Abstract: The inventors' working hypothesis relies on the original observations that mesenchymal MAPKi resistant cells display markers of fibrosis, acquire a myofibroblast-like phenotype and extracellular matrix (ECM) remodelling activities. In addition to increased remodelling of the ECM, pro-fibrotic responses induced by MAPK-targeted therapy include enhanced actin cytoskeleton plasticity, high sensitivity to mechanical cues and the establishment of an inflammatory microenvironment that contribute to therapy escape. The inventor's reason that approaches aimed at manipulating this abnormal fibrotic-like response induced by targeted therapy may represent rationale combination strategies to normalize the fibrous stroma, enhance drug efficacy and overcome resistance in BRAE mutant melanoma. Here the inventors investigated the impact of Nintedanib, an EMA/FDA-approved anti-fibrotic drug, as a repurposed drus in combination with targeted therapy on melanoma cell viability and tumor growth.

Abstract: Agents for the treatment of patients having non-small cell lung cancer and methods of diagnostics related include an inhibitor of miR 24 3p, a locked nucleic acid, including methods of predicting response to platinum-based chemotherapy, for patients having, or suspected of having, non-small cell lung cancer.

Abstract: The present invention relates to the use of the miRNA expression profile, particularly of miR-199a-5p, and the target genes regulated thereby for the diagnosis, prognosis and use of miR-199a-5p inhibitors for treating fibroproliferative disorders.

Abstract: The present invention relates to the use of the miRNA expression profile, particularly of miR-199a-5p, and the target genes regulated thereby for the diagnosis, prognosis and use of miR-199a-5p inhibitors for treating fibroproliferative disorders.

Abstract: The present invention relates to at least one nucleic acid (i) comprising or consisting of or (ii) encoding a nucleic acid comprising or consisting of, a sequence selected from the group consisting of: 1) SEQ ID NO: 1, SEQ ID NO: 2, SEQ ID NO: 3, and SEQ ID NO: 4, and 2) a sequence derived from SEQ ID NO: 1 to 4 by substitution deletion or insertion of at least one nucleotide, provided that a nucleic acid consisting of the sequence derived from SEQ ID NO: 1 to 4 is liable to induce HIV-1 expression in latent HIV-1-infected cells, for use as a medicament, in particular for treating retrovirus infections.

Abstract: The present invention relates to a method for evaluating the regenerative and/or differentiation capacity of ciliated epithelial tissue in a vertebrate subject, in particular a mammal, preferably a human, and to the use of microRNA in treating illnesses associated with a dysfunction of multiciliated epithelial cells.

Abstract: The present invention relates to the use of the miRNA expression profile, particularly of miR-199a-5p, and the target genes regulated thereby for the diagnosis, prognosis and use of miR-199a-5p inhibitors for treating fibroproliferative disorders.

Abstract: The present invention relates to a method for evaluating the regenerative and/or differentiation capacity of ciliated epithelial tissue in a vertebrate subject, in particular a mammal, preferably a human, and to the use of microRNA in treating illnesses associated with a dysfunction of multiciliated epithelial cells.

Abstract: The present invention relates to at least one nucleic acid (i) comprising or consisting of or (ii) encoding a nucleic acid comprising or consisting of, a sequence selected from the group consisting of: 1) SEQ ID NO: 1, SEQ ID NO: 2, SEQ ID NO: 3, and SEQ ID NO: 4, and 2) a sequence derived from SEQ ID NO: 1 to 4 by substitution deletion or insertion of at least one nucleotide, provided that a nucleic acid consisting of the sequence derived from SEQ ID NO: 1 to 4 is liable to induce HIV-1 expression in latent HIV-1-infected cells, for use as a medicament, in particular for treating retrovirus infections.