The use of fluorescence laparoscopy in the resection of splenic tissue replantation in the right lobe of the liver: A case report and literature review.

BACKGROUND: Ectopic replantation and regeneration of splenic tissue fragments following splenic trauma or splenectomy is known as replantation of splenic tissue. It typically takes place in the abdominal cavity, however, splenic tissue replantation in the liver is extremely rare and difficult to diagnose. It is often misdiagnosed as a liver tumor and removed. CASE PRESENTATION: We present the case of a patient with a history of traumatic splenectomy 15 years prior to the replantation of splenic tissue in the liver. A 4 cm mass in the liver was found during the most recent physical examination, and a computed tomography scan indicated the possibility of a malignant tumor. The tumor was then removed using fluorescence laparoscopy. CONCLUSION: There is a possibility of intrahepatic replantation of splenic tissue in patients who have had a splenectomy in the past, have recently discovered an intrahepatic space-occupying lesion, and do not have any high-risk factors for liver cancer. Unnecessary surgery can be avoided if 99mTc-labeled red blood cells imaging using mass puncture or radionuclide examination provides a clear preoperative diagnosis. Globally, there are no reports of the use of fluorescence laparoscopy in resecting replanted splenic tissue in the liver. Specifically, in the current case, there was no indocyanine green uptake in the mass, and only a small amount was found in the normally functioning liver tissue surrounding the tumor.

Cell division cycle associated 8: A novel diagnostic and prognostic biomarker for hepatocellular carcinoma.

The cell division cycle associated 8 (CDCA8) is a crucial component of the chromosome passenger complex (CPC). It has been implicated in the regulation of cell dynamic localization during mitosis. However, its role in hepatocellular carcinoma (HCC) is not clearly known. In this study, data of 374 patients with HCC were retrieved from the Cancer Genome Atlas (TCGA) database. Pan analysis of Gene Expression Profiling Interactive Analysis (GEPIA) database was performed to profile the mRNA expression of CDCA8 in HCC. Then, the Kaplan-Meier plotter database was analysed to determine the prognostic value of CDCA8 in HCC. In addition, samples of tumour and adjacent normal tissues were collected from 88 HCC patients to perform immunohistochemistry (IHC), reverse transcription-quantitative polymerase chain reaction (qRT-PCR) and Western blotting. The results obtained from bioinformatic analyses were validated through CCK-8 assay, EdU assay, colony formation assay, cell cycle assays and Western blotting experiments. Analysis of the Kaplan-Meier plotter database showed that high expression of CDCA8 may lead to poor overall survival (OS, p = 4.06e-05) in patients with HCC. For the 88 patients with HCC, we found that stages and grades appeared to be strongly linked with CDCA8 expression. Furthermore, the high expression of CDCA8 was found to be correlated with poor OS (p = 0.0054) and progression-free survival (PFS, p = 0.0009). In vitro experiments revealed that inhibition of CDCA8 slowed cell proliferation and blocked the cell cycle at the G0/G1 phase. In vivo experiments demonstrated that inhibition of CDCA8 inhibited tumour growth. Finally, blockade of CDCA8 reduced the expression levels of cyclin A2, cyclin D1, CDK4, CDK6, Ki67 and PCNA. And, there is an interaction between CDCA8 and E2F1. In conclusion, this research demonstrates that CDCA8 may serve as a biomarker for early diagnosis and prognosis prediction of HCC patients. In addition, CDCA8 could be an effective therapeutic target in HCC.

Novel long noncoding RNA Linc1749808 promotes hepatocellular carcinoma metastasis by negatively regulating miR-206.

Notably, a growing number of long noncoding RNAs (lncRNAs) have been recognized to play critical roles in hepatocellular carcinoma (HCC) progression. In this study, we identified a new lncRNA, Linc1749808 (ID: XR_001749808.1) based on microarray data from HCC tissues. Linc1749808 levels in 72 HCC tissues and paracancerous samples were detected by qRT-PCR. The interaction between Linc1749808 and microRNA-206 (miR-206) was assessed by bioinformatic analysis and luciferase assays. Linc1749808 depletion assays, Transwell assays, and miR-206-inhibitor rescue experiments were performed to examine the role of the Linc1749808/miR-206 axis in HCC cells. Our results showed that Linc1749808 was highly expressed in both HCC tissues and cell lines. Linc1749808 expression was significantly correlated with microvascular invasion, metastasis, and prognosis. After the knockdown of Linc1749808, the metastatic potential of 97H and HepG2 cells was attenuated in vitro and in vivo, but the proliferative capacity did not significantly change. Furthermore, Linc1749808 was found to act as a sponge of miR-206. Inhibition of miR-206 counteracted the effect of Linc1749808 knockdown in 97H cells by regulating YAP1 and epithelial-mesenchymal transition (EMT). In summary, these findings show that Linc1749808 can exacerbate the metastasis of HCC by sponging miR-206.

Prognostic significance of regional lymphadenectomy in T1b gallbladder cancer: Results from 24 hospitals in China.

BACKGROUND: Whether regional lymphadenectomy (RL) should be routinely performed in patients with T1b gallbladder cancer (GBC) remains a subject of debate. AIM: To investigate whether RL can improve the prognosis of patients with T1b GBC. METHODS: We studied a multicenter cohort of patients with T1b GBC who underwent surgery between 2008 and 2016 at 24 hospitals in 13 provinces in China. The log-rank test and Cox proportional hazards model were used to compare the overall survival (OS) of patients who underwent cholecystectomy (Ch) + RL and those who underwent Ch only. To investigate whether combined hepatectomy (Hep) improved OS in T1b patients, we studied patients who underwent Ch + RL to compare the OS of patients who underwent combined Hep and patients who did not. RESULTS: Of the 121 patients (aged 61.9 ± 10.1 years), 77 (63.6%) underwent Ch + RL, and 44 (36.4%) underwent Ch only. Seven (9.1%) patients in the Ch + RL group had lymph node metastasis. The 5-year OS rate was significantly higher in the Ch + RL group than in the Ch group (76.3% vs 56.8%, P = 0.036). Multivariate analysis showed that Ch + RL was significantly associated with improved OS (hazard ratio: 0.51; 95% confidence interval: 0.26-0.99). Among the 77 patients who underwent Ch + RL, no survival improvement was found in patients who underwent combined Hep (5-year OS rate: 79.5% for combined Hep and 76.1% for no Hep; P = 0.50). CONCLUSION: T1b GBC patients who underwent Ch + RL had a better prognosis than those who underwent Ch. Hep + Ch showed no improvement in prognosis in T1b GBC patients. Although recommended by both the National Comprehensive Cancer Network and Chinese Medical Association guidelines, RL was only performed in 63.6% of T1b GBC patients. Routine Ch + RL should be advised in T1b GBC.

Expression and prognostic analyses of the insulin-like growth factor 2 mRNA binding protein family in human pancreatic cancer.

BACKGROUND: Despite advances in early diagnosis and treatment, cancer remains the leading cause of mortality worldwide. The insulin-like growth factor 2 mRNA binding protein (IGF2BP) family has been reported to be involved in a variety of human malignant tumours. However, little is known about their expression and prognostic value in human pancreatic cancer. Therefore, we performed a detailed cancer versus normal differential analysis. METHODS: The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA) databases were used to analyse the mRNA expression levels of the IGF2BP family in various cancers, including pancreatic cancer. Then, the LinkedOmics and GEPIA databases were used to assess the relation between the expression levels of IGF2BPs and overall survival (OS). Then, univariate and multivariate Cox regression analyses were performed, and subgroups based on grade and stage were analysed. The signalling pathways associated with IGF2BP2 and IGF2BP3 were then investigated via gene set enrichment analysis (GSEA). RESULTS: IGF2BP2 and IGF2BP3 were associated with each subset of OS based on grade and stage. Further clinical correlation analysis of IGF2BP2 and IGF2BP3 confirmed that IGF2BP2 and IGF2BP3 are fundamental factors in promoting pancreatic cancer progression. CONCLUSION: IGF2BP2 and IGF2BP3 are key factors in promoting the progression of pancreatic cancer and are closely related to overall survival.

Effect and mechanism of RNAi targeting WWTR1 on biological activity of gastric cancer cells SGC7901.

Gastric cancer (GC) is one of the most common malignancies in the world. It is essential to develop novel targets and therapeutic approaches for GC, which requires identification of novel functional molecules. WW­domain containing transcription regulator 1 (WWTR1) may activate many transcriptional factors and exhibit an important role in the development of various tissues in mammals. The results of the present study demonstrated that mRNA and protein levels of WWTR1 are increased in GC tissues and cell lines. The SGC7901 cell line was selected to perform RNA interference (RNAi) targeting WWTR1, and for subsequent study. Compared with control groups (cells without any treatment) and mock groups (cells treated with nonspecific siRNA), cell proliferation of siWWTR1 cells (cells treated with WWTR1 siRNA) was detected using a Cell Counting Kit­8 assay at 12, 24 and 48 h, and decreased in a time­dependent manner. Cell cycle and apoptosis status were determined by flow cytometry, and it was demonstrated that G1/S transition was blocked in the cell cycle and apoptosis promoted in siWWTR1 cells, compared with control and mock cells. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to detect the mRNA and protein levels of cell cycle and apoptosis­associated factors. The expression of Cyclin D1, cancer Myc and B cell lymphoma/leukemia­2 (Bcl­2) decreased and Bcl­2 associated X protein increased significantly in siWWRT1 cells, at the mRNA and protein level, compared with control and mock cells. With the exception of the Hippo pathway, siWWTR1 regulated downstream factors, including mothers against decapentaplegic homolog family member 3 (SMAD3) and inhibitor of DNA binding 1, HLH protein (ID1), HLH protein in the transforming growth factor (TGF)­ß pathway. The expression of asparagine synthetase was decreased whereas ID1, SMAD3 (proteins that participate in intracellular TGF­ß transduction) and betacellulin increased notably in siWWRT1 cells. In conclusion, WWTR1 promotes cell proliferation and inhibits apoptosis of GC cells by regulating cell cycle/apoptosis­associated factors, and effectors in the TGF­ß pathway.

MYO9B gene polymorphisms are associated with the risk of inflammatory bowel diseases.

Myosin IXB (MYO9B) gene polymorphisms have been extensively investigated in terms of their associations with inflammatory bowel disease (IBD), with contradictory results. The aim of this meta-analysis was to evaluate associations between MY09B gene polymorphisms and the risk of IBD, Crohn's disease (CD) and ulcerative colitis (UC). Eligible studies from PubMed, Embase, and CNKI databases were identified. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. Ten studies published in eight papers reporting 8,975 cases and 9,482 controls were included in this meta-analysis. Five MY09B gene polymorphisms were evaluated: rs1545620, rs962917, rs1457092, rs2305764, and rs2305767. Our data suggested that the rs1545620 polymorphism was associated with a decreased risk of IBD. A similar result was found for rs2305767 and UC. The rs962917 single nucleotide polymorphism (SNP) increased the risk of IBD, CD and UC. Moreover, rs1457092 increased the risk of IBD and UC. Rs2305764 was also associated with an increased risk of IBD. Furthermore, stratification analyses indicated that rs1545620 decreased the risk of IBD, while rs962917 increased the risk of IBD, CD and UC in Caucasian populations. To sum up, our data indicate that these five SNPs in MY09B are significantly associated with the risk of IBD.

Semi-mature MyD88-silenced bone marrow dendritic cells prolong the allograft survival in a rat model of intestinal transplantation.

BACKGROUND: Semi-mature dendritic cells (DCs) may induce tolerance rather than immunity. However, little is known about the regulatory mechanism by which these DCs induce transplant tolerance. Myeloid differentiation factor 88 (MyD88) is a key adaptor of Toll-like receptor signaling, which plays a critical role in DC maturation. Activation of MyD88-silenced immature DCs results in the generation of semi-mature DCs. We explored the possibility of using these DCs to induce intestinal transplant tolerance in rats. METHODS: MyD88 expression was silenced in bone marrow DCs (F344 rats) using small interfering RNAs for 24 hours, at which point, lipopolysaccharide (LPS) was added to the culture for another 48 hours. These cells were analyzed for their in vitro and in vivo tolerizing capacities. RESULTS: Semi-mature DCs expressing moderate levels of MHC class II and low levels of co-stimulatory molecules were found to produce interleukin (IL)-10, while IL-12 production was decreased. In vitro co-culture with completely allogeneic T cells from Wistar rats led to a significant decrease in alloreactive T-cell responses. In vivo, the transfer of semi-mature DCs (1 × 10(6) cells) followed by the transplantation of fully mismatched intestinal grafts (F344 rats) led to significantly prolonged survival compared to rats receiving immature and mature DCs. Serum from semi-mature DC-treated rats contained lower concentrations of the pro-inflammatory cytokines IL-2 and interferon-γ 5 days after transplantation. CONCLUSION: Semi-mature DCs may promote inducible allograft tolerance and this study suggests a new strategy by which to facilitate the induction of transplant tolerance.

[Effect of surgical manipulation on the dissemination of cancer cells into peripheral blood in patients with gastric cancer and its risk factor analysis].

OBJECTIVE: To evaluate the effect of surgical manipulation on the dissemination of cancer cells into blood circulation in patients with gastric cancer and to analyze its risk factors. METHODS: This study included 45 consecutive patients with gastric cancer undergoing curative resection and 13 control cases (10 healthy persons and 3 patients with peptic ulcer receiving gastrectomy). Peripheral blood was obtained preoperatively and just after surgical manipulation. The mRNA levels of carcinoembryonic antigen (CEA) from the blood samples were assayed by reverse transcription-polymerase chain reaction(RT-PCR) and compared between the 2 groups. RESULTS: CEA mRNA was negative in all control cases. Of the 45 gastric cancer patients, the preoperative positive rate of CEA mRNA was 8.9%, while the postoperative positive rate was 48.9%, which was significantly higher than that of preoperation (P=0.000). Multivariable Logistic regression analysis showed that operative duration (P=0.014) and tumor depth (P=0.010) were independent risk factors for cancer cell dissemination. Furthermore, the operative duration in patients with positive postoperative CEA mRNA was markedly longer than that in patients with negative postoperative CEA mRNA (P=0.000), and positive rate of postoperative CEA mRNA in advanced gastric cancer was higher compared with that in early gastric cancer (P=0.034). CONCLUSIONS: Surgical manipulation of curative gastrectomy can provoke dissemination of cancer cells into blood circulation, and the operative duration and tumor invasion depth may be 2 of the risk factors for cancer cell dissemination.