Objective To investigate the reverse effects of zoledronic acid on the malignant phenotype of Bel-7402 human hepatocarcinoma cells.Methods The AFP secretary amount of the cells was determind with RIA,and thespecfic activities of tyrosine-?-ketoglutarate transaminase(TAT),ornithine carbamyl transferase(OCT) and alkaline phospharase(ALP),?-glutamgl transpeptidase(?-GT) and aldolase(ALD) were assayed by enzymological methods.Results Treating with 0.05?g/ml zoledronic acid,the proliferation of the cells,the secretary amount of AFP,and the specific activities of ?-GT and ALD significantly decreased(P

Objective To evaluate the preventive effect of compound matrine injection on hepatic lesion caused by chemotherapy. Methods 178 patients after gastric and colorectal cancer resection were enrolled into three groups randomly. 56 patients in group A received MFOLFOX6 regimen treatment only, 62 patients in group B received both normal treatment and combined compound matrine injection,60 patients in group C received both normal treatment and glutathione. The change of liver function were observed. Results There was no the hepatotoxicity of Ⅲ-Ⅳ degree in all groups;the incidence of bilirubin and transaminase increasing in group B and C was significantly lower than that group A(P ＜0.05), but the incidence of ALP/GGT increasing showing no significant difference among the three groups; 72.7 % of the incidence of hepatic lesion in group A happened firstly before the seventh cycle,it was 27.3 % and 33.3 % respectively in group B and group C, the time of the emerging of hepatotoxicity in group B and C was markedly delayed than that group A (P ＜0.05); there was not significant difference between group B and group C in both bilirubin and transaminase increasing and the time of the emerging of hepatotoxicity (P ＞0.05). Conclusion Compound matrine injection can prevent and postpone the happening of hepatic lesion caused by adjuvant chemotherapy after digestive tract cancer resection, The result is equal to glutathione. Compound matrine injection also has antineoplastic effects, so the clinical superiority is more obvious.

Purpose:To study effect of peripheral blood lymphocyte subsets in autologous LAK cell treatment of advanced lung adenocarcinoma and to discuss the prognosis.Methods:21 surgically resected cases, were confirmed as primary lung adenocarcinoma stage Ⅲ or Ⅳ. The patients had received the treatment of IL 2 and two kinds of autologous LAK cells, every 2～3 months, for two years. The results of the three groups death in 2 years and survival over 2 years were analysed statistically as a whole.Results:In total,CD4 + decreased, t =2.817, P

Objective To investigate the abnormality of electrocardiography (ECG) of patients with neoplasms after different chemotherapy. Methods The abnormality of ECG data in 632 patients with neoplasms after different chemotherapy in our hospital was analyzed. Results The changes of ST-T was found in 352 cases (55.70 %), arrhythmia in 197 cases (31.2 %), low QRS in 91 cases (14.4 %), cardiac infarction in 2 cases (0.32 %). Conclusion Different chemotherapy can induce abnormality of ECG, especially combined with anthracycline. Pay attention to potential cardiotoxicity of chemotherapeutics and do regular examination of ECG is very important.

Background and purpose:EGFR-TKI (EGFR-tyrosine kinase inhibitors), represented by geiftinib and erlotinib, have exhibited signiifcant antiproliferative effects against non-small cell lung cancer (NSCLC) with low toxicity.EGFR gene mutation was discovered to be a predictive biomarker for EGFR-TKI treatment. Although the efifcacy of EGFR-TKI is limited toEGFR wild-type patients, it is still noticeable suggesting that some other mechanisms are responsible for it. The current study is aimed at evaluating the expression of phosphorylated EGFR in advanced NSCLC, investigating its relationship withEGFR mutations and EGFR-TKI efifcacy.Methods:EGFR gene mutations were detected by denaturing high performance liquid chromatography (DHPLC) in 205 stageⅢB-ⅣNSCLC patients. The expressions of phosphorylated tyrosine 1068 (pTyr1068) and 1173 (pTyr1173) were detected by immunohistochemistry.Results:The positive expressions of pTyr1068 and pTyr1173 were 80.0% (164/205) and 57.6% (95/165) respectively. None of them were related to clinical pathological characteristics (age, gender, pathological type, smoking status, disease stage).EGFR gene mutation rate was 44.9% (92/205), which was only related to smoking status (P=0.024) compared to other clinical pathological characteristics.EGFR gene mutations were poorly related to pTyr1068 expression (P<0.001) and not related to pTyr1173 expression (P=0.297). The objective response rate (ORR),disease control rate (DCR), and progressive free survival (PFS) of EGFR-TKI treatment in patients withEGFR mutations were 48.3% (43/89), 80.9% (72/89) and 8 months (95%CI: 6.11-11.42) respectively, which were signiifcantly higher than that ofEGFR wild-type patients [ORR=16.2% (17/105,P<0.001); DCR=56.2%(59/105,P<0.001); Median PFS: 2.1 months, (95%CI: 0.89-3.24;P=0.001)]. Superior ORR: DCR and PFS appeared in patients with pTyr1068 positive expression compared to negative [ORR: 37.7% (58/154)vs 5.0% (2/40,P<0.001); DCR: 74.7% (115/154)vs 40.0% (16/40,P<0.001); Median PFS: 7.0 monthsvs 1.2 months,P<0.001)]. Inversely, the patients with pTyr1173 positive expression had lower ORR, DCR and shorter PFS [ORR: 27.8% (25/90)vs 37.9%(25/66,P=0.123); DCR: 64.4% (58/90)vs 83.3% (55/66,P=0.007); Median PFS: 4.8 monthsvs 7.7 months (P=0.016)]. In subgroup ofEGFR wild-type patients, positive expression of pTyr1068 was 69.0% (69/100).EGFR wild-type patients with pTyr1068 positive expression had a prolonged PFS and elevated ORR and DCR compared to negative [median PFS: 3.6 monthsvs 1.2 months (P<0.001); ORR: 23.2%vs 3.2% (P=0.010); DCR: 69.6%vs 35.5% (P=0.001)]. Sixteen patients with pTyr1068 positive expression who responded to EGFR-TKI treatment in this subgroup had a remarkable PFS [median PFS: 15.6 months (95%CI:7.28-23.9)]. Multiple factor analysis showed that the expression of pTyr1068 was an independence predictor factor for EGFR-TKI treatment (OR=0.24, 95%CI: 0.16~0.37,P<0.001). Conclusion:Phosphorylation at Tyr1068 of EGFR might be a potential predictive factor for clinical response and survival of EGFR-TKI treatment in patients with advanced NSCLC, especially inEGFR wild-type patients.

Objective:To evaluate the efficacy and adverse reaction caused by Capecitabine compared with S-1 as maintenance treat-ments for patients with advanced gastric cancer (AGC) after first-line induction chemotherapy. Methods:A total of 130 AGC patients who did not suffer disease progression after first-line chemotherapies, including XELOX (four to six cycles), SOX (four to six cycles), and mFOLFOX6 regimen (six to eight cycles), were randomized into three groups. The Capecitabine group (Cap) received maintenance che-motherapy with Capecitabine (1 000 mg/m2 twice daily for 14 days, 21 days/cycle), while the S-1 group (S1) received S-1 (40, 50, or 60 mg according to the body surface area and orally administered twice a day for 14 days, 21 days/cycle). The control group was consid-ered as the observation group. Patients with maintenance treatments received drugs until disease progression or observation of intol-erant toxicity. Results:A total of 44, 33, and 53 patients received XELOX, SOX, and mFOLFOX6 regimens, respectively. The overall DCR was 63.1%. Among the 82 patients, 35, 28, and 19 belonged to the Cap, S1, and observation groups, respectively. The comparison be-tween the efficacy of treatments in the Cap and S1 groups did not show statistically significant differences (P=0.678). The median time of progression was 8.5 months in the Cap group and 9.0 months in the S1 group (P>0.05). Both groups showed better responses than the observation group, which demonstrated a median progression of 6.0 months (P<0.001). The median overall survivals were 14.5, 15.0, and 14.0 months in the Cap, S-1, and observation groups, respectively (P=0.188). The most common adverse effects observed among the patients with maintenance treatments included myelo-suppression, gastrointestinal reaction, fatigue, hand-foot syndrome, and stomatitis. No death occurred in relation to the therapy. Conclusion:The effectiveness of Capecitabine and S-1 as maintenance chemotherapies in AGC patients after the first-line induction chemotherapy are similar, and both can prolong the time of disease pro-gression with low toxicity.

Background and purpose:Tetrandrine is a natural compound whose role in retinoblastoma remains unclear. This study investigated the effects of tetrandrine (Tet) on human retinoblastoma cells.Methods:CCK-8 assays were performed to analyze the effects of Tet on viability of retinoblastoma cells. The apoptosis rate was determined by Annexin V/PI assays. After staining with 2′,7′-dichlorolfuorescin diacetate (DCFH-DA), cellular reactive oxygen species (ROS) was measured by lfow cytometry. Akt and p-Akt were detected by Western blot.Results:Tet inhibited cell viability of retinoblastoma cells. After treatment with Tet (4, 8, 10 and 20μmol/L) for 24h, cell viability inhibition rates of WERI-Rb-I were 5.7%, 25.0%, 55.1% and 84.9%, whereas inhibition rates of Y79 cells were 2.4%,2.9%, 23.8% and 54.2% (P<0.01). In cells treated with 10μmol/L of Tet for 12, 24 and 48 h, cell viability inhibition rates of WERI-Rb-I were 6.0%, 45.5% and 74.7%, whereas inhibition rates of Y79 cells were 2.9%, 19.4% and 43.3% (P<0.01). Tet induced retinoblastoma cell apoptosis. After treatment with Tet (10 μmol/L) for 24 and 48 h, apoptosis rates of WERI-Rb-I were (23.70±1.75)% and (34.83±3.15)%, respectively, whereas apoptosis rates of Y79 cells were (9.62±2.69)% and (14.97±1.50)%, respectively (P<0.01). Apoptosis inhibitor Z-VAD-FMK attenuated Tet-induced cell death (P<0.05). ROS levels were indeed increased in cells treated with Tet (10 μmol/L) for 6 and 12 h (P<0.01), while N-Acetyl-L-cysteine (NAC) decreased Tet-induced ROS (P<0.01). After ROS was inhibited by NAC, apoptosis rate was decreased compared with the control (P<0.01). Further study indicated that Tet inhibited PI3K/Akt pathway in retinoblastoma cells.Conclusion:Tet induces cell apoptosis via increasing ROS synthesis and inhibiting PI3K/Akt pathway.

A new clinical teaching mode of standardized treatment in colorectal cancer for fellows in training is reported here with good results. This one-year program included medical ethics education, humanistic management, pre job training, clinical thinking mode, surgery teaching, and computerized teaching. This new clinical teaching mode with distinct features is effective and introduced in this article.
Colorectal Neoplasms ; Education, Medical, Graduate ; Humans