Anti-Human BCL2 Polyclonal Antibody

The prognosis of diffuse large B-cell lymphoma (DLBCL) havingMYCrearrangement (MYC-R), including double hit lymphoma (DHL), is poor by standard immunochemotherapy. To evaluate the significance of hematopoietic stem cell transplantation (SCT) for DLBCL withMYC-R, we retrospectively analyzed Japanese SCT registry data. In total, 54 patients with DLBCL withMYC-R were identified from 4336 registered adult DLBCL patients. Detailed clinical and cytogenetic information was obtained for 48 patients. The median age at diagnosis of the 48 patients was 54.5 (range 21-67) years. Twenty-six (54%) patients hadMYC-R only (single hit), and 22 (46%) hadMYC-R and BCL2, and/or BCL6 rearrangement (double/triple hit). In 12 patients who received auto-SCT during the first complete response (CR), both the 2-year overall survival (OS) and progression-free survival (PFS) rates were 75.0% (95% confidence interval [CI], 40.8%-91.2%). In 20 patients who received auto-SCT after relapsed or refractory state, the 2-year OS and PFS rates were 68.2% (95% CI, 41.9%-84.5%) and 59.6% (95% CI, 35.1%-77.4%), respectively. In 17 patients who received allo-SCT, only 4 patients underwent SCT in CR. The 2-year OS and PFS rates were 29.4% (95% CI, 10.7%-51.1%) and 17.6% (95% CI, 4.3%-38.3%), respectively. The rate of non-relapse mortality at 1 year was 41.2% (95% CI, 17.1%-64.0%) in this group. The outcomes of single hit and double or triple hit were not different. These findings suggest that auto-SCT may be effective forMYC-R DLBCL, including DHL patients of chemosensitive relapsed or refractory state. Since most patients received allo-SCT not in CR, the outcome of allo-SCT was unsatisfactory due to high non-relapse mortality and early relapse. To clarify the role of allo-SCT forMYC-R DLBCL, further accumulation of patients is necessary.

Background Nano-sized extracellular vesicles secreted by cells play key roles in intercellular crosstalk, and appear to be an excellent biocompatible material as therapeutic cargoes in vivo. Previously, we have demonstrated that miR-204-5p is a key tumor suppressor that could inhibit tumor growth, metastasis and chemoresistance. Methods A HEK293T cell line stably expressing miR-204-5p (293T-miR-204) was constructed by lentivirus transduction. Fluorescence real-time quantitative PCR (qPCR) was applied to measure the expression of miR-204-5p. CCK-8 and colony formation assays were used to evaluate the in vitro anticancer effects, and the flow cytometry was used to detect apoptosis. The in vivo therapeutic effects of exosomal miR-204-5p were evaluated using a xenograft mouse model. Western blots were used to detect the protein levels of CD63, Flotillin-2, RAB22A and Bcl2. The protein levels of RAB22A and Bcl2 in tumor tissues were measured by immunohistochemistry staining. Results MiR-204-5p was clearly upregulated in CRC cells after coculturing with 293T-miR-204 cell-derived conditioned medium (CM) or exosomes. CCK-8 and colony formation assays showed that the cell proliferation ability of CRC cells was clearly inhibited by 293T-miR-204 cell-derived CM or exosomes. The inhibitory effects of exosomal miR-204-5p on cell proliferation were further confirmed in other types of cancers. Exosomal miR-204-5p could induce apoptosis and increase the sensitivity of cancer cells to the chemotherapeutic drug-5-fluorourcil. In addition, exosomal miR-204-5p inhibited the tumor growth in mice. Western blot assay and IHC staining showed that the protein levels of miR-204-5p targets were clearly decreased in cancer cells or xenograft tissues treated with exosomal miR-204-5p. Conclusions In this study, we confirmed that exosomal miR-204-5p could efficiently inhibit cancer cell proliferation, induce apoptosis and increase chemosensitivity by specifically suppressing the target genes of miR-204-5p in human cancer cells.