ArticleSignal transduction and targeted therapy2025
Anti-BCL2 therapy eliminates giant congenital melanocytic nevus by senolytic and immune induction.
Article in Signal transduction and targeted therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Precision Medicine in Dermatology: MEK Inhibition and MAPK Pathway Modulation for Congenital Melanocytic Nevi.Biomedicines · 2026Review
- USP5 Stabilizes TGFBR1 to Drive Vascular Smooth Muscle Cell Senescence and Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- High Mobility Group Protein B1 Mediates the Role of the Neutrophil Extracellular Traps in the Progression of Acute Myocardial Infarction.Cardiovascular drugs and therapy · 2026Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Giant congenital melanocytic nevus (GCMN) is a RAS/RAF mutation-driven syndrome characterized by extensive melanocytic lesions, posing psychological challenges and a lifelong risk of malignancy. Existing treatments like surgical resection and laser therapy fail to fully remove lesions, and MAPK inhibitors show limited efficacy. This study identified a predominant population of senescent cells and a minority of proliferative cells in GCMN, necessitating dual-targeted strategies. We found that the anti-apoptotic protein BCL2 is expressed in both senescent and proliferative cells from GCMN patients with various gene mutations. Coexpression of P16 and BCL2 indicated a phenotype of growth arrest and cell survival. BCL2 inhibitors (BCL2i) showed significant cytotoxicity to GCMN cells in vitro. Hypopigmentation and GCMN cell clearance were observed in patient-derived xenograft models and in Nras
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