Abstract: Inventors have shown that salinomycin and its derivatives such as AM23, through lysosomal iron accumulation, reduced proliferation/survival of uveal melanoma cells harboring different genetic background. Accordingly, salinomycin and its derivates ironomycin represent valuable therapeutic strategies to treat melanoma and uveal melanoma. The present invention relates to a method for treating melanoma in a subject in need thereof comprising a step of administering said subject with a therapeutically effective amount of an iron metabolism disruptor.

Abstract: The pigmentation disorders alter people's quality of life, the effectiveness of treatments is limited resulting in unsatisfactory outcomes, and there is a high therapeutic demand. The inventors tested BCH and JPH203 on a more physiological model, using reconstructed human epidermis and confirmed a strong inhibition of pigmentation demonstrating the clinical potential of SLC7A5 inhibition and positioning BCH and JPH203 as depigmenting agents suitable for cosmetic or dermatologic intervention in hyperpigmentation diseases. Thus, the invention relates to a method for treating hyperpigmentation disorder in a subject in need thereof comprising administering said subject with a therapeutically effective amount of JPH203.

Abstract: The present invention relates to a method for treating a subject suffering from melanoma resistant by administering to said subject an inhibitor of NAMPT. Using a global metabolic profiling, inventors have showed that in addition to glycolysis, the BRAF inhibitor, PLX4032, promoted a complex metabolic rewiring of melanoma cells, including protein catabolism and fatty acid synthesis. Importantly, they observed that PLX4032 reduced the levels of nicotinamide adenine dinucleotide (NAD+), an important redox co-factor in numerous metabolic processes, including glycolysis, tricarboxylic acid cycle (TCA) cycle, glutamate metabolism and fatty acid betaoxidation. Pharmacological or genetic inhibition of NAMPT impaired melanoma cell growth, whereas the overexpression of NAMPT dampened the antiproliferative effect of PLX4032. In vivo, the inhibition of NAMPT also prevented the xenograft development of PLX4032-sensitive and -resistant melanoma cells, identifying NAMPT as a potential target for BRAFi-resistant melanomas.

Abstract: The present invention relates to a mutant of MITF which is useful as a marker for predisposition to the development of cancer and to uses thereof in diagnosis and preventive treatments, sumoylation being reduced or absent in this mutant.

Abstract: The present invention relates to a mutant of MITF which is useful as a marker for predisposition to the development of cancer and to uses thereof in diagnosis and preventive treatments, sumoylation being reduced or absent in this mutant.