Gene Polymorphisms of Patients with Lymphoma-Associated Hemophagocytic Syndrome in Longyan area, Fujian Province / 中国实验血液学杂志

OBJECTIVE@#To analyze the gene polymorphisms of patients with lymphoma-associated hemophagocytic syndrome in Longyan area, Fujian province.@*METHODS@#A total of 125 patients with lymphoma-associated hemophagocytic syndrome in Longyan, Fujian province, admitted to Longyan First Hospital from May 2017 to November 2020 were selected. Peripheral venous blood was collected from all the patients, and the genotypes of perforin 1 (PRF1) and interleukin-10 (IL-10) gene loci were detected by PCR-fluorescence probe method, and the correlation between PRF1 and IL-10 gene polymorphisms and lymphoma-associated hemophagocytic syndrome was analyzed.@*RESULTS@#The mutation frequencies of PRF1 gene loci rs885821 (C>T), rs885822 (C>T), rs1889490 (G>A) in patients with lymphoma-associated hemophagocytic syndrome were 10.40%, 78.8% and 64.4%, respectively. The mutation frequencies of rs1800872 (A>C), rs1800871 (C>T) and rs1800896 (G>A) of IL-10 loci were 56.0%, 45.2% and 77.6%, respectively.@*CONCLUSION@#PRF1 and IL-10 gene loci were polymorphic in patients with lymphoma-associated hemophagocytic syndrome in Longyan area, Fujian province. Alleles C and G of PRF1 and IL-10 were risk factors, and alleles T and A were protective factors.

Small interfering RNA-mediated OCT4 gene silencing inhibits the proliferation and induces apoptosis of pancreatic cancer cell line PANC1 / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the effects of small interfering RNA (siRNA)-mediated silencing of octamer binding factor 4 (OCT4) gene on the proliferation and apoptosis of pancreatic carcinoma cell line PANC1 in vitro.</p><p><b>METHODS</b>Chemically synthesized siRNA against human OCT4 was transfected into PANC1 cells via Lipofectamine(TM)2000. The expression of OCT4 mRNA in the cells was detected using RT-PCR, and the protein expressions of OCT4 and PARP were assayed using Western blotting. The changes in the cell proliferation were evaluated using CCK8 method. Flow cytometry was used to detect the apoptosis of the transfected cells.</p><p><b>RESULTS</b>siRNA transfection significantly suppressed the expression of OCT4 gene, which activated the expression of PARP in PANC1 cells (P<0.05). CCK8 method demonstrated a significant inhibition of cell proliferation by OCT4 siRNA transfection, which also resulted in significantly increased apoptotic rate of the cells (P<0.05).</p><p><b>CONCLUSION</b>siRNA-mediated OCT4 gene silencing can inhibit the proliferation and induce apoptosis of pancreatic carcinoma PANC1 cells, and this study provides a basis for further functional study of OCT4 gene.</p>

In vitro induced and expanded Epstein Barr virus-specific cytotoxic T lymphocytes can specifically kill nasopharyngeal carcinoma cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To establish a method for efficient induction and expansion of Epstein Barr virus (EBV)-specific cytotoxic T lymphocytes (CTL) in vitro and evaluate the possibility of using this strategy for treatment of nasopharyngeal carcinoma (NPC).</p><p><b>METHODS</b>EBV-transformed B lymphoblastoid cells (BLCLs) were used as the antigen stimuli and antigen-presenting cells. EBV-specific CTL was induced by co-culture of the autologous peripheral blood mononuclear cells (PBMCs) and the irradiated BLCLs, and expanded with a cocktail method consisting of OKT-3, irradiated homologous PBMC, and IL-2. The specific activity of the CTL against the NPC cells was measured with MTT assay.</p><p><b>RESULTS</b>EBV-specific CTL was successfully induced and expanded by 600 folds. The killing efficiency of the CTL was 76% for autologous BLCLs, 13% for homologous BLCLs, 51% for autologous NPC cells, and 27% for homologous CNE cell line, and after expansion, the corresponding killing efficiencies were 63%, 25%, 49%, and 33%, respectively. The non-specific killing only slightly increased after the expansion.</p><p><b>CONCLUSION</b>EBV-specific CTL can be successfully induced and expanded in vitro for specific killing of autologous NPC cells, suggesting the potential of this strategy in the treatment of NPC.</p>