T-Cell Lymphomas Emerging as Epineoplasms in Mice Bearing Transplanted Polyoma Virus-induced Salivary Gland Tumors1

A subset of salivary epithelial tumors induced by mouse polyoma virus (PyV) has been designated lymphoepithelioma on the basis of a prominent lymphocytic component. Serial transplantation of this variant has previ ously been observed to result in lymphoma development. A recent repe tition of this phenomenon allowed us to characterize the lymphoma cell populations with regard to phenotypic markers and PyV content. Lymphomas emerged in recipients of the third, fifth, sixth, and seventh transplant generations of the lymphoepithelioma. Most lymphomas were widely disseminated in hematopoietic and lymphoreticular tissues, and other sites as well. Flow cytometric analysis of lymphocyte populations from lymphomas in six recipients revealed that, while all lymphomas expressed phenotypic markers of immature cortical thymocytes, i.e., Thy-1, Pgp-1, .Hid, and CDS, they were not uniform with regard to other T-cell markers, notably CD4 and CDS. Varying levels of T-cell receptor markers CD3 and a/ß, as well as interleukin 2 receptor, were also noted. DNA blot analysis failed to detect PyV in lymphoma cells at a sensitivity level capable of detecting less than one intact copy per cell. It appears improbable the lymphoma was directly induced by PyV. Hy potheses invoking other mechanisms of lymphoma development are outlined.