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JNCI Monographs 2008 2008(39):37-40; doi:10.1093/jncimonographs/lgn015
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Published by Oxford University Press 2008.

Genetic and Environmental Cofactors of Myc Translocations in Plasma Cell Tumor Development in Mice

Siegfried Janz

Affiliation of author: Laboratory of Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD

Correspondence to: Siegfried Janz, Laboratory of Genetics, National Cancer Institute, Bldg 37, Rm 2B10, Bethesda, MD 20892-4256 (e-mail: sj4s{at}nih.gov).

Peritoneal plasmacytomagenesis in inbred BALB/c mice affords an experimental model system for the study of the mechanism by which naturally occurring Myc (c-myc) translocations collaborate with host susceptibility factors and environmental influences in tumor development. Mouse plasmacytoma is initiated in ~80% of cases by a balanced chromosomal T(12;15)(Igh-Myc) translocation that results in a mode of Myc deregulation that renders the survival and outgrowth of the translocation-bearing tumor precursor exquisitely dependent upon factors provided by sustained inflammation (IL-6) and gut flora microbes. Tumor susceptibility genes of BALB/c, such as weak efficiency alleles of genes encoding p16Ink4a and Frap (mTOR), are also required for plasmacytoma, although the pathways linking these genes with deregulated Myc and the environment have not yet been elucidated. The findings in mouse plasmacytoma may be relevant for hematopoietic neoplasms in human beings, in which leukemia- and lymphoma-associated chromosomal translocation (LLA-CT) is much more frequent than subsequent neoplasia. Just like T(12;15)-carrying B-lymphocytes and plasma cells in mice, the malignant transformation of LLA-CT–bearing blood cells in humans may be a rare occurrence that requires several genetic and environmental cofactors to take place.


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