Cem. Voorter et al., LOSS OF CHROMOSOME-11 AND CHROMOSOME-11P Q IMBALANCES IN BLADDER-CANCER DETECTED BY FLUORESCENCE IN-SITU HYBRIDIZATION/, International journal of cancer, 65(3), 1996, pp. 301-307
To identify chromosomal imbalances in non-diploid transitional-cell ca
rcinoma (TCC) of the bladder we performed double-target in situ hybrid
ization (FISH), using the centromeric probe for chromosome 11 together
with 2 cosmid probes located on the 11p and 11q arm in the proximity
of the telomere. The FISH protocol was optimized to ensure a highly ef
ficient and reproducible detectability of all 3 targets. As a conseque
nce, it was possible to calculate ratios between the number of spots o
btained with cosmid and centromere probes. Furthermore, the number of
chromosomes 11 present was compared with the DNA index and the chromos
ome ploidy as obtained with other chromosome centromere probes. In thi
s study we found that: (i) in 54 diploid TCCs a monosomy for chromosom
e 11 was detected in only one case; (ii) chromosome 11 was completely
lost in 9 of 16 non-diploid TCCs; (iii) in 8 of these 16 non-diploid t
umors an imbalance was observed between the 11p and 11q arm, in 4 of t
hese cases a complete loss of chromosome 11 being observed in addition
; (iv) the copy number counted for 11q was always identical to the 11
centromere number, except in one case, indicating a loss of 11p in the
cases with imbalances. In total, 13 of 16 non-diploid TCCs (81%) show
ed either a loss of a complete chromosome 11, of (part of) the 11p arm
, or both. Therefore we concluded that during tetra- or aneuploidizati
on in TCCs, (part of) chromosome 11 is lost. In addition, our results
indicate that under-representation of chromosome 11p occurs in the maj
ority of the tumor cells, supporting the idea that loss of these seque
nces is an important step in the development of TCC. (C) 1996 Wiley-Li
ss, Inc.