## Abstract New Zealand Black (NZB) mice, an inbred strain characterized by immunological dysfunction and lymphoreticular malignancy, also develop populations of aneuploid spleen cells. In detailed cytogenetic analyses performed on 10 NZBs, the chromosomally abnormal cells were found to be clonally
Neoplastic behavior of chromosomally abnormal clones in New Zealand black mice
✍ Scribed by J. M. Friedman; Philip J. Fialkow; Jean Bryant; A. L. Reddy; Armi C. Salo
- Publisher
- John Wiley and Sons
- Year
- 1978
- Tongue
- French
- Weight
- 579 KB
- Volume
- 22
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
Abstract
Old New Zealand Black (NZB) mice frequently develop reticulum‐cell sarcoma and clones of aneuploid cells in their spleens. In order to define the relationship between neoplasms and chromosomal abnormalities, the pattern of distribution of aneuploid cells was studied to see if it corresponds to that expected of the malignancy, and chromosomally aberrant or normal spleen cells were transplanted into syngeneic newborn recipients. The results indicate that aneuploid cells arise focally but may disseminate widely in an affected mouse. A strong association was found between spleen‐cell aneuploidy in a transplantation donor and both aneuploidy and histological evidence of reticulum‐cell sarcoma in young recipients. Chromosomal aberrations in young recipients were always of donor origin. On the basis of these data, it seems likely that aneuploid clones which arise in the spleens of old NZB mice usually are at least potentially neoplastic.
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## Abstract A longitudinal study of 40 New Zealand Black (NZB) mice and 20 BALB/c control animals was performed. A significant association was observed between the presence of acquired spleen‐cell aneuploidy at some time during life and development of histological evidence of reticulum‐cell neoplas
## Abstract Polyclonal B cell activation is a hallmark of the immune dysregulation in New Zealand Black (NZB) mice. We have previously shown that the splenic B cell activation is associated with increased CD80 expression. Here we show that abnormal expansions of CD80‐expressing GC, CD5^+^, marginal