Background: Hepatic cysts in located posterior segments close to the diaphragm (IVa, VII, and VIII) reportedly have a high recurrence rate. Presently, laparoscopic omentoplasty is the accepted technique; developed from laparoscopic deroofing, which places a viable pedicle flap of omentum to prevent cyst closure. However, potential adhesions have made laparoscopic omentoplasty less favorable. In this paper, we report on an improved surgical technique involving lauromacrogol sclerosis directly under laparoscopic fenestration. We also review and evaluate the efficacy and feasibility of this refined surgical approach.Methods: Data from 49 patients admitted to the Department of Hepatobiliary Surgery at the Affiliated Hospital of Jiangnan University from October 2015 to June 2020 with simple hepatic cysts located in the IVa, VII, and VIII segments were retrospectively analyzed. All patients were symptomatic before admission.They were separated into two groups based on the surgical approach they had received; refined laparoscopic lauromacrogol sclerotherapy or laparoscopic omentoplasty, and were compared and evaluated in terms of the postoperative cyst volume and quality of life.Results: No significant differences in sex, age, preoperative cyst volume, surgery duration, hospital stay, and bleeding volume were reported. There were no deaths or major complications in both groups. The postoperative cyst volume was significantly reduced in the laparoscopic lauromacrogol sclerotherapy group (2.48 cm) compared to the laparoscopic omentoplasty group (3.90 cm). This study evaluated both the immediate and medium-term results with a 3-12 months follow-up period for all patients. The cyst volume change in the laparoscopic lauromacrogol sclerotherapy group was found to be significantly greater than that of the laparoscopic omentoplasty group. The feedback regarding quality of life did not vary significantly between the two groups, except for general health and health change, where patients who received laparoscopic sclerotherapy responded with higher scores. Conclusions:Our results indicate that laparoscopic lauromacrogol sclerotherapy surgery was safe and effective in patients with IVa, VII and VIII segment simple hepatic cysts.

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RAS plays an important role in the carcinogenesis of colorectal epithelial cells, but RAS mutations are only present, at most, in approximately 50% of patients. In order to compare the gene mutation profiles of patients with or without a KRAS mutation, the clinicopathological data of 858 patients and NGS test results of 1697 patients with colorectal cancer were used in this analysis. In 858 patients, the mutation rate of KRAS was 50.8% (i.e., 436/858). Only 2 out of 349 (0.5%) KRAS mutant patients had a BRAF mutation, while 25 out of 422 (5.9%) KRAS wild-type patients had a BRAF mutation (p < 0.0001). The median OS of patients with a mutant or wild-type KRAS were 83.47 months and not reached, respectively (HR: 0.8147; 95% CI: 0.6271–1.051; p = 0.1153). The NGS results showed that in RAS mutant patients, genes with a high mutation rate mainly included APC, TP53, PIK3CA, Smad4, and Fbxw7, and in RAS wild-type patients, genes with a high mutation rate mainly included TP53, APC, LRP1B, MYC, and BRAF. The mutation rates of BRAF and EGFR in the RAS wild-type group were 15% and 9%, respectively, while they were only 3% in the RAS mutant group. The mutation rate of PIK3CA in the RAS mutant group was 31%, while that in the RAS wild-type group was 14%. The mutation rate of APC was 72.2% (i.e., 687/952). The mutation rate of the gene, RNF43, in the APC wild-type group was 5.23 times higher than that in the APC mutant group, and the gene, NSD1, in the APC wild-type group was 0.07 times higher than that in the APC mutant group. The mutation rate of TP53 was 78.2% (i.e., 744/952). The mutation rate of MLH1 in the TP53 wild-type group was 8.42 times higher than that in the TP53 mutant group, which was significantly higher than that in the TP53 mutant group. Generally, the gene mutation profiles were significantly different between KRAS mutation and wild-type colorectal cancer patients. A single gene mutation may be sufficient to cause the dysfunction of a signal transduction pathway, and APC, TP53, or RAS are not necessary for the carcinogenesis of sporadic colorectal cancer.