Correlation of chromosomal imbalances by comparative genomic hybridization and expression of EGFR, PTEN, p53, and MIB-1 in diffuse gliomas

We present the first data on our comparative genomic hybridization (CGH)–based strategy for the analysis of ancient DNA (aDNA) samples extracted from fetuses preserved in the Meckel Anatomical Collection in Halle, Germany. The collection contains numerous differently fixed ancient samples of fetal malformations collected from the middle of the 18th to the early 19th century. The main objective of this study is to establish a “standard” aDNA extraction and amplification protocol as a prerequisite for successful CGH analyses to detect or exclude chromosomal imbalances possibly causative for the malformations described for the fetuses.

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Genome-wide survey for chromosomal imbalances in ganglioglioma using comparative genomic hybridization

Cancer Genetics and Cytogenetics ◽

10.1016/s0165-4608(01)00611-2 ◽

2002 ◽

Vol 134 (1) ◽

pp. 71-76 ◽

Cited By ~ 29

Author(s):

Xiao-Lu Yin ◽

Angela Bik-Yu Hui ◽

Jesse Chung-Sean Pang ◽

Wai Sang Poon ◽

Ho-Keung Ng

Keyword(s):

Comparative Genomic Hybridization ◽

Comparative Genomic ◽

Genomic Hybridization ◽

Chromosomal Imbalances ◽

Genome Wide ◽

Genome Wide Survey

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Chromosomal imbalances in Korean intrahepatic cholangiocarcinoma by comparative genomic hybridization

Cancer Genetics and Cytogenetics ◽

10.1016/j.cancergencyto.2004.05.007 ◽

2005 ◽

Vol 157 (1) ◽

pp. 37-41 ◽

Cited By ~ 20

Author(s):

Kyung-Ok Uhm ◽

Young-Nyun Park ◽

Ji-Young Lee ◽

Dong-Seop Yoon ◽

Sun-Hwa Park

Keyword(s):

Comparative Genomic Hybridization ◽

Intrahepatic Cholangiocarcinoma ◽

Comparative Genomic ◽

Genomic Hybridization ◽

Chromosomal Imbalances

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Chromosomal imbalances identified by comparative genomic hybridization in sporadic parathyroid adenomas

Acta Endocrinologica ◽

10.1530/eje.0.1460209 ◽

2002 ◽

pp. 209-213 ◽

Cited By ~ 12

Author(s):

JL Garcia ◽

JC Tardio ◽

NC Gutierrez ◽

MB Gonzalez ◽

JM Hernandez ◽

...

Keyword(s):

Comparative Genomic Hybridization ◽

Genetic Gain ◽

Chromosome 9 ◽

Comparative Genomic ◽

Chromosome 11 ◽

Genomic Hybridization ◽

Genomic Amplification ◽

Chromosomal Imbalances ◽

Parathyroid Adenomas ◽

Gains And Losses

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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