HDAC8 and Melanoma Resistance to BRAF Inhibitor Tx

Researchers identify mechanism of resistance to BRAF inhibitors in melanoma 15 April 2019 Melanoma in skin biopsy with H&E stain – this case may

approved BRAF inhibitors produce high response rates and improve overall survival in patients with BRAF V600E/K mutant melanoma, but are linked to pathologies associated with paradoxical ERK1/2 activation in wild-type. BRAF cells. To overcome this limitation, a next-generation paradox breaking raf inhibitor (plx8394) has been designed. Here we.

This link between HDAC8 and drug resistance suggested to the researchers that drugs targeting HDACs may be able to overcome cellular resistance mechanisms to BRAF inhibitors.

Melanoma is a deadly skin disease well known for resistance to chemotherapies and immunomodulating therapies. PLX4032 is a selective BRAF inhibitor and, in clinical trials, has consistently.

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Melanoma cells have the ability to switch to a dedifferentiated, invasive phenotype in response to multiple stimuli. Here we show that exposure of melanomas to multiple stresses including BRAF-MEK inhibitor therapy, hypoxia, and UV irradiation leads to an increase in histone deacetylase 8 (HDAC8) activity and the adoption of a drug-resistant phenotype.

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Underlies Resistance of Melanoma Cells to BRAF Inhibitors via JAK1 Deregulation Graphical Abstract. Houston, TX 77030,USA 5Melanoma Research Center, Wistar Institute. Downregulation of the ubiquitin ligase rnf125 Underlies Resistance of Melanoma Cells to BRAF Inhibitors via JAK1.

Although BRAF and MEK inhibitors have proven clinical benefits in melanoma, most patients develop resistance. We report a de novo MEK2-Q60P mutation and BRAF gain in a melanoma from a patient who progressed on the MEK inhibitor trametinib and did not respond to the BRAF inhibitor dabrafenib. We also identified the same MEK2-Q60P mutation along with BRAF amplification in a xenograft tumor.

This link between HDAC8 and drug resistance suggested to the researchers that drugs targeting HDACs may be able to overcome cellular resistance mechanisms to BRAF inhibitors. The researchers performed a series of mouse experiments and found that co-treatment with both HDAC and BRAF inhibitors inhibited melanoma tumor growth better than either.

Here, we report that RIP1 was upregulated and contributed to both intrinsic and acquired resistance of melanoma cells to BRAF. Inhibitor Vemurafenib, the MEK inhibitor Trametinib, and the selective.

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