scholarly journals Activation of c-Jun predicts a poor response to sorafenib in hepatocellular carcinoma: Preliminary Clinical Evidence

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Wei Chen ◽  
Weikai Xiao ◽  
Kunsong Zhang ◽  
Xiaoyu Yin ◽  
Jiaming Lai ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Clinical Evidence ◽  
Poor Response

scholarly journals Beyond the Usual Suspects: Hepatitis E Virus and Its Implications in Hepatocellular Carcinoma

Cancers ◽  
2021 ◽  
Vol 13 (22) ◽  
pp. 5867
Author(s):  
Mara Klöhn ◽  
Jil Alexandra Schrader ◽  
Yannick Brüggemann ◽  
Daniel Todt ◽  
Eike Steinmann
Keyword(s):  
Hepatocellular Carcinoma ◽  
Viral Hepatitis ◽  
Hepatitis E Virus ◽  
Clinical Evidence ◽  
Hepatitis E ◽  
Clinical Spectrum ◽  
Immunocompromised Patients ◽  
Virus Infections ◽  
The Relationship ◽  
Liver Infection

Hepatitis E virus infections are the leading cause of viral hepatitis in humans, contributing to an estimated 3.3 million symptomatic cases and almost 44,000 deaths annually. Recently, HEV infections have been found to result in chronic liver infection and cirrhosis in severely immunocompromised patients, suggesting the possibility of HEV-induced hepatocarcinogenesis. While HEV-associated formation of HCC has rarely been reported, the expansion of HEV’s clinical spectrum and the increasing evidence of chronic HEV infections raise questions about the connection between HEV and HCC. The present review summarizes current clinical evidence of the relationship between HEV and HCC and discusses mechanisms of virus-induced HCC development with regard to HEV pathogenesis. We further elucidate why the development of HEV-induced hepatocellular carcinoma has so rarely been observed and provide an outlook on possible experimental set-ups to study the relationship between HEV and HCC formation.

scholarly journals Hepatocellular Carcinoma Immunopathogenesis: Clinical Evidence for Global T Cell Defects and an Immunomodulatory Role for Soluble CD25 (sCD25)

2009 ◽  
Vol 55 (2) ◽  
pp. 484-495 ◽  
Author(s):  
Roniel Cabrera ◽  
Miguel Ararat ◽  
Mengde Cao ◽  
Yiling Xu ◽  
Clive Wasserfall ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
T Cell ◽  
Clinical Evidence ◽  
Soluble Cd25

scholarly journals Hepatic resection for hepatocellular carcinoma in patients with Child–Pugh's A cirrhosis: is clinical evidence of portal hypertension a contraindication?

HPB ◽  
2013 ◽  
Vol 15 (1) ◽  
pp. 78-84 ◽  
Author(s):  
Roberto Santambrogio ◽  
Michael D. Kluger ◽  
Mara Costa ◽  
Andrea Belli ◽  
Matteo Barabino ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Portal Hypertension ◽  
Hepatic Resection ◽  
Clinical Evidence

scholarly journals DNA Hypermethylation Modification Promotes the Development of Hepatocellular Carcinoma by Depressing the Tumor Suppressor Gene ZNF334

2021 ◽  
Author(s):  
Da-peng Sun ◽  
Xiao-jie Gan ◽  
Lei Liu ◽  
Yuan Yang ◽  
Dong-yang Ding ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Dna Methylation ◽  
Tumor Suppressor ◽  
Liver Cancer ◽  
Tumor Suppressor Gene ◽  
Clinical Evidence ◽  
Early Stage ◽  
Suppressor Gene ◽  
Dna Hypermethylation ◽  
Dysplastic Nodules

Abstract Background: DNA methylation plays a pivotal role in the development and progression of tumors, but studies focused on the dynamic changes of DNA methylation in the development of hepatocellular carcinoma (HCC) are rare. This manuscript is aimed to construct pre- and early DNA methylation maps of liver cancer of the same genetic background, as well as to reveal the mechanism of epigenetics regulating gene expression during the development of liver cancer, thus providing new targets and clinical evidence for early diagnosis and shedding lights on the precise treatment for liver cancer. Methods: The study includes 5 patients who were chronic hepatitis B virus infected, clinically diagnosed as primary liver cancer and pathologically diagnosed as early liver cancer with liver dysplastic nodules. Liver fibrosis tissues, dysplastic nodules and early HCC tissues from these patients have been used to measure DNA methylation. Results: We report significant differences in the DNA methylation spectrum of three types of tissues. In the early stage of HCC, DNA hypermethylation of tumor suppressor genes is predominant. Additionally, DNA hypermethylation in the early stage of HCC changes the binding of transcription factor P53 to the promoter of tumor suppressor gene ZNF334, and inhibits the expression of ZNF334 at the transcription level. Furthermore, through a series of in vivo and in vitro experiments, we have clarified the exacerbation effect of tumor suppressor gene ZNF334 deletion in the occurrence of HCC. Combined with clinical data, we found that the overall survival and disease-free survival of patients with high ZNF334 expression are longer than the lower one. Conclusions: We constructed a sequential map of DNA methylation modification during the occurrence of HCC, and clarified the biological function and regulatory mechanism of the tumor suppressor gene ZNF334, which is regulated by related DNA methylation sites, and also provide new targets and clinical evidence for the early diagnosis and precise treatment of liver cancer.

Updated use of TACE for hepatocellular carcinoma treatment: How and when to use it based on clinical evidence

2019 ◽  
Vol 72 ◽  
pp. 28-36 ◽  
Author(s):  
Jean-Luc Raoul ◽  
Alejandro Forner ◽  
Luigi Bolondi ◽  
Tan To Cheung ◽  
Roman Kloeckner ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Clinical Evidence

scholarly journals Hyperactivation of HER2-SHCBP1-PLK1 axis promotes tumor cell mitosis and impairs trastuzumab sensitivity to gastric cancer

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wengui Shi ◽  
Gengyuan Zhang ◽  
Zhijian Ma ◽  
Lianshun Li ◽  
Miaomiao Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Clinical Evidence ◽  
Poor Response ◽  
Her2 Positive ◽  
Patient Response ◽  
Trastuzumab Therapy ◽  
Poor Patient ◽  
Clinical Challenge ◽  
New Strategy ◽  
Cell Mitosis

AbstractTrastuzumab is the backbone of HER2-directed gastric cancer therapy, but poor patient response due to insufficient cell sensitivity and drug resistance remains a clinical challenge. Here, we report that HER2 is involved in cell mitotic promotion for tumorigenesis by hyperactivating a crucial HER2-SHCBP1-PLK1 axis that drives trastuzumab sensitivity and is targeted therapeutically. SHCBP1 is an Shc1-binding protein but is detached from scaffold protein Shc1 following HER2 activation. Released SHCBP1 responds to HER2 cascade by translocating into the nucleus following Ser273 phosphorylation, and then contributing to cell mitosis regulation through binding with PLK1 to promote the phosphorylation of the mitotic interactor MISP. Meanwhile, Shc1 is recruited to HER2 for MAPK or PI3K pathways activation. Also, clinical evidence shows that increased SHCBP1 prognosticates a poor response of patients to trastuzumab therapy. Theaflavine-3, 3’-digallate (TFBG) is identified as an inhibitor of the SHCBP1-PLK1 interaction, which is a potential trastuzumab sensitizing agent and, in combination with trastuzumab, is highly efficacious in suppressing HER2-positive gastric cancer growth. These findings suggest an aberrant mitotic HER2-SHCBP1-PLK1 axis underlies trastuzumab sensitivity and offer a new strategy to combat gastric cancer.

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