scholarly journals Amplification at 9p in Cervical Carcinoma by Comparative Genomic Hybridization

2001 ◽  
Vol 22 (3) ◽  
pp. 159-163 ◽  
Author(s):  
Kowan J. Jee ◽  
Young Tak Kim ◽  
Kyu Rae Kim ◽  
Yan Aalto ◽  
Sakari Knuutila
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Comparative Genomic Hybridization ◽  
Copy Number ◽  
Comparative Genomic ◽  
Malignant Cells ◽  
Genomic Hybridization ◽  
Carcinoma Of Cervix ◽  
Chromosome Arm ◽  
Copy Number Changes

DNA copy number changes were studied by comparative genomic hybridization on 10 tumor specimens of squamous cell carcinoma of cervix obtained from Korean patients. DNA was extracted from paraffin‐embedded sections after removal of non‐malignant cells by microdissection technique. Copy number changes were found in 8/10 tumors. The most frequent changes were chromosome 19 gains (n=6) and losses on chromosomes 4 (n=4), 5 (n=3), and 3p (n=3). A novel finding was amplification in chromosome arm 9p21‐pter in 2 cases. Gains in 1, 3q, 5p, 6p, 8q, 16p, 17, and 20q and losses at 2q, 6q, 8p, 9q, 10p, 11, 13, 16q, and 18q were observed in at least one of the cases.

scholarly journals DNA copy number changes in diffuse large B-cell lymphoma--comparative genomic hybridization study

Blood ◽  
1996 ◽  
Vol 87 (12) ◽  
pp. 5269-5278 ◽  
Author(s):  
O Monni ◽  
H Joensuu ◽  
K Franssila ◽  
S Knuutila
Keyword(s):  
Comparative Genomic Hybridization ◽  
Copy Number ◽  
B Cell Lymphoma ◽  
Comparative Genomic ◽  
Genomic Hybridization ◽  
Primary Tumors ◽  
Large B Cell Lymphoma ◽  
Recurrent Tumors ◽  
Copy Number Changes ◽  
High Level

We studied DNA copy number changes in diffuse large B-cell lymphoma using comparative genomic hybridization analysis on 20 primary tumors and on 12 recurrent tumors excised after chemotherapy or radiotherapy. Twenty-nine (91%) of the cases showed abnormal copy number karyotypes. Chromosomal regions at X (41%), 1q (38%), 7 (31%), 3 (24%), 6p (21%), 11 (21%), 12 (21%), and 18 (21%) were most frequently gained, and the most common losses involved 6q (38%), X (21%), 1p (14%), and 8p (10%). High-level amplifications were observed at 6p23-ter, 10p12–14, 17p1l.2, 18q21-ter, and Xq22-ter, all but 18q appearing only in the recurrent tumors. Gains (median, 2; range, 0 to 10) were more frequent than losses (median, 1; range, 0 to 7; P = .0004). The median number of aberrations found in the recurrent tumors (6.5) was greater than that in the primary tumors (2; P = .01). The copy number changes found in the recurrent tumors were more random than those found in the primary tumors, which were mainly located in the most frequently affected regions. Our findings are in line with those observed using conventional cytogenetic analysis, but especially novel high-level amplifications were detected. Southern blot analysis showed BCL2 amplification, but not translocation t(14;18)(q32;q21), in cases in which a gain at 18q was detected by comparative genomic hybridization, which strongly suggests that, in addition to translocation, gene amplification is another mechanism for the overexpression of the BCL2 protein.

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