ReviewCancer research2013
mRNA splicing variants: exploiting modularity to outwit cancer therapy.
Review in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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.
Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Roles and mechanisms of aberrant alternative splicing in melanoma - implications for targeted therapy and immunotherapy resistance.Cancer cell international · 2024Review
- Differential Splicing of Skipped Exons Predicts Drug Response in Cancer Cell Lines.Genomics, proteomics & bioinformatics · 2021Article
- PTBP1 is necessary for dendritic cells to regulate T-cell homeostasis and antitumour immunity.Immunology · 2021Article
- Association of altered folylpolyglutamate synthetase pre-mRNA splicing with methotrexate unresponsiveness in early rheumatoid arthritis.Rheumatology (Oxford, England) · 2021Article
- SRPK1 acetylation modulates alternative splicing to regulate cisplatin resistance in breast cancer cells.Communications biology · 2020Article
- ZRANB2 and SYF2-mediated splicing programs converging on ECT2 are involved in breast cancer cell resistance to doxorubicin.Nucleic acids research · 2020Article
- Methionyl-tRNA Synthetase is a Useful Diagnostic Marker for Lymph Node Metastasis in Non-Small Cell Lung Cancer.Yonsei medical journal · 2019Article
- Isoforms S and L of MRPL33 from alternative splicing have isoform‑specific roles in the chemoresponse to epirubicin in gastric cancer cells via the PI3K/AKT signaling pathway.International journal of oncology · 2019Article
- Splicing factor SRSF1 promotes gliomagenesis via oncogenic splice-switching of MYO1B.The Journal of clinical investigation · 2019Article
- SRSF1 modulates PTPMT1 alternative splicing to regulate lung cancer cell radioresistance.EBioMedicine · 2018Article
- The absence of a novel intron 19-retainingOncotarget · 2018Article
- Developing new targeting strategy for androgen receptor variants in castration resistant prostate cancer.International journal of cancer · 2017Article
- Allosteric alterations in the androgen receptor and activity in prostate cancer.Endocrine-related cancer · 2017Review
- Methionyl-tRNA synthetase overexpression is associated with poor clinical outcomes in non-small cell lung cancer.BMC cancer · 2017Article
- Variant 2 of KIAA0101, antagonizing its oncogenic variant 1, might be a potential therapeutic strategy in hepatocellular carcinoma.Oncotarget · 2017Article
- Aberrant RNA splicing in cancer; expression changes and driver mutations of splicing factor genes.Oncogene · 2016Review
- Cloning of multiple ERα mRNA variants in killifish (Fundulus heteroclitus), and differential expression by tissue type, stage of reproduction, and estrogen exposure in fish from polluted and unpolluted environments.Aquatic toxicology (Amsterdam, Netherlands) · 2015Article
- Alternative RNA structure-coupled gene regulations in tumorigenesis.International journal of molecular sciences · 2014Review
- The splicing factor RBM4 controls apoptosis, proliferation, and migration to suppress tumor progression.Cancer cell · 2014Article
- Modulation of alternative splicing contributes to cancer development: focusing on p53 isoforms, p53β and p53γ.Cell death and differentiation · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Systemic cancer therapy has traditionally exploited vulnerabilities in cancer cells, a strategy which has become more precise with the identification and targeting of driver oncogenes. However, persistent tumor growth due to primary (de novo) or secondary (acquired) resistance limits therapeutic efficacy for many patients. Alternative splicing is important for increasing the diversity of the cellular proteome, and is a process frequently deregulated during cancer development and progression. In cancer cells, diverse splicing alterations have been identified that eliminate protein domains or enzymatic activities required for efficacy of cancer therapies, promote gain of novel signaling functions that circumvent cancer therapies, and uncouple signaling pathways from upstream regulatory points that are blocked by cancer therapies. The mechanisms underlying these splicing changes range from stable alterations in gene sequence/structure to deregulation of splicing regulatory factors. In this review, the role of splice variants in cancer therapy resistance will be discussed, with examples of how mechanistic understanding of these processes has led to the development of novel strategies for therapy resensitization.
Indexed as
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What OpenQuestion holds
Registered trials
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.