Targeted inhibition of the DAPKs (Death-associated protein kinase 1 and 3) reduces the proportion of slow-proliferating/senescent-like HuR Low cells and the adaptive response of the whole melanoma-cell population to BRAF inhibition.
A team from the UNIGE and the HUG has succeeded in identifying a drug-targetable mechanism whose blockage reduces the capacity of melanoma cells to adapt. and resist to treatment. Targeted inhibition of the DAPKs (Death-associated protein kinase 1 and 3) reduces the proportion of slow-proliferating/senescent-like HuR Low cells and the adaptive response of the whole melanoma-cell population to BRAF inhibition. UNIGE / Rastine Merat - The advent of small-molecule targeted therapies, a decade ago, revolutionized the treatment of metastatic melanoma, provided that the tumors carry the mutations to respond to these treatments. However, despite a remarkable initial response that can be seen in a majority of patients, most of them will undergo relapse even after spectacular initial responses. These relapses are due to "dormant" persistent cells, unresponsive to treatment. A team from the University of Geneva and the University Hospitals of Geneva (HUG) has shown that these cells under-express a protein called HuR.
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