ReviewDrug development research2026
Alternative Splicing in Cyclin-Dependent Kinase 4/6 Inhibitor Resistance in Estrogen Receptor-Positive Breast Cancer.
Review in Drug development research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Alternative Splicing in Cyclin-Dependent Kinase 4/6 Inhibitor Resistance in Estrogen Receptor-Positive Breast Cancer.Drug development research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Breast cancer is one of the leading causes of cancer-related deaths among women worldwide, with estrogen receptor-positive (ER+) breast cancer being the most common subtype. Cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) have become a crucial therapeutic approach for this type of cancer. However, ER+ breast cancer frequently develops resistance to CDK4/6i, limiting therapeutic efficacy. Alternative splicing is a key post-transcriptional regulatory mechanism that may drive such resistance. In this review, we comprehensively analyzed the literature on the molecular mechanisms and key signaling pathways associated with CDK4/6i resistance in ER+ breast cancer and introduced the role of alternative splicing, with a particular focus on its function in tumor drug resistance. Available evidence suggests that splicing dysregulation may influence resistance through multiple pathways, including cell-cycle control, epithelial-mesenchymal transition, growth factor and RAS/MAPK signaling, and immune-related programs. Recent work has also suggested that reduced expression of the splicing regulator NSRP1 may be associated with CDK4/6i resistance through altered NSD2 splicing and activation of interferon signaling, although this mechanism currently requires further independent validation. Collectively, these findings support alternative splicing as a promising but still evolving area of investigation in CDK4/6i resistance. This work provides deeper insights into the role of alternative splicing in CDK4/6i resistance and offers a theoretical foundation for developing novel therapeutic approaches. Future research may focus on developing drugs that precisely modulate specific splicing events or combining CDK4/6i with splicing modulators to reverse or delay resistance.
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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 Socratic graph.