Related Experiment Videos
The myb oncogene.
1Jonsson Comprehensive Cancer Center, University of California, School of Medicine, Los Angeles 90024.
Gene Amplification and Analysis
|January 1, 1986
Summary
The c-myb gene, crucial in cell growth, can cause leukemia when altered by viruses. Research explores its nuclear functions, cell cycle regulation, and role in human cancers.
Area of Science:
- Molecular Biology
- Genetics
- Oncology
Background:
- The c-myb gene is a highly conserved, single-copy gene.
- It is independently transduced by avian acute leukemia viruses (AMV and E26) and activated by insertional mutagenesis in hematopoietic tumors.
- Truncation of the c-myb coding region is a common feature in retroviral activations.
Purpose of the Study:
- To investigate the function of c-myb gene products, which are nuclear proteins.
- To understand the regulation of c-myb expression, particularly its cell cycle dependence.
- To explore the role of c-myb in leukemogenesis and human malignancies.
Main Methods:
- Analysis of retroviral activations of c-myb.
- Studying c-myb gene products' association with the nuclear matrix, half-lives, and DNA binding in vitro.
- Investigating c-myb expression patterns in different cell types and tissues.
- Utilizing new experimental systems, including a myb-related gene in Drosophila and murine myb studies.
Main Results:
- c-myb gene products are nuclear proteins with short half-lives that bind DNA, suggesting roles in DNA replication or transcription.
- c-myb expression is cell cycle dependent in many cell types but not in the thymus.
- v-myb transformation's hematopoietic specificity is not fully understood, but hematopoietic growth factors are implicated.
Conclusions:
- The c-myb gene and its viral counterparts are implicated in leukemogenesis.
- Further research is needed to define myb protein function, understand expression regulation, identify transforming alterations, and determine its role in human cancers.