Application of Laparoscopic Partial Splenectomy with Total Blood Flow Occlusion in Benign Splenic Lesions.

Laparoscopic partial splenectomy (LPS) is gradually becoming the preferred method for treating benign splenic lesions. However, due to the abundant blood supply and its soft, fragile tissue texture, especially when the lesion is located near the splenic hilum or is particularly large, performing partial splenectomy (PS) in clinical practice is extremely challenging. Therefore, we have been continuously exploring and optimizing hemorrhage control methods during PS, and we here propose a method to perform LPS with complete spleen blood flow occlusion.

Ten-year experience of laparoscopic partial splenectomy for patients with splenic benign lesions.

Background: The increasing comprehension of spleen function has led to the gradual endorsement of laparoscopic partial splenectomy (LPS) as a treatment option for benign spleen lesions. However, it is important to note that the LPS technique remains challenging. This study explores the standardized process and surgical techniques in LPS, aiming to promote the application of this technique.

Multi-omics integrated analyzed the origin of intrahepatic mucinous cholangiocarcinoma: a case report.

Intrahepatic mucinous cholangiocarcinoma (IMCC) is a rare subtype of intrahepatic cholangiocarcinoma (IHCC). Limited data describe the genetic characteristics of IMCC and insights on its pathogenesis are lacking. Here, we employed a multi-omics approach to analyze somatic mutations, transcriptome, proteome and metabolome of tumor tissue obtained from a case of IMCC in order to clarify the pathogenesis of IMCC.

SHARPIN promotes cell proliferation of cholangiocarcinoma and inhibits ferroptosis via p53/SLC7A11/GPX4 signaling.

SHARPIN is a tumor-associated gene involved in the growth and proliferation of many tumor types. A function of SHARPIN in cholangiocarcinoma (CCA) is so far unclear. Here, we studied the role and function of SHARPIN in CCA and revealed its relevant molecular mechanism.

TGF-β1 induced deficiency of linc00261 promotes epithelial-mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3.

Emerging evidence suggests that long non-coding RNAs (lncRNAs) play important roles in the metastasis and recurrence of hepatocellular carcinoma (HCC). A kinds of lncRNAs were found to be involved in regulating epithelial-mesenchymal transition (EMT) or stem-like traits in human cancers, however, the molecular mechanism and signaling pathways targeting EMT and stemness remains largely unknown. Previously, we found that linc00261 was down-regulated in HCC and associated with multiple worse clinical pathological parameters and poor prognosis.

Epigenetically silenced linc00261 contributes to the metastasis of hepatocellular carcinoma via inducing the deficiency of FOXA2 transcription.

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. In recent decades, long non-coding RNAs (lncRNAs) have attracted increasing attention and have been reported to play important roles in human cancers, making them ideal candidates for precise disease assessment and treatment. Our previous study found that the loss of linc00261 was significantly correlated with the malignant biological behaviors of HCC, particularly MVI, and serves as an excellent independent prognostic factor for recurrence-free survival.

Pseudogene Annexin A2 Pseudogene 1 Contributes to Hepatocellular Carcinoma Progression by Modulating Its Parental Gene ANXA2 via miRNA-376a-3p.

Background: Pseudogenes are defined as key regulators in cancer initiation and progression. But their biological function and clinical significance in hepatocellular carcinoma (HCC) remain to be elucidated. In the current study, we identified a novel pseudogene, Annexin A2 pseudogene 1 (ANXA2P1), in HCC and explored its underlining molecular mechanism.

Deficiency of pseudogene UPAT leads to hepatocellular carcinoma progression and forms a positive feedback loop with ZEB1.

Hepatocellular carcinoma (HCC) is a common disease worldwide. Accumulating reports have evidenced the internal connection between epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs), as well as their significance in metastasis and post-operative recurrence. In this study, we investigated an interesting ubiquitin-proteasome pathway associated pseudogene of AOC4, also known as UPAT, and showed that it was downregulated in 39.

MALAT1 functions as a competing endogenous RNA to regulate SMAD5 expression by acting as a sponge for miR-142-3p in hepatocellular carcinoma.

Background: Long non-coding RNAs are involved in the pathology of various tumors, including hepatocellular carcinoma. The expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is increased in numerous types of tumors and is involved in tumor cell proliferation, migration, invasion and apoptosis. MALAT1 level was reported to be upregulated in hepatocellular carcinoma tissues, but its roles and the specific molecular mechanisms are still unclear.

Frizzled 2-induced epithelial-mesenchymal transition correlates with vasculogenic mimicry, stemness, and Hippo signaling in hepatocellular carcinoma.

Prior observation has indicated that Frizzled 2 (FZD2)-induced epithelial-mesenchymal transition (EMT) could be a key step in metastasis and early recurrence of hepatocellular carcinoma (HCC). However, the mechanism underlying tumor development and progression due to aberrant FZD2 expression is poorly defined. Here, we provide evidence that FZD2 is a driver for EMT, cancer stem cell properties, and vasculogenic mimicry (VM) in HCC.

Circulating Tumor Cell Phenotype Indicates Poor Survival and Recurrence After Surgery for Hepatocellular Carcinoma.

Background: Circulating tumors cells (CTCs) may be a promising prognostic marker for patients with malignant tumors. However, there are few reports regarding its value for hepatocellular carcinoma (HCC) patients.

Aims: To investigate CTCs with epithelial and mesenchymal phenotypes as a potential prognostic biomarker for HCC patients.

[Expression of Wnt5b in patients with HBV-related hepatocellular carcinoma and its clinical significance].

Objective: To investigate the expression of Wnt5b in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) tissues and its correlation with the clinicopathological parameters.

Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemical staining were employed to measure Wnt5b mRNA and protein expressions in two groups of HBV-related HCC patients (100 cases in each) selected from a cohort of 289 cases with HBV-related HCC using simple random sampling method. The correlation of Wnt5b expression with the clinicopathological parameters and the prognosis of HCC patients was analyzed.

Loss of tumor suppressor miR-126 contributes to the development of hepatitis B virus-related hepatocellular carcinoma metastasis through the upregulation of ADAM9.

Hepatocellular carcinoma is the most common histological type of primary liver cancer, which represents the second leading cause of cancer-related mortality. MiR-126 was reported to be downregulated in hepatocellular carcinoma tissues, compared with its levels in noncancerous tissues. However, baseline miR-126 expression levels in hepatitis B virus-related hepatocellular carcinoma patients who did not undergo pre-operational treatment remains unknown since hepatitis B virus infection and pre-operational transcatheter arterial chemoembolization were shown to upregulate miR-126 expression.

NVM-1 predicts prognosis and contributes to growth and metastasis in hepatocellular carcinoma.

Novel metastasis-promoting gene 1 (NVM-1) has a significantly elevated protein level in a variety of tumor tissues and is involved in metastasis. However, its functions in hepatocellular carcinoma (HCC) are not clear. The current study aimed to investigate the functions of NVM-1 in cell proliferation, apoptosis, and epithelial-mesenchymal transition in HCC.

Elevated UHRF1 expression contributes to poor prognosis by promoting cell proliferation and metastasis in hepatocellular carcinoma.

Ubiquitin-like with plant homeodomain and ring finger domains, 1 (UHRF1) is overexpressed in a variety of tumor tissues and is negatively correlated with prognosis of patients with cancers, yet so far, a comprehensive study of UHRF1 in hepatocellular carcinoma (HCC) has not been conducted. The present study was designed to explore the expression of UHRF1, associated clinical implications, and its possible functions in HCC. Reverse transcription-polymerase chain reaction and immunohistochemical staining were used to detect UHRF1 expression in HCC specimens including cancerous and noncancerous tissues.

[Positive circulating tumor cells in the peripheral blood may indicate a poor prognosis in patients with hepatocellular carcinoma].

Objective: To assess the value of detecting peripheral blood circulating tumor cells (CTCs) in the diagnosis and treatment of hepatocellular carcinoma (HCC).

Methods: A total of 296 patients diagnosed with HCC admitted in our department from July 2013 to January 2015 were analyzed, with 39 patients with benign liver disease serving as the control group. The distribution of CTCs in the peripheral blood of HCC patients were detected by CanPatrol(TM) CTCs, and its relationship with the clinical features and prognosis of the patients were analyzed.

Methylenetetrahydrofolate dehydrogenase 2 overexpression is associated with tumor aggressiveness and poor prognosis in hepatocellular carcinoma.

Background: Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) is the key enzyme in the transformation of folic acid metabolites. MTHFD2 overexpression plays a key role in the progression of human cancers, and depletion of MTHFD2 has shown potential antitumor activities in several types of cancer. However, the role of MTHFD2 in hepatocellular carcinoma (HCC) has not been investigated.

Dramatic antitumor effects of the dual mTORC1 and mTORC2 inhibitor AZD2014 in hepatocellular carcinoma.

The mammalian target of rapamycin (mTOR) has emerged as a critical effector in cell growth, proliferation, survival, angiogenesis, and autophagy through direct interaction with mTORC1 (mTOR complex 1) and mTORC2 (mTOR complex 2). The mTOR axis is aberrantly activated in about 50% of human hepatocellular carcinoma (HCC) cases and thus has become an attractive target for drug development in this disease. Allosteric inhibitors of mTORC1, rapamycin and its derivatives have been used to study in patients with HCC but have not shown significant clinical utility, likely because of the lack of inhibition of mTORC2.