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Purpose: The aim of this study is to compare the short-term and pathological outcomes of TPLRC (Three-port laparoscopic right hemicolectomy) and FPLRC (Five-port laparoscopic right hemicolectomy), using propensity score matching analysis. Methods: One hundred and sixty-eight patients who accepted laparoscopic right hemicolectomy with either three ports or five ports from January 2013 to October 2017 were non-randomly selected and analyzed retrospectively. Propensity score matching model was used to eliminate the patients' selection bias between two groups. Results: A total of 168 patients were involved. After propensity score matching, 39 for each group were compared. The number of harvested lymph nodes was significantly larger in the TPLRC group than in the FPLRC group (18.36 ± 8.58 vs. 14.90 ± 6.63, p = 0.048). A lower mean operative time was observed in the TPLRC group (136.24 ± 26.78 vs. 168.64 ± 43.68 min, p < 0.001). A less blood loss in the TPLRC group (62.44 ± 55.17, 135.54 ± 139.11 ml, p = 0.003). No significant differences in the other short-term outcomes between the two groups. Conclusions: TPLRC is a safe and feasible surgical procedure with similar results of FPLRC in short-term clinical outcomes. TPLRC has the advantages of shorter operative time, less blood loss and larger number of harvested lymph nodes. A randomized prospective clinical trial of long-term outcomes of TPLRC is required to further prove the present results. [ABSTRACT FROM AUTHOR]

Objectives: Colorectal cancer (CRC), one of the most aggressive gastrointestinal malignancies, is a frequently diagnosed life-threatening cancer worldwide. Most CRC patients have poor prognosis mainly because of frequent metastasis and recurrence. Thus, it is crucial to find out some new biomarkers and to show deeper insights into the mechanisms of CRC. MLLT10, Myeloid/lymphoid or mixed-lineage leukemia translocated to 10, also known as AF10, a recurrent MLL partner. In this study, we found that MLLT10 promotes CRC tumor invasion and metastasis both in vitro and in vivo. Methods: Here, the expression of MLLT10 was evaluated by immunohistochemistry. Then, the plasmid and lentivirus particles for MLLT10 overexpression or knockdown were designed and constructed into SW620 and HT29 cells. Finally, cell proliferation assay, cell adhesion assay, transwell migration, and invasion assay were used to detect the migration and invasion ability of MLLT10 in CRC cells. A tail vein injection assay was employed to evaluate the role of MLLT10 in tumor metastases. Results: MLLT10 expression was significantly higher in CRC tissues than in noncancerous tissues and was associated with some clinicopathological factors. In vitro, the overexpression of MLLT10 promoted CRC cell migration and invasion, while after MLLT10 was knocked down, the opposite results were observed. Furthermore, we used animal metastasis models to detect the function of MLLT10 in vivo, the results are same with the outcomes in vitro. In lung metastasis sites, the knockdown of MLLT10 in SW620 cells significantly inhibited Vimentin expression, whereas the E-Cadherin was increased. Conclusions: These results indicate that MLLT10 regulates the metastasis of CRC cells via EMT. [ABSTRACT FROM AUTHOR]