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1.
Chinese Medical Journal ; (24): 2460-2468, 2016.
Article in English | WPRIM | ID: wpr-307391

ABSTRACT

<p><b>BACKGROUND</b>Perineural invasion (PNI) is a histopathological characteristic of pancreatic cancer (PanCa). The aim of this study was to observe the treatment effect of continuous low-dose-rate (CLDR) irradiation to PNI and assess the PNI-related pain relief caused by iodine-125 ( 125 I) seed implantation.</p><p><b>METHODS</b>The in vitro PNI model established by co-culture with dorsal root ganglion (DRG) and cancer cells was interfered under 2 and 4 Gy of 125 I seeds CLDR irradiation. The orthotopic models of PNI were established, and 125 I seeds were implanted in tumor. The PNI-related molecules were analyzed. In 30 patients with panCa, the pain relief was assessed using a visual analog scale (VAS). Pain intensity was measured before and 1 week, 2 weeks, and 1, 3, and 6 months after 125 I seed implantation.</p><p><b>RESULTS</b>The co-culture of DRG and PanCa cells could promote the growth of PanCa cells and DRG neurites. In co-culture groups, the increased number of DRG neurites and pancreatic cells in radiation group was significantly less. In orthotopic models, the PNI-positive rate in radiation and control group was 3/11 and 7/11; meanwhile, the degrees of PNI between radiation and control groups was significant difference (P < 0.05). At week 2, the mean VAS pain score in patients decreased by 50% and significantly improved than the score at baseline (P < 0.05). The pain scores were lower in all patients, and the pain-relieving effect was retained about 3 months.</p><p><b>CONCLUSIONS</b>The CLDR irradiation could inhibit PNI of PanCa with the value of further study. The CLDR irradiation could do great favor in preventing local recurrence and alleviating pain.</p>


Subject(s)
Animals , Humans , Mice , Rats , Apoptosis , Radiation Effects , Cell Line, Tumor , Coculture Techniques , Dose-Response Relationship, Radiation , Ganglia, Spinal , Cell Biology , Iodine Radioisotopes , Therapeutic Uses , Mice, SCID , Neoplasm Recurrence, Local , Radiotherapy , Pancreatic Neoplasms , Radiotherapy
2.
Chinese Journal of Epidemiology ; (12): 794-799, 2005.
Article in Chinese | WPRIM | ID: wpr-295662

ABSTRACT

<p><b>OBJECTIVE</b>To explore the relationship between methylenetetrahydrofolate reductase (MTHFR) gene polymorphism and microsatellite instability (MSI) in patients with gastric cancer.</p><p><b>METHODS</b>MTHFR gene C677T and A1298C polymorphism were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and MSI was examined with PCR.</p><p><b>RESULTS</b>MTHFR gene C677T and A1298C polymorphisms were analyzed on 122 gastric cancers and 110 normal controls The genotype frequencies of MTHFR 677CC, 677CT and 677TT were 47.5%, 39.3% and 13.1% on patients with gastric cancer, and 48.5%, 42.6%, 8.9% in the controls respectively. There was no significant difference of genotype frequency between the two groups (P > 0.05). The individuals with 677CT genotype, 677TT genotype and 677CT + TT genotype exhibited significantly reduced risk (OR = 0.38,95% CI: 0.15-0.98; OR = 0.26,95% CI: 0.03-2.18 and OR = 0.36,95% CI: 0.07-0.98) of developing gastric cardia cancer compared with those harboring the wild-type(677CC). The individuals with 677TT genotype having a 3.03-fold (95% CI: 1.07-8.65) increased risk of developing gastric corpus cancer. The genotype frequency of MTHFR 1298AA, 1298AC and 1298CC were 59.8%, 36.1% and 4.1% in gastric cancer patients, and 57.4%, 7.6%, 5.0% in the controls, respectively. The distribution of MTHFR A1298C genotype was not significantly different between gastric cancer and controls (P > 0.05). The individuals with 1298CC genotype had a reduced risk of developing gastric antrum cancer (OR = 0.41- fold, 95% CI: 0.03-2.18, 0.05-3.72) when comparing with those having 1298AA genotype. Patients with MSI+ gastric cancer had an increased frequency of the MTHFR 677TT genotype when comparing with those suffering from MSI- gastric cancer (P = 0.009) and with controlled subjects (P = 0.008). There was no significant association found between MTHFR A1298C polymorphism and MSI (P>0.05).</p><p><b>CONCLUSION</b>Polymorphism of MTHFR C677T was associated with increased risk on gastric corpus cancer and reduced risk on gastric cardia cancer. The polymorphism of MTHFR A1298C was associated with reduced risk for gastric antrum cancer while MSI pathway was possibly involved in the development of gastric cancer with MTHFR 677TT genotype.</p>


Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Case-Control Studies , Gene Frequency , Genotype , Methylenetetrahydrofolate Reductase (NADPH2) , Genetics , Microsatellite Instability , Polymorphism, Genetic , Stomach Neoplasms , Genetics
3.
Chinese Journal of Hepatology ; (12): 676-679, 2003.
Article in Chinese | WPRIM | ID: wpr-339122

ABSTRACT

<p><b>OBJECTIVE</b>To observe the anti-tumor effect of combination TNF-related apoptosis-inducing ligand (TRAIL) with aspirin on liver cancer cell line, SMMC-7721.</p><p><b>METHODS</b>The survival fraction of SMMC-7721 cells was measured by MTT assay, apoptosis rate and cell cycle was determined by flow cytometry, and the expression of apoptosis-related gene was identified by western blot.</p><p><b>RESULTS</b>The survival fraction of SMMC-7721 cells treated with 300 ng/ml TRAIL, 3 mmol/L or 10 mmol/L aspirin alone was 82.76%, 81.34% and 71.29% respectively, and the survival fractions of SMMC-7721 cells treated with TRAIL and 3 mmol/L or 10 mmol/L aspirin were 43.54% and 37.8% respectively. The apoptosis rates of SMMC-7721 cells induced by TRAIL and 3 mmol/L or 10 mmol/L aspirin were higher than that induced by TRAIL or aspirin alone (34.76% and 38.56% vs 21.25%, 1.89% and 6.08%), and G0/G1 arrest was observed under TRAIL and aspirin. The expression of Bcl-2 in SMMC-7721 cells treated by 3 mmol/L or 10 mmol/L aspirin decreased markedly, but no effect on Bax.</p><p><b>CONCLUSION</b>The cooperative anti-tumor effect of aspirin and TRAIL may be related to the inhibition of the expression of Bcl-2 by aspirin</p>


Subject(s)
Humans , Antineoplastic Combined Chemotherapy Protocols , Pharmacology , Apoptosis , Apoptosis Regulatory Proteins , Aspirin , Pharmacology , Cell Survival , Membrane Glycoproteins , Pharmacology , Proto-Oncogene Proteins c-bcl-2 , TNF-Related Apoptosis-Inducing Ligand , Tumor Cells, Cultured , Tumor Necrosis Factor-alpha , Pharmacology
4.
Chinese Journal of Oncology ; (12): 538-541, 2003.
Article in Chinese | WPRIM | ID: wpr-271086

ABSTRACT

<p><b>OBJECTIVE</b>To observe the sensitivity change of SMMC-7721 cells transfected with antisense DNMT1 gene fragment to tumor necrosis factor related apoptosis inducing ligand (TRAIL) and its mechanism.</p><p><b>METHODS</b>Cell survival rate was measured by trypan blue, apoptosis rate by TUNEL method and the expression of bcl-2, bax and bad by flow cytometry.</p><p><b>RESULTS</b>Cell survival rate of SMMC-7721 cells transfected with antisense DNMT1 gene fragment was markedly lower than that transfected with sense DNMT1 gene fragment or empty vector (P < 0.05 and 0.01), but the apoptosis rate was on the contrary (P < 0.05 or 0.01). The expression of bax and bad (especially the former), but not bcl-2 of SMMC-7721 cells transfected with antisense DNMT1 gene fragment was markedly higher than those of SMMC-7721 cells transfected with sense DNMT1 gene fragment or empty vector.</p><p><b>CONCLUSION</b>The sensitivity of SMMC-7721 cells to TRAIL can be enhanced by the transfection of antisense DNMT1 gene fragment, which may be related to the increase of bax and bad expression.</p>


Subject(s)
Humans , Antisense Elements (Genetics) , Genetics , Apoptosis , Apoptosis Regulatory Proteins , Carrier Proteins , Cell Line, Tumor , DNA (Cytosine-5-)-Methyltransferase 1 , DNA (Cytosine-5-)-Methyltransferases , Genetics , Flow Cytometry , Liver Neoplasms , Metabolism , Pathology , Membrane Glycoproteins , Pharmacology , Proto-Oncogene Proteins , Proto-Oncogene Proteins c-bcl-2 , TNF-Related Apoptosis-Inducing Ligand , Tumor Necrosis Factor-alpha , Pharmacology , bcl-2-Associated X Protein , bcl-Associated Death Protein
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