Abstract
Constitutive over-expression of myc oncogenes in the stem cell compartment of the bursa-of Fabricius of chickens provides an in-vivo model system for analysis of the mechanisms of myc-induced, multi-staged neoplastic change. The biology, molecular biology and genetics of this system has recently been reviewed (Neiman 1994a). Briefly, the lymphoid population of embryonic follicles of the bursa is composed of large cycling lymphoblasts expressing surface IgM (Thompson et al. 1987a) This population includes a compartment of stem cells that can clonally reconstitute ablated bursal follicles in transplantation experiments (Pink et al. 1985). Deregulated expression of a myc oncogene within this stem cell compartment, either due to integration of an avian leukosis virus (ALV) near c-myc (Hayward et al. 1981) or due to ex-vivo infection of embryonic bursal lymphoblasts with a v-myc transducing myelocytomatosis virus (HB1)(Neiman et al. 1985; Thompson et al. 1987a), initiates neoplastic change in bursal follicles. This change is signaled by the replacement of the lymphoid cells of the follicle with a monomorphic population of pyroninophilic lymphoblasts producing a histologically distinctive lesion called a transformed follicle (TF)(Cooper et al. 1960; Neiman et al. 1980a, b; Baba and Humphries 1985).
Published Version
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