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Renal Neoplastic Response to Leukosis Virus Strains BAI A (Avian Myeloblastosis Virus) and MC29¹

Department of Surgery, Duke University Medical Center, Durham, North Carolina 27706 [J. W. B., J. F. C., D. B., U. H.], and Life Sciences Research Laboratories, Life Sciences, Inc., St. Petersburg, Florida 33710 [J. W. B., D. B., G. E. H.]

Previous reports described the induction of avian renal neoplasms by leukosis virus strains BAI A [avian myeloblastosis virus (AMV)] and MC29, and illustrated morphological characteristics of the tumors. Continued studies in this work confirm evidence of the origin of the tumors from embryonal cells residual in the posthatched chick. The work further emphasizes differences in histopathology of the neoplasms caused by the two viruses and reveals differences in the histopathogenesis of the respective growths. Embryonal rests may consist of two types of cells, those of epithelial characteristics and a second element of differentiation between nephroblastema (mesenchyme) and epithelium and designated here as nephromesoblastoma. Infection by AMV induces tumors of epithelial characteristics and, in addition, derivatives of nephromesoblastoma consisting of cartilage, bone, areas of keratinization, and sarcoma. Keratinized structures in the nephroblastoma originate from nephromesoblastoma. In contrast, MC29 virus induces only epithelial growths representing principally aberrant and malformed glomerular and tubular structures with occasional cartilage derived from epithelial cells. MC29 tumors are completely lacking in nephromesoblastoma tissue and contain no bone, sarcoma, or keratinized formations. In MC29 tumors, occasional cartilage was derived from epithelium. Tumors caused by AMV exhibit the complex structure of nephroblastoma with all of the features of the growth in humans (Wilms' tumor). The neoplasms induced by both AMV and MC29 exhibit marked aberration, distortion, and malformation in the differentiation of the cells growing out from the embryonal rests representing rare manifestations of cell genetic influence inherent in the primordial growth of nephroblastema. The results thus illustrate fundamental differences in cellular composition and capacity to respond to etiologically different leukosis viruses.

¹ This work was supported by USPHS Research Grant C-4572; by Contracts NIH-71-2132 and NO1-CP-33291 within the Virus Cancer Program of the National Cancer Institute, NIH, USPHS; and by the Dorothy Beard Research Fund.

² Present address: Life Sciences Research Laboratories, St. Petersburg, Fla. 33710.

³ Present address: Cornell University, Ithaca, N. Y. 14850. Portions of the work reported here were taken from a dissertation submitted to Duke University, Durham, N. C., in partial fulfillment of the requirements for the Ph.D. degree.

⁴ Present address: National Cancer Institute, Bethesda, Md. 20014.

Received 7/23/75. Accepted 10/22/75.