Role of 1q trisomy in tumorigenicity, growth, and metastasis of human leukemic B-cell clones in nude mice.

In order to investigate the association between various karyotypes of human tumor cells and biological behavior of tumors such as tumorigenicity, rate of growth, and the capacity to form metastasis, six chromosomally distinctive clones were isolated from an Epstein-Barr virus-transformed human chronic lymphocytic leukemic B-cell line which progressively grew and metastasized in irradiated nude mice. When inoculated into nude mice one clone (D10-1) with the karyotype of 46,XY,dup(1)(q11----q32) was more tumorigenic, grew faster, and produced more metastases than the other five clones. When mixtures of different clone-derived cells were grown in vitro or inoculated s.c. into nude mice the proportion of D10-1 cells was higher than their expected numbers in the cultures, s.c. tumors, and splenic and lymph nodal metastases. The growth and metastatic potential of the D10-1 clone were inhibited when cells from this clone were mixed with one or more clones that had slower growth. Duplication of 1q has been observed as a secondary aberration in human hematological malignancies and solid cancers. Our results demonstrate that duplication of the chromosome segment of 1q11----1q32 is associated with advantages in proliferation and metastasis formation.