
Akihide YoshimiCancer RNA Research Unit, National Cancer Center Research Institute, Tokyo, Japan.ORCID https://orcid.org/0000-0002-0664-7281
National Cancer Centre Japan · JP

Funding

Brain Science FoundationJapan Agency for Medical Research and Development JP20jm0210085h0002Japanese Foundation for Multidisciplinary Treatment of CancerJapanese Society of HematologyJapan Society for the Promotion of Science 19K24691Japan Society for the Promotion of Science 21H04828Kato Memorial Bioscience FoundationLeukemia and Lymphoma SocietyNarishige Neuroscience Research FoundationNational Cancer Center Research and Development Funds 2020-A-2Novartis FoundationThe Japan Neurosurgical SocietyTokyo Biochemical Research FoundationUehara Memorial Foundation
6 · The paper itself

Abstract

There has been accumulating evidence that RNA splicing is frequently dysregulated in a variety of cancers and that hotspot mutations affecting key splicing factors, SF3B1, SRSF2 and U2AF1, are commonly enriched across cancers, strongly suggesting that aberrant RNA splicing is a new class of hallmark that contributes to the initiation and/or maintenance of cancers. In parallel, some studies have demonstrated that cancer cells with global splicing alterations are dependent on the transcriptional products derived from wild-type spliceosome for their survival, which potentially creates a therapeutic vulnerability in cancers with a mutant spliceosome. It has been c. 10 y since the frequent mutations affecting splicing factors were reported in cancers. Based on these surprising findings, there has been a growing interest in targeting altered splicing in the treatment of cancers, which has promoted a wide variety of investigations including genetic, molecular and biological studies addressing how altered splicing promotes oncogenesis and how cancers bearing alterations in splicing can be targeted therapeutically. In this mini-review we present a concise trajectory of what has been elucidated regarding the pathogenesis of cancers with aberrant splicing, as well as the development of therapeutic strategies to target global splicing alterations in cancers.

Indexed as

Antineoplastic AgentsHumansMutationNeoplasmsOligonucleotides, AntisenseRNA-Binding ProteinsRNA SplicingRNA Splicing FactorsSpliceosomesAntineoplastic AgentsOligonucleotides, AntisenseRNA-Binding ProteinsRNA Splicing Factorsantisense oligonucleotidecancerRNA binding proteinSF3bsplicing factor

Identifiers

PMID34812550
PMCPMC8819303
OpenAlexW3216095492

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.