During the course of a multifaceted study of clonality in murine neoplasms we observed two B-lymphoid malignancies. Results of studies with the X-chromosome-linked enzyme phosphoglycerate kinase strongly suggest that these tumors had a clonal origin. Each of them had trisomy 15. This chromosomal abnormality has been found consistently in many murine thymic neoplasms, and has been thought to be specific to tumors of thymic origin. However, the occurrence of trisomy 15 in each of the only two B-cell malignancies thus far detected in our studies indicates that it may occur in B-lymphoid progenitors as well.

Fibroblasts from New Zealand Black mouse fetuses manifest increased frequency of chromosomal breaks and interchanges after exposure to ultraviolet radiation when compared with cells from BABL/c fetuses. This chromosomal instability is similar to what has been reported in cells from patients with xeroderma pigmentosum and may be related to the chromosomally abnormal clones and malignancy previously reported in adult New Zealand Black mice.