TL;DR
This work unveils an unforeseen tumor-suppressing role for mTORC2 in the early adaptation phase of BRAF V600E melanoma cells to targeted therapy and identifies the NAMPT-ETC axis as a potential therapeutic vulnerability of low RICTOR tumors.
The use of BRAF inhibitors (BRAFi) for the targeted inhibition of the MAPK pathway represents a cornerstone of treatment for BRAFV600E-mutant melanoma. However, the rapid emergence of drug resistance remains a major clinical challenge. Mounting evidence indicates that therapy resistance is driven by both phenotypic pla...
The therapeutic landscape of advanced melanoma has been transformed by immune checkpoint inhibitors and BRAF/MEK inhibitors, resulting in substantial improvements in response rates and overall survival. However, both primary and acquired resistance remain frequent, commonly driven by MAPK pathway reactivation and activ...
The RAS/MAPK pathway is among the most frequently dysregulated in human cancer, predominantly driven by activating mutations across RAS and BRAF in a broad spectrum of tumor types. The recent clinical validation of direct inhibitors of RAS, long considered undruggable, has reenergized the field and renewed focus on tar...
Cutaneous melanoma remains a global health challenge. Although BRAF/MEK-targeted therapies and immune checkpoint inhibitors (ICIs) have improved outcomes in advanced disease, durable responses remain difficult to achieve for most patients. Therapeutic resistance represents the central barrier to long-term disease contr...
Background/Aim: Advanced melanoma treatment remains debated, particularly in patients with B-Raf proto-oncogene serine/threonine kinase (BRAF) V600 mutations eligible for both immune checkpoint inhibitors (ICI) and BRAF/MEK inhibitors. Additional biomarkers are needed to improve treatment selection. Mutations of the te...
Combined BRAF/MEK and PSGL-1 targeting provides a durable anti-tumor response through enhanced functionality and a memory-like phenotype in CD8⁺ T cell subsets.
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