Malignant melanoma (MM) is among the most lethal cutaneous neoplasms, frequently tied to metastasis and poor outcomes. Neural cell adhesion molecule L1 (L1CAM) is a protein that has been associated with poor prognosis in several cancer types, but its association with MM is poorly understood.
Kinnate Biopharma Inc. has synthesized mitogen-activated protein kinase kinase (MAP2K; MEK; MAPKK) inhibitors reported to be useful for the treatment of cancer.
Selenoprotein O (SELENOO) is an antioxidant mitochondrial enzyme that transfers AMP from ATP to protein substrates in a post-translational process known as AMPylation.
Researchers at the University of California San Diego have uncovered a key mechanism underlying the treatment resistance of melanoma with the BRAF V600E mutation through pathways involved in focal adhesion and extracellular matrix (ECM) remodeling. These two processes remodel the tumor cell environment in melanoma through the RAF/MEK cell signaling pathway. However, the combined use of FAK inhibitors with a RAF-MEK clamp overcame this resistance.
New research has uncovered a complex interplay between extracellular matrix (ECM) structure and the transcriptional responses of cancer cells, showing how they alter their gene expression to ‘escape’ from ECM.
The tumor microenvironment plays a crucial role in the resistance of solid tumors to immunotherapy. In particular, fibroblast activation protein (FAP)-expressing cancer-associated fibroblasts have been shown to contribute to immune evasion.
Glucocorticoid-induced tumor necrosis factor receptor (GITR) and its ligand, GITRL, are involved in immune response regulation. GITR is mainly expressed in activated T cells while GITRL is primarily found in antigen-presenting cells.
New research has uncovered a complex interplay between extracellular matrix (ECM) structure and the transcriptional responses of cancer cells, showing how they alter their gene expression to ‘escape’ from ECM. The findings will make it easier to identify tumors that are likely to metastasize at an early stage.
New research has uncovered a complex interplay between extracellular matrix (ECM) structure and the transcriptional responses of cancer cells, showing how they alter their gene expression to ‘escape’ from ECM. The findings will make it easier to identify tumors that are likely to metastasize at an early stage.
