Identification of cooperating oncogenes in E mu-myc transgenic mice by provirus tagging

M van Lohuizen ¹, S Verbeek , B Scheijen

⁰Division of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam.

Cell +

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May 31, 1991

View abstract on PubMed

Summary

Moloney murine leukemia virus (Mo-MLV) infection accelerates B cell lymphomagenesis in E mu-myc mice. Provirus tagging identified four cooperating oncogenes: pim-1, bmi-1, pal-1, and bla-1.

Area Of Science

Oncology
Molecular Biology
Genetics

Background

E mu-myc transgenic mice are models for B cell lymphomagenesis.
Moloney murine leukemia virus (Mo-MLV) infection accelerates tumor development in these mice.
Identifying cooperating genes is crucial for understanding B cell transformation.

Purpose Of The Study

To identify genes cooperating with the E mu-myc transgene in B cell transformation using provirus tagging.
To characterize novel proviral insertion sites and their encoded proteins.

Main Methods

Provirus tagging in E mu-myc transgenic mice infected with Mo-MLV.
Analysis of proviral insertion sites in pre-B cell lymphomas.
Bioinformatic analysis of the bmi-1 gene and its protein product.

Main Results

Four common proviral insertion loci (pim-1, bmi-1, pal-1, bla-1) were identified in 35%, 35%, 28%, and 14% of tumors, respectively.
bmi-1, pal-1, and bla-1 represent novel common proviral insertion sites.
The bmi-1 gene encodes a conserved nuclear protein with transcriptional regulator motifs, including a zinc finger.

Conclusions

Provirus tagging is effective for identifying cooperating oncogenes in lymphomagenesis.
The identified loci, particularly bmi-1, pal-1, and bla-1, are significant in B cell transformation.
Further research is needed to assign genes to pal-1 and bla-1 and to elucidate their roles.

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