Objective To investigate the expression of β-catenin and Oct-4 in colonal carcinoma and explore the relationship with recurrence and metastasis after operation. MethodsImmunohistochemical analysis was used to evaluate the expression of β-catenin and Oct-4.The correlation of β-catenin and Oct-4 expression with tumor cell differentiation,T stage,N stage and metastasis was analyzed.The gene expression of Oct-4 was examined by RT-PCR in 20 frozen tumor tissues and normal tissues adjacent to tumor.Results Thirty-five patients had metastasis. The positive rates of β-catenin and Oct-4 expression were significantly higher in metastasis group than in the non-metastasis group (65.71％ vs 31.11％,51.43 ％vs 13.33 ％,x2 =9.843,P =0.002,x2 =13.605,P =0.001).Expression of β-catenin and Oct-4 was not associated with differentiation,T stage or N stage.The positive expression rate of Oct-4 in colonal carcinoma tissues was significantly higher than that in normal tissues.Metastatic rates in patients with positive expression of β-catenin and Oct-4 was higher than that in negative expression.The survival analysis showed that time of metastasis was significantly different in two groups of patients (P ＜0.05).Conclusion The expression of β-catenin and Oct-4 in tumor tissues is related to metastasis of colonal cancer after surgery and might be used to predict metastasis of colonal cancer after operation.

Primary esophageal small cell carcinoma (PESCC) is a rare disease first described by McKeown in 1952. PESCC is characterized by high malignancy, distant metastasis, and poor prognosis. The incidence of PESCC has significantly increased world-wide in recent years. However, practice guidelines that concern the histological origin, clinical diagnosis methods, therapies, and prog-nosis of PESCC are still not well established because of the paucity of cases and lack of large prospective randomized research. This ar-ticle aims to outline recent advances in the clinical and therapeutic aspects of PESCC as well as review the different opinions concerned to better understand PESCC and solve clinical problems.

Objective To compare the short-term efficacy and adverse effects of docetaxe or oxaliplatin combined with capecitabine in the treatment of late-staged gastric cancer in aged patients. Methods Eighty-two aged patients with late-staged gastric cancer were randomly divided into two groups,of which 38 patients were treated group) ,and 44 patients were treated with oxaliplatin (100 mg/m2 ivgtt on 1st day) and eapecitabine (2000 mg/1 cycle). Results There is no failure of follow-up. In the docetaxe group,the effective rate was 52.63% (20/38) and 54.55 % (24/44) for the docetaxe and oxaliplatin group,respectively (P>0.05). The median progression-free survival(PFS) in the docetaxe group (6.1 months) was similar to that in the oxaliplatin group (6.3 months) (P>0.05). Gastrointestinal response,myelosuppression and neurotoxicity (Ⅰ or Ⅱ level) were the most common ad-verse effects observed in both groups (P>0.05). No chemotherapy-related death was observed. Conclusions The short-term efficacy of decetaxe or oxaliplatin combined with capecitabine in the treatment of late-staged gastric cancer in aged patients is similar,and the adverse effects are all within tolerance limits.

Background and purpose:Rectal small cell carcinoma is high malignant tumor and prone to early metastasis. It is rare in the clinical and its prognosis is poor. The aim of this article was to analyze clinical characteristics and summarize the diagnosis,treatment and prognosis of rectal small cell carcinoma.Methods:Clinical data of 16 cases with rectal small cell carcinoma conifrmed by pathology from Jan. 2001 to Jan. 2013 in the Tumor Hospital Affiliated to Zhengzhou University Hospital were analyzed retrospectively.Results:Among the 16 rectal small cell carcinoma patients (mean age is 58.5 years), 9 were male, 7 were female; 4 cases in stageⅡ, 7 cases in stageⅢ and 5 cases in stageⅣ. Ten cases underwent surgical treatment, of which 6 cases underwent radical surgery, 4 cases underwent palliative surgery;6 cases received chemotherapy alone, 2 cases received chemoradiotherapy, 2 cases did not receive any treatment postoperatively. Five cases were lost opportunity for operation, of which 3 cases underwent chemotherapy alone and 2 cases underwent chemoradiotherapy. One case did not receive any treatment. Among 10 cases of resection of the lesions, 5 cases had vascular invasion and 7 cases had local lymph node metastasis. All patients received 7-65 months of follow-up. The median survival was 15.4 months. The 6 months, 1 year, 2 years, 3 years and 5 years survival rates were 58.4%, 46.2%, 26.6%, 13.1% and 6.2% respectively. The prognosis of patients was associated with tumor staging, presence of vascular invasion and lymph node metastasis, and type of operation (P<0.05); but not related to age, gender and tumor size (P>0.05).Conclusion:The biologic behavior of rectal small cell carcinoma which is a rare disease and similar to small cell lung cancer, and its prognosis is poor. Treatment methods include surgery, radiotherapy and chemotherapy. The overall result is poor.

Objective To investigate the effects of mechanism of silent information regulator of transcription 1 (SIRT1) in the drug-resistance of colonic cancer.Methods The clinical data of 25 colonic cancer patients with 5-Fu-resistance and 30 colonic cancer patients with chemosensitivity who were admitted to the Henan Tumor Hospital from December 2012 to December 2013 were retrospectively analyzed.The specimens of colonic cancer were collected for study.(1) The protein expression of SIRT1 in patients with drug-resistance or chemotherapeutic sensitivity was tested by immunohistochemical staining.The protein expression of SIRT1 in the HCT116 and HCT1 16/5-FU cells was detected by Western blot.(2)HCT116/5-FU cells were interfered by siRNA and divided into the blank control group (cells untreated),the empty vector group (cells treated by siRNA) and the SIRT1 silence group (cells treated by SIRT1 siRNA).The protein expression of the HCT116/5-FU cells were inhibited by the c-Jun N-terminal kinase (JNK) and then divided into the SP600125 group [cells were treated by JNK signaling pathway inhibitor SP60012 (concentration:30 μmol/L)for 12 hours],the DMSO group [cells were treated by DMSO (cells were treated by 0.1％ DMSO for 12 hours] and the control group (cells were treated by cell culture media).(3) Serine in the SIRT1 ser47 was mutated to alanine or aspartic acid,and mutations S47A (S47A group,serine to alanine) and S47D (S47D group,serine to aspartic acid) ; Untransfected HCT116/5-FU cells were in the S47 wild type group,and apCMV-3Tag-3 cells transfected by empty vector were served as negative control; all the HCT116/5-FU cells were interfered by 5-FU (concentration:8 μmol/L) for 12 hours.HTC116 cells and HTC116/5-FU cells were treated by SIRT1 inhibitor resveratrol at concentrations of 0,1,10,50,100 nmol/L and SIRT1 activator niacinamide at concentrations of 0,1,2,3,4,5 ng/L.Cell proliferation was detected by MTF.(4) Cell apoptosis was detected by flow cytometry.(5) The expressions of related genes were detected by real-time PCR.(6)The expressions of related proteins were detected by western blot.The count data were analyzed using the chi-square test.The measurement data with normal distribution were presented as (x) ± s.The comparison among groups were analyzed using the one-way analysis of variance and LSD-t test.The pairwise comparisons were analyzed using the t text.Results (1) The results of immunohistochemical staining were as follows.The positive expressions of SIRT1 in patients with chemotherapeutic sensitivity and drug-resistance were 16.7％ (5/30) and 92.0％ (23/25),respectively,with significant difference (x2 =30.965,P ＜ 0.05).The relative mRNA and protein expressions of SIRT1 in HCT116/5-FU cells with drug-resistance were 1.870 ± 0.100 and 1.660 ± 0.109,which were significantly higher than 1.000 ± 0.070 and 1.000 ± 0.050 in HCT116/5-FU cells without drug-resistance (t =11.721,8.963,P ＜ 0.05).(2) The results of MTT were as follows.The proliferation rates of HCT116/5-FU cells treated by resveratrol at concentrations of 0,1,10,50 nmol/L were 100％ ±12％,105％± 14％,129％ ± 10％ and 144％ ± 17％,which were significantly higher than 41％ ± 10％,49％ ±11％,74％ ± 16％ and 105％ ± 17％ of HCT116 cells which were treated by reseratrol at the same contrations (t =8.226,-7.236,6.673,3.510,P ＜0.05).The proliferation rates of HCT116/5-FU cell treated by niacinamide at concentrations of 0,1,2 ng/L were 87％ ± 12％,78％ ± 12％,69％ ± 11％,which were significantly higher than 36％ ± 6％,32％± 5％,30％± 6％ of HCT116 cells which were treated by niacinamide at the same concentrations (t =-8.593,-8.006,-7.000,P ＜ 0.05).The proliferation rates of HCT116/5-FU cells in the blank control group,the empty vector group and the SIRT1 silence group were 100％± 8％,99％ ±9％,37％ ± 6％,with significant differences among the 3 groups (F =66.597,P ＜ 0.05),and the proliferation rate of HCT116/5-FU cells in the SIRT1 silence group was significantly lower than that in the blank control group (t =10.113,P ＜0.05).(3) The results of flow cytometry were as follows.The apoptotic rates of HCT116/5-FU cells in the SIRT1 silence group,the empty vector group and the blank control group were 60％ ± 5％,36％ ± 4％,35％ ±4％,with significant differences among the 3 groups (F =36.549,P ＜ 0.05),and the apoptotic rates of HCT1 16/5-FU cells in the SIRT1 silence group were significantly higher than that in the blank control group and the empty vector group (t =-7.215,-7.084,P ＜0.05).(4)The results of RT-PCR were as follows.The relative expression rates of P-gp mRNA in the HCT116/5-FU cells in the SIRT1 silence group,the empty vector group and the blank control group were 0.320 ± 0.030,0.990 ± 0.060,1.000 ± 0.090,with significant differences among the 3 groups (F =10.107,P ＜ 0.05),and the relative expression rate of P-gp mRNA in the SIRT1 silence group was significantly lower than that in the blank control group (t =11.463,P ＜ 0.05).The relative expression rates of P-gp mRNA in the HCT116/5-FU cells in the SP600125 group,the DMSO group and the control group were 0.240 ±.0.040,0.990 ± 0.100,1.000 ± 0.070,with significant difference among the 3 groups (F =19.002,P＜0.05),and the relative expression rates of P-gp mRNA in the SP600125 group was significantly lower than that in the control group (t =7.301,P ＜0.05).(5) The results of western blot were as follows.The relative expression rates of p-JNK protein in the HCT116/5-FU cells in the blank control group,the empty vector group and the SIRT1 silence group were 1.000 ± 0.090,1.090 ± 0.020,0.080 ± 0.010,with significant difference among the 3 groups (F =12.130,P ＜ 0.05).The ratios of p-SIRT1-S27/T-SIRT1,p-SIRT1-T530/T-SIRT1,p-SIRT1-S47/T-SIRT1 were 1.158 ±0.140,1.209 ±0.150,3.760 ±0.150 in HCT116 cells treated by 5-FU,and 1.120 ±0.109,1.130 ±0.100,2.160 ±0.110 in HCT116 cells treated by DMSO,with significant differences (F =9.763,10.261,P ＜0.05).The ratios of p-SIRT1-S47/T-SIRT1 in HCT116 cells treated by 5-FU and DMSO were 3.760 ± 0.150 and 2.160 ± 0.110,which were significantly higher than 0.940 ± 0.040 and 1.121 ± 0.110 in HCT116/5-FU cells (t =14.721,21.335,P ＜ 0.05).(6) The proliferation rates of HCT116/ 5-FU cells in the S47 wild type group,the negative control group,the S47A group and the S47D group were 41％± 31％,39％ ± 4％,64％ ± 2％ and 26％ ± 5％,with significant differences among the 4 groups (F =6.371,P ＜ 0.05).Conclusions SIRT1 promotes the proliferation of drug-resistant colonic cancer cells and increases the expression of P-gp via JNK signaling pathway,there by enhances cellular drug resistance.SIRT1 S47 is the critical site for 5-FU-resistance in HCT116/5-FU cells.

Objective To investigate the relationship between RAD51 135G ＞ C polymorphism and prognosis in triple-negative breast cancer patients by retrospective analysis.Methods The clinical data of 62 triplenegative breast cancer patients were collected.The 62 cases underwent standard chemotherapy and radiotherapy after tumor resection from Jan.2004 to Dec.2010 in Affiliated Cancer Hospital of Zhengzhou University.RAD51 135G ＞ C polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RELP) technology.The survival curve about progress free and overall survival time were then made.Results The median progress free and overall survival time in triple-negative breast cancer patients with or with-out RAD51 135G ＞ C polymorphism were(77.00 ±5.55)and(89.00 ± 10.40) months vs(99.00 ±4.26)and (103.00 ±4.30) months.The difference had statistical significance(P =0.039 and 0.015 respectively).Conclusion RAD51 135G ＞ C polymorphism is related with prognosis of triple-negative breast cancer patients,which might be a prognostic factor for breast cancer.

BACKGROUNDChemotherapy is an important treatment for un-resectable lung cancer patients. The aim of this study is to investigate effects and safety of weekly paclitaxel/cisplatin as first-line chemotherapy in un-resectable non-small cell lung cancer (NSCLC).

METHODSThirty-eight initially treated patients (male/female: 20/18) with un-resectable NSCLC were enrolled for the study. They were at ages ranging from 33 to 82 years old with ECOG PS of 0 to 2. Paclitaxel 80mg/m² was given by intravenous infusion on 1st and 8th day, and cisplatin 25mg/m² on 2th to 6th days, 3 to 4 weeks was one cycle. The responses and toxicity of chemotherapy were evaluated after six cycles and the patients were followed up.

RESULTSIn 38 patients, partial response and complete response were observed in 21 cases and 1 case, respectively with overall response rate of 57.9%. The response rate in cases with ECOG of 0 to 1 was significantly higher than those with ECOG PS of 2 (69.0% vs 22.2%). Median survival time was 14 months and 1-, 2- and 3-year survival rate were 63.8%, 29.5% and 16.2% respectively. Main Toxicities were leucopenia and alopecia, and all patients could tolerate the side effects and there was no drug-related death associated with myelotoxicity.

CONCLUSIONSRegimen of paclitaxel/cisplatin was efficient and safe as the first-line treatment for un-resectable NSCLC patients.

Background and purpose: In recent years indirubin-3'-monoxime has been found to be capable of inhibiting some cell proliferation in vitro and in vivo studies, but human colon cancer HT-29 cells, therefore the purpose in this paper was to study the effect of indirubin-3'-monoxime on proliferation and apoptosis of HT-29 cells and its associated mechanism. Methods: HT-29 cells were treated with indirubin-3'-monoxime. The proliferative status of cells was measured by methabenzthiazuron (MTT) assay, flow cytometry (FCM) was used to measure the apoptosis rate. RT-PCR was used to measure the transcription of apoptosis suppressor gene bcl-2, survivin and apoptosis promoting gene Bar. Results: Indimbin-3'-monoxime inhibited growth of HT-29 cells in a dose-dependent and time-dependent manner (F=11.25, P<0.01). The apoptosis rate increased after the treatment by indirubin-3'-monoxime at 10 μmol/L. There were significant differences between different time groups (F=195.25, P<0.01). The transcription of survivin (F=78.75, P<0.01) and Bax (F=87.61, P<0.01) mRNA in HT-29 cells were increased; the transcription of bcl-2 was significantly decreased (F=95.82, P<0.01). Conclusion: Indirubin-3'-monoxime has obviously inhibited proliferation and induce apoptosis of colon cancer HT-29 cells, its mechanism may be related to decrease the bcl-2/Bax ratio.

BACKGROUND:Abdominal incision healing is not only related with the patient’s own situation, but also closely related with the surgeon's suture technique, suture method, choice of stitches. ＜br> OBJECTIVE:To compare the absorbable sutures and silk sutures for abdominal incision. ＜br> METHODS:Total y 153 colorectal cancer patients, including 91 males and 62 females, aged 30-82 years, were randomly divided into observation group (n=78) and control group (n=75). An abdominal midline incision was made in al patients receiving radical surgery of colorectal cancer. The Vicryl suture and silk suture were respectively used in the observation and control groups for abdominal incision closure. Suturing time, length of hospital stay, incision infection, disruption of wound, fat liquefaction of wound and rejection were compared between two groups. ＜br> RESULTS AND CONCLUSION:The suturing time and length of hospital stay were less in the observation group than the control group (P＜0.05). In the observation group, there were three cases of incision infection, but no incision dehiscence and rejection occurred;in the control group, there were 10 cases of incision infection, 4 cases of incision dehiscence, and 5 cases of rejection. A significant difference was found in the incision infection, dehiscence and rejection between the two groups (P＜0.05). Hospitalization expenses and fat liquefaction of incision had no difference between the two groups. these findings indicate that the Vicryl plus as an absorbable suture is simple, effective and safe that can promote wound healing and reduce complications.

Objective: To explore the clinical characteristics, treatment strategy and prognosis of adenoid cystic carcinoma of the head and neck (ACCHN). Methods: A retrospective analysis of the clinical and follow-up treatment of 79 patients with ACCHN from June 2008 to July 2017 was conducted in the Cancer Hospital of Zhengzhou University. Results: A total of 79 ACCHN cases, including 31 males and 48 females. The age ranged from 19 to 77 (median, 52). The clinical manifestations of ACC were related to the locations of primary tumor.The mean size of the tumor was 2.6 cm (range from 1.5 to 7.7 cm). 50 of 79 patients with a definitive pathological diagnosis received surgical resection. 59 cases received chemotherapy and 62 cases received radiotherapy. With a median follow-up of 55 months, the 5-year, 10-year survival rate of these patients were 69.6% and 54.4%, respectively. Conclusions ACCHN is an uncommon neoplasm with the characteristics of epithelial nerve growth, being inclined to distant metastasis, and high early misdiagnosis rate. The clinical manifestation, imaging and pathological result are need to be combined together to diagnose ACCHN.