Influence of psychological intervention on pain and immune functions of patients receiving lung cancer surgery.

OBJECTIVE: To observe the influence of psychological intervention on pain, immune system and adrenocortical functions of patients receiving lung cancer surgery. METHODS: We selected 124 patients who received surgery for treating stage I or II lung cancer and divided into experimental group and control group. The experimental group received comprehensive psychological intervention while the control group was given conventional nursing intervention. Pain of patients in two groups was evaluated by visual analog scale (VAS). Before and after intervention, CD3(+), CD4(+), CD8(+), CD4(+)/CD8(+) and free cortisol level in serum were measured. Moreover, QLQ-C30, a life quality measurement scale developed by European Organization for Research and Treatment of Cancer (EORTC) was used. RESULTS: Compared to control group, VAS of patients in experimental group remarkably decreased before anesthesia, 6 hour, 12 hour 24 hour and 48 hour after surgery (P<0.05), and moreover, OLQ-C30 score and various factor scores (except physical symptoms) in experimental group were much higher (P<0.05). No statistical significant difference was found in immune index between two groups before intervention (P>0.05). Differences of CD3(+) and CD4(+) before and after intervention were both statistically significant (P<0.05), so did free cortisol level (P<0.05). CONCLUSION: Comprehensive psychological intervention can effectively relieve pain, improve immune functions and enhance quality of life for patients suffering from lung cancer surgery.

Single Nucleotide Polymorphisms in the Acylphosphatase 2 Gene and The SNP-SNP Interactions on the Risk of Breast Cancer in Chinese Han Women.

INTRODUCTION: The purpose of this study was to investigate the impact of single nucleotide polymorphisms (SNPs) in the acylphosphatase 2 gene and the SNP-SNP interactions on breast cancer (BC) risk in Chinese Han women. PATIENTS AND METHODS: A logistic regression model was used to examine the association between SNPs and BC risk. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. Generalized multifactor dimensionality reduction was employed to analyze the SNP-SNP interaction. RESULTS: Logistic regression analysis showed that BC risk was significantly higher in carriers with the rs1682111-A allele than those with the TT genotype (TA + AA vs. TT; adjusted OR, 1.47; 95% CI, 1.21-1.92). In addition, we also found that BC risk was significantly higher in carriers with the rs10439478-C allele than those with the AA genotype (AC + CC vs. AA); adjusted OR, 1.67; 95% CI, 1.29-2.11. We found a significant 2-locus model (P = .0010) involving rs1682111 and rs10439478; the cross-validation consistency of this model was 10 of 10, and the testing accuracy was 60.11%. Participants with the TA or AA of rs1682111 and the AC or CC of rs10439478 genotype have the highest BC risk, compared with subjects with the TT of rs1682111 and the AA of rs10439478 genotype (OR, 2.52; 95% CI, 1.67-3.44), after covariate adjustment for gender, age, age at menarche, number of children, and body mass index. CONCLUSIONS: Minor allele of rs1682111 and rs10439478 and its interaction were associated with increased BC risk.

MMI-166, a selective matrix metalloproteinase inhibitor, promotes apoptosis in human pancreatic cancer.

MMI-166 is a third-generation selective matrix metalloproteinase (MMP) inhibitor that prevents tumor invasion and metastasis by downregulating the activity of MMP-2 and MMP-9. However, MMI-166's effect in pancreatic cancer cells has not been widely studied. Initially, we treated SW1990, human pancreatic cancer cells, with 0, 50 or 100 µg/ml of MMI-166 for 24 h. Apoptosis in the cells was then observed by inverted fluorescence microscope and flow cytometry; the apoptosis rate was dependent on MMI-166 concentration. We then injected nude mice with SW1990 cells. Volume of the resulting xenograft tumors in nude mice treated with MMI-166 was far less than that of the control group, whereas their apoptotic index was much greater. Expression of MMP-2, MMP-9, c-myc and survivin were markedly lower in tumors from the treated mice than in the control group. In cell experiments, MMP-2 and MMP-9 activities were downregulated by MMI-166 compared with controls, as were both mRNA and protein levels of MMP-2, MMP-9 and c-myc, although survivin expression did not differ. These results show that MMI-166 can induce apoptosis of pancreatic cancer cells in vitro and in vivo. The mechanism may be related to downregulation of c-myc by MMI-166.