Effect of Transumbilical Single-Port Laparoscopic-Assisted Duhamel Operation on Serum CRP and IL-6 Levels in Children with Hirschsprung's Disease.

Objective: To explore the clinical intervention effect of transumbilical single-port laparoscopic-assisted Duhamel operation on children with Hirschsprung's disease (HD) and to analyze the effect of treatment on children with serum C-reactive protein (CRP) and interleukin-6 (IL-6) effects. Methods: Retrospectively select 80 children with HD who underwent surgery in our hospital from May 2017 to May 2020 as the research subjects and they are classified as group A according to the difference of the children's surgical procedures (receiving transumbilical single-port laparoscopic-assisted Duhamel surgery, 40 cases) and group B (receiving conventional laparoscopic surgery, 40 cases), compare the perioperative period (operating time, intraoperative blood loss, surgical posthospitalization, and postoperative gastrointestinal function recovery time), early postoperative complications (perianal dermatitis, urinary retention, enterocolitis, and anastomotic leakage), and late postoperative complications (anastomotic stenosis, dirty stool, recurrence of constipation, and enterocolitis), compare the differences in the levels of CRP and IL-6 between the two groups of children before and after the operation, and conduct a 1-year follow-up of the two groups of children to compare the long-term defecation status. Results: The surgical time of children in group A, postoperative hospitalization time, and postoperative gastrointestinal function recovery time were significantly shorter than those of group B, and the differences between groups were statistically significant (P < 0.05). A group of patients: the total incidence of postearly complications was 5.00% lower than 22.50% (P < 0.05) in group B (P < 0.05), and the total incidence of previous complications after group A of patients was 10.00% lower than 27.50% of group B (P < 0.05). The two groups of serum CRP and IL-6 in two groups were not statistically significant (P > 0.05), and the serum CRP and IL-6 levels of children in group A after surgery were 3 days. It is obviously lower than those in group B, and the differences between groups have statistical significance (P < 0.05). At 1 month after surgery, the average bowel movement time in group A is significantly lower than those of group B (P < 0.05); during the 1-12 months, the difference between the defecation frequency group of the group A and group B did not have statistically significance (P > 0.05). Conclusion: Transumbilical single-port laparoscopic assistant Duhamel operation of HD has a good intervention effect, compared to traditional laparoscopic surgery, the operation time, postoperative hospitalization time, and postoperative gastrointestinal function recovery time, and also help to reduce postoperative near-long complications The incidence improves the stress reactions and long-term defecation functions in children.

Coexpression of receptor tyrosine kinase AXL and EGFR in human primary lung adenocarcinomas.

AXL has been identified as a tyrosine kinase switch that causes resistance to inhibitors targeting epidermal growth factor receptor (EGFR) signaling in non-small cell lung cancer (NSCLC). However, the relationship between 2 receptor tyrosine kinases, AXL and EGFR, and the relevance of AXL expression with EGFR mutation status in treatment-naive human NSCLCs remain uncertain. In this study, we evaluated the coexpression pattern of AXL, EGFR, and pEGFR(1068) in 109 lung adenocarcinoma patients with or without an EGFR mutation. There were 68 (62.4%) patients with tumors harboring EGFR mutations such as 19 del and/or L858R; 2 patients were T790M positive. The expression of AXL, EGFR, and pEGFR(1068) was detected in 60 (55%), 68 (62.4%), and 57 (52.3%) of 109 patients, respectively. The positive rates of EGFR and pEGFR(1068) were associated with the L858R mutation alone or with the 19 del and L858R mutation status. Further analysis indicated that the percentage of AXL(+)/EGFR(+)/pEGFR(1068) coexpression in 68 EGFR-activating mutations patients was significantly higher than that in 39 EGFR wild-type patients (30.9% versus 10.3%, P=.015). Furthermore, in the subgroup of AXL(+) patients (35 mutation(+) and 23 wild-type patients), the coexpression rates of AXL(+)/pEGFR(1068+) and AXL(+)/EGFR(+)/pEGFR(1068+) in patients with EGFR mutations were significantly higher compared with those in wild-type patients (both P<.05). Our study emphasized that the AXL and EGFR receptor tyrosine kinases were coexpressed in a subgroup of treatment-naive lung adenocarcinomas with or without EGFR mutations. Anti-AXL therapeutics delivered up front in combination with an EGFR inhibitor might prevent or delay resistance in patients with AXL-positive, EGFR-mutant, or wild-type NSCLC.

Pim-1 kinase is a target of miR-486-5p and eukaryotic translation initiation factor 4E, and plays a critical role in lung cancer.

BACKGROUND: Pim-1 kinase is a proto-oncogene and its dysregulation contributes to tumorigenesis and progression of a variety of malignancies. Pim-1 was suggested as a therapeutic target of cancers. The functional relevance of Pim-1 and the mechanism underlying its dysregulation in lung tumorigenesis remained unclear. This study aimed to investigate if Pim-1 has important functions in non-small-cell lung cancer (NSCLC) by: 1) evaluating the clinicopathologic significance of Pim-1 through analysing its expression in 101 human NSCLCs tissues using quantitative PCR, Western Blot and immunohistochemical studies, 2) determining its role in NSCLC and drug resistance using in vitro assays, and 3) investigating the regulatory mechanism of Pim-1 dysregulation in lung tumorigenesis. RESULTS: Pim-1 was upregulated in 66.2% of the lung tumor tissues and its expression was significantly related to advanced stage (P = 0.019) and lymph node metastasis (P = 0.026). Reduced Pim-1 expression suppressed NSCLC cell growth, cell cycle progression and migration in vitro. Pim-1 was a novel target of miR-486-5p determined by luciferase report assay, and ectopic miR-486-5p expression in cancer cells reduced Pim-1 expression. Furthermore, eukaryotic translation initiation factor 4E (eIF4E) controlled the synthesis of Pim-1 in NSCLC cells, and its expression was positively associated with that of Pim-1 in NSCLC tissue specimens (r = 0.504, p < 0.001). The downregulated miR-486-5p and upregulated eIF4E in NSCLC cells led to the overexpression of Pim-1 by relieving the inhibitory effect of the 3'-UTR or 5'-UTR of Pim-1 mRNA, respectively. Moreover, Pim-1 knockdown sensitized NSCLC cells to cisplatin and EGFR tyrosine kinase inhibitor, gefitinib. CONCLUSIONS: Pim-1 kinase could be a critical survival signaling factor in NSCLC, and regulated by miR-486-5p and eIF4E. Pim-1 kinase may provide a potential target for diagnosis and treatment for lung cancer.