Primary polyoma virus-induced murine thymic epithelial tumors. A tumor model of thymus physiology

G. P. Hoot, J. R. Kettman

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

Thymic tumors were induced in C3H/Bittner mice by neonatal inoculation with polyoma virus. The objective of this study was to identify the phenotypes of the cells within the tumors and to attempt to determine the origin of the neoplastic cell population(s). At the ultrastructural level, the neoplastic cells resembled normal thymic epithelium with tonofilaments and desmosomes. Immunoperoxidase staining demonstrated the presence of cytokeratin, Ia(k), β2-microglobulin, asialo-GM1, the thymic cortical epithelial marker ER-TR4, and the medullary epithelial marker ER-TR5. Islands of normal cortical thymocytes supported by residual normal cortical epithelium and acid phosphatase-positive cortical macrophages were interspersed in the tumors. Residual islands of normal medullary architecture with nonspecific esterase-positive IDCs were rarely identified in tumors. Most lymphocytes in the tumors were normal immature cortical thymocytes with the phenotype Tdt+, PNA+, Thy1.2(bright), Ly-1(dull), H-2K(k dull), ThB+, J11d+, and Lyt-2+L3T4+. Lymphocytes in the tumors were steroid-sensitive like normal thymocytes. The proportions of Lyt-2+L3T4- and Lyt-2-L3T4+ cells were generally larger in the tumors than in normal thymus and reflected the higher frequency of lymphocytes in the tumors capable of proliferating in vitro in response to Con A plus IL-2. The data were consistent with the hypothesis that the neoplasia originates from thymic epithelium that is interspersed with normal, developing thymic lymphocytes.

Original languageEnglish (US)
Pages (from-to)679-695
Number of pages17
JournalAmerican Journal of Pathology
Volume135
Issue number4
StatePublished - 1989

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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