Identification of gains and losses of DNA sequences in primary bladder cancer by comparative genomic hybridization

1995 ◽  
Vol 12 (3) ◽  
pp. 213-219 ◽  
Author(s):  
Anne Kallioniemi ◽  
Olli-P. Kallioniemi ◽  
Gil Citro ◽  
Guido Sauter ◽  
Sandy Devries ◽  
...  
Author(s):  
Jadwiga Szymanska ◽  
Maija Tarkkanen ◽  
Tom Wiklund ◽  
Martti Virolainen ◽  
Carl Blomqvist ◽  
...  

2000 ◽  
Vol 121 (1) ◽  
pp. 67-72 ◽  
Author(s):  
Rienstein Shlomit ◽  
Aviram-Goldring Ayala ◽  
Daniely Michal ◽  
Amerigleo Ninett ◽  
Simoni Frida ◽  
...  

1996 ◽  
Vol 89 (1) ◽  
pp. 7-13 ◽  
Author(s):  
Paula Kivipensas ◽  
Anna-Maria Björkqvist ◽  
Ritva Karhu ◽  
Katarina Pelin ◽  
Kaija Linnainmaa ◽  
...  

Blood ◽  
1995 ◽  
Vol 85 (12) ◽  
pp. 3610-3618 ◽  
Author(s):  
M Bentz ◽  
K Huck ◽  
S du Manoir ◽  
S Joos ◽  
CA Werner ◽  
...  

In chronic B-cell leukemias, fluorescence in situ hybridization has greatly improved the ability to detect certain chromosomal aberrations, as cells in all phases of the cell cycle are analyzed. To obtain a comprehensive view of chromosomal gains and losses, we applied the recently developed technique of comparative genomic hybridization (CGH) to 28 patients with chronic B-cell leukemias. CGH results were compared with those obtained by chromosome banding analysis and interphase cytogenetics. In 19 of the 28 cases, chromosomal imbalances were detected, including amplified DNA sequences in three instances. The most common aberrations included gains of chromosomal material on 8q and 12 as well as losses of 6q, 11q, 13q, and 17p. In 13 cases, CGH revealed chromosomal gains and losses not detected by banding analysis. In 8 of these 13 cases, discrepancies were further investigated using other methods, and in all instances, the CGH findings were confirmed. A limitation of detecting small deleted regions by CGH was found in one example of 18p. In conclusion, our data show that the results of banding analysis in chronic B-cell leukemias often do not reflect the chromosomal changes in the predominant cell clone. This may be one explanation for the as yet poor correlation between cytogenetic findings and clinical course in this group of neoplasms.


Blood ◽  
1998 ◽  
Vol 91 (8) ◽  
pp. 3007-3010 ◽  
Author(s):  
Juan C. Cigudosa ◽  
Pulivarthi H. Rao ◽  
M. Jose Calasanz ◽  
M. Dolores Odero ◽  
Joseph Michaeli ◽  
...  

Clonal chromosomal changes in multiple myeloma (MM) and related disorders are not well defined, mainly due to the low in vivo and in vitro mitotic index of plasma cells. This difficulty can be overcome by using comparative genomic hybridization (CGH), a DNA-based technique that gives information about chromosomal copy number changes in tumors. We have performed CGH on 25 cases of MM, 4 cases of monoclonal gammopathy of uncertain significance, and 1 case of Waldenstrom's macroglobulinemia. G-banding analysis of the same group of patients demonstrated clonal chromosomal changes in only 13 (43%), whereas by CGH, the number of cases with clonal chromosomal gains and losses increased to 21 (70%). The most common recurrent changes detected by CGH were gain of chromosome 19 or 19p and complete or partial deletions of chromosome 13. +19, an anomaly that has so far not been detected as primary or recurrent change by G-banding analysis of these tumors, was noted in 2 cases as a unique change. Other recurrent changes included gains of 9q, 11q, 12q, 15q, 17q, and 22q and losses of 6q and 16q. We have been able to narrow the commonly deleted regions on 6q and 13q to bands 6q21 and 13q14-21. Gain of 11q and deletion of 13q, which have previously been associated with poor outcome, can thus be detected by CGH, allowing the use of this technique for prognostic evaluation of patients, without relying on the success of conventional cytogenetic analysis.


2002 ◽  
pp. 209-213 ◽  
Author(s):  
JL Garcia ◽  
JC Tardio ◽  
NC Gutierrez ◽  
MB Gonzalez ◽  
JM Hernandez ◽  
...  

OBJECTIVE: To identify chromosomal gains and losses in sporadic parathyroid adenomas (PAs). METHODS: Fourteen sporadic PAs were studied by comparative genomic hybridization (CGH). RESULTS: The fourteen studied PAs showed chromosomal imbalances. All cases except one exhibited two or more abnormalities. Chromosomal gains were found in all cases, and three cases (21%) also presented chromosomal losses. Genomic amplification was not observed. Chromosome 9 was involved in ten cases. Recurrent genetic gain was found on 9p22-24 and on 9q34, each in 6 of 14 cases (43%). Other recurrent gains included Xq26 in 6 PAs (43%) and 4q21-28 and 8p22-23, each in 4 of 14 cases (29%). Regions of recurrent genetic loss involved whole chromosome 11 and 20q12-13, each in 2 of 14 cases (14%). CONCLUSIONS: Our findings show chromosomal imbalances in all sporadic PAs studied by CGH, partly confirming previous reports, with the exception that we observed more chromosomal gains than losses. Several regions (9p22-24, 9q34, Xq26, 4q21-28, and 8p22-23) probably deserve further investigation in order to discard the presence of genes involved in parathyroid tumorigenesis.


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