ArticleJournal of virology1997
Minimal truncation of the c-myb gene product in rapid-onset B-cell lymphoma.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Selection for avian leukosis virus integration sites determines the clonal progression of B-cell lymphomas.PLoS pathogens · 2017Article
- Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas.mBio · 2015Article
- Myb proteins: angels and demons in normal and transformed cells.Frontiers in bioscience (Landmark edition) · 2011Review
- RNA processing control in avian retroviruses.Frontiers in bioscience : a journal and virtual library · 2008Review
- 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
- The negative regulator of splicing element of Rous sarcoma virus promotes polyadenylation.Journal of virology · 2006Article
- Silent point mutation in an avian retrovirus RNA processing element promotes c-myb-associated short-latency lymphomas.Journal of virology · 2003Article
- Functional genomic analysis reveals distinct neoplastic phenotypes associated with c-myb mutation in the bursa of Fabricius.Oncogene · 2003Article
- Review
- Article
- Efficient polyadenylation of Rous sarcoma virus RNA requires the negative regulator of splicing element.Nucleic acids research · 2002Article
- Tumorigenic N-terminal deletions of c-Myb modulate DNA binding, transactivation, and cooperativity with C/EBP.Oncogene · 2001Article
- Functional analysis of carboxy-terminal deletion mutants of c-Myb.Journal of virology · 1999Article
- Transformation by v-Myb.Oncogene · 1999Review
- Identification of protein instability determinants in the carboxy-terminal region of c-Myb removed as a result of retroviral integration in murine monocytic leukemias.Journal of virology · 1999Article
- The role of overlapping U1 and U11 5' splice site sequences in a negative regulator of splicing.RNA (New York, N.Y.) · 1999Article
- Genetic determinant of rapid-onset B-cell lymphoma by avian leukosis virus.Journal of virology · 1997Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Oncogenic activation of c-myb by insertional mutagenesis has been implicated in rapid-onset B-cell lymphomas induced by the nonacute avian leukosis virus EU-8. In these tumors, proviruses are integrated either upstream of the c-myb coding region or within the first intron of c-myb. Tumors with either type of integration contained identical chimeric mRNAs in which the viral 5' splice site was juxtaposed to the 3' splice site of c-myb exon 2 and myb exon 1 was eliminated. Both classes of integrations generated truncated Myb proteins that were indistinguishable by Western analysis. In contrast to most other examples of c-myb activation, the truncation consisted of only 20 N-terminal amino acids and did not disrupt either the DNA binding domain near the N terminus or the negative regulatory domain near the C terminus of Myb. The significance of the 20-amino-acid Myb truncation to tumorigenesis was tested by infection of chicken embryos with retroviral vectors expressing different myb gene products. While virus expressing either wild-type c-myb or c-myb mutated at the N-terminal casein kinase II sites was only weakly oncogenic at 10 weeks, the minimally truncated myb virus induced a high incidence of rapid-onset tumors, including B-cell lymphomas, sarcomas, and adenocarcinomas.
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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.