Objective:To explore the possibility and methods of surgical treatment(ST) for huge primary liver cancer(HPLC).Methods:The clinical data of 86 HPLC were analyzed retrospectively and the main challenges as well as their counter measures during ST are concluded.Results:Among the 86 cases,there were 10 cases which complicated with portal vein(PV),and 5 cases with IVC thrombus respectively;there were 76 cases with HBV cirrhosis,2 HCV cirrhosis,there were 60 and 26 cases of primary and secondary hepatectomy in which included regular right(9 cases),left hemihepatectomy(8 cases)and combined hepatectomy(69 cases).Six cases received PV embolism before surgery.There were 10 and 5 cases of cancer thrombus extraction from PV and IVC respectively.In this group,81 patients were cured,and the perioperative mortality was 5.8%(5/86).The postoperative one—year survival rate for the patients was 77.9%.Conclusions:ST for HPLC is safe and acceptable.Full of preoperative assessment,careful intraoperative exploration,and surgical skill played a key roles.

Pituitary tumors are usually benign but can occasionally exhibit hormonal and proliferative behaviors. Dysregulation of the G1/S restriction point largely contributes to the over-proliferation of pituitary tumor cells. F-box protein S-phase kinase-interacting protein-2 (SKP2) reportedly targets and inhibits the expression of p27(Kip1), a well-known negative regulator of G1 cell cycle progression. In this study, SKP2 expression was found to be upregulated while p27(Kip1) expression was determined to be downregulated in rat and human pituitary tumor cells. Furthermore, SKP2 knockdown induced upregulation of p27(Kip1) and cell growth inhibition in rat and human pituitary tumor cells, while SKP2overexpression elicited opposite effects on p27(Kip1) expression and cell growth. The expression of microRNA-186 (miR-186) was reported to be reduced in pituitary tumors. Online tools predicted SKP2 to be a direct downstream target of miR-186, which was further confirmed by luciferase reporter gene assays. Moreover, miR-186 could modulate the cell proliferation and p27(Kip1)-mediated cell cycle alternation of rat and human pituitary tumor cells through SKP2. As further confirmation of these findings, miR-186 and p27(Kip1) expression were downregulated, while SKP2 expression was upregulated in human pituitary tumor tissue samples; thus, SKP2 expression negatively correlated with miR-186 and p27(Kip1) expression. In contrast, miR-186 expression positively associated with p27(Kip1) expression. Taken together, we discovered a novel mechanism by which miR-186/SKP2 axis modulates pituitary tumor cell proliferation through p27(Kip1)-mediated cell cycle alternation.
Animals ; Cell Cycle ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p27 ; Genes, Reporter ; Humans ; Luciferases ; Pituitary Neoplasms ; Rats ; Up-Regulation