Karyotypic evolution of four novel mouse mammary carcinoma cell lines: Identification of marker chromosomes by fluorescence in situ hybridization.

FABRIS VICTORIA; CAROLINE A. LAMB; KECK CATHERINE; ALDAZ MARCELO C; MERANI SUSANA; CLAUDIA LANARI

CANCER GENETICS AND CYTOGENETICS

ELSEVIER SCIENCE INC

Año: 2003 vol. 142 p. 36 - 45

0165-4608

We studied the karyotypes of four different mammary carcinoma cell lines derived from a medroxy-progesterone acetate (MPA)-induced mouse mammary carcinoma using G-banding and fluorescence in situ hybridization. All the cell lines showed the same four marker chromosomes (M1-M4) as the parental tumor and also acquired new markers. M1 and M2 are Robertsonian translocations between chromosomes 1 and 10 and 2 and 17. M3 is an acrocentric marker derived from chromosomes 4, 5, and 12; M4 is derived from chromosomes 6 and 8. The parental tumor disclosed a modal number of 39, with a trisomy of chromosomes 3, 4, 10, and 11 and monosomies of 9, 13, and 16. MC4-L1 and MC4-L3 lines had a chromosome number similar to that of the parental tumor in early passages, which increased to the triploid range in late passages. MC4-L5 showed a near-diploid modal number in both early and late passages. MC4-L2 cells had a high chromosome number even in early passages. To our knowledge, this is the first study in which a complete characterization of the cytogenetics of murine mammary carcinoma cell lines and of their parental tumor is described. No associations between changes in ploidy, invasiveness, or hormone dependence were found. Conversely, the presence of one exclusive marker chromosome, a translocation between chromosomes 1 and 18 (M5), in the most aggressive and in vivo hormone-independent line suggests that this rearrangement may be associated with these biologic features. The constant presence of common marker chromosomes in both the parental tumor and the derived cell lines suggests that they are involved in the maintenance of this tumor phenotype.