Minimal truncation of the c-myb gene product in rapid-onset B-cell lymphoma? Academic Article uri icon

Overview

MeSH Major

  • Avian Leukosis Virus
  • Lymphoma, B-Cell
  • Proto-Oncogene Proteins
  • Trans-Activators

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.

publication date

  • September 4, 1997

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC191928

PubMed ID

  • 9261372

Additional Document Info

start page

  • 6526

end page

  • 33

volume

  • 71

number

  • 9