Melanoma articles from across Nature Portfolio

Super-enhancers (SEs) drive specific gene expression programmes underlying different cancer cell states offering opportunities for therapeutic _targeting. Here, the authors suggest _targeting SE-dependent genes with synthetic ecteinascidins in tumors with heterogeneous transcriptional landscapes.

In an ongoing adaptive-design trial exploring different combinations of neoadjuvant immunotherapies including the anti-PD-1 agent pembrolizumab, the anti-TIGIT agent vibostolimab and the oncolytic virus gebasaxturev, neoadjuvant pembrolizumab-based regimens elicited encouraging clinical responses in patients with resectable melanoma.

The molecular regulation of endothelial cells (ECs) in metastasis remains unclear. Here, the authors use single-cell RNA-seq to examine the reprogramming of lung ECs in mouse models of melanoma metastasis, revealing that PIM3 protects capillary integrity and that its inhibition increases vascular leakage and metastatic colonisation.

In this Journal Club, Chakrabarti discusses a method to dissect the molecular architecture of inheritable gene expression (memory) states that mark cells that transition into drug-tolerant persister cells in melanoma.

In this Journal Club, Sabarinathan discusses a study suggesting immunoproteasome expression as a potential biomarker of response to immune checkpoint inhibition in melanoma.

In a recent study published in Cell, Chhabra et al. identify age- and sex-dependent changes in skin fibroblasts that drive melanoma aggressiveness, with aged male fibroblasts promoting a slow-cycling, invasive state and resistance to _targeted therapy in melanoma cells.

Evidence-based reductions in cancer treatment that still preserve outcomes can result in an improved quality of life for patients and optimized healthcare resourcing. Using melanoma as an example, we define treatment deintensification, outlining barriers to its implementation, as well as existing guidance.

Aminoacyl-tRNA synthetases can promote or suppress cancer progression by regulating codon-dependent translation. A study now shows that valine aminoacyl-tRNA synthetase (VARS) promotes therapeutic resistance of melanoma to MAPK pathway inhibitors by enhancing translation of valine-enriched genes, including the fatty acid oxidation gene HADH.