Abstract: The response of subjects suffering from cancer to MAPK inhibitors is dramatically impaired by secondary resistances and rapid relapse. So far, the molecular mechanisms driving these resistances are not completely understood. The inventors show that expression of 10 SLITRK6 (SLIT and NTRK-like family, member 6) is induced by a MAPK inhibitor (e.g. Vemurafenib) and the inhibition of its induction in presence of the MAPK inhibitor induces synthetic lethality. Thus, the only inhibition of SLITRK6 by an inhibitor ot activity or expression should potentiate the antitumor effect of the MAPK inhibitors and avoid the emergence of a resistance to those compounds. Furthermore the specific expression of 15 SLITRK6 also paves the way of strategies based on depletion of the residual cancer cells by targeting them with anti-SLITRK6 antibodies capable of mediating ADCC or antibody-drug conjugates binding to SLITRK6.

Abstract: A detection apparatus detects at least one chemical species in the sweat of a human or animal subject, the at least one chemical species being selected from the group consisting of nitrogen oxide NO, nitrite ion NO2— and hydrogen peroxide H2O2. The apparatus has a collection element that is intended to be positioned in an investigation zone of an epidermis of the subject, and a detection device has at least one fluid circuit that is coupled to the collection element in order to direct at least one flow of sweat from the investigation zone and an electrochemical sensor having electrodes that are arranged in the fluid circuit, the electrochemical sensor being configured to produce a signal that represents a concentration of the at least one chemical species in the flow of sweat and a signal that represents a flow speed of the flow of sweat.

Abstract: The present invention relates to methods and kits for detection protein-protein interactions.

Abstract: Resistance to kinase inhibitors exemplifies the greatest hindrance to effective treatment of cancer patients. Recent studies have suggested that the onset of said resistance might not only be explained by a drug selection of pre-existing resistant sub-clones as it what was generally assumed, but may also arise de novo from a small population of drug-tolerant cells (DTC) that initially resists the treatment by entering a slow cycling state. Thus, targeting these DTC should be a new promising approach to hamper the emergence of secondary resistance to kinase inhibitors. The inventors now demonstrate that farnesyltransferase (but not geranylgeranyl transferase) inhibition can prevent the emergence of said resistance in different oncogenic contexts. In particular, the inventors determined invitro the efficacy of farnesyltransferase inhibitor (i.e. Tipifarnib) in combination with erlotinib in several EGFR-mutated cell lines.

Abstract: The response of subjects suffering from cancer to MAPK inhibitors is dramatically impaired by secondary resistances and rapid relapse. So far, the molecular mechanisms driving these resistances are not completely understood. The inventors show that expression of 10 SLITRK6 (SLIT and NTRK-like family, member 6) is induced by a MAPK inhibitor (e.g. Vemurafenib) and the inhibition of its induction in presence of the MAPK inhibitor induces synthetic lethality. Thus, the only inhibition of SLITRK6 by an inhibitor of activity or expression should potentiate the antitumor effect of the MAPK inhibitors and avoid the emergence of a resistance to those compounds. Furthermore the specific expression of 15 SLITRK6 also paves the way of strategies based on depletion of the residual cancer cells by targeting them with anti-SLITRK6 antibodies capable of mediating ADCC or antibody-drug conjugates binding to SLITRK6.

Abstract: Active forms of specific anti Rho GTPase conformational single domain antibodies are useful in the therapeutic and diagnostic fields. In particular, single domain antibodies wherein the amino acid sequences of CDR1-IMGT, CDR2-IMGT and CDR3-IMGT have at least 90% of identity with the amino acid sequences of the CDR1-IMGT, CDR2-IMGT and CDR3-IMGT of the H12, B6, 4P75, 4SP1, 4SNP36, 4SNP61, 5SP10, 5SP11, 5SP58, 5SNP47, 5SNP48, 5SNP65, B20, B15, B5, B71, E3, A6, G12, NB61, 212B, 111B or 404F (hs2dAb) are defined in Table B.

Abstract: The present invention relates to the combination of a Dbait molecule with a protein kinase inhibitor for treating cancer.

Abstract: The present invention relates to active form specific anti-Rho GTPase conformational single domain antibodies and their uses in particular in the therapeutic and diagnostic fields. In particular, the present invention relates to a single domain antibody wherein the amino acid sequences of CDR1-IMGT, CDR2-IMGT and CDR3-IMGT have at least 90% of identity with the amino acid sequences of the CDR1-IMGT, CDR2-IMGT and CDR3-IMGT of the H12, B6, 4P75, 4SP1, 4SNP36, 4SNP61, 5SP10, 5SP11, 5SP58, 5SNP47, 5SNP48, 5SNP65, B20, B15, B5, B71, E3, A6, G12, NB61, 212B, 111B or 404F (hs2dAb) single domain antibody which are defined in Table B.

Abstract: The present invention relates to active form specific anti-Rho GTPase conformational single domain antibodies and their uses in particular in the therapeutic and diagnostic fields. In particular, the present invention relates to a single domain antibody wherein the amino acid sequences of CDR1-IMGT, CDR2-IMGT and CDR3-IMGT have at least 90% of identity with the amino acid sequences of the CDR1-IMGT, CDR2-IMGT and CDR3-IMGT of the H12, B6, 4P75, 4SP1, 4SNP36, 4SNP61, 5SP10, 5SP11, 5SP58, 5SNP47, 5SNP48, 5SNP65, B20, B15, B5, B71, E3, A6, G12, NB61, 212B, 111B or 404F (hs2dAb) single domain antibody which are defined in Table B.

Abstract: A method of tracking a physiological state in a subject by studying the NO emission curve thereof measured by a sensing element on the epidermis thereof over a predefined activity sequence.

Abstract: The present invention relates to methods and kits for detection protein-protein interactions.

Abstract: The present invention relates to methods and kits for detection protein-protein interactions.

Abstract: The present invention relates to active form specific anti-Rho GTPase conformational single domain antibodies and their uses in particular in the therapeutic and diagnostic fields. In particular, the present invention relates to a single domain antibody wherein the amino acid sequences of CDR1-IMGT, CDR2-IMGT and CDR3-IMGT have at least 90% of identity with the amino acid sequences of the CDR1-IMGT, CDR2-IMGT and CDR3-IMGT of the H12, B6, 4P75, 4SP1, 4SNP36, 4SNP61, 5SP10, 5SP11, 5SP58, 5SNP47, 5SNP48, 5SNP65, B20, B15, B5, B71, E3, A6, G12, NB61, 212B, 111B or 404F (hs2dAb) single domain antibody which are defined in Table B.

Abstract: The response of subjects suffering from cancer to MAPK inhibitors is dramatically impaired by secondary resistances and rapid relapse. So far, the molecular mechanisms driving these resistances are not completely understood. The inventors show that expression of 10 SLITRK6 (SLIT and NTRK-like family, member 6) is induced by a MAPK inhibitor (e.g. Vemurafenib) and the inhibition of its induction in presence of the MAPK inhibitor induces synthetic lethality. Thus, the only inhibition of SLITRK6 by an inhibitor of activity or expression should potentiate the antitumor effect of the MAPK inhibitors and avoid the emergence of a resistance to those compounds. Furthermore the specific expression of 15 SLITRK6 also paves the way of strategies based on depletion of the residual cancer cells by targeting them with anti-SLITRK6 antibodies capable of mediating ADCC or antibody-drug conjugates binding to SLITRK6.

Abstract: The present invention relates to methods and kits for detection protein-protein interactions.

Abstract: The present invention relates to active form specific anti-Rho GTPase conformational single domain antibodies and their uses in particular in the therapeutic and diagnostic fields. In particular, the present invention relates to a single domain antibody wherein the amino acid sequences of CDR1-IMGT, CDR2-IMGT and CDR3-IMGT have at least 90% of identity with the amino acid sequences of the CDR1-IMGT, CDR2-IMGT and CDR3-IMGT of the H12, B6, 4P75, 4SP1, 4SNP36, 4SNP61, 5SP10, 5SP11, 5SP58, 5SNP47, 5SNP48, 5SNP65, B20, B15, B5, B71, E3, A6, G12, NB61, 212B, 111B or 404F (hs2dAb) single domain antibody which are defined in Table B.

Abstract: The invention relates to a gene expression inducing fusion protein comprising a) a ribonucleic acid linking peptide domain and a post-transcriptional gene expression activator domain and b) a domain enabling cytoplasmic membrane delocalization. The invention also relates to a modulatable permanent external method for controlling gene expression induction by modulating the state of post-translational modulation of the gene expression inducing fusion protein for the expression of said gene.

Abstract: Method of preparing a lipoprotein modified by incorporation of at least one lipophilic active substance other than a triglyceride, characterized by incorporation of said active substance into an emulsion of a lipid phase in a continuous aqueous phase, by adding to the emulsion, with stirring, an original lipoprotein and at least one lipid transfer protein, allowing the mixture to incubate, and, using known methods, isolating the lipoprotein into which the active substance is incorporated; a lipoprotein thus obtained, and pharmaceutical or cosmetic composition containing such a modified lipoprotein.