Strain Code 01R25 [RFM/UnN]
Origin and Characteristics
To N from Oak Ridge National Laboratories, 1980.
- Neoplastic diseases occurred in 88% of aging virgin females: reticulum cell sarcoma
(67%) and lung tumors (26%) were most common; thymic lymphomas (8%), pituitary adenomas
(7%), and Harderian gland tumors (3%) were the only other tumors with an incidence
greater than 1%; mammary tumors were absent. (108)
- Murine myeloid leukemia was serially passaged by spleen cell inoculation to provide
a possible model for human acute myelocytic leukemia; the original cell donor developed
leukemia after irradiation. Leukemic cells obtained early in the course of the disease
were less malignant than those obtained from preterminal mice. The leukemia was
most sensitive to alkytlating agents, but also responsive to antimetabolites. (554)
- Antilymphocyte globulin administration reduced the incidence and increased the latency
of lymphomas induced by whole body irradiation. (033)
- Corynebacterium parvum inoculation prolonged the survival of RFM mice bearing
myeloid leukemia induced by leukemia cell passage. Silica abrogated the effects
of C. parvum, and polyvinyl pyridine-N-oxide prevented the inhibitory effects
of silica, indicating a critical role for macrophages. (062)
- Tumors were induced more effectively with neutrons than with gamma rays. Gamma rays
increased the incidence of thymic lymphoma and ovarian tumors, but the incidence
of reticulum cell sarcoma and lung adenoma decreased. Neutron irradiation effects
were similar, but lung adenomas were increased. (744)
- Glomerulosclerosis was found in almost all aging virgin females and was severe in
90%; uterine hyperplasia (87%), mammary hyperplasia (39%), adrenal cortical atrophy
(52%), auricular thrombosis (35%), hemopoietic hyperplasia (33%), arteriosclerosis
(21%), and fatty liver (21%) were the other diseases of moderate to high frequency.
- A fatal host versus graft syndrome characterized by depletion of peripheral T lymphocytes
was initiated by perinatal inoculations of (T6 X RFM)F1 spleen cells.
The syndrome may serve as a model for immunodeficiency syndromes of Nezelof type.