A technique of laparoscopic gastrectomy with lymph node dissection for early invasive gastric cancer is described. A definitive answer concerning the appropriate level of lymph node dissection and the role of laparoscopic gastrectomy in the treatment of more advanced gastric cancer remains to be defined.

Patients with extrahepatic cholangiocarcinoma (EHCC) have a poor prognosis; postoperative survival depends on cancer progression and therapeutic resistance. The mechanism of EHCC progression needs to be clarified to identify ways to improve disease prognosis. Stathmin1 (STMN1) is a major cytosolic phosphoprotein that regulates microtubule dynamics and is associated with malignant phenotypes and chemoresistance in various cancers. Recently, STMN1 was reported to interact with p27, an inhibitor of cyclin-dependent kinase complexes. Eighty EHCC cases were studied using immunohistochemistry and clinical pathology to determine the correlation between STMN1 and p27 expression; RNA interference to analyze the function of STMN1 in an EHCC cell line was also used. Cytoplasmic STMN1 expression correlated with venous invasion (P = 0.0021) and nuclear p27 underexpression (P = 0.0011). Patients in the high-STMN1-expression group were associated with shorter recurrence-free survival and overall survival than those in the low-expression group. An in vitro protein-binding assay revealed that cytoplasmic STMN1 bound to p27 in the cytoplasm, but not in the nucleus of EHCC cells. Moreover, p27 accumulated in EHCC cells after STMN1 suppression. STMN1 knockdown inhibited proliferation and increased the sensitivity of EHCC cells to paclitaxel. STMN1 contributes to a poor prognosis and cancer progression in EHCC patients. Understanding the regulation of p27 by STMN1 could provide new insights for overcoming therapeutic resistance in EHCC.

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Extrahepatic cholangiocarcinoma (EHCC) is a cancer with a poor prognosis, and the postoperative survival of patients depends on the existence of invasion and metastasis. The epithelial-tomesenchymal transition (EMT) is an important step in EHCC invasion and metastasis. Forkhead box protein C2 (FOXC2) is a transcription factor that has been reported to induce the EMT. Therefore we examined the correlation between FOXC2 expression and clinical pathological factors, and analysed the function of FOXC2. The expression of FOXC2 in 77 EHCC cases was investigated by immunohistochemical staining, and the relationship between FOXC2 expression and clinicopathological factor was assessed. Knockdown by small interfering RNA (siRNA) was performed to determine the roles of FOXC2 in EHCC cell line. FOXC2 expression correlated with lymph node metastasis (P = 0.0205). Patients in the high FOXC2 expression group had a poorer prognosis than the patients in the low FOXC2 expression group. Moreover, FOXC2 knockdown inhibited cell motility and invasion, and decreased the expression of EMT markers (N-cadherin, and matrix metalloproteinase (MMP) -2) and Angiopietin-2 (Ang-2). The EMT inducer FOXC2 contributes to a poor prognosis and cancer progression. FOXC2 may be a promising molecular target for regulating EHCC metastasis. (Cancer Sci 2013; 104: 1427-1432 T he incidence and mortality of cholangiocarcinoma, a cancer with a poor prognosis, are rising worldwide.(1) The 5-year survival rates for cholangiocarcinoma is 10-40% overall.(2) Cholangiocarinoma is categorized into intrahepatic or extrahepatic cholangicarinoma, extrahepatic cholangiocarcinoma (EHCC), the latter of which consists of either a hilar tumor or a bile duct tumor. Surgical therapy is the only effective curative treatment of EHCC, and the postoperative survival has been shown to be dependent on the existence of invasion and lymph node metastasis.(3,4) Therefore, to improve patient prognoses, it is essential to elucidate the mechanisms of invasion and metastasis in EHCC.The epithelial to mesenchymal transition (EMT), whereby epithelial cells alter their morphology to resemble mesenchymal cells, is required for the invasion and metastasis of cancer cells. Epithelial to mesenchymal transition was first proposed as a central differentiation process in embryogenic morphogenesis.(5) Embryonic cells lose E-cadherin expression and acquire cellular rearrangements for their conversion into the motile fibroblastic cells that are integral to embryonic development, and these cells can migrate from their original position to establish new colonies. A number of reports have supported EMT as an essential mechanism that prompts the detachment of cancer cells from a primary site and permits their migration, invasion, and metastasis. (6,7) However, several reports have demonstrated that N-cadherin expression is more important for cancer metastasis than the expression of E-cadherin and or EMT inducers. (8,9) Previously, we described EMT in a cholangiocarcinoma cell line using recombinant tra...

A high platelet count on POD 7 was associated with a good response to splenectomy, but age at surgery, the time interval between diagnosis and splenectomy, and prior responses to corticosteroid were not. We suggest that long-term outcomes of splenectomy can easily be predicted by platelet counts on POD 7.