Academic literature on the topic 'Liver diseases, HCC,MerTK'
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Journal articles on the topic "Liver diseases, HCC,MerTK"
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Hammitt, Laura, Dean Quinn, Ewa Janczewska, Francisco J. Pasquel, Richard Tytus, K. Rajender Reddy, Katia Abarca, et al. "1050. Phase 3 Trial to Evaluate the Safety, Tolerability, and Immunogenicity of V114 Followed by 23valent Pneumococcal Polysaccharide Vaccine 6 Months Later in At-risk Adults Aged 18–49 Years (PNEU-DAY): A Subgroup Analysis by Baseline Risk Factors." Open Forum Infectious Diseases 8, Supplement_1 (November 1, 2021): S616—S617. http://dx.doi.org/10.1093/ofid/ofab466.1244.
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Abstract Background Risk factors (RFs) for pneumococcal disease (PD) in immunocompetent individuals include comorbidities, behavioral habits, or living in a community with increased risk of PD transmission. RF stacking of comorbidities is associated with a higher incidence of PD, approaching that of immunocompromised individuals. Pneumococcal vaccination of certain adults is recommended with the 23-valent pneumococcal polysaccharide vaccine (PPSV23) alone/sequentially with pneumococcal conjugate vaccine (PCV). V114, an investigational 15-valent PCV, contains 2 epidemiologically important serotypes (STs), 22F and 33F, in addition to the 13 STs in 13-valent PCV (PCV13). Methods PNEU-DAY was a Phase 3 study evaluating V114 or PCV13 administered on Day 1, and PPSV23 given 6 months later, in adults aged 18–49 years with or without RFs. This subgroup analysis assessed safety, tolerability, and immunogenicity of V114 and PCV13 based on the number of baseline PD RFs, which included chronic liver, lung, and heart disease, diabetes mellitus, tobacco use, and alcohol consumption. Adverse events (AEs; overall and solicited) were collected after each vaccination. Immunogenicity assessment was based on ST-specific opsonophagocytic activity (OPA) at 30 days after each vaccination. Subgroup analyses were conducted by RF group (0, 1, or ≥2 RFs for PD). Results Among the 1515 participants randomized to V114 (n=1135) or PCV13 (n=380), 25.2% had no RFs, 54.7% had 1 RF and 20.1% had ≥2 RFs for PD at baseline. The proportions of participants with solicited AEs following V114/PCV13 and PPSV23 were comparable across the 3 subgroups, with injection-site pain, myalgia, and fatigue being the most common. V114 and PCV13 were immunogenic in all subgroups based on OPA geometric mean titers (GMTs) at 30 days post-vaccination for the 13 shared STs (Figure); in addition, V114 induced a robust immune response to the 2 unique STs (22F, 33F) in all subgroups. PPSV23 following PCV was immunogenic for all 15 STs contained in V114 across all subgroups. Figure. Serotype-specific OPA GMTs at baseline and 30 days post-vaccination with V114 and PCV13 by number of baseline risk factors (per-protocol population) Conclusion V114 administered alone/sequentially with PPSV23 is well tolerated and immunogenic for all 15 vaccine STs, including those not contained in PCV13, in immunocompetent adults aged 18–49 years, regardless of the number of baseline RFs. Disclosures Laura Hammitt, MD, MedImmune (Grant/Research Support, Scientific Research Study Investigator, Research Grant or Support)Merck & Co., Inc. (Grant/Research Support, Scientific Research Study Investigator, Research Grant or Support)Novavax (Grant/Research Support, Scientific Research Study Investigator, Research Grant or Support)Pfizer (Grant/Research Support, Scientific Research Study Investigator, Research Grant or Support) Francisco J. Pasquel, MD, MPH, Boehringer Ingelheim (Consultant)Dexcom (Grant/Research Support)Eli Lilly & Company (Consultant)Insulet (Grant/Research Support)Merck & Co., Inc. (Consultant, Grant/Research Support) K. Rajender Reddy, MD, BMS (Grant/Research Support)Deciphera (Advisor or Review Panel member)Gilead (Grant/Research Support)Grifols (Grant/Research Support)HCC-TARGET (Grant/Research Support)Intercept (Grant/Research Support)Mallinckrodt (Grant/Research Support, Advisor or Review Panel member)NASH-TARGET (Grant/Research Support)Pfizer (Advisor or Review Panel member)Sequana (Grant/Research Support) Ron Dagan, MD, Medimmune/AstraZeneca (Grant/Research Support, Scientific Research Study Investigator, Research Grant or Support)MSD (Consultant, Grant/Research Support, Scientific Research Study Investigator, Advisor or Review Panel member, Research Grant or Support, Speaker’s Bureau)Pfizer (Consultant, Grant/Research Support, Scientific Research Study Investigator, Advisor or Review Panel member, Research Grant or Support, Speaker’s Bureau) Rachel Dawson, D.O. MPH, Merck & Co., Inc. (Employee, Shareholder) Jennifer McCauley, BSc, Merck & Co., Inc. (Employee) Kyeongmi Cheon, Ph.D., Merck & Co., Inc. (Employee, Shareholder) Alison Pedley, PhD, Merck & Co., Inc. (Employee) Tina Sterling, BS, Merck & Co., Inc. (Employee, Shareholder) Gretchen Tamms, B.S., Merck Sharp and Dohme (Employee, Shareholder) Luwy Musey, MD, Merck & Co., Inc. (Employee) Ulrike K. Buchwald, MD, MS, Merck & Co., Inc. (Employee)TB Alliance (Employee)
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Lleo, Ana, Ynto S. de Boer, Rodrigo Liberal, and Massimo Colombo. "The risk of liver cancer in autoimmune liver diseases." Therapeutic Advances in Medical Oncology 11 (January 2019): 175883591986191. http://dx.doi.org/10.1177/1758835919861914.
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Hepatocellular carcinoma (HCC), the dominant primary malignancy of the liver, has almost invariably a fatal outcome that can be averted only by early diagnosis and treatment. While the close association of HCC with chronic viral hepatitis and alcohol abuse has impacted favourably on screening and treatment of this deadly tumour, at the same time it has long obscured the etiologic role of autoimmune liver diseases. Recently, a systematic analysis of 25 published cohorts disclosed a 3.1 × 1000 patients/year incidence of HCC in autoimmune hepatitis patients that tripled in those with cirrhosis. HCC is also a sequela of primary biliary cholangitis, where the incidence is more relevant in males, those with advanced liver disease and nonresponders to ursodeoxycholic acid therapy. Cholangiocarcinoma (CCA), the second ranking primary cancer of the liver, is also on the rise with its intrahepatic pattern, in part reflecting an association with chronic liver diseases of diverse aetiology. In the USA and northern Europe, perihilar CCA is a frequent complication of primary sclerosing cholangitis, a cholestatic disorder thought to be immune mediated. International Guidelines clearly recommend HCC screening with abdominal ultrasonography every 6 months in autoimmune cirrhotic patients. While surveillance of patients with autoimmune liver disorders who are at risk of HCC affects both early diagnosis and radical therapy of this tumour, this is not the case for CCA, where early diagnosis is challenged by the lack of sensitive and accurate tests for screening.
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Hedrich, Viola, Kristina Breitenecker, Leila Djerlek, Gregor Ortmayr, and Wolfgang Mikulits. "Intrinsic and Extrinsic Control of Hepatocellular Carcinoma by TAM Receptors." Cancers 13, no. 21 (October 29, 2021): 5448. http://dx.doi.org/10.3390/cancers13215448.
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Hepatocellular carcinoma (HCC) is the major subtype of liver cancer, showing high mortality of patients due to limited therapeutic options at advanced stages of disease. The receptor tyrosine kinases Tyro3, Axl and MerTK—belonging to the TAM family—exert a large impact on various aspects of cancer biology. Binding of the ligands Gas6 or Protein S activates TAM receptors causing homophilic dimerization and heterophilic interactions with other receptors to modulate effector functions. In this context, TAM receptors are major regulators of anti-inflammatory responses and vessel integrity, including platelet aggregation as well as resistance to chemotherapy. In this review, we discuss the relevance of TAM receptors in the intrinsic control of HCC progression by modulating epithelial cell plasticity and by promoting metastatic traits of neoplastic hepatocytes. Depending on different etiologies of HCC, we further describe the overt role of TAM receptors in the extrinsic control of HCC progression by focusing on immune cell infiltration and fibrogenesis. Additionally, we assess TAM receptor functions in the chemoresistance against clinically used tyrosine kinase inhibitors and immune checkpoint blockade in HCC progression. We finally address the question of whether inhibition of TAM receptors can be envisaged for novel therapeutic strategies in HCC.
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Junior, Yin-Siew Lai, Huyen Thi Nguyen, Farrah P. Salmanida, and Ko-Tung Chang. "MERTK+/hi M2c Macrophages Induced by Baicalin Alleviate Non-Alcoholic Fatty Liver Disease." International Journal of Molecular Sciences 22, no. 19 (September 30, 2021): 10604. http://dx.doi.org/10.3390/ijms221910604.
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Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide. An accumulation of fat, followed by inflammation, is the major cause of NAFLD progression. During inflammation, macrophages are the most abundant immune cells recruited to the site of injury. Macrophages are classified into “proinflammatory” M1 macrophages, and “anti-inflammatory” M2 macrophages. In NAFLD, M1 macrophages are the most prominent macrophages that lead to an excessive inflammatory response. Previously, we found that baicalin could polarize macrophages into anti-inflammatory M2c subtype macrophages with an increased level of MERTK expression. Several studies have also shown a strong correlation between MERTK expression and cholesterol efflux, efferocytosis, as well as phagocytosis capability. Therefore, in this study, we aim to elucidate the potential and efficacy of mononuclear-cell (MNC)-derived MERTK+/hi M2c macrophages induced by baicalin as a cell-based therapy for NAFLD treatment. In our results, we have demonstrated that a MERTK+/hi M2c macrophage injection to NAFLD mice contributes to an increased level of serum HDL secretion in the liver, a decline in the circulating CD4+CD25− and CD8+CD25− T cells and lowers the total NAFLD pathological score by lessening the inflammation, necrosis, and fibrosis. In the liver, profibrotic COL1A1 and FN, proinflammation TNFα, as well as the regulator of lipid metabolism PPARɣ expression, were also downregulated after injection. In parallel, the transcriptomic profiles of the injected MERTK+/hi M2c macrophages showed that the various genes directly or indirectly involved in NAFLD progression (e.g., SERPINE1, FADS2) were also suppressed. Downregulation of cytokines and inflammation-associated genes, such as CCR5, may promote a pro-resolving milieu in the NAFLD liver. Altogether, cell-based therapy using MERTK+/hi M2c macrophages is promising, as it ameliorates NAFLD in mice.
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Jiang, Kun, and Barbara A. Centeno. "Primary Liver Cancers, Part 2." Cancer Control 25, no. 1 (January 1, 2018): 107327481774465. http://dx.doi.org/10.1177/1073274817744658.
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Hepatocellular carcinoma (HCC) and primary intrahepatic cholangiocarcinoma (ICC) have been increasing in incidence worldwide and are leading causes of cancer death. Studies of the molecular alterations leading to these carcinomas provide insights into the key mechanisms involved. A literature review was conducted to identify articles with information relevant to current understanding of the etiologies and molecular pathogenesis of HCC and ICC. Chronic inflammatory diseases are the key etiological risk factors for both HCC and ICC, although other diseases play a role, and for many ICCs, an underlying risk factor is not identified. Mutations in catenin beta 1 ( CTNBB1) and tumor protein 53 (P53) are the main genetic alterations in HCC. Isocitrate dehydrogenases 1 and 2 (IDH1/2), KRAS protooncogene GTPase (KRAS), a RAS Viral Oncogene Homolog in neoroblastoma (NRAS) and P53 are primary genetic alterations in ICC. In both diseases, the mutational landscape is dependent on the underlying etiology. The most significant etiologies and genetic processes involved in the carcinogenesis of HCC and ICC are reviewed.
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Nguyen, Xuan-vinh Kevin, Jason Zhang, Ken Lee Chin, Stephen Bloom, and Amanda J. Nicoll. "Is Hepatocellular Carcinoma in Fatty Liver Different to Non-Fatty Liver?" Nutrients 14, no. 18 (September 19, 2022): 3875. http://dx.doi.org/10.3390/nu14183875.
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Background: Non-alcoholic fatty liver disease (NAFLD) has become the most prevalent liver disease in Australia and is recognised to play a role in the development of hepatocellular carcinoma (HCC). There are no clear guidelines regarding screening for HCC in NAFLD. The aim of this retrospective study was to compare the characteristics and survival rates of NAFLD-HCC to patients with non-NAFLD-HCC to help guide future research in this area. Methods: A total of 152 HCC patients with either NAFLD (n = 36) or non-NAFLD (n = 116) were retrospectively analysed from the HCC database and medical records. Chi-square and independent t-test were used to compare baseline characteristics and Kaplan–Meier curves and Cox models were used for survival analysis. Results: Patients with NAFLD-HCC were more likely to be diagnosed due to symptoms rather than through screening, and at an older age, compared with non-NAFLD HCC. The median survival rates were lower in NAFLD-HCC (17.2 months) than in those with non-NAFLD-HCC (23.5 months). Conclusion: There is a rise in the number of HCC cases in patients with NAFLD, and this has significant implications for hepatologists as they are presented with more advanced diseases and have poorer outcomes. Future studies on HCC will need to identify this group earlier in order to have an impact on the HCC survival rate.
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Rizzo, Giacomo Emanuele Maria, Giuseppe Cabibbo, and Antonio Craxì. "Hepatitis B Virus-Associated Hepatocellular Carcinoma." Viruses 14, no. 5 (May 7, 2022): 986. http://dx.doi.org/10.3390/v14050986.
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Hepatitis B virus (HBV) is DNA-based virus, member of the Hepadnaviridae family, which can cause liver disease and increased risk of hepatocellular carcinoma (HCC) in infected individuals, replicating within the hepatocytes and interacting with several cellular proteins. Chronic hepatitis B can progressively lead to liver cirrhosis, which is an independent risk factor for HCC. Complications as liver decompensation or HCC impact the survival of HBV patients and concurrent HDV infection worsens the disease. The available data provide evidence that HBV infection is associated with the risk of developing HCC with or without an underlying liver cirrhosis, due to various direct and indirect mechanisms promoting hepatocarcinogenesis. The molecular profile of HBV-HCC is extensively and continuously under study, and it is the result of altered molecular pathways, which modify the microenvironment and lead to DNA damage. HBV produces the protein HBx, which has a central role in the oncogenetic process. Furthermore, the molecular profile of HBV-HCC was recently discerned from that of HDV-HCC, despite the obligatory dependence of HDV on HBV. Proper management of the underlying HBV-related liver disease is fundamental, including HCC surveillance, viral suppression, and application of adequate predictive models. When HBV-HCC occurs, liver function and HCC characteristics guide the physician among treatment strategies but always considering the viral etiology in the treatment choice.
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Chen, Shen, Yi Tang, Wanjun Fang, Taiping He, Xu Chen, and Peiwen Zhang. "CoQ10 Promotes Resolution of Necrosis and Liver Regeneration After Acetaminophen-Induced Liver Injury." Toxicological Sciences 185, no. 1 (October 20, 2021): 19–27. http://dx.doi.org/10.1093/toxsci/kfab123.
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Abstract Coenzyme Q10 (CoQ10) which acts as an electron transporter in the mitochondrial respiratory chain has many beneficial effects on liver diseases. In our previous research, CoQ10 has been found to attenuate acetaminophen (APAP)-induced acute liver injury (ALI). However, whether CoQ10 administration is still effective at the late stage of APAP overdose is still unknown. In this study, we aimed to test CoQ10 efficacy at the late stage of APAP overdose. C57BL/6J mice were intraperitoneally treated with APAP to induce liver injury. CoQ10 (5 mg/kg) was given to mice at 16 h after APAP treatment. The results showed that while CoQ10 treatment at 16 h post-APAP overdose had no effects on the expression of ROS generated genes or scavenged genes, it still significantly decreased necrosis of hepatocytes following APAP-induced ALI. Moreover, CoQ10 increased MerTK+ macrophages accumulation in the APAP-overdose liver and inhibition of MerTK signaling partly abrogated the protective role of CoQ10 treatment on the hepatic necrosis. CoQ10 treatment also significantly enhanced hepatocytes proliferation as shown in the increased 5-bromodeoxyuridine incorporation in the APAP-intoxicated mice liver section. In addition, CoQ10 treatment increased hepatic Proliferating Cell Nuclear Antigen (PCNA) and Cyclin D1 expression and promoted activation of the β-catenin signaling in APAP-overdose mice. To conclude, these data provide evidence that CoQ10 treatment is still effective at the late stage of APAP-induced ALI and promotes resolution of necrosis and liver regeneration following ALI.
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Kim, Young-Ah, Kwan-Kyu Park, and Sun-Jae Lee. "LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma." International Journal of Molecular Sciences 21, no. 8 (April 20, 2020): 2883. http://dx.doi.org/10.3390/ijms21082883.
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Long non-coding RNAs (lncRNAs) are emerging as important contributors to the biological processes underlying the pathophysiology of various human diseases, including hepatocellular carcinoma (HCC). However, the involvement of these molecules in chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD) and viral hepatitis, has only recently been considered in scientific research. While extensive studies on the pathogenesis of the development of HCC from hepatic fibrosis have been conducted, their regulatory molecular mechanisms are still only partially understood. The underlying mechanisms related to lncRNAs leading to HCC from chronic liver diseases and cirrhosis have not yet been entirely elucidated. Therefore, elucidating the functional roles of lncRNAs in chronic liver disease and HCC can contribute to a better understanding of the molecular mechanisms, and may help in developing novel diagnostic biomarkers and therapeutic targets for HCC, as well as in preventing the progression of chronic liver disease to HCC. Here, we comprehensively review and briefly summarize some lncRNAs that participate in both hepatic fibrosis and HCC.
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Rajapaksha, Indu. "Liver Fibrosis, Liver Cancer, and Advances in Therapeutic Approaches." Livers 2, no. 4 (November 2, 2022): 372–86. http://dx.doi.org/10.3390/livers2040028.
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Chronic liver diseases (CLDs) that lead to hepatic fibrosis, cirrhosis, and/or hepatocellular carcinoma (HCC) have become a major cause of illness and death worldwide. The main causative factors for CLDs are chronic viral infections, excessive alcohol consumption, non-alcoholic fatty liver disease (NAFLD), and cholestatic diseases. The primary approach to managing cirrhosis should be removing the causative agent, and the secondary approach should address fibrogenesis. Liver cancer is also a leading cause of death worldwide, and many therapeutic approaches exist to treat the disease. However, liver transplantation remains the last treatment option for cirrhosis and liver cancer. Thus, this review discusses the pathophysiology of liver fibrosis, its progression to cirrhosis and HCC, and current therapeutic options available to treat the diseases with potential therapeutic options that will be available in the near future.
Dissertations / Theses on the topic "Liver diseases, HCC,MerTK"
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Roth, Alexander David. "Modeling Liver Diseases Using Hepatic Cell Microarrays." Cleveland State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=csu1544719407531728.
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Jariwala, Nidhi H. "Characterization of Staphylococcal nuclease and tudor domain containing protein 1 (SND1) as a molecular target in Hepatocellular carcinoma and Non-alcoholic steatohepatitis." VCU Scholars Compass, 2017. https://scholarscompass.vcu.edu/etd/5183.
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CHARACTERIZATION OF STAPHYLOCOCCAL NUCLEASE AND TUDOR DOMAIN CONTAINING PROTEIN 1 (SND1) AS A MOLECULAR TARGET IN HEPATOCELLULAR CARCINOMA AND NON-ALCOHOLIC STEATOHEPATITIS
Nidhi Jariwala, PhD
A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Integrative Life Sciences
Virginia Commonwealth University, 2017
Devanand Sarkar, M.B.B.S., PhD.
Associate Professor, Department of Human and Molecular Genetics
Virginia Commonwealth University
Richmond, Virginia
SND1, a subunit of the miRNA regulatory complex RISC, has been implicated as an oncogene in hepatocellular carcinoma (HCC). Oncoprotein SND1 regulates gene expression at a post-transcriptional level in multiple cancers including hepatocellular carcinoma (HCC). In the present study, we characterize oncogenic functions of SND1 in HCC employing a novel transgenic mouse model (Alb/SND1) and present SND1 as a potential molecular target in HCC management. We show that Alb/SND1 mice develop spontaneous HCC with partial penetrance and exhibit more highly aggressive HCC induced by chemical carcinogenesis. Livers from Alb/SND1 mice exhibit a relative increase in inflammatory markers and spheroid-generating tumor initiating cells (TiC). Mechanistic investigations defined roles for Akt and NF-κB signaling pathways in promoting TiC formation in Alb/SND1 mice. Intravenous administration of the selective SND1 inhibitor 3', 5'-deoxythymidine bisphosphate (pdTp) inhibited tumor formation without effects on body weight or liver function. We conclude that SND1 drives pro-oncogenic transcriptomic and proteomic changes in hepatocyte resulting in aggressive HCC. SND1 specific RNA interactome is identified with RNA immunoprecipitation sequencing (RIPSeq) approach. With an adjusted p value of2-fold enrichment over control, 282 mRNAs were identified to significantly associate with SND1 protein. We focused on the tumor suppressor Protein Tyrosine Phosphatase non-receptor type 23 (PTPN23) because its regulation by SND1 and its role in HCC are not known. In current study, we confirm that SND1 post-transcriptionally downregulates PTPN23. Pursuing functional studies with tetracycline inducible overexpression system, we validate that PTPN23 inhibits tyrosine kinase signaling, proliferation, epithelial to mesenchymal transition, migration, invasion and in vivo tumorigenesis.
Alb/SND1 mice also manifest steatosis and fibrosis at one year of age. Coupled with a pro-inflammatory hepatic phenotype, we conclude that Alb/SND1 livers present NASH. High fat diet causes severe NASH and aggressive NASH induced HCC in Alb/SND1 mice. Serum and hepatic lipid profiling shows that hepatocyte specific SND1 overexpression associate with elevated triglyceride and cholesterol LDL levels. Contrarily, hepatocyte specific deletion of SND1 (SND1ΔHEP) in vivo, significantly protects against age dependent steatosis. Association of SND1 in NASH pathology is novel discovery and we present preliminary evidence confirming role of SND1 in promoting NASH.
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Robertson, Chadia L. "Analysis of the Role of Astrocyte Elevated Gene-1 in Normal Liver Physiology and in the Onset and Progression of Hepatocellular Carcinoma." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3573.
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First identified over a decade ago, Astrocyte Elevated Gene-1 (AEG-1) has been studied extensively due to early reports of its overexpression in various cancer cell lines. Research groups all over the globe including our own have since identified AEG-1 overexpression in cancers of diverse lineages including cancers of the liver, colon, skin, prostate, breast, lung, esophagus, neurons and neuronal glia as compared to matched normal tissue. A comprehensive and convincing body of data currently points to AEG-1 as an essential component, critical to the progression and perhaps onset of cancer. AEG-1 is a potent activator of multiple pro-tumorigenic signal transduction pathways such as mitogen-activated protein extracellular kinase (MEK)/ extracellular signal-regulated kinase (ERK), phosphotidyl-inositol-3-kinase (PI3K)/Akt/mTOR, NF-κB and Wnt/β-catenin pathway. In addition, studies show that AEG-1 not only alters
global gene and protein expression profiles, it also modulates fundamental intracellular processes, such as transcription, translation and RNA interference in cancer cells most likely by functioning as a scaffold protein.
The mechanisms by which AEG-1 is overexpressed in cancer have been studied extensively and it is clear that multiple layers of regulation including genomic amplification, transcriptional, posttranscriptional, and posttranslational controls are involved however; the mechanism by which AEG 1 itself induces its oncogenic effects is still poorly understood. Just as questions remain about the exact role of AEG-1 in carcinogenesis, very little is known about the role of AEG-1 in regulating normal physiological functions in the liver. With the help of the Massey Cancer Center Transgenic/Knockout Mouse Core, our lab has successfully created a germline-AEG-1 knockout mouse (AEG-1-/-) as a model to interrogate AEG-1 function in vivo. Here I present the insights gained from efforts to analyze this novel AEG-1-/- mouse model. Aspects of the physiological functions of AEG-1 will be covered in chapter two wherein details of the characterization of the AEG-1-/- mouse are described including the role of AEG-1 in lipid metabolism. Chapter three discusses novel discoveries about the specific role of AEG-1 in mediating hepatocarcinogenesis by modulating NF-κB, a critical inflammatory pathway.
First identified over a decade ago, Astrocyte Elevated Gene-1 (AEG-1) has been studied extensively due to early reports of its overexpression in various cancer cell lines. Research groups all over the globe including our own have since identified AEG-1 overexpression in cancers of diverse lineages including cancers of the liver, colon, skin, prostate, breast, lung, esophagus, neurons and neuronal glia as compared to matched normal tissue. A comprehensive and convincing body of data currently points to AEG-1 as an essential component, critical to the progression and perhaps onset of cancer. AEG-1 is a potent activator of multiple pro-tumorigenic signal transduction pathways such as mitogen-activated protein extracellular kinase (MEK)/ extracellular signal-regulated kinase (ERK), phosphotidyl-inositol-3-kinase (PI3K)/Akt/mTOR, NF-κB and Wnt/β-catenin pathway. In addition, studies show that AEG-1 not only alters
global gene and protein expression profiles, it also modulates fundamental intracellular processes, such as transcription, translation and RNA interference in cancer cells most likely by functioning as a scaffold protein. The mechanisms by which AEG-1 is overexpressed in cancer have been studied extensively and it is clear that multiple layers of regulation including genomic amplification, transcriptional, posttranscriptional, and posttranslational controls are involved however; the mechanism by which AEG 1 itself induces its oncogenic effects is still poorly understood. Just as questions remain about the exact role of AEG-1 in carcinogenesis, very little is known about the role of AEG-1 in regulating normal physiological functions in the liver. With the help of the Massey Cancer Center Transgenic/Knockout Mouse Core, our lab has successfully created a germline-AEG-1 knockout mouse (AEG-1-/-) as a model to interrogate AEG-1 function in vivo. Here I present the insights gained from efforts to analyze this novel AEG-1-/- mouse model. Aspects of the physiological functions of AEG-1 will be covered in chapter two wherein details of the characterization of the AEG-1-/- mouse are described including the role of AEG-1 in lipid metabolism. Chapter three discusses novel discoveries about the specific role of AEG-1 in mediating hepatocarcinogenesis by modulating NF-κB, a critical inflammatory pathway.
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Mirella, Pastore. "Ruolo della tirosin-chinasi Mer nella progressione delle malattie epatiche croniche e nello sviluppo del carcinoma epatocellulare." Doctoral thesis, 2019. http://hdl.handle.net/2158/1157292.
Full textBook chapters on the topic "Liver diseases, HCC,MerTK"
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Torimura, Takuji, Takato Ueno, Motoaki Kin, Riko Ogata, Michio Sata, and Kyuichi Tanikawa. "VEGF Participates in Neovascularization and Sinusoidal Capillarization in HCC." In Liver Diseases and Hepatic Sinusoidal Cells, 274–87. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-67935-6_23.
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Zigmond, Ehud, and Daniel Shouval. "Viral alcoholic and fatty liver diseases." In Oxford Textbook of Global Public Health, edited by Roger Detels, Quarraisha Abdool Karim, Fran Baum, Liming Li, and Alastair H. Leyland, 249–68. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198816805.003.0074.
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Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, alcohol, and non-alcoholic fatty liver disease (NAFLD) are major risk factors in the development of chronic liver disease (CLD), cirrhosis, and hepatocellular carcinoma (HCC). Various estimates have been proposed regarding the global prevalence of HBV and HCV carriers. According to a recent Polaris Observatory HCV Collaborators and the World Health Organization (WHO) burden estimates that 257 and 71 million people are living in the world with HBV and HCV infection, respectively, leading to an annual death from cirrhosis/liver failure and HCC of ~900,000 and ~400,000, respectively. Alcohol consumption, which is a major risk factor for CLD and HCC, is responsible for about 3.3 million deaths annually worldwide and for 5.1% of the global burden of disease as measured in disability-adjusted life years (DALYs). In recent years NAFLD and non-alcoholic steatohepatitis (NASH) associated with the metabolic syndrome, have captured the attention of hepatologists, public health experts, and the pharma industry alike. Indeed, the incidence of NAFLD and NASH and its complications including cirrhosis and HCC, is rising to epidemic proportions in the Western population, and constitute a major health problem worldwide.
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Darmadi, Darmadi, Riska Habriel Ruslie, and Cennikon Pakpahan. "Vascular Endothelial Growth Factor (VEGF) in Liver Disease." In Tumor Angiogenesis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103113.
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Vascular endothelial growth factor (VEGF) is the most potent stimulating factor for angiogenesis. Its expression is related to inflammation and hypoxia. In normal conditions, VEGF is important in the wound healing process. The binding of VEGF with its receptors triggers angiogenesis and lymphangiogenesis and increases vascular permeability. Liver diseases comprise acute and chronic ones. Liver diseases cause inflammation and hypoxia, which increase VEGF level. If they occur chronically, persistent high VEGF levels will promote the risk of chronic liver diseases, including hepatic viral infections, alcoholic and nonalcoholic fatty liver diseases, liver cirrhosis, and finally hepatocellular carcinoma (HCC). High VEGF level is also associated with progressive disease course and poorer outcomes. Tissue remodeling by replacement of normal liver tissue with fibrous tissue occurs. Due to the importance of VEGF in angiogenesis and liver diseases, therapeutic agents targeting VEGF have been developed. Drugs that neutralize VEGF and modulate VEGF receptors have been approved for treating various disorders, including liver disease. Additionally, VEGF is a promising modality for diagnosing liver cirrhosis and HCC. VEGF may also be utilized to predict the outcome of the liver and to monitor the therapeutic response of patients.
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Abu-Zaid, Ahmed, Lynn Alkhatib, Judie Noemie Hoilat, Sana Samer Kadan, Abdulaziz Mohammed Eshaq, Ahmed Mubarak Fothan, Abdulrahman Mohammed Bakather, et al. "Past, Present, and Future Perspectives on the Systemic Therapy for Advanced Hepatocellular Carcinoma (HCC) — A Comprehensive Review." In Recent Advances in Liver Diseases and Surgery. InTech, 2015. http://dx.doi.org/10.5772/60991.
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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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Kale, Aditya. "Hepatocellular Carcinoma: Diagnosis and Surveillance." In Hepatocellular Carcinoma - Challenges and Opportunities of a Multidisciplinary Approach [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99839.
Full textAbstract:
Hepatocellular carcinoma arises commonly on the background of liver cirrhosis. Patients presenting with clinical symptoms have advanced stage and often are unsuitable for curative therapies. Diagnosis of hepatocellular carcinoma is commonly performed by multiphase computed tomography (CT) and / or magnetic resonance imag¬ing scans (MRI). Contrast enhanced ultrasound and MRI with hepatobiliary contrast agents are better in characterizing small lesions. Tumor markers play an adjunct role in diagnosis. For HCC in cirrhotic liver biopsy is seldom required and diagnosis is based on typical imaging features of non-rim arterial phase hyperenhancement and washout on delayed phase and pseudocapsule appearance. This is due to differential blood supply of liver parenchyma, regenerative nodules and tumor. Biopsy is only required in noncirrhotic liver, vascular liver diseases, atypical imaging features. Surveillance programs involving high risk groups can help in early detection of lesions which are amenable for curative therapies. Biannual ultrasound with or without alfa fetoprotein are commonly used surveillance tests. Multidisciplinary teams provide platform for care coordination, reassessments of clinical course, and fine changes in treatment plans required for management of this complex group of patients.
Conference papers on the topic "Liver diseases, HCC,MerTK"
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Al-Kababji, Ayman Jamal, Faycal Bensaali, and Sarada Prasad Dakua. "Segmenting Liver Volume for Surgical Analysis." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0100.
Full textAbstract:
Introduction: Almost two million people worldwide die annually due to hepatic-related diseases. Half of these diseases are attributed to cirrhosis and the other half are related to hepatitis and hepatocellular carcinoma (HCC). The liver is also a metastasis hub from adjacent organs. This research aims to create an accurate high-quality delineation of the human liver and prepare them to be 3D printed for medical analysis to help aid medical practitioners in pre-procedural planning. Materials and Methods: Convolutional neural networks (ConvNets) are used to perform the liver tissues delineation. A famous ConvNet, named U-net, is used as the basis benchmark architecture that is also known for its great outcomes in the medical segmentation field. Contrast-enhanced computerized tomography (CT) scans are used from the famous Medical Segmentation Decathlon Challenge (Task 8: Hepatic Vessel), abbreviated as MSDC-T8. It contains 443 CT scans, which is considered the largest dataset that contains both the tumors and vessels ground-truth segmentation. Some researchers also generated the liver masks for this dataset, making it a complete dataset that contains all the relevant tissues’ ground-truth masks. Results: Currently, the liver delineation has been successfully done with very high DICE = 98.12% (higher than the state-of-the-art results DICE = 97.61%), where a comparison between two famous schedulers namely, ReduceLRonPlateau and OneCycleLR has been conducted. Moreover, the 3D liver volume creation has also been completed and built via the marching cube algorithm. Conclusions/Future Directions: The developed ConvNet can segment livers with high confidence. The tumor(s) and vessels tissues segmentation are also under investigation now. Moreover, newly devised self-organized neural networks (Self-ONN) look promising and will be investigated soon. Lastly, a GUI will be built so that the medical practitioner can just insert the CT volume and get the 3D liver volume with all the segmented tissues.