Relevant bibliographies by topics / Highly Upregulated in Liver Carcinoma

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Highly Upregulated in Liver Carcinoma'

Author: Grafiati
Published: 6 September 2023
Last updated: 7 September 2023

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Journal articles on the topic "Highly Upregulated in Liver Carcinoma"

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Wadkin, James C. R., Daniel A. Patten, Sivesh K. Kamarajah, Emma L. Shepherd, Vera Novitskaya, Fedor Berditchevski, David H. Adams, Chris J. Weston, and Shishir Shetty. "CD151 supports VCAM-1-mediated lymphocyte adhesion to liver endothelium and is upregulated in chronic liver disease and hepatocellular carcinoma." American Journal of Physiology-Gastrointestinal and Liver Physiology 313, no. 2 (August 1, 2017): G138—G149. http://dx.doi.org/10.1152/ajpgi.00411.2016.

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CD151, a member of the tetraspanin family of receptors, is a lateral organizer and modulator of activity of several families of transmembrane proteins. It has been implicated in the development and progression of several cancers, but its role in chronic inflammatory disease is less well understood. Here we show that CD151 is upregulated by distinct microenvironmental signals in a range of chronic inflammatory liver diseases and in primary liver cancer, in which it supports lymphocyte recruitment. CD151 was highly expressed in endothelial cells of the hepatic sinusoids and neovessels developing in fibrotic septa and tumor margins. Primary cultures of human hepatic sinusoidal endothelial cells (HSECs) expressed CD151 at the cell membrane and in intracellular vesicles. CD151 was upregulated by VEGF and HepG2 conditioned media but not by proinflammatory cytokines. Confocal microscopy confirmed that CD151 colocalized with the endothelial adhesion molecule/immunoglobulin superfamily member, VCAM-1. Functional flow-based adhesion assays with primary human lymphocytes and HSECs demonstrated a 40% reduction of lymphocyte adhesion with CD151 blockade. Inhibition of lymphocyte adhesion was similar between VCAM-1 blockade and a combination of CD151/VCAM-1 blockade, suggesting a collaborative role between the two receptors. These studies demonstrate that CD151 is upregulated within the liver during chronic inflammation, where it supports lymphocyte recruitment via liver endothelium. We propose that CD151 regulates the activity of VCAM-1 during lymphocyte recruitment to the human liver and could be a novel anti-inflammatory target in chronic liver disease and hepatocellular cancer prevention. NEW & NOTEWORTHY Chronic hepatitis is characterized by lymphocyte accumulation in liver tissue, which drives fibrosis and carcinogenesis. Here, we demonstrate for the first time that the tetraspanin CD151 supports lymphocyte adhesion to liver endothelium. We show that CD151 is upregulated in chronic liver disease and hepatocellular carcinoma (HCC) and is regulated on endothelium by tissue remodeling and procarcinogenic factors. These regulatory and functional studies identify CD151 as a potential therapeutic target to treat liver fibrosis and HCC.
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Jiang, Xue, and Weiwei Liu. "Long Noncoding RNA Highly Upregulated in Liver Cancer Activates p53-p21 Pathway and Promotes Nasopharyngeal Carcinoma Cell Growth." DNA and Cell Biology 36, no. 7 (July 2017): 596–602. http://dx.doi.org/10.1089/dna.2017.3686.

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Yang, Shuang, Jian Zhou, Weiwu Gao, Xia Yang, Di Yang, Zhiqiang Tian, Yuzhang Wu, Mengjie Zhang, Yi Zhang, and Bing Ni. "Multifunctional YY1 in Liver Diseases." Seminars in Liver Disease 37, no. 04 (November 2017): 363–76. http://dx.doi.org/10.1055/s-0037-1607451.

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AbstractThe transcription factor Yin Yang 1 (YY1) is a multifunctional protein that can activate or repress gene expression, depending on the cellular context. While YY1 is ubiquitously expressed and highly conserved between species, its role varies among the diverse cell types and includes proliferation, differentiation, and apoptosis. Upregulated YY1 expression is found in pathogenic conditions, such as human hepatocellular carcinoma and hepatitis B virus infection, and its roles in the molecular pathogenic mechanisms in liver (i.e., fibrosis, carcinogenesis, viral-induced injury) are currently being elucidated. The most recent studies have revealed that YY1 is deeply involved in such dysregulated cellular metabolisms as glycometabolism, lipid metabolism, and bile acid metabolism, which are all involved in various diseases. In this review, we will summarize the current knowledge on YY1 in liver diseases, providing a focused discussion on the characterized and probable underlying mechanisms, as well as a reasoned evaluation of the potential for YY1-mediated pathology as drug targets in liver disease therapies.
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Henderson, James M., Michelle S. W. Xiang, Jiali Carrie Huang, Stefanie Wetzel, Linxuan Jiang, Jack H. Lai, Wengen Wu, et al. "Dipeptidyl Peptidase Inhibition Enhances CD8 T Cell Recruitment and Activates Intrahepatic Inflammasome in a Murine Model of Hepatocellular Carcinoma." Cancers 13, no. 21 (November 1, 2021): 5495. http://dx.doi.org/10.3390/cancers13215495.

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The mRNA expression of the dipeptidyl peptidase 4 (DPP4) gene family is highly upregulated in human hepatocellular carcinoma (HCC) and is associated with poor survival in HCC patients. Compounds that inhibit the DPP4 enzyme family, such as talabostat and ARI-4175, can mediate tumour regression by immune-mediated mechanisms that are believed to include NLRP1 activation. This study investigated the expression and activity of the DPP4 family during the development of HCC and evaluated the efficacy of ARI-4175 in the treatment of early HCC in mice. This first report on this enzyme family in HCC-bearing mice showed DPP9 upregulation in HCC, whereas intrahepatic DPP8/9 and DPP4 enzyme activity levels decreased with age. We demonstrated that ARI-4175 significantly lowered the total number of macroscopic liver nodules in these mice. In addition, ARI-4175 increased intrahepatic inflammatory cell infiltration, including CD8+ T cell numbers, into the HCC-bearing livers. Furthermore, ARI-4175 activated a critical component of the inflammasome pathway, caspase-1, in these HCC-bearing livers. This is the first evidence of caspase-1 activation by a pan-DPP inhibitor in the liver. Our data suggest that targeting the DPP4 enzyme family may be a novel and effective approach to promote anti-tumour immunity in HCC via caspase-1 activation.
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Ruan, Lingjuan, Lifei Huang, Lilai Zhao, Qiang Wang, Xiaocheng Pan, Anmin Zhang, Qiuping Bai, and Zongjun Lv. "The Interaction of lncRNA-HEIH and lncRNA-HULC with HBXIP in Hepatitis B Patients." Gastroenterology Research and Practice 2018 (December 4, 2018): 1–6. http://dx.doi.org/10.1155/2018/9187316.

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Hepatitis B virus (HBV) infection is a major risk factor for the development of hepatic cirrhosis (HC) and hepatocellular carcinoma (HCC), which are associated with very high morbidity and mortality rates worldwide. Many studies have shown that long noncoding RNAs (lncRNAs) that are highly expressed in HCC (lncRNA-HEIH) and highly upregulated in liver cancer (lncRNA-HULC) have been implicated in the development and progression of hepatitis B-related HC and HCC. In this study, reverse transcription and quantitative PCR were used to detect the expression of lncRNA-HEIH and lncRNA-HULC and western blot analysis to detect the expression of hepatitis B X-interacting protein (HBXIP). RNA immunoprecipitation was used to detect the interaction of HBXIP with lncRNA-HULC and lncRNA-HEIH. The results showed that lncRNA-HEIH, lncRNA-HULC, and HBXIP were upregulated in hepatitis B patients, particularly those with hepatitis B-related HCC. Both lncRNA-HEIH and lncRNA-HULC interacted with HBXIP. These results suggest that lncRNA-HEIH and lncRNA-HULC interact with HBXIP in hepatitis B-related diseases.
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Huynh, Kenneth N., Sriram Rao, Bradley Roth, Theodore Bryan, Dayantha M. Fernando, Farshid Dayyani, David Imagawa, and Nadine Abi-Jaoudeh. "Targeting Hypoxia-Inducible Factor-1α for the Management of Hepatocellular Carcinoma." Cancers 15, no. 10 (May 12, 2023): 2738. http://dx.doi.org/10.3390/cancers15102738.

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Hypoxia-inducible factor 1 alpha (HIF-1α) is a transcription factor that regulates the cellular response to hypoxia and is upregulated in all types of solid tumor, leading to tumor angiogenesis, growth, and resistance to therapy. Hepatocellular carcinoma (HCC) is a highly vascular tumor, as well as a hypoxic tumor, due to the liver being a relatively hypoxic environment compared to other organs. Trans-arterial chemoembolization (TACE) and trans-arterial embolization (TAE) are locoregional therapies that are part of the treatment guidelines for HCC but can also exacerbate hypoxia in tumors, as seen with HIF-1α upregulation post-hepatic embolization. Hypoxia-activated prodrugs (HAPs) are a novel class of anticancer agent that are selectively activated under hypoxic conditions, potentially allowing for the targeted treatment of hypoxic HCC. Early studies targeting hypoxia show promising results; however, further research is needed to understand the effects of HAPs in combination with embolization in the treatment of HCC. This review aims to summarize current knowledge on the role of hypoxia and HIF-1α in HCC, as well as the potential of HAPs and liver-directed embolization.
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Li, Duguang, Junhai Pan, Yiyin Zhang, Yirun Li, Shengxi Jin, Cheng Zhong, Peng Chen, et al. "C8orf76 Modulates Ferroptosis in Liver Cancer via Transcriptionally Up-Regulating SLC7A11." Cancers 14, no. 14 (July 13, 2022): 3410. http://dx.doi.org/10.3390/cancers14143410.

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Hepatocellular carcinoma (HCC) is a common malignant tumor worldwide. Chromosome 8 open reading frame 76 (C8orf76), a novel gene located in the nucleus, is highly expressed in many tumor types. However, the specific mechanisms and functions of C8orf76 in HCC remain unclear. Here, we reported for the first time that C8orf76 gene expression levels were frequently upregulated in liver cancer and significantly correlated with HCC development. C8orf76 downregulation induced G1-S arrest and inhibited cell proliferation. Intriguingly, C8orf76 deficiency could accelerate erastin or sorafenib-induced ferroptosis through increasing lipid reactive oxygen species (ROS) levels. Moreover, although C8orf76 overexpression did not affect tumorigenesis under normal conditions, it increased resistance to lipid disturbance and ferroptosis triggered by erastin or sorafenib, which further facilitated HCC cell growth and tumor progression. Mechanistically, C8orf76 bound to the promoter region of the solute carrier family 7 member 11 (SLC7A11) gene and upregulated SLC7A11 transcriptionally. SLC7A11-dependent cystine import led to sufficient GSH synthesis and lipid peroxidation inhibition, thus accelerating tumor growth. Our study indicated that C8orf76 could be a novel marker for HCC diagnosis. In addition, a better comprehensive understanding of the potential role of C8orf76 in HCC helped us develop novel therapeutic strategies for this intractable cancer.
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Kim, Wantae, Sanjoy Kumar Khan, Yuchen Liu, Ruoshi Xu, Ogyi Park, Yong He, Boksik Cha, Bin Gao, and Yingzi Yang. "Hepatic Hippo signaling inhibits protumoural microenvironment to suppress hepatocellular carcinoma." Gut 67, no. 9 (September 2, 2017): 1692–703. http://dx.doi.org/10.1136/gutjnl-2017-314061.

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ObjectiveHippo signalling is a recently identified major oncosuppressive pathway that plays critical roles in inhibiting hepatocyte proliferation, survival and hepatocellular carcinoma (HCC) formation. Hippo kinase (Mst1 and Mst2) inhibits HCC proliferation by suppressing Yap/Taz transcription activities. As human HCC is mainly driven by chronic liver inflammation, it is not clear whether Hippo signalling inhibits HCC by shaping its inflammatory microenvironment.DesignWe have established a genetic HCC model by deleting Mst1 and Mst2 in hepatocytes. Functions of inflammatory responses in this model were characterised by molecular, cellular and FACS analysis, immunohistochemistry and genetic deletion of monocyte chemoattractant protein-1 (Mcp1) or Yap. Human HCC databases and human HCC samples were analysed by immunohistochemistry.ResultsGenetic deletion of Mst1 and Mst2 in hepatocytes (DKO) led to HCC development, highly upregulated Mcp1 expression and massive infiltration of macrophages with mixed M1 and M2 phenotypes. Macrophage ablation or deletion of Mcp1 in DKO mice markedly reduced hepatic inflammation and HCC development. Moreover, Yap removal abolished induction of Mcp1 expression and restored normal liver growth in the Mst1/Mst2 DKO mice. Finally, we showed that MCP1 is a direct transcription target of YAP in hepatocytes and identified a strong gene expression correlation between YAP targets and MCP-1 in human HCCs.ConclusionsHippo signalling in hepatocytes maintains normal liver growth by suppressing macrophage infiltration during protumoural microenvironment formation through the inhibition of Yap-dependent Mcp1 expression, providing new targets and strategies to treat HCCs.
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Correia de Sousa, Marta, Nicolas Calo, Cyril Sobolewski, Monika Gjorgjieva, Sophie Clément, Christine Maeder, Dobrochna Dolicka, et al. "Mir-21 Suppression Promotes Mouse Hepatocarcinogenesis." Cancers 13, no. 19 (October 4, 2021): 4983. http://dx.doi.org/10.3390/cancers13194983.

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The microRNA 21 (miR-21) is upregulated in almost all known human cancers and is considered a highly potent oncogene and potential therapeutic target for cancer treatment. In the liver, miR-21 was reported to promote hepatic steatosis and inflammation, but whether miR-21 also drives hepatocarcinogenesis remains poorly investigated in vivo. Here we show using both carcinogen (Diethylnitrosamine, DEN) or genetically (PTEN deficiency)-induced mouse models of hepatocellular carcinoma (HCC), total or hepatocyte-specific genetic deletion of this microRNA fosters HCC development—contrasting the expected oncogenic role of miR-21. Gene and protein expression analyses of mouse liver tissues further indicate that total or hepatocyte-specific miR-21 deficiency is associated with an increased expression of oncogenes such as Cdc25a, subtle deregulations of the MAPK, HiPPO, and STAT3 signaling pathways, as well as alterations of the inflammatory/immune anti-tumoral responses in the liver. Together, our data show that miR-21 deficiency promotes a pro-tumoral microenvironment, which over time fosters HCC development via pleiotropic and complex mechanisms. These results question the current dogma of miR-21 being a potent oncomiR in the liver and call for cautiousness when considering miR-21 inhibition for therapeutic purposes in HCC.
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Xie, Hui, Hongwei Ma, and Danqiu Zhou. "Plasma HULC as a Promising Novel Biomarker for the Detection of Hepatocellular Carcinoma." BioMed Research International 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/136106.

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Hepatocellular carcinoma (HCC) is a leading cause of cancer death in many Asian and African countries. Lack of early diagnosis tools is one of the clinical obstacles for effective treatment of HCC. Thus, enhanced understanding of the molecular changes associated with HCC is urgently needed to develop novel strategies for the diagnosis and treatment of this dismal disease. While aberrant expression of long noncoding RNAs (lncRNAs) has been functionally associated with certain cancers, the expression profiles and biological relevance of lncRNAs in HCC remain unclear. Highly upregulated in liver cancer (HULC) lncRNA has been implicated in the regulation of hepatoma cell proliferation. In this study, we demonstrate that HULC expression is significantly higher in HCC tumors compared to normal liver tissues. Among the tumor tissues, higher HULC expression is positively associated with Edmondson histological grades or with hepatitis B (HBV) positive status. Moreover, HULC lncRNA is detected with higher frequency in the plasma of HCC patients compared to healthy controls. Higher HULC detection rates are observed in the plasma of patients with higher Edmondson grades or with HBV+ status. These findings indicate for the first time that the expression of HULC in plasma can be used as a noninvasive promising novel biomarker for the diagnosis and/or prognosis of HCC.
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Dissertations / Theses on the topic "Highly Upregulated in Liver Carcinoma"

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Sharma, Geetika. "Regulation of Hepatitis C Virus life-cycle by lncRNA HULC: crosstalk with other host factors." Thesis, 2018. https://etd.iisc.ac.in/handle/2005/5253.

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Hepatitis C virus (HCV) is a positive sense single-stranded RNA virus. It belongs to the family Flaviviridae and the genus hepacivirus. Following the receptor-mediated endocytosis, HCV genome is released into the cytoplasm, where it is first translated in association with ER. The translated viral proteins signal re-distribution of cellular membranes to form a membranous web structure. This membranous structure makes the site of viral replication. This not only acts as a closed site where all the required factors can be ‘concentrated’ to achieve efficient replication, it also helps the virus escape immune surveillance. HCV infected cell is also triggered to synthesize increased amount of lipid. This assists in the efficient assembly and release of HCV particle via VLDL release pathway. Increased lipid synthesis also contributes to HCV-induced hepato-steatosis. Taken together, the study suggests a novel role of HULC in HCV life-cycle. It also uncovers the novel association of HULC and hnRNPC1/C2 and its impact on HCV replication. At this stage it can be considered that HULC acts as a double-edged sword, on one side benefitting the HCV particle release, but on the other exhibiting its antiviral effect
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Books on the topic "Highly Upregulated in Liver Carcinoma"

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Price, Jennifer Cohen, Priyanka Amin, and Antoine Douaihy. Hepatitis C and HIV Co-Infection. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0043.

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Chronic infection with hepatitis C virus (HCV) is a leading cause of end-stage liver disease and is the most common indication for liver transplantation in the United States. Because of shared risk factors, individuals living with HIV infection are disproportionately affected by HCV. Moreover, co-infection with HIV accelerates the natural history of chronic HCV infection, increasing the risk of cirrhosis, hepatocellular carcinoma, hepatic decompensation, and death. Highly effective medications such as direct-acting antivirals (DAA) to cure HCV are now available and have the potential to profoundly improve the health of HIV-HCV-co-infected individuals. However, addressing the many gaps in the HCV care cascade is necessary to fully achieve the benefits of these drugs. This chapter reviews the natural history of HIV-HCV co-infection, the psychiatric comorbidities associated with HCV infection, the evolution of HCV treatment, and the barriers to care that HIV-HCV-co-infected individuals continue to face.
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Book chapters on the topic "Highly Upregulated in Liver Carcinoma"

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Liu, Shihai. "Emerging Immunotherapy: Liver Cancer Microenvironment for Treatment." In Liver Cancer - Genesis, Progression and Metastasis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106021.

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Hepatocellular carcinoma (HCC) is a highly prevalent primary liver carcinoma and the main cause of deaths (linked with cancer) across the globe. Despite advancements in prevention strategies, testing, and technological advances in diagnosis and treatment, the occurrence and fatality rate of HCC continue to rise. In recent decades, the approval of immune checkpoint inhibitors (ICIs) has transformed palliative treatment for liver cancer. However, the majority of patients with liver cancer do not respond to these treatments. Herein, we elaborated the microenvironment of the liver cancer and candidate immunotherapies based on activating the antitumor activity of myeloid, NK and T cells, chimeric antigen receptors-T or -NK cells, vaccines, oncolytic viruses, and combination therapies, as well as the challenges and opportunities of immunotherapies in liver cancer. This review also explores the rationale, molecular foundation, and supporting preclinical evidence for immunotherapies in HCC, available clinical evidence, and current immunotherapeutic clinical studies.
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O’Grady, John G. "Liver transplantation." In Oxford Textbook of Medicine, edited by Jack Satsangi, 3100–3107. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0322.

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Liver transplantation is an established treatment for liver conditions that broadly fall into the categories of acute liver failure, end-stage chronic liver disease, primary hepatic malignancy, and metabolic disease. The expected 1-year survival rate is over 90% and some patients are alive more than 40 years after transplantation. Disease severity scores for cirrhosis heavily influence selection of patients with cirrhosis for transplantation. The prototype is the MELD (Model for End-Stage Liver Disease) score, based on serum bilirubin, serum creatinine, and INR: a score of 16 is considered the threshold that confers benefit from liver transplantation. Hepatocellular carcinoma accounts for most of the malignancy group and selection is largely determined by tumour bulk assessed by the number and size of lesions. Immunosuppression strategies based on tacrolimus, with or without other drugs including mTOR (mechanistic target of rapamycin) inhibitors, antiproliferative agents, or prednisolone, are highly effective in preventing loss of the graft through classical rejection processes. Recurrence of original disease is the main cause of loss of graft function, with recurrence of hepatitis C a particularly challenging problem, although new direct-acting antiviral agents are likely to radically improve outcomes. Technical problems can also result in graft loss due to hepatic artery thrombosis or diffuse ischaemic cholangiopathy, especially in livers harvested from donors after cardiac death. Anastomotic biliary strictures are the commonest technical complication, with 15 to 20% of patients requiring some form of endoscopic or surgical intervention. There is a considerably increased risk of myeloproliferative disease and skin cancers in transplant recipients, as well as aetiology-specific risk. Many patients die having achieved a normal life expectancy, and death with a functioning graft is the commonest terminal scenario.
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Wen, Qirong, Qingfa Zeng, and Ting Li. "Impaired Autophagy and Exosomes Release by Long-Term mTOR Pathway Activation Promotes Hepatocellular Carcinoma Occurrence and Invasion." In Cell Death and Disease [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.107668.

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Mammalian target of rapamycin (mTOR) is highly expressed in various types of hepatocellular carcinoma (HCC). Clinically, HCC cases without inflammation and cirrhosis are also increasingly common, especially in patients with nonalcoholic fatty liver disease, more and more patients develop HCC, which is only characterized by hepatic steatosis. However, the molecular mechanisms underlying the development of non-inflammatory HCC remain unclearly. Our previous study demonstrated that overactivation of mTOR pathway in the liver promotes de novo lipid synthesis and eventually spontaneous formation of non-inflammatory HCC. The continuous activation of mTOR pathway, on the one hand, promotes the de novo synthesis of lipids, resulting in the production of a large amount of lipid in the liver; on the other hand, it inhibits autophagy, resulting in the inability of lipid to be removed in time and accumulate in the liver. Accumulated lipid peroxidation eventually develops into HCC. In addition, the continuously activated mTOR pathway inhibited the release of exosomes by reducing the expression of Rab27A, and in vitro experiments confirmed that hepatoma cells after Rab27A knockout were more prone to invasion and metastasis. The reduced release of exosomes may impair intercellular communication, especially with immune cells, thereby making HCC more prone to invasion and metastasis with less inflammation.
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Lupsor-Platon, Monica, Teodora Serban, and Alexandra Iulia Silion. "Noninvasive Assessment of HCV Patients Using Ultrasound Elastography." In Elastography - Applications in Clinical Medicine [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102294.

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Among patients with chronic hepatitis C (CHC) infection, extensive research showed that fibrosis progression is a proper surrogate marker for advanced liver disease, eventually leading to dramatic endpoints such as cirrhosis and hepatocellular carcinoma. Therefore, there is growing interest in the use of noninvasive methods for fibrosis assessment in order to replace liver biopsy (LB) in clinical practice and provide optimal risk stratification. Elastographic techniques, such as Vibration Controlled Transient Elastography (VCTE), point-shear wave elastography (p-SWE), and 2D-SWE have shown promising results in this regard, with excellent performance in diagnosing hepatic cirrhosis, and great accuracy for steatosis detection through the Controlled Attenuation Parameter embedded on the VCTE device. In addition, the recent introduction of highly efficient direct-acting antivirals (DAAs) led to viral eradication and a significant decrease in liver damage, lowering the risk of hepatic decompensation, and HCC. Therefore, CHC patients need proper noninvasive and repeatable methods for adequate surveillance, even after treatment, as there still remains a risk of portal hypertension and HCC. However, the usefulness for monitoring fibrosis after the sustained virological response (SVR) needs further research.
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Adesina, Evaristus, Olusola Oyero, Nelson Okorie, Charity Ben-Enukora, and Babatunde Adeyeye. "Risk Communication for Viral Hepatitis Management Among Migrants." In Research Anthology on Improving Health Literacy Through Patient Communication and Mass Media, 15–32. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-6684-2414-8.ch002.

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The burden of viral hepatitis is high with huge mortality and morbidity on human population. The increasing migration of people from areas highly prevalent of viral hepatitis poses a unique threat to the healthcare systems of the host nations. The deficient universal standards for screening, vaccination, and treatment of viral hepatitis have therefore made the burden of chronic liver disease and hepatocellular carcinoma to increase among migrant populations globally. This study examines the role of risk communication in managing viral hepatitis among migrants at the different levels of pre-departure phase, travel phase, destination phase, interception phase and the return phase. The study concluded on the need for concerted effort by national governments to develop a national communication policy with comprehensive risk communication strategies on viral hepatitis management among migrants.
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Adesina, Evaristus, Olusola Oyero, Nelson Okorie, Charity Ben-Enukora, and Babatunde Adeyeye. "Risk Communication for Viral Hepatitis Management Among Migrants." In Handbook of Research on the Global Impact of Media on Migration Issues, 235–52. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-0210-5.ch014.

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The burden of viral hepatitis is high with huge mortality and morbidity on human population. The increasing migration of people from areas highly prevalent of viral hepatitis poses a unique threat to the healthcare systems of the host nations. The deficient universal standards for screening, vaccination, and treatment of viral hepatitis have therefore made the burden of chronic liver disease and hepatocellular carcinoma to increase among migrant populations globally. This study examines the role of risk communication in managing viral hepatitis among migrants at the different levels of pre-departure phase, travel phase, destination phase, interception phase and the return phase. The study concluded on the need for concerted effort by national governments to develop a national communication policy with comprehensive risk communication strategies on viral hepatitis management among migrants.
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Shahid, Imran, and Qaiser Jabeen. "HCV-Host Interactions: A Plethora of Genes and their Intricate Interplay Part 1: Virus Specific Factors." In Hepatitis C Virus-Host Interactions and Therapeutics: Current Insights and Future Perspectives, 1–25. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815123432123010004.

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Hepatitis C virus (HCV) interaction with host cells is pivotal for natural disease course starting from asymptomatic acute infection to progress into persistent chronic infection and subsequent extrahepatic manifestations, including fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The HCV infection biology in infected host cells via virus attachment, virus genome replication, mRNA translation, new virion formation, and egress from infected cells involves highly coordinated participation of the virus- and host-specific proteins, a plethora of genes, and cell signaling cascade. The progression of persistent chronic hepatitis C (CHC) infection to hepatic fibrosis, cirrhosis, and HCC involves viral invasion strategies against host immune system defense mechanisms as well as impeding healthy metabolic and signaling networks of the liver cells. Thereby, HCV-induced liver injury via chronic inflammatory processes that fail to resolve is responsible for decompensated cirrhosis and on occasion, hepatocarcinogenesis in infected individuals. With the latest advancement and rapid expansion of our knowledge in hepatology, the human liver is deciphered as an immunologically distinct organ with its specialized physiological niche. The relationship between human hepatocytes and different components of the immune system is quite complex and dynamic. The immunopathogenesis of various viral infections demonstrates that the immune system plays an essential role to determine the progression of many hepatic diseases through immune cell communication and cell signaling networks. In this book chapter, we overview HCV host interactions and their intricate interplay with complex crosstalk to propagate less fetal acute HCV infection to CHC and subsequent hepatocarcinogenesis (i.e. HCC) in infected individuals.
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Conference papers on the topic "Highly Upregulated in Liver Carcinoma"

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Suh, CH, HA Kim, WY Baek, JY Jung, SH Lee, and SS Kim. "118 The liver x receptor is highly upregulated in monocyte derived macrophage and potentiates tlr-driven cytokine release according to genotype of -1830 t > c polymorphism." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.118.

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