Melanoma and MAPK Pathways

This study shows that combining ICMT and MAPK inhibitors suppresses RAC1P29S-driven resistance in BRAFV600E melanoma by inhibiting TAZ activity.

This study shows that combining palbociclib and crizotinib enhances senescence and immune recognition in melanoma cells regardless of BRAF/NRAS status, reducing tumor growth.

The paper identifies a novel interaction between BRAFV600E and TP53 in melanoma, suggesting that BRAFV600E inactivates TP53, explaining the rarity of TP53 alterations in this cancer type.

This paper identifies Midkine as a factor that disrupts melanoma dormancy by suppressing NR2F1 and altering signaling pathways, showing that targeting both Midkine and NR2F1 can limit metastasis and extend survival in mouse models.

This study identifies TRIM24 as an epigenetic regulator that promotes melanoma cell dedifferentiation and treatment resistance, with potential as a druggable target.

The paper identifies a kinase-independent role of MEK1/2 in stabilizing and maturing CRAF through direct binding, independent of catalytic activity.

This study identifies KDM5B's role in regulating the PRDX/TXN ROS detoxification system in melanoma DTPs, showing that PRDX inhibition increases ROS vulnerability and delays resistance to MAPK inhibition.

This study identifies that vemurafenib resistance in BRAFV600E melanomas is linked to metabolic pathway choices and Wnt/β-catenin signaling, with varying tolerance thresholds affecting mitochondrial and pentose phosphate pathway utilization.

The paper identifies off-target activation of GCN2 by BRAF and EGFR inhibitors, showing it limits cancer cell proliferation.

This study identifies SOX10 enhancer elements in melanoma that drive phenotype plasticity and drug resistance by modulating SOX10 expression and NTRK1 upregulation.

This study reveals how ARID1A-mediated transcriptional rewiring drives resistance to MAPK inhibitors in melanoma by altering signalling pathways, immune interactions, and receptor dynamics, highlighting potential targets for combinatorial therapies.

The paper identifies FK866, a NAMPT inhibitor, as effective against drug-naive and -resistant melanoma cells in various culture conditions without affecting healthy cells.

The paper identifies a BMP-dependent attractor state in melanoma precursor cells that precedes neural crest fate and is associated with ID1 expression in human melanoma.

This study analyzes acral melanoma genomes and transcriptomes from Mexican patients, finding ancestry-related mutation patterns and survival differences.

This study investigates the role of ERBB4 heterodimers in driving the proliferation of BRAF-WT&RAS/NF1-mutant melanoma cell lines and shows that dominant-negative mutants of ERBB2 and EGFR inhibit clonogenic growth in some but not all cell lines.

This study identifies CDK12/13 as key regulators of TRIB2 stability in melanoma and presents three classes of compounds that effectively eliminate TRIB2 with higher potency than afatinib.

This study identifies RhoA activation as a driver of glucose uptake and proliferation in MAPK inhibitor-resistant melanoma cells through ROCK-mediated IRS1 and PI3K pathway activation.

The paper presents a proteogenomic approach to identify resistance-specific alterations in melanoma PDX models treated with MAPK inhibitors using custom curated databases.

The paper shows that increased antioxidant capacity in BRAF-mutated melanoma cells reduces sensitivity to BRAF inhibitors and suggests targeting redox pathways could improve treatment outcomes.