ArticleJournal of virology1989
RAV-1 insertional mutagenesis: disruption of the c-myb locus and development of avian B-cell lymphomas.
Article in Journal of virology, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 68 citations in OpenAlex.
- Article
- Endogenous Avian Leukosis Virus in Combination with Serotype 2 Marek's Disease Virus Significantly Boosted the Incidence of Lymphoid Leukosis-Like Bursal Lymphomas in Susceptible Chickens.Journal of virology · 2019Article
- Telomerase reverse transcriptase expression elevated by avian leukosis virus integration in B cell lymphomas.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Functional genomic analysis reveals distinct neoplastic phenotypes associated with c-myb mutation in the bursa of Fabricius.Oncogene · 2003Article
- What retroviruses teach us about the involvement of c-Myc in leukemias and lymphomas.Leukemia · 2002Review
- Tumorigenic N-terminal deletions of c-Myb modulate DNA binding, transactivation, and cooperativity with C/EBP.Oncogene · 2001Article
- Review
- Regulation of the resident chromosomal copy of c-myc by c-Myb is involved in myeloid leukemogenesis.Molecular and cellular biology · 2000Article
- Reassessing the role of C-MYB in tumorigenesis.Oncogene · 1999Review
- Genetic determinant of rapid-onset B-cell lymphoma by avian leukosis virus.Journal of virology · 1997Article
- Minimal truncation of the c-myb gene product in rapid-onset B-cell lymphoma.Journal of virology · 1997Article
- Retroviral insertional activation of the c-myb proto-oncogene in a Marek's disease T-lymphoma cell line.Journal of virology · 1996Article
- FAETL motif required for leukemic transformation by v-Myb.Journal of virology · 1996Article
- Lymphoid leukosis viruses, their recognition as 'persistent' viruses and comparisons with certain other retroviruses of veterinary importance.Veterinary research communications · 1996Review
- Casein kinase II phosphorylation site mutations in c-Myb affect DNA binding and transcriptional cooperativity with NF-M.Molecular and cellular biology · 1995Article
- Modulation of c-Myb-induced transcription activation by a phosphorylation site near the negative regulatory domain.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Mutations in the DNA-binding and transcriptional activation domains of v-Myb cooperate in transformation.Journal of virology · 1995Article
- Overexpression of C-terminally but not N-terminally truncated Myb induces fibrosarcomas: a novel nonhematopoietic target cell for the myb oncogene.Molecular and cellular biology · 1994Article
- Recognition of specific DNA sequences by the c-myb protooncogene product: role of three repeat units in the DNA-binding domain.Proceedings of the National Academy of Sciences of the United States of America · 1993Article
- Mechanism of c-myc regulation by c-Myb in different cell lineages.Molecular and cellular biology · 1993Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Infection of young chickens with RAV-1, a subgroup A isolate of avian leukosis virus, results in the development of lymphoid leukosis, a B-cell lymphoma characterized by provirus insertion into the c-myc locus. We report here that when 12- to 13-day-old embryos rather than 1-day-old chickens were infected with RAV-1, a novel B-cell lymphoma developed in which proviral insertions had activated expression of the c-myb gene. These tumors expressed elevated levels of a 4.5-kilobase myb-containing mRNA transcript that contained c-myb sequences not found in v-myb. The c-myc locus in these tumors appeared normal. The biological properties of the activated myb lymphoma were distinct from those of lymphoid leukosis. Metastatic disease developed within 7 weeks of infection. Distinct intermediate pathogenic stages with preneoplastic and primary neoplastic lesions were not detected. Although bursal tissues appeared to be nonmalignant on gross examination, Southern analyses of bursal DNA revealed the presence of tumor with the same clonal origin as abdominal lymphoma masses. The dependence on embryonic infection for development of activated myb lymphoma suggests that the target cells in which c-myb is activated are found only in embryos and are distinct from those cells that give rise to lymphoid leukosis.
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