Objective To explore the efficacy with prognostic value of postoperative prophylactic hyperthermic intraperitoneal chemotherapy (HIPEC) for locally advanced gastric cancer with clinical stage cT3-4NxM0. Methods A retrospective collection and analysis of clinical data was conducted from 60 patients with locally advanced gastric cancer (cT3-4NxM0) who underwent D2 radical surgery between January 2016 and December 2021 at our department. Patients who underwent prophylactic HIPEC were classified into the HIPEC group (n=30), while patients who did not undergo prophylactic HIPEC were clssified into the control group (n=30). Both groups of patients routinely were treated with postoperative adjuvant systemic chemotherapy. The median survival time, and overall survival rate of the two groups were compared through follow-up, and the risk factors affecting the overall survival rate were analyzed. Results The median survival time of the HIPEC group was 51.0 months (95% CI: 40.7-61.3), which was higher than that of the control group with 30.0 months (95% CI: 16.3-43.7). The 3-year and 5-year overall survival rates of the HIPEC group (66.7%, 53.3%)were higher than those of the control group（56.7%, 43.3%） (P=0.019). Prophylactic HIPEC was the protective factor affecting the overall survival rate of postoperative patients with locally advanced gastric cancer (P=0.021). Conclusions For patients with locally advanced cT3-4NxM0 gastric cancer, prophylactic HIPEC plays an important role in prolonging the median survival time, hence impro-ving the overall survival rate of patients.

OBJECTIVETo evaluate the gene therapeutic efficiency of apoptosis-inducing ligand (TRAIL) related to tumor necrosis factor on human colon cancer cell line HT29.

METHODSHuman colon cancer cell line HT29 was transfected with adenovirus-mediated TRAIL gene Ad/GT-TRAIL. The morphological changes, cell growth and apoptosis were measured by phase contrast microscope, MTT method and flow cytometry.

RESULTSObvious morphological changes in HT29 cells was induced by Ad/GT-TRAIL and Ad/PGK-GV16. The cell suppression percentage and the percentage of apoptotic cells were 54.3% and 11.1%, respectively. When used in combination with Ad/PGK-GV16, HT29 was suppressed to 82.7% and the percentage of apoptotic cells was 24.6%. This result showed significantly enhanced therapeutic efficiency on HT29 and thus inhibiting of its growth (P < 0.05).

CONCLUSIONAd/GT-TRAIL is able to induce apoptosis of HT29 and inhibit its growth. Ad/GT-TRAIL shows significantly enhanced therapeutic efficiency for HT29 when used in combination with Ad/PGK-GV16.

Adenoviridae ; genetics ; Apoptosis ; genetics ; physiology ; Apoptosis Regulatory Proteins ; Cell Division ; genetics ; physiology ; Colonic Neoplasms ; genetics ; pathology ; therapy ; Genetic Therapy ; methods ; Genetic Vectors ; genetics ; HT29 Cells ; Humans ; Membrane Glycoproteins ; genetics ; physiology ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Necrosis Factor-alpha ; genetics ; physiology

Objective To study the bystander effect of tumor necrosis factor related apoptosis inducing ligand(TRAIL) gene and it's mechanism. Methods Full length cDNA of human TRAIL was transfected into SMMC7721 with binary adenoviral vectors system. RT PCR was used to determine the expression of TRAIL gene. By MTT assay the effects of the TRAIL gene on the proliferation of SMMC7721 was studied; The apoptosis inducing ability of TRAIL gene on SMMC7721 was tested by fluorescence activated cell sorting (FACS). Bystander effect by testing the proliferation of the mixed cells of SMMC7721/TRAIL and SMMC7721 with different ratios, and the mechanism of bystander effect by testing the proliferation of SMMC7721 cultured with media of SMMC7721/TRAIL without cell components were also studied. Results TRAIL gene expressed by binary adenoviral vector system was able to inhibit proliferation(91.2%) and induce apoptosis(29.07%) of SMMC7721, significant difference between TRAIL gene and the other three controls were observed(PBS, LacZ, Bax)( P

AIM: To explore the influence of Chrysanthemum morifolium Ramat on TNF-related apoptosis inducing ligand (TRAIL)-mediated apoptosis in human colon cancer cell line DLD-1 and its possible mechanism. METHODS: Adenovirus-mediated TRAIL gene AD/hTERT-gTRAIL was applied either alone or by combination with Chrysanthemum morifolium Ramat in human colon DLD-1 cell line. Cell growth and apoptosis were measured by inverted microscope, MTT method and flow cytometry. The expression of TRAIL mRNA, TRAIL-Rs mRNA and TRAIL protein expression after exposure to Chrysanthemum morifolium Ramat were measured by semi-quantitive RT-PCR and FACS, respectively. RESULTS: The suppression percentages and apoptotic rate of DLD-1 by Ad/hTERT-gTRAIL alone were 31.4% and 13.5%, respectively. Combination of TRAIL gene transfection with Chrysanthemum morifolium Ramat, the suppression and the apoptosis rate raised to 93.1% and 45.4%, respectively (P

AIM:To evaluate effects of different chemotherapeutic agents on reversing the acquired resistance to TRAIL gene and clarify the involved mechanisms in DLD1-TRAIL/R colon cancer cells.METHODS: Human colon cancer cell line DLD1-TRAIL/R cells that were resistant to TRAIL-expressing adenovector(Ad/gTRAIL) were treated with Ad/gTRAIL combined with different chemotherapeutic agents.Then,the cell viability was measured by MTT method,and apoptotic signaling conditions,including activation of caspase-3 and caspase-8,expression of Bax and Bcl-XL,were measured by Western blotting analysis.RESULTS: In vitro data showed that several chemotherapeutic agents,including 5-fluorouracil(5-FU) and mitomycin c(MMC),overcome the acquired resistance to TRAIL gene in DLD1-TRAIL/R colon cancer cells.The combination of Ad/gTRAIL and 5-FU effectively suppressed tumor growth in vivo in subcutaneous tumors established from DLD1-TRAIL/R cells.Further data showed that treatment with the combination of Ad/gTRAIL and 5-FU or MMC led to enhance the activation of caspase-3.Moreover,MMC but not 5-FU induced overexpression of Bax gene that was sufficient to overcome the resistance to TRAIL gene in DLD1-TRAIL/R cells.CONCLUSION: Chemotherapeutic agents,such as 5-FU and MMC,overcome the acquired resistance to TRAIL gene in DLD1-TRAIL/R cells.The candidate mechanisms for MMC but not 5-FU to overcome this resistance might involve the induction of over-expressed Bax protein in DLD1-TRAIL/R cells.