ArticlemBio2015
Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas.
Article in mBio, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- lncRNA ch-MYC-AS1 restricts ALV-J replication by disrupting the ANXA2-C-Myc oncogenic axis.Microbiology spectrum · 2026Article
- Methodological landscape in the field of integration site identification of retroviruses and retroviral vectors.Frontiers in bioengineering and biotechnology · 2025Review
- Critical role for ribonucleoside-diphosphate reductase subunit M2 in ALV-J-induced activation of Wnt/β-catenin signaling via interaction with P27.Journal of virology · 2023Article
- Proviral ALV-LTR Sequence Is Essential for Continued Proliferation of the ALV-Transformed B Cell Line.International journal of molecular sciences · 2022Article
- A point mutation in HIV-1 integrase redirects proviral integration into centromeric repeats.Nature communications · 2022Article
- rigrag: high-resolution mapping of genic targeting preferences during HIV-1 integration in vitro and in vivo.Nucleic acids research · 2021Article
- Mutations altering acetylated residues in the CTD of HIV-1 integrase cause defects in proviral transcription at early times after integration of viral DNA.PLoS pathogens · 2020Article
- Gp37 Regulates the Pathogenesis of Avian Leukosis Virus Subgroup J via Its C Terminus.Journal of virology · 2020Article
- Isolation and Identification of Subgroup J Avian Leukosis Virus Inducing Multiple Systemic Tumors in Parental Meat-Type Chickens.Frontiers in veterinary science · 2020Article
- An Improved Sequencing-Based Bioinformatics Pipeline to Track the Distribution and Clonal Architecture of Proviral Integration Sites.Frontiers in microbiology · 2020Article
- A novel recombinant avian leukosis virus isolated from gamecocks induced pathogenicity in Three-Yellow chickens: a potential infection source of avian leukosis virus to the commercial chickens.Poultry science · 2019Article
- Multifunctional miR-155 Pathway in Avian Oncogenic Virus-Induced Neoplastic Diseases.Non-coding RNA · 2019Review
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- A Novel Long Non-Coding RNA in the hTERT Promoter Region Regulates hTERT Expression.Non-coding RNA · 2017Article
- Selection for avian leukosis virus integration sites determines the clonal progression of B-cell lymphomas.PLoS pathogens · 2017Article
- Article
- Integration of ALV intoOncotarget · 2017Article
- Article
- Avian Leukosis Virus Activation of an Antisense RNA Upstream of TERT in B-Cell Lymphomas.Journal of virology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledAvian leukosis virus (ALV) induces B-cell lymphoma and other neoplasms in chickens by integrating within or near cancer genes and perturbing their expression. Four genes--MYC, MYB, Mir-155, and TERT--have previously been identified as common integration sites in these virus-induced lymphomas and are thought to play a causal role in tumorigenesis. In this study, we employ high-throughput sequencing to identify additional genes driving tumorigenesis in ALV-induced B-cell lymphomas. In addition to the four genes implicated previously, we identify other genes as common integration sites, including TNFRSF1A, MEF2C, CTDSPL, TAB2, RUNX1, MLL5, CXorf57, and BACH2. We also analyze the genome-wide ALV integration landscape in vivo and find increased frequency of ALV integration near transcriptional start sites and within transcripts. Previous work has shown ALV prefers a weak consensus sequence for integration in cultured human cells. We confirm this consensus sequence for ALV integration in vivo in the chicken genome. IMPORTANCE: Avian leukosis virus induces B-cell lymphomas in chickens. Earlier studies showed that ALV can induce tumors through insertional mutagenesis, and several genes have been implicated in the development of these tumors. In this study, we use high-throughput sequencing to reveal the genome-wide ALV integration landscape in ALV-induced B-cell lymphomas. We find elevated levels of ALV integration near transcription start sites and use common integration site analysis to greatly expand the number of genes implicated in the development of these tumors. Interestingly, we identify several genes targeted by viral insertions that have not been previously shown to be involved in cancer.
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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.