RELATIONSHIP BETWEEN LYMPH NODE METASTASES IN ESOPHAGEAL CARCINOMA AND ITS PROGNOSIS

Objective: To study the relationship between lymph node metastases in esophageal carcinoma and its prognosis. Methods: We obtained 1500 resected lymph nodes from the specimen of 86 patients with resected esophageal carcinoma and checked these lymph nodes by routine histopathology. Additiionally, frozen tissue sections of 540 lymph nodes classified as tumor-free by routine histopathology were screened for micrometastases by immunohistology with the monoclonal antibody Ber-EP4. Results: Forty-two patients (49%) had pN0 disease, and 61 patients (71%) had lymph node micrometastases detected by immunohistochemistry, skip metastases detected by routine histopathology were present in 26%(11/42) of pN0 and 41%(18/44) of pN1 patients. Skipping of micrometastases detected by immunohistochemistry was found in 71%(61/86). Twenty-six of 42 patients (62%) with tumor staged as pN0 and 35 of 44 patients (80%) with stage pN1 had nodal micrometastasis. The presence of micrometastases was associated with a significantly decreased relapse-free time and overall survival (P<0.0001 and P=0.004, respectively). Conclusion: Lymph node skip metastases are a frequent event in esophageal carcinoma. Extensive lymph node sampling, in conjunction with immunohistochemical detection, will lead to accurate staging and prognosis.

Optimal therapeutic dose and time window of picroside II in cerebral ischemic injury

A preliminary study from our research group showed that picroside II inhibited neuronal apop- tosis in ischemic penumbra, reduced ischemic volume, and improved neurobehavioral function in rats with cerebral ischemia. The aim of the present study was to validate the neuroprotective effects of picroside II and optimize its therapeutic time window and dose in a rat model of cerebral ischemia. We found that picroside Ⅱ inhibited cell apoptosis and reduced the expression of neuron-specific enolase, a marker of neuronal damage, in rats after cerebral ischemic injury. The optimal treatment time after ischemic injury and dose were determined, respectively, as follows： （1） 2.0 hours and 10 mg/kg according to the results of toluidine blue staining; （2） 1.5 hours and 10 mg/kg according to early apoptotic ratio by flow cytometry; （3） 2.0 hours and 10 mg/kg according to immunohistochemical and western blot analysis; and （4） 1.5 hours and 10 mg/kg according to reverse transcription polymerase chain reaction. The present findings suggest that an intraperitoneal injection of 10 mg/kg picroside II 1.5-2.0 hours after cerebral ischemic injury in rats is the optimal dose and time for therapeutic benefit.

Detection of multidrug resistant gene 1 in pancreatic cancer

BACKGROUND: The results are conflicting in detecting P-glycoprotein (P-gp) in pancreatic cancer. The aim of this study was to detect the expression of multidrug resis- tant gene 1 ( MDR1) in pancreatic cancer cell lines. METHODS: MDR1 mRNA and P-gp were detected by re- verse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical assay (IHC) in three pancreatic cancer cell lines SW1990, CAPAN-1 and P3. P-gp func- tions were evaluated through the rhodamine extrusion test. RESULTS: Two of the three cell lines expressed MDR1 po- sitively at different levels. The rhodamine extrusion test showed that the percentage of positive cells in MDR(+) cells was significantly lower than that in MDR1 (-) cells. The results of IHC, RT-PCR and the rhodamine extrusion test were consistent with each other. CONCLUSION: All of these methods are reliable in the de- tection of MDR1 in pancreatic cancer tissue, thus providing a guide for clinical chemotherapy of pancreatic cancer.