ABSTRACT
To study a possible role(s) played by the trisomy and pentasomy of chromosome 13 in murine mammary tumors, we examined, in eight cloned established cell lines derived from a single BALB/c mammary tumor induced by MTV, a correlation between the presence of trisomy or pentasomy 13 and transformation parameters and in vivo tumorigenicity in syngeneic mice. We found that cell lines with a higher incidence of trisomy or pentasomy 13 in cells of diploid and tetraploid chromosome numbers, respectively, grew to a much higher cell density in flasks than did those with low incidence, and they formed tumors in syngeneic BALB/c mice, whereas those with a low incidence of trisomy or pentasomy 13 were poorly tumorigenic. The presence in the tumorigenic cells of trisomy or pentasomy 13 was not correlated with their growth in soft agar. Furthermore, other chromosomes manifested a wide range of copy numbers in the presence of trisomy or pentasomy 13, indicating that no chromosomes counteracted chromosome 13 to prevent the tumorigenicity. In light of the tumorigenic growth of the cells that maintain gene dosage of chromosome 13 at different ploidy levels, the possibility of the yeast G1 cyclin-like roles played by the gene(s) residing on chromosome 13 in murine mammary tumorigenesis is discussed.
Subject(s)
Chromosome Aberrations , Chromosomes, Human, Pair 13 , Mammary Neoplasms, Experimental/genetics , Trisomy , Animals , Humans , Karyotyping , Mammary Neoplasms, Experimental/microbiology , Mammary Tumor Virus, Mouse , Mice , Mice, Inbred BALB C , Ploidies , Tumor Cells, CulturedABSTRACT
A total of five hepatic cell lines were established from SV40-T transgenic mice at different stages of development. Karyotype analysis performed on these cell lines revealed 1) chromosomal instability manifested by numerous karyotypic alterations, 2) non-random numerical changes of chromosome number 18 and 3) frequent occurrence of marker chromosomes in four of the five lines. These findings indicate that genetic abnormalities occur very frequently in hepatocytes of the transgenic mice, most probably caused by the mutagenic action of T-antigen, raising the possibility that they play essential roles in initiation and progression in this model of murine hepatocarcinogenesis.
Subject(s)
Antigens, Viral, Tumor/genetics , Chromosome Aberrations , Liver/ultrastructure , Simian virus 40/immunology , Animals , Cell Division , Cell Line , Female , Karyotyping , Male , Mice , Mice, Inbred C57BL , Mice, Nude , Mice, Transgenic , PloidiesABSTRACT
The chromosome analysis of mammary tumors of mice by the Giemsa banding procedures yielded the following results: (1) Mammary tumors induced by urethan displayed the same chromosome aberration of trisomy of chromosome 13 as spontaneous mammary tumors; (2) By analyzing tumor cells with translocated chromosomes, genes assumed to be involved in mammary tumor development were mapped in the proximal region of chromosome 13; (3) Polyploid tumor cells manifested heteromorphism among homologous chromosomes which segregated regularly. The analysis of its segregation indicated that trisomy of chromosome 13 was derived from endomitosis and loss of a chromosome. The possible mechanisms of the genesis of the endomitosis were put forth based on a probable role of replicator played by a long terminal repeat of the viral mammary tumor genome integrated into chromosome 13.
Subject(s)
Mammary Neoplasms, Experimental/genetics , Trisomy , Animals , Female , Karyotyping , Mammary Neoplasms, Experimental/chemically induced , Mice , Mice, Inbred BALB C , Mitosis , UrethaneABSTRACT
Karyotype analyses were conducted on spontaneous mammary tumors of 11 GR, 2 C3H, and 2 noninbred Swiss mice with the use of trypsin-Giemsa banding procedures. All tumors manifested trisomy of chromosome No 13 in most cells, and all except 1 tumor had cells with a model chromosome number of 40.
Subject(s)
Mammary Neoplasms, Experimental/genetics , Trisomy , Animals , Chromosome Aberrations , Female , Mice , Mice, Inbred C3H , X ChromosomeABSTRACT
Karyotypes of spontaneous thymomas of AKR mice were determined by trypsin-Giemsa banding methods. Trisomy of chromosome 15 occurred in 10 of 11 leukemic mice. Seven of the thymomas were predominantly trisomic for chromosome 15, one was trisomic for chromosome 12, and one exhibited multiple trisomies of chromosomes 3, 12, 15, and 17. Trisomy was not found in the norm-l AKR tissues examined.
