Publications by authors named "Bi Xiang Zhang"

Article Synopsis
  • Liver metastases often occur in advanced cancer stages, posing a major clinical challenge due to their complex interactions with immune cells in the liver.
  • These immune cells contribute to the growth of metastases by interacting with tumor cells and liver components, creating supportive environments for the tumors.
  • Despite current treatments being largely ineffective, researchers are actively investigating new immune-based therapies tailored for patients with liver metastases.
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Previous research has revealed that platelets promote tumor metastasis by binding to circulating tumor cells (CTCs). However, the role of platelets in epithelial-mesenchymal transition (EMT) of cancer cells at the primary tumor site, the crucial initial step of tumor metastasis, remains to be elucidated. Here, we found that platelet releasate enhanced EMT and motility of hepatocellular carcinoma (HCC) cells via AMPK/mTOR-induced autophagy.

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Background: Adequate evaluation of degrees of liver cirrhosis is essential in surgical treatment of hepatocellular carcinoma (HCC) patients. The impact of the degrees of cirrhosis on prediction of post-hepatectomy liver failure (PHLF) remains poorly defined. This study aimed to construct and validate a combined pre- and intra-operative nomogram based on the degrees of cirrhosis in predicting PHLF in HCC patients using prospective multi-center's data.

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Thermal ablative techniques such as radiofrequency and microwave ablation are minimally invasive and cost-effective approaches that are currently being adopted as alternatives to surgical resection for primary and metastatic liver malignancies. However, they are considered to be relatively contraindicated for tumors in high-risk locations due to technical difficulties and a perceived increased risk of perioperative complications. Several techniques, including artificial ascites, non-touch multibipolar ablation, and laparoscopically assisted ablation, can be used to improve the outcomes of ablation for high-risk tumors.

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Article Synopsis
  • Metastasis is the leading cause of cancer deaths, particularly in hepatocellular carcinoma (HCC), and is linked to high blood platelet counts and tumor expression of ADAM10, which indicate poor patient prognosis.
  • Research showed that platelets increase ADAM10 expression in tumor cells through the TLR4/NF-κB signaling pathway, leading to the shedding of CX3CL1 and promoting cancer cell migration and invasion.
  • The study highlights the potential of targeting the TLR4/ADAM10/CX3CL1 axis as a strategy to inhibit platelet-driven metastasis in HCC, supported by findings from both in vitro and in vivo mouse models.
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Glycolytic reprogramming is one of the most important features of cancer and plays an integral role in the progression of cancer. In cancer cells, changes in glucose metabolism meet the needs of self-proliferation, angiogenesis and lymphangiogenesis, metastasis, and also affect the immune escape, prognosis evaluation and therapeutic effect of cancer. The n6-methyladenosine (m6A) modification of RNA is widespread in eukaryotic cells.

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Background: Liver cancer is now the fourth most common cancer in China. The most important factor in decreasing the overall survival is recurrence. Nearly 40%-70% of patients would be detected with intrahepatic or extrahepatic recurrence in 5 years after R0 resection.

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Cancer stem cells (CSCs) have been blamed as the main culprit of tumor initiation, progression, metastasis, chemoresistance, and recurrence. However, few anti-CSCs agents have achieved clinical success so far. Here we report a novel derivative of lonidamine (LND), namely HYL001, which selectively and potently inhibits CSCs by targeting mitochondria, with 380-fold and 340-fold lower IC values against breast cancer stem cells (BCSCs) and hepatocellular carcinoma stem cells (HCSCs), respectively, compared to LND.

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Cancer stem cells (CSCs) have been recognized as the culprit for tumor progression, treatment resistance, metastasis, and recurrence while redox homeostasis represents the Achilles' Heel of CSCs. However, few drugs or formulations that are capable of elevating oxidative stress have achieved clinical success for eliminating CSCs. Here, we report hydroxyethyl starch stabilized copper-diethyldithiocarbamate nanoparticles (CuET@HES NPs), which conspicuously suppress CSCs not only in vitro but also in numerous tumor models in vivo.

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Background: Intrahepatic cholangiocarcinoma (ICC) is a highly malignant biliary tumor. Patients with unresectable and advanced ICC have a poor prognosis with current gemcitabine-based chemotherapy. Combination therapy strategies based on immunotherapy have achieved promising results in various tumor types.

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Metadherin (MTDH) is a well-established oncogene in various cancers including Hepatocellular Carcinoma (HCC). However, the precise mechanism through which MTDH promotes cancer-related signaling pathways in HCC remains unknown. In this study, we identified DDX17 as a novel binding partner of MTDH.

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Background: Intrahepatic cholangiocarcinoma (ICC) is the second most common liver malignancy after hepatocellular carcinoma (HCC), with a dismal prognosis and high heterogeneity. The oncological advantages of anatomical resection (AR) and nonanatomical resection (NAR) in HCC have been studied, but surgical strategies for ICC remain controversial with insufficient investigations.

Materials And Methods: From Jan 2013 to Dec 2016, 3880 consecutive patients were retrospectively reviewed from a single center.

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Objective: This study evaluated the antitumor activity and safety of pemigatinib in previously treated Chinese patients with advanced cholangiocarcinoma and fibroblast growth factor receptor 2 (FGFR2) fusions or rearrangements.

Background: Pemigatinib provided clinical benefits for previously treated patients with cholangiocarcinoma carrying FGFR2 fusions or rearrangements and was approved for this indication in multiple countries.

Methods: In this ongoing, multicenter, single-arm, phase II study, adult patients with locally advanced or metastatic cholangiocarcinoma carrying centrally confirmed FGFR2 fusions or rearrangements who had progressed on ≥1 systemic therapy received 13.

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Background And Aims: Conflicting results are often observed in the prognosis of patients with ruptured hepatocellular carcinoma (rHCC), and there are currently very few studies on the long-term postoperative outcomes of ruptured hepatocellular carcinoma patients. This study aimed to distinguish between the postoperative prognosis of rHCC patients with cirrhosis (rHCC-C) and those without cirrhosis (rHCC-NC) using some serum markers.

Methods: We collected the data of 151 rHCC patients treated at our centers from January 2010 to March 2021.

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Objective: To compare the short- and long-term outcomes of robot-assisted (RALR), laparoscopic (LLR), or open liver resection (OLR) in the treatment of Barcelona Clinic Liver Cancer (BCLC) stage 0-A hepatocellular carcinoma (HCC).

Summary Background Data: Following the Balliol IDEAL classification, long-term oncological outcomes can be used to evaluate the value of minimally invasive techniques in the treatment of HCC, and to assess whether they should become a standard practice.

Methods: Data from prospective cohorts of patients with BCLC stage 0-A HCC who underwent curative liver resection using OLR, LLR, or RALR at Tongji Hospital were reviewed.

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Background: Hepatocellular carcinoma (HCC) accompanied by a tumor thrombus is very common. However, the treatment strategy is controversial and varies by the location of the thrombus.

Case Summary: We report herein a case of HCC with a tumor thrombus in the suprahepatic inferior vena cava (IVC), which was successfully treated by hepatectomy combined with thrombectomy following sorafenib chemotherapy.

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Background: Ingestion of fish bones leading to gastric perforation and inducing abscess formation in the caudate lobe of the liver is very rare.

Case Presentation: A 67-year-old man presented to our hospital with a 2-day history of subxiphoid pain. There were no specific symptoms other than pain.

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18[Formula: see text]-glycyrrhetinic acid (GA) is the active ingredient of the traditional Chinese medicinal herb Glycyrrhizae radix et rhizoma. We previously demonstrated that GA inhibited tumor growth in hepatocellular carcinoma (HCC). However, the effect of GA on transforming growth factor-[Formula: see text] (TGF-[Formula: see text]-induced epithelial-mesenchymal transition (EMT) and metastasis were still unclear.

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Background: Aberrant TAK1 (transforming growth factor β-activated kinase 1) activity is known to be involved in a variety of malignancies, but the regulatory mechanisms of TAK1 remain poorly understood. GRAMD4 (glucosyltransferase Rab-like GTPase activator and myotubularin domain containing 4) is a newly discovered p53-independent proapoptotic protein with an unclear role in HCC (hepatocellular carcinoma).

Results: In this research, we found that GRAMD4 expression was lower in HCC samples, and its downregulation predicted worse prognosis for patients after surgical resection.

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Hepatocellular carcinoma (HCC) is the most common type of liver cancer with a high mortality rate worldwide. The percentage of HCC patients with vascular invasion is high. However, tumor thrombus in the hepatic vein (HVTT) has a lower incidence than tumor thrombus in the portal vein (PVTT).

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Aberrant mechanical properties and immunosuppression are the two key factors that limit the antitumor efficacy of T cell immune checkpoint blockade inhibitors, e.g., programmed cell death-1 antibody (PD-1 Ab), against solid tumors in the clinic.

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Rationale: Esophageal carcinoma is an aggressive cancer with extremely poor therapeutic outcomes due to its high metastatic potential and a significant risk of recurrence after radical resection. Liver is the most common metastatic target organ of esophageal carcinoma, followed by the lungs, bones, and brain. Few cases of solitary pancreatic and hepatic metastases of esophageal carcinoma have been reported.

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During the past decades, drugs targeting transforming growth factor-β (TGFβ) signaling have received tremendous attention for late-stage cancer treatment since TGFβ signaling has been recognized as a prime driver for tumor progression and metastasis. Nonetheless, in healthy and pre-malignant tissues, TGFβ functions as a potent tumor suppressor. Furthermore, TGFβ signaling plays a key role in normal development and homeostasis by regulating cell proliferation, differentiation, migration, apoptosis, and immune evasion, and by suppressing tumor-associated inflammation.

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The TGF-β receptor kinase inhibitors (TRKI) have been reported to inhibit tumorigenicity in colon cancer. However, there is no direct evidence showing that these inhibitors function through inhibiting the TGF-β- mediated tumor-promoting effects in vivo. We established a TGF-β inducible reporter system by inserting a luciferase reporter gene to the vector downstream of TGF-β-inducible promoter elements, and transfected it into colon cancer cell lines.

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Type-2 11β-hydroxysteroid dehydrogenase (HSD11B2) is a key enzyme which converts cortisol to inactive cortisone and is involved in tumor progression and metastasis. Several studies have shown that the promotion of tumor progression and metastasis by HSD11B2 resulted from its physiological function of inactivating glucocorticoids (GC). However, the underlying molecular mechanisms by which HSD11B2 drives metastasis, in addition to inactivating GC, are still unclear.

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