Christine L.Y. Lee

Cytogenetic Abnormalities Associated with Renal Cell Carcinoma

Cytogenetic analysis was performed on 23 renal cell carcinomas (21 sporadic and 2 associated with von Hippel-Lindaus disease). Clonal chromosomal abnormalities were found in 19 of 21 of the sporadic tumors. The most frequent abnormalities were a loss or rearrangement of material in 3p (11 of 21 cases) or an extra chromosome 7 (7 of 21 cases). Correlation between specific chromosomal abnormalities and clinical presentation was absent with the exception of trisomy 7 and -Y, which occurred only in patients more than 60 years old. An increasing number of cytogenetic abnormalities were associated with a greater likelihood of renal vein and/or capsule involvement. Both patients with von Hippel-Lindaus disease had tumors with a normal karyotype.

Detection of a novel t(6;15)(q21;q21) in a pediatric Wilms tumor

We report a novel cytogenetic finding in a favorable histology Wilms tumor occurring in a 4-month-old boy. Karyotypic analysis demonstrated a t(6;15)(q21;q21) in all tumor cells examined. This was confirmed using fluorescence in situ hybridization analysis. Molecular analysis of this rearrangement may provide clues to understanding the pathobiology of Wilms tumor.

The emergence and establishment of a clonal subline with partial duplication of chromosome 1q from a tumorigenic human chronic lymphocytic leukemic B-cell line

Sequential analysis was performed on a tumorigenic human B-cell chronic lymphocytic leukemia cell line in which the initial population consisted of two abnormal clones, one with trisomy 12 (47%), the other with duplication of 1q; that is, 46,XY,dup(1)(q11----q32) (10%), and rest of the population had a normal karyotype. The clone with 1q+ marker expanded steadily and after 11 weeks became the only proliferating cell population in vitro and remained so till the end of an observation period of 75 weeks. All tumors recovered from nude mice that were inoculated with this newly established subline had retained the 1q+ marker. All the secondary clones also carried this aberration.

Retardation in tumor growth and metastasis demonstrated in a human CLL B-cell line after the acquisition of an extra chromosome 11☆

In this study we described the isolation of a subclonal EBV-transformed human CLL B-cell line with retarded growth rate and metastatic potential from its clonal parent (D10-1), which was karyotyped: 46.XY.dup(1)(q11----q32). The subclone, designated D10-1C, was isolated by limiting dilution of D10-1 following selection in 8-azaguanine-supplemented medium. Chromosome analysis of D10-1C revealed a constitution of 47,XY, + 11.dup(1)(q11----q32). This is the first demonstration that partial trisomy 1q-associated growth advantage in human cancer cells can be retarded by the presence of an additional dose of chromosome 11. Human chromosome 11 had been shown to be responsible for the suppression of tumor development. Whether the same suppressor genes are involved in D10-1C remains to be elucidated. The procedure described here for the enrichment and isolation of a growth-retarded mutant from D10-1 may be applicable in other malignant cell systems.