ArticleJournal of virology2013
B cells in chronically hepatitis C virus-infected individuals lack a virus-induced mutation signature in the TP53, CTNNB1, and BCL6 genes.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- B Cell Differentiation and the Origin and Pathogenesis of Human B Cell Lymphomas.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Carcinogenic mechanisms of virus-associated lymphoma.Frontiers in immunology · 2024Review
- Hepatitis Virus-associated Non-hodgkin Lymphoma: Pathogenesis and Treatment Strategies.Journal of clinical and translational hepatology · 2023Review
- Hepatitis C Virus (HCV)-Ribonucleic Acid (RNA) As a Biomarker for Lymphoid Malignancy with HCV Infection.Cancers · 2023Review
- Article
- Clinical practice: hepatitis C virus infection, cryoglobulinemia and cryoglobulinemic vasculitis.Clinical and experimental medicine · 2019Review
- The value of detecting immunoglobulin gene rearrangements in the diagnosis of B-cell lymphoma.Oncotarget · 2017Article
- Hepatitis C virus - associated B cell non-Hodgkin's lymphoma.World journal of gastroenterology · 2016Review
- Hepatitis C virus-associated B-cell non-Hodgkin's lymphomas: what do we know?Therapeutic advances in hematology · 2016Review
- Role of hepatitis C virus in B cell lymphoproliferations.Virologica Sinica · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) is considered to have a causative role in B-cell lymphoproliferative diseases, including B-cell lymphomas, in chronic virus carriers. Previous data from in vitro HCV-infected B-cell lines and peripheral blood mononuclear cells from HCV-positive individuals suggested that HCV might have a direct mutagenic effect on B cells, inducing mutations in the tumor suppressor gene TP53 and the proto-oncogenes BCL6 and CTNNB1 (β-catenin). To clarify whether HCV indeed has a mutagenic effect on B cells in vivo, we analyzed naive and memory B cells from the peripheral blood of four chronic HCV carriers and intrahepatic B cells from the livers of two HCV-positive patients for mutations in the three reported target genes. However, no mutations were found in the TP53 and CTNNB1 genes. For BCL6, which is a physiological target of the somatic hypermutation process in germinal-center B cells, the mutation levels identified were not higher than those reported in the respective B-cell subsets in healthy individuals. Hence, we conclude that in chronic HCV carriers, the virus does not generally induce mutations in the cancer-related genes TP53, CTNNB1, and BCL6 in B cells. Based on these findings, new targets have to be investigated as potential mediators of HCV-associated B-cell lymphomagenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.