Update on Hepatocellular Carcinoma: a Brief Review from Pathologist Standpoint

Soylu, Neşe Karadağ

doi:10.1007/s12029-020-00499-5

Cited by 23 publications

(19 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1). 13,14 iCCA is thought to originate from cholangiocytes and unlike HCC, is not normally associated with classical risk factors of chronic liver disease, except for primary sclerosing cholangitis. 5,15,16 A limited number of transcriptomic studies have reported several iCCA subclasses (i.e.…”

Section: Introductionmentioning

confidence: 99%

Combined hepatocellular-cholangiocarcinoma: An update

Beaufrère

Caldéraro²,

Paradis

2021

Journal of Hepatology

123

131

View full text Add to dashboard Cite

Combined hepatocellular-cholangiocarcinoma (cHCC-CCA) is a tumour that exhibits both hepatocytic and biliary differentiation. Classical risk factors for hepatocellular carcinoma (HCC) seem to also predispose patients to the development of cHCC-CCA. The pathological definition of cHCC-CCA has significantly evolved over time. The last 2019 WHO classification highlighted that the diagnosis of cHCC-CCA should be primarily based on morphology using routine stainings, with additional immunostaining used to refine the identification of subtypes. Among them, "intermediate cell carcinoma" is recognised as a specific subtype, while "cholangiolocellular carcinoma" is now considered a subtype of iCCA. Increasing molecular evidence supports the clonal nature of cHCC-CCA and parallels its biphenotypic histological appearance, with genetic alterations that are classically observed in HCC and/or iCCA. That said, the morphological diagnosis of cHCC-CCA is still challenging for radiologists and pathologists, especially on biopsy specimens. Identification of cHCC-CCA's cell of origin remains an area of active research. Its prognosis is generally worse than that of HCC, and similar to that of iCCA. Resection with lymph node dissection is unfortunately the only curative option for patients with cHCC-CCA. Thus, there remains an urgent need to develop specific therapeutic strategies for this unique clinical entity.

show abstract

Section: Introductionmentioning

confidence: 99%

Combined hepatocellular-cholangiocarcinoma: An update

Beaufrère

Caldéraro²,

Paradis

2021

Journal of Hepatology

123

131

View full text Add to dashboard Cite

show abstract

“…Hepatocellular carcinoma (HCC) is a common type of cancer with poor prognosis, and this disease is a major healthy burden around the world [ 1 , 2 ]. The well-known risk factors for HCC include genetic metabolic diseases, toxins (e.g., aflatoxin), hepatitis B virus and hepatitis C virus hepatitis, and alcoholic and nonalcoholic fatty liver disease [ 3 ]. Generally, patients with HCC are prone to be diagnosed at an advanced stage due to the absence of pathognomonic symptoms, contributing to a poor prognosis [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Extracellular Vesicle-Encapsulated MicroRNA-375 from Bone Marrow-Derived Mesenchymal Stem Cells Inhibits Hepatocellular Carcinoma Progression through Regulating HOXB3-Mediated Wnt/β-Catenin Pathway

Liu

Fan

et al. 2022

Analytical Cellular Pathology

View full text Add to dashboard Cite

Nowadays, microRNA-375 (miR-375) has been implicated in many types of cancers, including hepatocellular carcinoma (HCC), and the functions of miRNAs encapsulated by extracellular vesicles (EV) in HCC progression have also been extensively investigated. In this research, we aimed to probe into the mechanism of EV-encapsulated miR-375 from bone marrow-derived mesenchymal stem cells (BM-MSCs) in HCC progression. At first, miR-375 expression in HCC tissues and cells was detected using RT-qPCR, and miR-375 was overexpressed to specify the effects of miR-375 on the malignant phenotype of HCC cells. miR-375 was downregulated in HCC, and overexpression of miR-375 suppressed HCC cell growth. Then, BM-MSCs and EV were isolated and identified, and, EV were cocultured with HCC cells for further functional assays. It was found that miR-375 encapsulated by EV could restrict the malignant phenotypes of HCC cells. Furthermore, the downstream genes and signaling cascades involved in HCC growth were investigated. HOXB3 was determined to be a downstream target of miR-375, and upregulation of miR-375 decreased Wnt1 and β-catenin protein expression. Furthermore, HOXB3 blocked the repressive effects of miR-375 on HCC cells and Wnt1 and β-catenin expression. This study highlights that miR-375 encapsulated by EV inhibits HCC development via modulating the HOXB3/Wnt/β-catenin axis.

show abstract

“…HCC is most commonly seen in the cirrhosis background. In addition, risk factors for HCC include hepatitis B and C, alcoholic and non‐alcoholic fatty liver disease, genetic metabolic diseases, and toxins 3 . Unfortunately, most HCC patients are diagnosed with advanced stages, and surgical treatment (resection and transplantation) and local chemotherapy have disappointing improvements in overall survival for advanced patients 4 .…”

Section: Introductionmentioning

confidence: 99%

Circular ribonucleic acid nei‐like deoxyribonucleic acid glycosylase 3 governs the microribonucleic acid ‐3150b‐3p/laminin subunit gamma 1 network to partially promote the development of hepatocellular carcinoma

Zhang

Jiang³

et al. 2021

Hepatology Research

View full text Add to dashboard Cite

Aim: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors, and its progression is implicated in the dysregulation of circular ribonucleic acids (RNAs). This study aimed to investigate the role of circular RNA nei-like DNA glycosylase 3 (circNEIL3) in HCC.Methods: Real-time quantitative PCR was used for expression analysis of circNEIL3, microRNA-3150b-3p (miR-3150b-3p) and laminin subunit gamma 1 (LAMC1) message RNA. MTT assay, colony formation assay, wound healing assay, transwell assay, and flow cytometry assay were performed for functional analyses on cell proliferation, migration, invasion, apoptosis, and cycle. The expression of marker proteins and LAMC1 protein was quantified by western blot. The interaction between miR-3150b-3p and circNEIL3 or LAMC1 was confirmed by dual-luciferase reporter assay or RNA immunoprecipitation assay. An animal study was performed to confirm the role of circNEIL3 in vivo.Results: CircNEIL3 was upregulated in tumor tissues and HCC cell lines. CircNEIL3 knockdown significantly suppressed HCC cell proliferation, migration and invasion and induced cell apoptosis and cell cycle arrest. MiR-3150b-3p was a target of circNEIL3, and its inhibition largely reversed the functional effects of circNEIL3 knockdown on cell behaviors. Moreover, LAMC1 served as a target of miR-3150b-3p, and its expression was elevated in HCC tissues and cells. LAMC1 overexpression recovered HCC cell proliferation, migration and invasion that were blocked by miR-3150b-3p restoration. Additionally, circNEIL3 knockdown inhibited tumor growth in mice. Conclusion:CircNEIL3 dysregulation was responsible for the partial development of HCC by regulating the miR-3150b-3p/LAMC1 regulatory network.

show abstract

Update on Hepatocellular Carcinoma: a Brief Review from Pathologist Standpoint

Cited by 23 publications

References 50 publications

Combined hepatocellular-cholangiocarcinoma: An update

Combined hepatocellular-cholangiocarcinoma: An update

Extracellular Vesicle-Encapsulated MicroRNA-375 from Bone Marrow-Derived Mesenchymal Stem Cells Inhibits Hepatocellular Carcinoma Progression through Regulating HOXB3-Mediated Wnt/β-Catenin Pathway

Circular ribonucleic acid nei‐like deoxyribonucleic acid glycosylase 3 governs the microribonucleic acid ‐3150b‐3p/laminin subunit gamma 1 network to partially promote the development of hepatocellular carcinoma

Contact Info

Product

Resources

About