The following is a summary of “Roles and mechanisms of aberrant alternative splicing in melanoma – implications for targeted therapy and immunotherapy resistance,” published in the March 2024 issue of Oncology by Chen et al.
In the landscape of melanoma treatment, despite notable strides in therapeutic approaches, the emergence of resistance to immunotherapy and the inherent off-target effects of targeted therapy have posed significant challenges, thereby attenuating the clinical benefits for afflicted patients. A critical facet of melanoma progression lies in the intricate orchestration of alternative splicing events, which orchestrate transcriptional reprogramming, ultimately shaping the disease trajectory.
Aberrant alternative splicing emerges as a pivotal player, intricately intertwined with the efficacy of immunotherapeutic interventions, targeted therapies, and the metastatic cascade characteristic of melanoma. Notably, deviations in the expression patterns of key splicing factors and their variants unveil potential avenues both as diagnostic biomarkers and as targets for therapeutic intervention, affording novel opportunities for personalized management strategies to enhance diagnostic accuracy, prognostication, and treatment efficacy in melanoma patients. Thus, a comprehensive elucidation of the multifaceted roles and underlying mechanisms governing alternative splicing in melanoma is imperative.
Within this framework, this review endeavors to furnish a meticulous synthesis of the splicing landscape in melanoma, unraveling the nuanced alterations intrinsic to this pathway during disease progression. Furthermore, by delineating the intricate interplay between aberrant splicing events and therapeutic resistance mechanisms, this review aims to furnish strategic insights into the development of innovative diagnostic modalities and therapeutic targets poised to mitigate resistance to targeted therapies and immunotherapy, thereby fostering the realization of more efficacious and personalized treatment paradigms tailored to the intricacies of melanoma biology.
Source: cancerci.biomedcentral.com/articles/10.1186/s12935-024-03280-x
