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Objective To evaluate the 7th edition American Joint Committee on Cancer/Union for International Cancer Control (AJCC/UICC) tumor node metastasis (TNM) staging system for gastric carcinoma with the 6th edition in Chinese population.Methods A total of 401 gastric cancer patients undergoing surgical resection was staged using the 6th and 7th edition AJCC TNM staging system,respectively.Homogeneity,discriminatory ability,and monotonicity of gradients of two systems were compared using linear trend x2 test,likelihood ratio x2 statistics,and akaike information criterion (AIC) calculations.To compare the accuracy of prognostic evaluation between the 6th and the 7th edition TNM staging system for gastric cancer.Results Significant difference in 5 years survival rate were observed according to the T/N classification using the 6th edition staging system,and there were similar survival curves between T1a and T1b according to the 7th T classification.There was not significant difference between the area under the curve (AUC) of the 6th and the 7th edition staging systems.Conclusions T staging and N classification according to the 7th edition showed better performance,but the 72 TNM staging system was not better in predictive accuracy.
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Metabonomics is a novel subject which develops after genomics,transcriptomics and proteomics.With its unique advantage,metabonomics has been used widely in screening diagnostic biomarker in a variety of tumors.At present,some diagnostic biomarkers are found in tissue,serum samples,urine samples and stool specimens of gastrointestinal cancer patients by metabonomics,which maybe helpful for the early diagnosis and individualized treatment of gastrointestinal cancer.
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Objective To explore the role of Beclin 1 and PTEN in gastric caicinoma genesis and the effects on prognosis.Methods The expression of Beclin 1 and PTEN in 199 gastric caicinoma specimens and corresponding adjacent noncancerous tissues were examined by tissue microarrays and immunohistochemistary,and the relation with gastric cancer was analyzed.The rate of Beclin 1 and PTEN expression in 15 fresh gastric carcinoma samples and corresponding adjacent noncancerous tissues were detected by Western blot.All the samples were from Changzheng Hospital.Results The Results of immunohistochemistary showed that the rates of Beclin 1 and PTEN positive expression in cancinoma tissues were 47.2％ (94/199) and 55.8％ (111/199),both were lower than that of adjacent noncancinoma tissues (94.5％,188/199 and 92.5％,184/199; P ＜ 0.01).The lower expression of Beclin 1 and PTEN in gastric carcinoma were associated with gender,differentiation degree,depth of tumor invasion,lymph node metastases and disease stage(P＜0.05).There was a positive correlation between Beclin 1 and PTEN expression in gastric carcinoma tissues (r =0.680,P＜0.01). The survival analysis indicated that Beclin 1 and PTEN were independent factors in determining the prognosis of gastric cancinoma patients.The 5-year survival rate of Beclin 1 positive patients was 67.0％ (63/94),and of negative patients was 33.3％ (35/105).The 5-year survival rate of PTEN positive patients was 71.2％ (79/111),and of negative patients was 21.6％ (19/88) ( all P＜0.001).The Results of Western blot indicated that the expression of Beclin 1 and PTEN in gastric carcinoma tissues were significantly lower than that in the adjacent noncarcinoma tissues ( all P＜0.001).Conclusion The abnormal expression of Beclin 1 and PTEN may be related to carcinogenesis and the development of gastric carcinoma.
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Phospholipase A2 (PLA2) is consisted of a large group of enzymes,which can hydrolyze Sn-2 ester bond of the phospholipids and have different structures and functions.According to the latest related researches,many subtypes of PLA2 express abnormally in a various of tumors and have a close relationship with cancer proliferation,apoptosis,invasion,metastasis and prognosis.Different subtypes have different effects on neoplasms.PLA2 can supply a new insight on cancer therapy.
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The hereditary diffuse gastric cancer (HDGC) is associated with CDHI (E-cadherin gene)germline mutations, and accounts for about one-third of the familial gastric cancer (FGC) cases. The other two thirds FGC cases which are not fit the diagnosis standard of HDGC remain lack of clear molecular diagnosis basis. The current disposal of prophylactic gastrectomy in FGC according to E-cadherins genetic counseling, has clinical significance only in part of HDGC.
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Objective:To investigate the understanding of cancer pain by medical doctors and its therapeutic status in Shanghai. Methods:We recruited 1 982 medical physicians from 106 secondary and tertiary hospitals in Shanghai city from January to March in 2007. The understanding and the therapeutic status of cancer pain were investigated by conducting a questionnaire survey and the results were statistically analyzed.Rusults:There were 52.3% physicians who believed that they understand the treatment protocol of the Three-step Analgesic Ladder regimen. The rate increased by 21.6 percentage point compared with the results in 1999. The understanding degree of oncologists was significantly better than non-oncologists. There were 16.8% physicians giving the correct answers on the three main principles of the dosage titration in analgesic management. The correct rate of oncologists was significantly higher than that of non-oncologists. Opium with strong analgesic effect had become the first choice for severe cancer pain, and the use of pethidine (Dolantin) for severe cancer pain decreased significantly.The pain was significantly relieved in 74.8% patients. The pain-relieving rate increased by 25.4 percentage point compared with the results in 1999. There were 81.1% medical doctors confirming the effect of pain treatment and among them oncologists were more optimistic to therapeutic outcome than others. There were 93.3% physicians who agreed that it was necessary to carry out the standardized training of cancer pain treatment and the requirement of non-oncologists were much emergent. The over-strict controls by the hospitals and the regulations were the main obstacles for using analgesic drugs.Conclusion:The understanding of medical doctors and the diagnostic and therapeutic levels of cancer pain were improved significantly compared with those in 1999. But more training of cancer pain treatment are still required to publicize the standardized therapy and overcome the obstacles of using analgesic drug.
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<p><b>BACKGROUND</b>Endostar™ (rh-endostatin, YH-16) is a new recombinant human endostatin developed by Medgenn Bioengineering Co. Ltd., Yantai, Shandong, P.R.China. Pre-clinical study indicated that YH-16 could inhibit tumor endothelial cell proliferation, angiogenesis and tumor growth. Phase I and phase II studies revealed that YH-16 was effective as single agent with good tolerance in clinical use.The current study was to compare the response rate , median ti me to progression (TTP) ,clinical benefit andsafety in patients with advanced non-small cell lung cancer ( NSCLC) , who were treated with YH-16 plus vi-norelbine and cisplatin (NP) or placebo plus NP.</p><p><b>METHODS</b>Four hundred and ninety-three histologically or cy-tologically confirmed stage IIIB and IV NSCLC patients , withlife expectancy > 3 months and ECOG perform-ance status 0-2 , were enrolledin a randomized ,double-blind ,placebo-controlled , multicenter trial ,either trialgroup : NP plus YH-16 (vinorelbine 25 mg/m² on day 1 and day 5 ,cisplatin 30mg/m² on days 2 to 4 , YH-167.5mg/m² on days 1 to 14) or control group : NP plus placebo (vinorelbine 25 mg/m² on day 1 and day 5 ,cis-platin 30 mg/m² on days 2 to 4 ,0.9% sodium-chloride 3 .75 ml on days 1 to 14) every 3 weeks for 2-6 cycles .The trial endpoints included response rate ,clinical benefit rate ,time to progression,quality of life and safety .</p><p><b>RESULTS</b>Of 486 assessable patients , overall response rate was 35.4% in trial group and 19.5% in controlgroup (P=0 .0003) . The median TTP was 6 .3 months and 3 .6 months for trial group and control group respectively (P < 0 .001) . The clinical benefit rate was 73 .3 %in trial group and 64.0% in control group (P=0 .035) .In untreated patients of trial group and control group ,the response rate was 40 .0% and 23.9%(P=0 .003) ,the clinical benefit rate was 76 .5 % and 65 .0 % (P=0 .023) ,the median TTP was 6 .6 and 3 .7months (P=0 .0000) ,respectively .In pretreated patients of trial group and control group ,the response ratewas 23.9% and 8.5%(P=0 .034) ,the clinical benefit rate was 65.2% and 61.7%(P=0 .68) ,the median TTP was 5 .7 and 3 .2 months (P=0 .0002) ,respectively . The relief rate of clinical symptoms in trial groupwas higher than that of those in control group ,but no significance existed (P > 0 .05) . The score of quality oflife in trial group was significantly higher than that in control group (P=0 .0155) after treatment . There were no significant differences in incidence of hematologic and non-hematologic toxicity , moderate and severe sideeffects betweentrial group and control group .</p><p><b>CONCLUSIONS</b>The addition of YH-16 to NP regimen results in significantly and clinically meaningful improvement in response rate , median time to tumor progression,and clinical benefit rate compared with NP alone in advanced NSCLC patients . YH-16 in combination with chemotherapy shows a synergic activity and a favorable toxic profile in advanced cancer patients .</p>
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Objective: To study the mechanism of inhibitory ef fect of ginsenoside Rg3 on tumor growth. Methods: The chick chor ioallantoic membrane(CAM) test and Lewis lung carcinoma model were used to inves tigate the inhibitory effect of Rg3 on tumor angiogenesis. Results: Rg3(0.1 or 0.5 mmol/L) obviously inhibited angiogenesis in the CAM. Treatmen t with Rg3 in vivo obviously inhibited Lewis lung carcinoma growth with the inhibition ratio from 23% to about 47%. We also observed that the angiogenesis in implanted Lewis lung carcinoma tissue decreased obviously after treated wit h Rg3 (5, 10, 20 mg/kg). Conclusion: Rg3 can obviously inhibit t he growth of Lewis lung cancer, the inhibitory effect partially due to the effec t of Rg3 inhibiting neovascularization induced by malignant tumor.
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Objective: To study the effect of arsenic trioxide (As2O3) on human pancreatic cancer cell proliferation and apoptosis (mainly early stage) in vitro. Methods: SW1990 cells line were trea ted with As2O3 at different concentration. Cell proliferation was evaluated by MTT and apoptosis by Annexin-Ⅴ-fluostaining, electron-microscopy, flow cytometry and immunocytochemical staining of Bcl-2 and Bax. Results: As2O3 and cisplatin had the same cytotoxity on SW1990. The cytotoxic effe ct on tumor cell was produced by induction of apoptosis. Twelve hours after cult ure with 10 μg/ml As2O3, much more SW1990 cells went into apoptosis than t he control. The apoptosis rate reached 24% after 48 h with the similar concentra tion of As2O3. Immunohistochemical study revealed that the expression of Bcl -2 was decreased after treated with As2O3. Conclusion: As 2O3 can depress the proliferation of SW1990 in vitro, mainly through the i nduction of apoptosis, and it is a potential agent for pancreatic cancer chemoth erapy.
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Now the targeted therapeutic drugs have become the hottest field in many kinds of cancer and appear to have the advantages of low toxicity and high efficiency. There are a lot of clinical trials on the efficiency and the side effects. This article focuses on the latest advances of the targeted drugs on digestive tract cancers.
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Although great achievement has been made on the diagnosis and treatment of malignant tumors,metastasis of tumor remains to be the major reason for treatment failure and death of their victims.The development of systematic biology and functional genomics give us a deeper understanding of the nature of metastasis at the molecular level.Based on the consensus reached on the metastasis mechanisms of cancer,including the genetic heterogeneity of cancer,pre-metastatic niche,epithelial-mesenchymal transition,anoikis resistance,angiogenesis and lymphangiogenesis,etc,the targeted therapy at molecular level should be emphasized,the treatment should target the tumor stem cells,and RNAi technique and other techniques should be used in clinical anti-metastatic therapy.
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Objective: To study the effect of arsenic trioxide (As 2O 3) on human pancreatic cancer cell proliferation and apoptosis (mainly early stage) in vitro . Methods: SW1990 cells line were treated with As 2O 3 at different concentration. Cell proliferation was evaluated by MTT and apoptosis by Annexin Ⅴ fluostaining, electron microscopy, flow cytometry and immunocytochemical staining of Bcl 2 and Bax. Results: As 2O 3 and cisplatin had the same cytotoxity on SW1990. The cytotoxic effect on tumor cell was produced by induction of apoptosis. Twelve hours after culture with 10 ?g/ml As 2O 3, much more SW1990 cells went into apoptosis than the control. The apoptosis rate reached 24% after 48 h with the similar concentration of As 2O 3. Immunohistochemical study revealed that the expression of Bcl 2 was decreased after treated with As 2O 3. Conclusion: As 2O 3 can depress the proliferation of SW1990 in vitro , mainly through the induction of apoptosis, and it is a potential agent for pancreatic cancer chemotherapy.