26S proteasome is an intracellular; ATP dependent enzymatic complex degrades ubiquitin-tagged proteins and maintains cellular homeostasis. The orderly degraded proteins including cyclins, caspases, Bcl-xL, p53, cell adhesion molecules are involved in cell-cycle progression, tumor suppression, DNA replication, inflammation, and apoptosis. So, proteasome inhibition is a target therapy for cancer to promote cell cycle arrest or apoptosis. Bortezomib (Velcade®, PS-341, and Millennium Pharmaceuticals, Inc.) is the first, selective, reversible, and only proteasome inhibitor for the treatment of multiple myeloma have been approved by U.S. Food and Drug Administration (FDA) in 2003. Bortezomib downregulates the interaction of multiple myeloma cells with bone marrow stromal cells, inhibits angiogenesis, and blocks cell cycle progression. Clinically, continuous dosage of bortezomib leads to few side effects.

Background: Despite the crucial role of integrin receptors in cancer pathogenesis and massive efforts towards establishing clinically relevant drugs, to the present no effective integrin antagonist for the treatment of malignant diseases has been introduced into the clinic.

Lenvatinib mesilate (lenvatinib) is an oral multiple-receptor tyrosine kinase inhibitor that selectively inhibits the kinase activities of Vascular Endothelial Growth Factor Receptor (VEGFR) 1-3, Fibroblast Growth Factor Receptor (FGFR) 1-4, Platelet-Derived Growth Factor Receptor (PDGFR) a, KIT, and RET. The VEGFR and FGFR signaling pathways are the master regulators of normal and tumor angiogenesis. Lenvatinib showed significant activity in patients with radioiodine-refractory thyroid cancer in a Phase III study and is used in the United States, the European Union, and Japan. Moreover, based on Phase II study, lenvatinib has been approved in the United States for the treatment of patients with advanced renal cell carcinoma in combination with everolimus. In addition, the efficacy of lenvatinib is being evaluated in other cancers, including hepatocellular carcinoma and endometrial cancer. The purpose of this study was to elucidate the mechanism underlying the clinical activities of lenvatinib by using in vitro and in vivo angiogenesis models.

Gamma-delta (?d) T cell neoplasms are a rare disease entity characterized by an aggressive clinical course [1,2]. The management of these neoplasms associated with high incidence of induction failures and poor clinical outcomes [3]. Here we present two cases of gamma-delta T cell acute lymphoblastic leukemia (?d T-ALL) successfully treated with chemotherapy and allogeneic stem cell transplant at our institution. We also review the literature and summarize what is known about this disease. In our experience, induction chemotherapy followed by allogeneic stem cell transplantation has been an effective strategy in producing durable remissions.

Increased neo antigens of cancer generated by mutations are reported to be associated with favorable prognosis of cancer patients. The interesting findings contradict the notions that cancers were caused by accumulation of gene mutations. The explanation of more efficient immuno surveillance provoked by the neo antigens contributes to the better outcomes also contradicts many more facts, i.e., the immuno surveillance in nature is inflammation which is a term of pathologist. The cancer related inflammation is widely accepted as a cancer promoting fact; more efficient immuno surveillance would result in more apoptosis of cancer cells. However, increased apoptosis were known to be associated with worse prognosis. Moreover, increasing evidence has shown that the expression of immune suppressing genes such as PD-1, PD-L1 and CTLA-4 were associated with better prognosis of cancer patients.

Primary oral leiomyosarcomas are exceptionally rare lesions often associated with poor prognosis. We report a case of leiomyosarcoma arising in the anterior mandibular gingiva, which is a non-prevalent site of occurrence. Clinically, the tumor was far from being firm and solid as it is usually described in the literature. Light microscopy failed to confirm the true nature of the lesion on the biopsy specimen.