Abstract: The present invention provides novel compounds of formula (I) and pharmaceutical compositions containing these compounds. The compounds of formula (I) can act as NF-?B-inducing kinase (NIK) inhibitors and, in particular, can induce the intracellular degradation of NIK, which renders these compounds highly advantageous for use in therapy, including in the treatment or prevention of cancer, inflammatory diseases and autoimmune diseases.

Abstract: The present invention relates to a compound of general formula (I), wherein R1 is OCH2CH2OCH3 or OCH3, R?1 is H or OH, R2 is Cl, F, Br or I, with the proviso that when: R1 is OCH2CH2OCH3 then R?1 is H, R1 is OCH3 then R?1 is OH, its pharmaceutically acceptable salts and/or optical isomers, tautomers, solvates or isotopic variations thereof. The invention also relates to said compounds for use in the treatment of cancer, namely solid tumor cancer, and preferably those selected from melanoma, colon, lung, pancreas, kidney, Merkel carcinoma, squamous cell carcinoma, prostate, breast and bladder. The invention also relates to a pharmaceutical composition comprising said compounds.

Abstract: The present invention relates to the identification of proteins of the WNT signaling pathway as therapeutic targets of pigmentation disorder and as biomarkers of pigmentation status. The invention in particular relates to products and methods for treating a hypopigmentation disorder. The invention also relates to products and methods for detecting, diagnosing, staging or monitoring the course of hypopigmentation disorder and is particularly suited for human subjects.

Abstract: The present invention relates to the identification of proteins of the WNT signaling pathway as therapeutic targets of pigmentation disorder and as biomarkers of pigmentation status. The invention in particular relates to products and methods for treating a hypopigmentation disorder. The invention also relates to products and methods for detecting, diagnosing, staging or monitoring the course of hypopigmentation disorder and is particularly suited for human subjects.

Abstract: The present invention relates to the identification of proteins of the WNT signaling pathway as therapeutic targets of pigmentation disorder and as biomarkers of pigmentation status. The invention in particular relates to products and methods for treating a hypopigmentation disorder. The invention also relates to products and methods for detecting, diagnosing, staging or monitoring the course of hypopigmentation disorder and is particularly suited for human subjects.

Abstract: The present invention relates to a method for treating hyperpigmentary skin disorder. By using normal human melanocytes (NHMs) and normal human keratinocytes (NHKs), which are infected with CLEC12B siRNA/shRNA/RNAi lentiviral particles, inventors have showed that decreasing CLEC12B expression significantly reduce the transfer of melanin to the keratinocytes. These results demonstrate that CLEC12B is specifically expressed in the skin by melanocytes and plays a key role in the transfer or melanosomes to the keratinocytes. Accordingly, the invention relates to a method for treating hyperpigmentary skin disorder in a subject in need thereof comprising a step of administering to said subject a therapeutically effective amount of a CLEC12B antagonist, wherein CLEC12B antagonist is polypeptide, more particularly a decoy.

Abstract: The present invention relates to a method for treating vitiligo in a subject in need thereof comprising a step of administering to said subject a therapeutically effective amount of an antagonist of CXCR3B. Inventors have demonstrated that in skin and blood samples obtained from vitiligo subjects the population of the innate immune system is increased (NK and ILC1 cells). For the first time, inventors have shown that melanocytes express CXCR3, more 10 particularly CXCR3B (RNA and protein expressions). They have shown that the expression of CXCR3B on melanocytes is responsible of the destruction of melanocytes upon local stimulation with CXCL10. Inventors have demonstrated for the first time that siRNA of CXCR3B or CXCR3B antagonist prevent the CXL10-induced apoptosis of melanocytes. This initial apoptosis of melanocyte triggers the secondary adaptive immunity against melanocytes 15 that further destroys the remaining melanocytes.

Abstract: The present invention relates to a compound of general formula (I), wherein R1 is OCH2CH2OCH3 or OCH3, R?1 is H or OH, R2 is Cl, F, Br or I, with the proviso that when: R1 is OCH2CH2OCH3 then R?1 is H, R1 is OCH3 then R?1 is OH, its pharmaceutically acceptable salts and/or optical isomers, tautomers, solvates or isotopic variations thereof. The invention also relates to said compounds for use in the treatment of cancer, namely solid tumor cancer, and preferably those selected from melanoma, colon, lung, pancreas, kidney, Merkel carcinoma, squamous cell carcinoma, prostate, breast and bladder. The invention also relates to a pharmaceutical composition comprising said compounds.

Abstract: The present invention relates to a compound of general formula (I)for use in the treatment of a disease selected from lymphomas and leukemia.

Abstract: The present invention relates to a compound of general formula (I): said compound being as defined in claim (1). The invention also relates to a pharmaceutical composition comprising: —a compound of general formula (I) as defined in claim (12) and, —at least one antibody selected from an anti-PD1 antibody, an anti-CTLA4 antibody, an anti-PD-L1 antibody and a mixture of two or more thereof. The invention also relates to a compound of general formula (I) as defined in claim (17) for use in the treatment of cancer, said cancer being preferably selected from melanoma, bladder, kidney, prostate, colon, lung, breast and blood cancer.

Abstract: The present invention relates to the identification of the glycogen synthase kinase-3 beta (GSK3B or GSK-3P) as a therapeutic target of pigmentation disorder and as biomarker of pigmentation status. The invention in particular relates to products and methods for treating a hypopigmentation disorder. The invention also relates to products and methods for detecting, diagnosing, staging or monitoring the course of hypopigmentation disorder and is particularly suited for human subjects.

Abstract: The present invention relates to the identification of the glycogen synthase kinase-3 beta (GSK3B or GSK-3P) as a therapeutic target of pigmentation disorder and as biomarker of pigmentation status. The invention in particular relates to products and methods for treating a hypopigmentation disorder. The invention also relates to products and methods for detecting, diagnosing, staging or monitoring the course of hypopigmentation disorder and is particularly suited for human subjects.

Abstract: The invention relates to nucleic acid sequences as well as to modified oligonucleotides (ODNs) comprising a p52 binding site derived from the EZH2 promoter region, as well as to compositions and methods for treating cancer. The invention relates to peptides derived from p52 as well as to compositions and methods for treating cancer. The invention also provides compositions and methods for inducing senescence in cancer cells (e.g. in epithelial cancer cells). The invention also provides compositions and methods for inhibiting expression of EZH2 in cancer cells. The invention further provides a new combination therapy as well as compositions and thereof for treating cancer.

Abstract: The present invention relates to the identification of proteins of the WNT signaling pathway as therapeutic targets of pigmentation disorder and as biomarkers of pigmentation status. The invention in particular relates to products and methods for treating a hypopigmentation disorder. The invention also relates to products and methods for detecting, diagnosing, staging or monitoring the course of hypopigmentation disorder and is particularly suited for human subjects.

Abstract: The invention relates to nucleic acid sequences as well as to modified oligonucleotides (ODNs) comprising a p52 binding site derived from the EZH2 promoter region, as well as to compositions and methods for treating cancer. The invention relates to peptides derived from p52 as well as to compositions and methods for treating cancer. The invention also provides compositions and methods for inducing senescence in cancer cells (e.g. in epithelial cancer cells). The invention also provides compositions and methods for inhibiting expression of EZH2 in cancer cells. The invention further provides a new combination therapy as well as compositions and thereof for treating cancer.

Abstract: A method of treating melanoma in a subject comprising administering an amount of SOX9 sufficient to treat melanoma is disclosed. A method of treating a hyperpigmentary condition in a subject comprising administering an amount of inhibitor of SOX9 activity sufficient to treat the condition is disclosed. A method of treating melanoma in a subject comprising administering an amount of SOX9 sufficient to treat melanoma is disclosed. A method of treating melanoma in a subject comprising increasing the amounts of retinoic acid and SOX9 in the subject by amounts sufficient to treat melanoma. A method of treating melanoma in a subject comprising administering an amount of prostaglandin D2 and retinoic acid sufficient to treat cancer is disclosed. A method of sensitizing a melanoma cell to RA comprising administering an amount of SOX9 sufficient to decrease PRAME expression is disclosed.

Abstract: The present disclosure is generally related to methods of inducing non-palmoplantar skin to develop a palmoplantar phenotype, for example, methods for increasing skin thickness, decreasing skin pigmentation, and/or decreasing hair growth. In particular, disclosed herein are methods of using topical administration of DKK1 to increase skin thickness, decrease skin pigmentation, or reduce hair growth. Also disclosed are topical DKK1 compositions for inducing non-palmoplantar skin to develop a palmoplantar phenotype.

Abstract: The present disclosure is generally related to methods of inducing non-palmoplantar skin to develop a palmoplantar phenotype, for example, methods for increasing skin thickness, decreasing skin pigmentation, and/or decreasing hair growth. In particular, disclosed herein are methods of using topical administration of DKK1 to increase skin thickness, decrease skin pigmentation, or reduce hair growth. Also disclosed are topical DKK1 compositions for inducing non-palmoplantar skin to develop a palmoplantar phenotype.

Abstract: The present disclosure is generally related to methods of inducing non-palmoplantar skin to develop a palmoplantar phenotype, for example, methods for increasing skin thickness, decreasing skin pigmentation, and/or decreasing hair growth. In particular, disclosed herein are methods of using topical administration of DKK1 to increase skin thickness, decrease skin pigmentation, or reduce hair growth. Also disclosed are topical DKK1 compositions for inducing non-palmoplantar skin to develop a palmoplantar phenotype.

Abstract: A method of treating a hypopigmentary condition in a subject comprising administering to the subject an amount of SOX9 sufficient to treat melanoma is disclosed. The hypopigmentary condition can be a result of surgery, trauma or vitiligo. A method of treating a hyperpigmentary condition in a subject comprising administering to the subject an amount of inhibitor of SOX9 activity sufficient to treat melanoma is disclosed. A method of treating melanoma in a subject comprising administering to the subject an amount of SOX9 sufficient to treat melanoma is disclosed. A method of treating melanoma in a subject comprising increasing the amounts of retinoic acid and SOX9 in the subject by amounts sufficient to treat melanoma. A method of treating melanoma in a subject comprising administering to the subject an amount of prostaglandin D2 (PGD2) and retinoic acid (RA) sufficient to treat cancer.