Anti-FYN monoclonal antibody, clone TQN358

ARHGEF16 is a recently identified Rho-family guanine nucleotide exchange factor (GEF) that has been implicated in the activation of Rho-family GTPases such as Rho G, Rac, and Cdc42. However, its functions in colon cancer cell proliferation and migration are not well understood. In this study, we showed that ARHGEF16 was highly expressed in clinical specimens of colon cancer. In colon cancer cells, ARHGEF16-stimulated proliferation and migration in vitro and in vivo. Furthermore, we identified a nonreceptor tyrosine kinase, FYN, as a novel partner of ARHGEF16. Knocking down FYN expression decreased ARHGEF16 protein level in colon cancer cells. We further demonstrated that ARHGEF16-induced colon cancer cell proliferation and migration were dependent on FYN since knockdown FYN abolished the ARHGEF16-induced proliferation and migration of colon cancer cells. The FYN-ARHGEF16 axis mediates colon cancer progression and is a potential therapeutic target for colon cancer treatment.

Objective: Mature T-cell lymphomas are a heterogeneous group of T-cell malignancies with a poor outcome. The discovery of new molecular biomarkers has led to the emergence of new drugs in recent years that target various signaling pathways. Methods: We examined all pertinent published patents through 2015 that analyzed novel methods for the diagnosis and treatment of T cell lymphoma, as well as related published and unpublished studies. Selection criteria were established before data collection. An exhaustive literature search was performed using MEDLINE and Science Direct databases. The search criteria were T-cell lymphoma, diagnosis, and treatment. Results: Recent papers have identified recurrent epigenetic factor mutations in RHOA and FYN kinase in PTCL allowing new perspectives for epigenetic-based therapy, molecular classification model using CD28, ABCA5 transporter, coiled-coil domain-containing protein 3, and angiogenic factor SMOC2 biomarkers for differentiating forms of lymphomas, as well as expression of receptors forTNFR-1, TNFR-2, and IL12p40/70 in CTCL. New therapeutic targets have been reported such as MicroRNAs 155 inhibitors and synthetic Toll-Like Receptor 7/8 agonists for treating CTCL, Anti CTLA-4 antibodies, anti-Killer cell immunoglobulin-like receptors 3DL2 and NK-p46 (NCR receptors) antibodies for treating PTCL, Cd1d antagonist-restricted gamma/delta-T cell lymphomas, antiEZH2, novel antihistone deacetylase, and NK cells engineered therapy. In the transplantation setting, the objective was to eradicate overcoming of the residual disease immunity and to induce an immune tolerance by anti-third part cells with a central memory T-lymphocyte phenotype. Conclusion: Therapeutic strategies based on a better molecular characterization of various histological types are certain to be used in the future.