In a phase I study in patientsS malignant cells with R / RB, 32765 PCI induced durable responses with minimal toxicity t. F Promotion of early clinical results with crizotinib anaplastic lymphoma kinase inhibitor in advanced chemoresistant SB-207499 lymphoma patients ALK were also observed. The benzimidazole AZD6244 is a new mitogen-activated protein kinase inhibitor of the second generation. Significant cell death was DLBCL cell lines prime Ren and cells in a xenograft model in vivo at concentrations achieved clinically shown. 5.7. JAK / STAT pathway. The Janus kinase 2 and signal transducer activators / channel transcription play an r Key in the proliferation and the pathogenesis of h Dermatological malignancies. A Phase I trial of the novel JAK 2 inhibitor, SB1518, has evidence of activity of t In patients with relapsed lymphoma made available. Degrasyn, a novel inhibitor smallmolecule the JAK / STAT pathway has been shown to act synergistically with bortezomib in vivo to prevent tumor growth and ridiculed Ngern the survival time in a mouse xenograft model of severe combined immunodeficiency Surface of MCL.
5.8. Toll Like Receptor JNJ-7706621 Agonist. PF 3512676 is a novel oligonucleotide TLR9 activation of antitumor agent with activity t Erh Ht only the pr Clinical efficacy of rituximab. Preferences INDICATIVE antitumor activity of t Found for the combination followed a phase I study in patients with recurrent NHL, indolent and aggressive, w During neutropenia of grade 3 or 4 in 4/50 patients. Evaluation of combination therapy with an agonist of TLR7 / 8 twice with rituximab, bortezomib or cyclophosphamide in human xenograft and syngeneic mouse lymphoma models show that the antitumor activity of T These substances h in the treatment of non-Hodgkin’s lymphoma and other dermatological malignancies could be improved with this strategy. The transforming growth factor-activated kinase 1 inhibitor, AZ TAK1, nachgewiesenerma S protein inhibitor X attached to inhibit apoptosis, caspase-9, and to activate apoptosis in cell lines MCL.
Immunostimulatory CpG oligodeoxynucleotides are potent activators of T-cell immunity T Cell-mediated cytotoxicity and t antibodydependent and confinement as immunotherapeutics for a variety of tumors Examines Lich BCL. Anti-CD20 antique Body, conjugated CpG has been shown that rituximab resistance BCL eradicate in a mouse model of syngeneic lymphoma. Can sartigen A recent manifestation of the divergent effects of CpG ODN on normal B cells from b A novel mechanism of action of CpG ODNs as therapeutic agents for the BCL. 5.9. Heat-shock proteins. Hsp chaperones are necessary for the proper functioning of involved proteins in cell growth and survival. Inhibition of these proteins Then causes increased FITTINGS degradation of key proteins Like kinases, protein signal transmitter and mutated oncogenic proteins. GOOD 70 showed a tricyclic coumarin derivatives Calophyllum brasiliense pronounced antiproliferative effects in MCL with mutant p53, a known negative prognostic factor for MCL, through inhibition of Hsp90. These results suggest that k 70 GOOD Nnte potentially useful for the treatment of MCL. The small molecule can AAG 17 cell death in a dose and zeitabh Induce-dependent mode by the cellular Whose content of proteins Including essential for survival Lich.