Early Versus Delayed Laparoscopic Cholecystectomy for Acute Cholecystitis with Mild Pancreatitis.

The safety and feasibility of early laparoscopic cholecystectomy (LC) for acute cholecystitis with mild pancreatitis were explored. A total of 973 patients with acute pancreatitis, including 651 mild cases and 322 moderate or severe cases were retrospectively studied from July 2014 to December 2018 in our department. And 426 mild pancreatitis cases with acute cholecystitis were enrolled in this study, of which 328 patients underwent LC during the same-admission (early LC group), and 98 patients underwent LC a period of time after conservative treatment (delayed LC group). Clinical characteristics, operative findings and complications were recorded and followed up. The two groups were comparable in age, gender, the grade of American Society of Anesthesiologist (ASA), biochemical findings and Balthazar computer tomography (CT) rating (P>0.05). The operation interval and hospital stay in early LC group were significantly shorter than in delayed LC group (5.83±1.62 vs. 41.36±8.44 days; 11.38±2.43 vs. 16.49±3.48 days, P<0.01). There was no significant difference in the average operation time between the two groups. No preoperative biliary related events recurred in early LC group but there were 21 cases of preoperative biliary related events in delayed LC group (P<0.01). There was no significant difference in conversion rate (3.85 vs. 5.10%, P=0.41) and surgical complication rate (3.95 vs. 4.08%, P=0.95) between early LC group and delayed LC group. During the postoperative follow-up period of 375 cases, biliary related events recurred in 4 cases in early LC group and 3 cases in delayed LC group (P=0.37). The effect of early LC during the same-admission is better than delayed LC for acute cholecystitis with mild pancreatitis.

Stage III should be subclassified into Stage IIIA and IIIB in the American Joint Committee on Cancer (8th Edition) staging system for pancreatic cancer.

AIM: To ascertain the prognostic role of the T4 and N2 category in stage III pancreatic cancer according to the 8th edition of the American Joint Committee on Cancer (AJCC) classification. METHODS: Patients were collected from the Surveillance Epidemiology and End Results (SEER) database (2004-2013) and were divided into three groups: T(1-3)N2, T4N(0-1), and T4N2. Overall survival (OS) and disease-specific survival (DSS) of patients were evaluated by the Kaplan-Meier method. RESULTS: For the first time, we found a significant difference in OS and DSS between T(1-3)N2/T4N(0-1) and T4N2 but not between T(1-3)N2 and T4N(0-1). A higher grading correlated with a worse prognosis in the T(1-3)N2 and T4N2 groups. CONCLUSION: Patients with stage T4N2 had a worse prognosis than those with stage T(1-3)N2/T4N(0-1) in the 8th edition AJCC staging system for pancreatic cancer. We recommend that stage III should be subclassified into stage IIIA [T(1-3)N2/T4N(0-1)] and stage IIIB (T4N2).

Association between polycystic ovary syndrome and the risk of pregnancy complications: A PRISMA-compliant systematic review and meta-analysis.

BACKGROUND: Polycystic ovary syndrome (PCOS) is inconsistently associated with increased risk of adverse pregnancy outcomes. The purpose of this meta-analysis was to summarize the evidence regarding the strength of the association between pregnancy in women with PCOS and pregnancy complications. METHODS: We systematically searched PubMed, EmBase, and the Cochrane Library to identify observational studies up to January 2016. The primary focus was pregnancy outcomes, including gestational diabetes mellitus (GDM), preeclampsia, pregnancy-induced hypertension (PIH), preterm delivery, cesarean delivery, oligohydramnios, and polyhydramnios. Effect estimates were pooled using the random-effects model. The analysis was further stratified by factors that could affect these associations. RESULTS: We included 40 observational studies that reported data on a total of 17,816 pregnancies with PCOS and 123,756 pregnancies without PCOS. Overall, PCOS in pregnancy was associated with greater risk of GDM, preeclampsia, PIH, preterm delivery, cesarean delivery, miscarriage, hypoglycemia, and perinatal death. However, PCOS in pregnancy had little or no effect on oligohydramnios, polyhydramnios, large-for-gestational age (LGA), small-for-gestational-age (SGA), fetal growth restriction (FGR), preterm premature membrane rupture, fasting blood glucose (FBG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglyceride, total cholesterol, congenital malformation, macrosomia, and respiratory distress syndrome. Subgroup analysis suggested that these associations might be influenced by study design and pre-BMI. CONCLUSION: PCOS in pregnancy is associated with a significantly increased risk of adverse pregnancy, fetal, and neonatal outcomes.

High expression of AP-4 predicts poor prognosis for hepatocellular carcinoma after curative hepatectomy.

The aim of this study was to evaluate the association between activating enhancer binding protein 4 (AP-4) tissue expression and patient prognosis in hepatocellular carcinoma (HCC). The levels of AP-4 mRNA and protein in tumor and para-tumor tissue were evaluated in 30 HCC cases by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Additionally, AP-4 protein expression in 112 HCC was analyzed by immunohistochemistry. The correlation of AP-4 expression and patients' clinicopathological parameters was evaluated. Survival analysis was performed using the Kaplan-Meier method and Cox's proportional hazards model. By RT-PCR and Western blot, the levels of AP-4 mRNA and protein were significantly higher in HCC, compared to that in para-tumor tissue (p < 0.001). Immunohistochemical staining revealed that AP-4 was highly expressed in 53.6 % of the HCC patients. The AP-4 expression level was closely associated with serum alpha fetoprotein elevation, tumor size, histological differentiation, tumor recurrence, tumor metastasis, and tumor stage. Kaplan-Meier survival analysis showed that a high expression level of AP-4 resulted in a significantly poor prognosis of HCC patients. Multivariate analysis revealed that AP-4 expression level was an independent prognostic parameter for the overall survival rate of HCC patients. These findings provide evidence that a high expression level of AP-4 serves as a biomarker for poor prognosis for HCC. Thus, we speculate that AP-4 may be a potential target of antiangiogenic therapy for HCC.

Overexpression of lysine specific demethylase 1 predicts worse prognosis in primary hepatocellular carcinoma patients.

AIM: To investigate the clinicopathological features and prognostic value of lysine specific demethylase 1 (LSD1) in hepatocellular carcinoma (HCC). METHODS: We examined LSD1 expression in 60 paired liver cancer tissues and adjacent noncancerous tissues by quantitative real time polymerase chain reaction (qRT-PCR) and Western blotting. In addition, we analyzed LSD1 expression in 198 HCC samples by immunohistochemistry. The relationship between LSD1 expression, clinicopathological features and patient survival was investigated. RESULTS: Immunohistochemistry, Western blotting, and qRT-PCR consistently confirmed LSD1 overexpression in HCC tissues compared to adjacent non-neoplastic tissues (P < 0.01). Additionally, immunostaining showed more LSD1-positive cells in the higher tumor stage (T3-4) and tumor grade (G3) than in the lower tumor stage (T1-2, P < 0.001) and tumor grade (G1-2, P < 0.001), respectively. Moreover, HCC patients with high LSD1 expression had significantly lower 5-year overall survival rates (P < 0.001) and lower 5-year disease-free survival rates (P < 0.001), respectively. A Cox proportional hazards model further demonstrated that LSD1 over-expression was an independent predictor of poor prognosis for both 5-year disease-free survival [hazards ratio (HR) = 1.426, 95%CI: 0.672-2.146, P < 0.001] and 5-year overall survival (HR = 2.456, 95%CI: 1.234-3.932, P < 0.001) in HCC. CONCLUSION: Our data suggest for the first time that the overexpression of LSD1 protein in HCC tissues indicates tumor progression and predicts poor prognosis.

Expression of ADAM8 and its clinical values in diagnosis and prognosis of hepatocellular carcinoma.

ADAM8 behaves as an active metalloprotease in vitro, hydrolyzing myelin basic protein and a variety of peptide substrates based on the cleavage sites of membrane-bound cytokines, growth factors, and receptors. Other studies have demonstrated overexpression of some ADAM family proteins in a variety of human tumors, but no report is available on the actual expression of ADAM8 and the correlation between clinicopathologic features and prognosis of hepatocellular carcinoma (HCC) patients. In this study, serum levels of ADAM8 were measured by ELISA in 126 patients with HCC, 50 patients with liver cirrhosis (LC), and 50 healthy individuals. The expression of ADAM8 in liver tissue was further studied using Western blotting in 126 patients with HCC and 50 with LC. The correlations between ADAM8 status and various clinicopathological parameters including survival were analyzed. Survival analysis was performed using the Kaplan-Meier method and Cox's proportional hazards model. The ELISA assay showed that the serum levels of ADAM8 in the HCC, LC, and healthy groups were 136.4 ± 34.5, 64.2 ± 20.1, and 63.2 ± 22.7 U/ml, respectively. Analysis of variance was used for inter-group comparison, and differences were found between the HCC group and the other two groups (both P < 0.001), while no difference was found between the LC group and the healthy group (P = 0.365). Western blotting assay showed that ADAM8 protein expression was detected in 62.7 % (79/126) HCC and in 32 % (16/50) LC tissues. Further, ADAM8 expression was associated closely with serum AFP elevation, tumor size, histological differentiation, tumor recurrence, tumor metastasis, and tumor stage. Kaplan-Meier survival analysis showed that patients with ADAM8-positive tumors had a shorter postoperative survival time than those with ADAM8-negative tumors (P < 0.001). Multivariate analysis revealed that ADAM8 expression was an independent prognostic parameter for the overall survival rate of HCC patients. These findings provide evidence that the expression of ADAM8 serves as a poor prognostic biomarker for HCC. ADAM8 may be a potential target of antiangiogenic therapy for HCC.

High RSF-1 expression correlates with poor prognosis in patients with gastric adenocarcinoma.

AIM: To investigate the expression and prognostic significance of RSF-1 in gastric adenocarcinoma. METHODS: RSF-1 expression was analyzed using immunohistochemical staining on tissue samples from a consecutive series of 287 gastric adenocarcinoma patients who underwent tumor resections between 2003 and 2006.The relationship between RSF-1 expression, clinicopathological factors, and patient survival was investigated. RESULTS: Immunohistochemical staining indicated that RSF-1 is highly expressed in 52.6% of gastric adenocarcinomas. RSF-1 expression levels were closely associated with tumor size, histological differentiation, tumor stage, and lymph node involvement. Kaplan-Meier survival analysis showed that high RSF-1 expression exhibited a significant correlation with poor prognosis for gastric adenocarcinoma patients. Multivariate analysis revealed that RSF-1 expression is an independent prognostic parameter for the overall survival rate of gastric adenocarcinoma patients. CONCLUSION: Our data suggest that RSF-1 plays an important role in gastric adenocarcinoma progression and that high RSF-1 expression predicts an unfavorable prognosis in gastric adenocarcinoma patients.

[Laparoscopic versus open surgery for D2 gastrectomy in advanced gastric cancer].

OBJECTIVE: To investigate the safety and feasibility of laparoscopic D2 gastrectomy for advanced gastric cancer. METHODS: The clinical data of 210 cases of laparoscopic gastrectomy and 180 cases of open gastrectomy for radical (D2) gastrectomy from May 2007 to Dec 2010 were analyzed retrospectively. RESULTS: A total of 206 cases underwent laparoscopic-assisted surgery with 4 conversions. Compared to the open group, the laparoscopic group was associated with less bleeding [(208±38) ml vs. (300±52) ml, P<0.05], quicker postoperative recovery of bowel function [(2.9±0.7) d vs. (3.9±1.8) d, P<0.05], shorter postoperative length of hospital stay[(12.8±6.2) d vs. (15.6±6.8) d, P<0.05], longer operative time [(258±42) min vs. (193±30) min, P<0.05]. The number of lymph node harvested was 20.5±1.9 in the laparoscopic group and 25.8±1.5 in the open group, and the postoperative complication rate was 8.1% (17/201) vs. 8.5% (15/180), and differences were not statistically significant (both P>0.05). The recurrence rate was 2.9% (6/210) and 2.8% (5/180), and the 3-year overall survival rate was 35.6% and 37.8%, the differences were not statistically significant (both P>0.05). CONCLUSIONS: Laparoscopic radical gastrectomy for gastric cancer is safe and effective, which can reach the same range of lymph node dissection as open gastric cancer surgery and similar survival rate.

Overexpression of HOXA1 correlates with poor prognosis in patients with hepatocellular carcinoma.

HOXA1 overexpression is sufficient for malignant transformation of nontumorigenic epithelial cells. It is known that HOXA1, which was upregulated in squamous cell carcinomas, affects both cell growth and death. The forced expression of HOXA1 in human breast cancer cells results in increased cell growth activity. However, it has not been reported in hepatocellular carcinoma (HCC). In this study, we used immunohistochemistry to compare HOXA1 protein expression in HCC and normal liver tissues and further analyzed HOXA1 protein expression in 156 clinicopathologically characterized HCC cases. We stably knocked down the endogenous expression level of HOXA1 in HepG2 cells with specific shRNA-expressing lentiviral vector. Following the successful establishment of stable cells, we examined in vitro cell growth by the MTT assay, anchorage-independent growth through a soft agar colony formation assay and cell migration/invasion by transwell and Boyden chamber assay. In addition, we also investigated in vivo tumor growth by xenograft transplantation of HepG2 cells into nude mice. Our results showed that the protein expression level of HOXA1 was markedly higher in HCC tissues than that in normal liver tissue (P = 0.019). In addition, a high expression level of HOXA1 protein was positively correlated with the T classification (P < 0.001), the N classification (P < 0.001), distant metastasis (P = 0.004), and the clinical stage (P < 0.001) of HCC patients. Patients with higher HOXA1 expression showed a significantly shorter overall survival time compared with patients with low HOXA1 expression. Multivariate analysis suggested that HOXA1 expression might be an independent prognostic indicator (P < 0.001) for the survival of patients with HCC. HOXA1-specific shRNA (shHOXA1) successfully knocked down HOXA1 endogenous expression in HepG2 cells. Compared to the parental and control shRNA-transfected (shCtrl) HepG2 cells, the shHOXA1 cells exhibited significantly reduced in vitro cell growth, anchorage-independent growth, and cell migration and invasion (P < 0.05). In vivo, the xenograft transplants from shHOXA1 cells gave rise to much smaller tumors compared with those from shCtrl cells. Collectively, high HOXA1 expression is associated with poor overall survival in patients with HCC. The downregulation of HOXA1 inhibits growth, anchorage-independent growth, and migration and invasion of HepG2 cells.

High RIN1 expression is associated with poor prognosis in patients with gastric adenocarcinoma.

The aim of this study was to investigate the expression and prognostic significance of RIN1 in gastric adenocarcinoma. RIN1 expression was analyzed using quantitative real-time PCR (qRT-PCR), Western blotting, and immunohistochemical staining on tissue samples from a consecutive series of 315 gastric adenocarcinoma patients who underwent tumor resections between 2003 and 2006. The relationship between RIN1 expression, clinicopathological factors, and patient survival was investigated. qRT-PCR results showed that the RIN1 mRNA expression was higher in tumor tissue samples than in the adjacent normal tissues, and a corresponding increase in protein expression was confirmed by Western blotting. Immunohistochemical staining indicated that RIN1 is highly expressed in 54.3 % of gastric adenocarcinomas. RIN1 expression levels were closely associated with tumor size, histological differentiation, tumor stage, and lymph node involvement. Kaplan-Meier survival analysis showed that high RIN1 expression exhibited a significant correlation with poor prognosis for gastric adenocarcinoma patients. Multivariate analysis revealed that RIN1 expression is an independent prognostic parameter for the overall survival rate of gastric adenocarcinoma patients. Our data suggest that RIN1 plays an important role in gastric adenocarcinoma progression and that a high RIN1 expression predicts an unfavorable prognosis in gastric adenocarcinoma patients.

Defunctioning stoma in low anterior resection for rectal cancer: a meta- analysis of five recent studies.

BACKGROUND/AIMS: The necessity of a defunctioning stoma in low anterior resection with total mesorectal excision for rectal cancer remains controversial. This meta-analysis evaluates the advantages of prophylactic stomas in patients undergoing low anterior resection and assesses postoperative outcomes of patients with or without a defunctioning stoma. METHODOLOGY: Studies and relevant literatures regarding the formation of defunctioning stomas after low anterior resection were searched through PubMed and Embase. The rates of anastomotic leakage and re-operation related to leakage with or without defunctioning stoma were pooled and compared using a meta-analysis. The risk ratios were calculated with 95% confidence intervals to evaluate the influence of defunctioning stomas. RESULTS: Five recent studies including 878 patients in total were included in this meta-analysis. These studies demonstrated that defunctioning stomas significantly reduced the rate of postoperative anastomotic leakage and reoperation after low anterior resection, the pooled risk ratio was 0.34 (95% CI=0.22-0.53, p<0.00001) and 0.27 (95% CI=0.16-0.48, p<0.00001), respectively. CONCLUSIONS: Defunctioning stomas can be useful to minimize the rate of anastomotic leakage and re-operation related to leakage. Furthermore, anorectal function was not affected. However, the influence of a defunctioning stoma on long-term mortality and the quality of life in patients treated for rectal cancer is inconclusive.

Diagnostic and prognostic value of the methylation status of secreted frizzled-related protein 2 in colorectal cancer.

PURPOSE: The aim of this study was to investigate the diagnostic and prognostic significance of the methylation status of secreted frizzled-related protein 2 (SFRP2) in colorectal cancer (CRC). METHODS: Methylation-specific PCR assay was performed to analyze SFRP2 promoter methylation in solid tissue, stool and serum samples collected from 169 CRC patients, 63 patients with advanced adenomas, 46 patients with non-adenomatous polyps and 30 normal healthy controls. RESULTS: Methylated SFRP2 was frequently detected in CRC tissues and precancerous lesions. The sensitivity of SFRP2 methylation levels in tissue, fecal and serum DNA for the detection of CRC was similar, ranging from 66.9 to 88.2%; however, serum SFRP2 methylation levels showed a markedly higher specificity in discriminating CRCs from benign adenomas than those of SFRP2 methylation levels in tumor and fecal DNA. Moreover, serum SFRP2 methylation was significantly associated with poor differentiation grade (P=0.019), serosal/subserosal invasion (P < 0.001), lymph node metastasis status (P < 0.001) and TNM stage (P < 0.001) of CRC. CRC patients with SFRP2 hypermethylation in tumor, stool and serum samples had a significantly shorter overall survival than those negative for SFRP2 methylation (P=0.0216, 0.0219, and 0.0255, respectively). Multivariate Cox regression analysis revealed that SFRP2 promoter methylation in tumor samples was an independent prognostic factor for overall survival. CONCLUSION: Our data suggest that serum SFRP2 methylation status represents a promising, non-invasive marker for CRC detection and staging. Hypermethylated SFRP2 may have prognostic relevance in patients with CRC.

Pharmacodynamic and pharmacokinetic study of pegylated liposomal doxorubicin combination (CCOP) chemotherapy in patients with peripheral T-cell lymphomas.

AIM: To investigate the pharmacodynamic and pharmacokinetic parameters of pegylated liposomal doxorubicin (PLD) combined with cyclophosphamide, vincristine, and prednisolone in patients with peripheral T-cell lymphomas (PTCL). METHODS: Seven chemonaive patients and four patients with relapsed peripheral T-cell lymphomas were treated with a CCOP regimen consisting of an intravenous administration of cyclophosphamide (750 mg/m(2)), vincristine (1.4 mg/m(2)), and PLD (30 mg/m(2)) on d 1, as well as an oral administration of prednisolone (60 mg/m(2)) on d 1-5. This regimen was repeated every 3 weeks for six cycles, and the clinical response and toxicity of the regimen were monitored. In addition, the plasma concentration of PLD at different time points was determined before and after treatment. The pharmacokinetics (PKs) software was used to estimate the pharmacokinetic parameters of PLD. RESULTS: The 11 PTCL patients received 35 treatment cycles. Three of them achieved complete response (CR), two partial response (PR), four stable disease (SD), and two progressive disease (PD). The overall response rate (ORR) was 45.5%, and the CR rate was 27.3%. In the 7 chemonaive patients, three achieved CR, two PR, one SD, and one PD. The ORR was 71.4%, and CR rate was 42.9%. The median follow-up time was 15 months, but 6 out of 11 patients were dead at the time of data analysis. The 1-year overall survival rate was 45.5%, and the median progression-free survival (PFS) rate was 6.5 [95% confidence interval (95% CI) 3.17-19.02] with a survival rate of 11.5 months (95% CI 6.65-16.36). The main toxicity was myelosuppression. Oral mucositis and hand-foot syndrome seldom occurred. The PLD plasma concentration from nine patients ranged from 1.7036 to 9.2207 mg·L(-1) after administration of the CCOP regimen (0-168 h). The pharmacokinetic parameters AUC(0-∞), CL, t(1/2), and V(d) were 910.76 mg/L·h, 0.043 L·h(-1)·m(-2), 68.40 h, and 3.56 L/m(2), respectively. CONCLUSION: The CCOP regimen was effective and well tolerated in patients with peripheral T-cell lymphomas. The results of the pharmacokinetic parameters showed that PLD had long retention time in blood circulation.

Phase II trial of gemcitabine plus cisplatin in patients with advanced non-small cell lung cancer.

AIM: To investigate the pharmacodynamics and pharmacokinetics of gemcitabine (dFdC) administered on d 1 and 5 plus cisplatin administered on d 1 in chemonaive patients with stage IIIB or IV non-small cell lung cancer (NSCLC). METHODS: In each combination cycle, gemcitabine was administered at a dose of 1250 mg/m(2) as a 30 min intravenous (iv) infusion on d 1 and 5 followed by cisplatin at a dose of 75 mg/m(2) as a 3 h iv infusion on d 1 every 3 weeks. There was an interval of 1 h between the two infusions. Clinical response and toxicity of the regimen were observed. Furthermore, the plasma concentrations of gemcitabine (dFdC) and its metabolite (dFdU) at different time points were detected during the first cycle of infusion. Pharmacokinetic software (PKS) was used to estimate the pharmacokinetic parameters of gemcitabine and its metabolite dFdU. RESULTS: A total of 28 patients was enrolled in the study. The median age was 54 years (range 27-75 years), and most patients were in good clinical condition. Twenty-seven patients received two or more treatment cycles. The overall clinical response rate was 33.3%. The median overall survival time was 13 months. The estimated median time to tumor progression (TTP) was 6.2 months, and the 1-year survival rate was 55.6%. Toxicities were tolerated. The main toxicity was myelosuppression; 35.7% of patients had grade 3/4 hematologic toxicities and 28.6% had grade 3/4 non-hematologic toxicities, which were commonly gastrointestinal responses. The pharmacokinetic parameters of dFdC and dFdU were not different between pre- and post-administration of gemcitabine on d 1 and 5. dFdU was minimal (0.729+/-0.637 microg/mL) before gemcitabine was infused on d 5, and gemcitabine was not present. CONCLUSION: The regimen is active and well tolerated in chemonaive patients with advanced NSCLC. After gemcitabine was administered on d 1 and 5, the pharmacokinetic parameters of dFdC and dFdU showed no difference from those before the infusion, and dFdU was minimal before gemcitabine was administered on d 5.

[Efficacy of salvage chemotherapy in the advanced non-small cell lung cancer patients who failed the treatment of chemotherapy and EGFR-TKI].

OBJECTIVE: Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) such as gefitinib and erlotinib are used as standard 2(nd)/3(rd) line therapy in previously treated advanced non-small cell lung cancer (NSCLC). However, the optimal treatment for patients who experienced disease progression after chemotherapy and EGFR-TKI is unclear. The aim of this study was to explore the efficacy and safety of a salvage chemotherapy in advanced NSCLC patients who failed the previous treatment of platinum-based chemotherapy and EGFR-TKI. METHODS: Clinicopathological data of 55 cases of advanced NSCLC patients who failure of first-line platinum-based chemotherapy and subsequent treatment with TKI were collected and analyzed. The patients were of PS = 0-2, and with normal vital organ function. Patients received salvage chemotherapy until disease progression or unacceptable toxicity or the patient refused to continue receiving treatment. A chart review assessed the key outcomes including the objective response rate (ORR), disease control rate (DCR) and progression-free survival (PFS). RESULTS: Fifty-five patients were enrolled in this study from march 2007 to october 2009. The median age of patients was 55 years (range: 34 - 72), 60.0% were males, PS 0-1 patients were 65.5%, stage IV patients were 100%; 34.5% had a TKI treatment duration ≥ 6 months. Twenty-four patients received pemetrexed as salvage chemotherapy, 21 received docetaxal and 10 had other chemotherapy. All patients were evaluable for efficacy. Among them, 7 (12.7%) patients achieved PR, 21 (38.2%) patients SD, and 27 (49.1%) patients PD, with ORR of 12.7% and DCR of 50.9%. The median follow-up duration was 5.5 months, and the median PFS was 2.0 months. The ORR and PFS were not significantly related with gender, PS and chemotherapy regimens (all P > 0.05), but patients with EGFR-TKI treatment ≥ 6 months achieved a significantly better ORR and DCR than those < 6 months (ORR: 21.1% vs. 8.3%, P = 0.012; DCR: 73.3% vs. 38.9%, P = 0.017), mPFS was significant longer in the patients received ≥ 6 months of EGFR-TKI (4.5 vs. 2.0 months, P = 0.008). The toxicity was acceptable and there were no treatment-related deaths. CONCLUSION: Advanced NSCLC patients failed with the previous treatment of first-line platinum-based chemotherapy and EGFR-TKI may benefit from salvage chemotherapy, especially in patients who received ≥ 6 months of EGFR-TKI. The toxicity of the salvage chemotherapy is acceptable.

[Efficacy of GDP regimen (gemcitabine, dexamethasone, and cisplatin) on relapsed or refractory aggressive non-Hodgkin's Lymphoma: a report of 24 cases].

BACKGROUND & OBJECTIVE: The prognosis of relapsed or refractory aggressive non-Hodgkin's lymphoma (NHL) after front-line therapy remains poor. The development of more effective and less toxic salvage regimens remains a major challenge. Gemcitabine is effective in treating lymphoma and, when combined with cisplatin, is effective for some solid tumors. This study was to evaluate the efficacy of GDP regimen (gemcitabine, dexamethasone, and cisplatin) on relapsed or refractory aggressive NHL, and observe the adverse events. METHODS: Patients with relapsed or refractory aggressive NHL, measurable disease, and had received previously at least one chemotherapy regimen were enrolled and treated with GDP regimen (gemcitabine 1000 mg/m2 on Days 1 and 8, dexamethasone 20-40 mg on Days 1-3, and cisplatin 25 mg/m2 on Days 1-3) every 3 weeks. The efficacy and adverse events were evaluated according to the WHO criteria. RESULTS: Twenty-four patients had received a total of 76 chemotherapy cycles, and were assessable for efficacy and adverse events. Five (20.8%) patients had complete response, 9 had partial response, 8 had stable disease, and 2 had progressive disease. The overall response rate (RR) was 58.3% for assessable patients; it was 57.1% for B-cell NHL patients and 60.0% for T-cell NHL patients (P=0.889). The median follow-up was 1.2 years. The 1-year overall survival rate was 41.7%; it was 42.9% in B-cell NHL patients and 40.0% in T-cell NHL patients (P=0.986). The occurrence rate was 37.5% for grade III/IV leucopenia, 25.0% for thrombocytopenia, and 16.7% for anemia in all patients. Non-hematologic toxicities were mild. There was no treatment-related death. Two patients proceeded to stem cell transplantation after salvage chemotherapy and obtained sufficient stem cells. CONCLUSION: GDP regimen is an effective and relatively nontoxic salvage chemotherapy regimen for relapsed or refractory aggressive NHL.

[Transabdominal ultrasound measurement of intravesical prostatic protrusion helps diagnosis of benign prostatic obstruction].

OBJECTIVE: To evaluate the measurement of intravesical prostatic protrusion (IPP) by transabdominal ultrasonography (TAUS) in the diagnosis of benign prostatic obstruction (BPO). METHODS: We studied the clinical data of 109 BPH patients referred for lower urinary tract symptoms (LUTS) from April 2005 to December 2006. IPP was measured by TAUS, urodynamic parameters such as Qmax and PdetQmax obtained by urodynamic studies and AG values calculated. The patients were divided into an obstruction and a non-obstruction group according to their AG values. RESULTS: IPP was found statistically different between the obstruction and non-obstruction groups (P<0.001) and positively correlated with the AG value (r=0.729, P=0.001). With the cutoff at IPP > or = 10 mm for the diagnosis of BPO, the sensitivity, specificity and accuracy of the diagnosis were 89.9%, 97.5% and 92.7%, respectively. CONCLUSION: The measurement of IPP by TAUS offers a valuable help for the diagnosis of BPO.

[MINE regimen for patients with relapsed or chemo-resistant invasive non-Hodgkin's lymphoma].

BACKGROUND & OBJECTIVE: Treatment of relapsed or refractory non-Hodgkin's lymphoma (NHL) remains problematic with no standard salvage chemotherapy regimen. This study was to evaluate the efficacy of MINE (mitoxantrone, mesna/ifosfamide and etoposide) regimen on relapsed or refractory NHL, and observe its toxicity. METHODS: Records of 38 patients with relapsed or refractory invasive NHL, treated with MINE regimen from Jan. 2001 to Jun. 2003, were reviewed. All patients had received at least 1 type of chemotherapy regimen (median, 2 types; range, 1-4 types) with a median of 6 chemotherapy cycles (range, 2-12 cycles). The patients received a median of 4 cycles (range, 2-6 cycles) of MINE regimen. RESULTS: The treatment outcome and adverse events of all patients were assessable. The overall response rate was 47.4%, with a complete response (CR) rate of 15.8%. The response rates were 57.7% in the 26 patients with B-cell lymphoma and 25.0% in the 12 patients with T-cell lymphoma. The 1- and 2-year survival rates were 34.2% and 7.9%, respectively. The major adverse event was myelosuppression: the prevalence of grade III-IV neutropenia was 39.5%, and that of grade III-IV thrombocytopenia was 13.1%. One patient suffered grade III liver toxicity. CONCLUSIONS: MINE regimen was effective for patients with relapsed or refractory invasive NHL, and its toxicity is well tolerated, but the response term is relatively short. Further clinical study on the application of MINE regimen is warranted.

Human p32 protein relieves a post-transcriptional block to HIV replication in murine cells.

In the mouse, replication of human immunodeficiency virus type 1 (HIV) is blocked at the levels of entry, transcription and assembly. For the latter effect, the amounts of unspliced viral genomic RNA could have an important function. Indeed, in murine cells, HIV transcripts are spliced excessively, a process that is not inhibited by the murine splicing inhibitor p32 (mp32). In marked contrast, its human counterpart, hp32, not only blocks this splicing but promotes the accumulation of viral genomic transcripts and structural proteins, resulting in the assembly and release of infectious virions. A single substitution in hp32 of Gly 35 to Asp 35, which is found in mp32, abrogates this activity. Thus, hp32 overcomes an important post-transcriptional block to HIV replication in murine cells.