Table 1.
HPKIA | p11 | none | ||||||||||||||||
p17 | +5p | +5q | +8p | +8q | −10p | +11 | +16 | +20 | +21q | +22q | ||||||||
p23 | −4 | +5q | −6q | +8q | +9 | −10p | +11 | +14q | +16 | +20 | ||||||||
p56 | +3q | (−4)* | +5 | −6 | +8q | +9 | −10p | +11 | +14q | +15q | +16 | +20 | ||||||
HPKII | p1 | none | ||||||||||||||||
p6 | −10p | +12q | +14q | +16q | +20q | |||||||||||||
p17 | −4q | +5 | +6p | −10p | +11 | +14q | −15 | +16 | +20 | +22q | −X | |||||||
p48 | −1q | −4 | +5p | −6q | +7p | −7q | −10p | +11 | +12q | +14q | 15 h | +16 | +20 | +22q | −Xp | −Xq | ||
HPKIII | p2 | none | ||||||||||||||||
p14 | +3q | +8 | −X | |||||||||||||||
p42 | +3q | −6q | −7q | +8 | +9q | −10 | +11 | +12q | +14q | +16 | +17 | +20 | −X | |||||
p55 | +3q | +8 | +9q | +11q | +12q | +14q | +16 | +17 | +20q | +22q | −X | |||||||
p72 | +3q | −4 | +5q | −6q | +7p | +8 | +9 | +11 | +12q | +14q | +16 | +17 | +20 | +22q | (−X)* | |||
HPKV | p0 | none | ||||||||||||||||
p12 | none | |||||||||||||||||
p22 | −3p | −10p | +10q | +17q | ||||||||||||||
p35 | −3p | +3q | −4 | −10p | +10q | +11q |
Even when only a portion of a chromosome arm was found imbalanced, the entire arm is listed. Details of the extension of an imbalanced region are presented in Fig. 2. p, passage upon virus transfection; h, high copy number amplification on chromosome band 15q23-q24; +, gained chromosome material [rev ish enh according to ISCN 1995 (62)]; −, lost chromosome material [rev ish dim according to ISCN 1995 (62)].
The CGH profile of these chromosomes shows a strong deviation from the balanced state and reaches the diagnostic threshold for deletion in only two (chromosome 4) and three (chromosome X) regions. However, the profile of the whole chromosome does not entirely exceeds this threshold, but, because this was the case in the previous time point analyzed, we report it here in parentheses.