In standard culture conditions, three human hepatoma cell lines, Hep3B, PLC/PRF/5 and HepG2, were characterised by a predominant transcription of only two (H2 and L) among the four genes involved in the synthesis of inter-alpha-trypsin inhibitor (ITI)-related proteins. Pulse-chase experiments followed by immuno-precipitation with specific anti-L and anti-H ITI antisera showed that the proteins synthesised displayed a restricted L and/or H2 antigenic reactivity. Furthermore, while Hep3B and PLC/PRF/5 lines only synthesised ITI precursors (mainly the L-form), HepG2 cells were able to secrete an ITI-like protein. Immunocytochemical analyses substantiated these results with uneven distribution of heavy and light-chain polypeptide reactivity among the cells. The use of hepatoma cell models for the study of protein synthesis and assembly must therefore be considered cautiously.
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http://dx.doi.org/10.1006/cbir.1995.1106 | DOI Listing |
Integr Cancer Ther
January 2025
National Centre for Radiation Research and Technology, Egyptian Atomic Energy Authority, Cairo, Egypt.
Objectives: Hepatocellular carcinoma (HCC) represents the third-most prevalent cancer in humans worldwide. The current study's objective is to search for the potentiality of H. Wendl () leaf extract in a nanoemulsion (NE) form in enhancing radiotherapy against HCC induced in rats using diethylnitrosamine (DEN).
View Article and Find Full Text PDFBioinform Adv
June 2024
Department of Pediatrics and Human Development, Michigan State University, Grand Rapids, MI 49503, United States.
Motivation: Bispecific antibodies (bsAbs) that bind to two distinct surface antigens on cancer cells are emerging as an appealing therapeutic strategy in cancer immunotherapy. However, considering the vast number of surface proteins, experimental identification of potential antigen pairs that are selectively expressed in cancer cells and not in normal cells is both costly and time-consuming. Recent studies have utilized large bulk RNA-seq databases to propose bispecific targets for various cancers.
View Article and Find Full Text PDFeGastroenterology
November 2024
School of Biological Sciences, Queen's University Belfast, Belfast, UK.
Metabolic dysfunction-associated steatotic liver disease (MASLD), previously referred to as non-alcoholic fatty liver disease, encompasses a broad range of hepatic metabolic disorders primarily characterised by the disruption of hepatic lipid metabolism, hepatic lipid accumulation and steatosis. Severe cases of MASLD might progress to metabolic dysfunction-associated steatohepatitis, characterised by hepatic inflammation, hepatocyte ballooning degeneration, activation of hepatic stellate cells (HSCs) and fibrogenesis. It may further progress to hepatocellular carcinoma.
View Article and Find Full Text PDFJ Hepatocell Carcinoma
January 2025
Department of Oncology, Ganzhou Hospital-Nanfang Hospital, Southern Medical University, Ganzhou, Jiangxi, People's Republic of China.
Purpose: The optimal timing for combining radiotherapy with immunotherapy in patients with hepatocellular carcinoma (HCC) remains uncertain and affects treatment efficacy and patient outcomes. This study aimed to evaluate and compare the efficacy and treatment-related adverse events (TRAEs) of synchronously administered radiotherapy and programmed cell death protein (PD)-1 inhibitors and sequential administration in patients with HCC.
Patients And Methods: We retrospectively enrolled 67 patients with HCC who were undergoing liver radiotherapy and PD-1 inhibitor therapy at two medical centers between July 2017 and April 2023.
World J Hepatol
January 2025
Shenzhen Branch, Guangdong Laboratory of Lingnan Modern Agriculture, Genome Analysis Laboratory of the Ministry of Agriculture and Rural Affairs, Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences, Shenzhen 518000, Guangdong Province, China.
In this review, we explore the application of next-generation sequencing in liver cancer research, highlighting its potential in modern oncology. Liver cancer, particularly hepatocellular carcinoma, is driven by a complex interplay of genetic, epigenetic, and environmental factors. Key genetic alterations, such as mutations in , , and , alongside epigenetic modifications such as DNA methylation and histone remodeling, disrupt regulatory pathways and promote tumorigenesis.
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