tretinoin and Hepatitis-C

tretinoin has been researched along with Hepatitis-C* in 6 studies

Reviews

1 review(s) available for tretinoin and Hepatitis-C

ArticleYear
Current strategies for chemoprevention of hepatocellular carcinoma.
    Oncology, 2002, Volume: 62 Suppl 1

    Hepatocellular carcinoma (HCC) develops frequently in the liver of patients with chronic hepatitis and cirrhosis caused by persistent infection with hepatitis B virus or hepatitis C virus in Asia. Several studies including ours have revealed that the risk of HCC increases in parallel with the progression of hepatic fibrosis associated with chronic hepatitis and liver cirrhosis. It may be delineated reasonably, therefore, that suppression of fibrosis by chemical (or biological) agents would be able to decrease the risk of HCC. We have demonstrated that antifibrotic agents, such as HOE 077, TJ-9 and interferon, can reduce the risk of HCC. Accordingly, antifibrotic agents are promising candidates for chemoprevention of HCC. The results of our study are discussed within the scope of the current state of the art as regards chemopreventing HCC.

    Topics: Animals; Antineoplastic Agents; Antiviral Agents; Carcinoma, Hepatocellular; Chemoprevention; Drugs, Chinese Herbal; Forecasting; Hepatitis B; Hepatitis C; Humans; Interferons; Liver Cirrhosis, Experimental; Liver Neoplasms; Pyridines; Tretinoin

2002

Other Studies

5 other study(ies) available for tretinoin and Hepatitis-C

ArticleYear
Aleukemic Acute Promyelocytic Leukemia: How Concomitant HIV, Hepatitis C, and Chronic Alcohol Use Disorder May Have Hidden an Underlying Malignancy.
    The American journal of case reports, 2023, Feb-10, Volume: 24

    BACKGROUND Acute promyelocytic leukemia (APL) is a rare subtype of acute myeloid leukemia (AML) and is characterized by a genetic translocation affecting the retinoic acid receptor-alpha gene, leading to blockage in the differentiation of granulocytic cells. The accumulation of promyelocytes in bone marrow leads to cytopenias and life-threatening coagulopathies. Definitive diagnosis is made with bone marrow biopsy. Differentiation of APL from other leukemias is important to appropriately treat with all-trans retinoic acid (ATRA) and arsenic trioxide. Patients with HIV are at a higher risk to develop AML. This article identifies how multiple comorbidities and social factors can contribute to difficulties in diagnosing AML. CASE REPORT We present a 67-year-old man with a past medical history of hypertension and substance use disorder who presented with progressive exertional dyspnea and was found to have HIV, chronic hepatitis C, and APL with pancytopenia. His bone marrow biopsy confirmed AML. This was a case of co-existing HIV and aleukemic leukemia. CONCLUSIONS APL can present with pancytopenia, weakness, failure to thrive, or bleeding complications, which can be similar to presentations of those diagnosed with HIV. Diagnosis of APL can be differentiated between hypergranular and hypogranular; our patient demonstrated APL with only 52% blasts, which can make for a challenging diagnosis. Given increased mortality of APL, immediate ATRA therapy is warranted. Aleukemic leukemia is a rare presentation typically accompanied by skin manifestations. Our case highlights the importance of having high clinical suspicion for malignancy in patients with comorbidities that can interfere with the classic presentation of leukemia.

    Topics: Aged; Alcoholism; Hepatitis C; HIV Infections; Humans; Leukemia, Promyelocytic, Acute; Male; Pancytopenia; Tretinoin

2023
All-trans retinoic acid inhibits HCV replication by downregulating core levels via E6AP-mediated proteasomal degradation.
    Biochemical and biophysical research communications, 2022, 02-26, Volume: 594

    Here, we found that all-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, strengthens the anti-viral defense mechanism of E6-associated protein (E6AP) that downregulates hepatitis C virus (HCV) Core levels via ubiquitin-dependent proteasomal degradation. For this effect, ATRA downregulated both protein and enzyme activity levels of DNA methyltransferase 1 and 3b and activated E6AP expression via promoter hypomethylation in HepG2 cells but not in Hep3B cells, in which p53 was absent. Ectopic p53 expression but not E6AP overexpression restored the ability of ATRA to downregulate HCV Core levels in Hep3B cells, suggesting a direct role of p53 in the E6AP-mediated ubiquitination of HCV Core. ATRA also downregulated HCV Core levels during HCV infection in Huh7D cells to inhibit virus replication, providing theoretical basis for the clinical application of ATRA against HCV infection.

    Topics: DNA Methylation; Dose-Response Relationship, Drug; Down-Regulation; Hep G2 Cells; Hepacivirus; Hepatitis C; Humans; Proteasome Endopeptidase Complex; Proteolysis; Tretinoin; Ubiquitin; Ubiquitin-Protein Ligases; Ubiquitination; Viral Core Proteins; Virus Replication

2022
Regulation of Hepatitis C Virus Infection by Cellular Retinoic Acid Binding Proteins through the Modulation of Lipid Droplet Abundance.
    Journal of virology, 2019, 04-15, Volume: 93, Issue:8

    Retinoid (vitamin A) is an essential diet constituent that governs a broad range of biological processes. Its biologically active metabolite, all-

    Topics: Antiviral Agents; Cell Line; Endoplasmic Reticulum; Hepacivirus; Hepatitis C; Humans; Lipid Droplets; Receptors, Retinoic Acid; Tretinoin

2019
An identification of the novel combination therapy for hepatitis C virus 1b infection by using a replicon system and human induced pluripotent stem cells.
    Hepatology (Baltimore, Md.), 2010, Volume: 51, Issue:1

    Topics: Hepatitis C; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Induced Pluripotent Stem Cells; Interferon-alpha; Quinolines; Replicon; Tretinoin; Virus Replication

2010
Acute promyelocytic leukaemia. Report of a meeting of Physicians and Scientists, University College London.
    Lancet (London, England), 1994, Dec-10, Volume: 344, Issue:8937

    Topics: Adult; DNA, Neoplasm; Hepatitis C; Humans; Leukemia, Promyelocytic, Acute; Male; Receptors, Retinoic Acid; Transfusion Reaction; Translocation, Genetic; Tretinoin

1994