TY - JOUR
T1 - Retardation in tumor growth and metastasis demonstrated in a human CLL B-cell line after the acquisition of an extra chromosome 11
AU - Lee, Christine L.Y.
AU - Lee, Spencer H.S.
AU - Ghose, Tarunendu
AU - Fernandez, Louis A.
AU - Colp, Patricia
N1 - Funding Information:
This work was supported in part by grants from the Medical Research Council (Canada).
PY - 1991/7/1
Y1 - 1991/7/1
N2 - 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.
AB - 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.
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U2 - 10.1016/0165-4608(91)90036-T
DO - 10.1016/0165-4608(91)90036-T
M3 - Article
C2 - 2065304
AN - SCOPUS:0025770547
SN - 0165-4608
VL - 54
SP - 101
EP - 108
JO - Cancer Genetics and Cytogenetics
JF - Cancer Genetics and Cytogenetics
IS - 1
ER -
