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Array Comparative Genomic Hybridization

Volume 973 of the series Methods in Molecular Biology pp 55-68

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Application of Array Comparative Genomic Hybridization in Chronic Myeloid Leukemia

  • Seonyang ParkAffiliated withDepartment of Internal Medicine, Diagnostic DNA Chip Center, Seoul National University College of Medicine Email author 
  • , Youngil KohAffiliated withDepartment of Internal Medicine, Diagnostic DNA Chip Center, Seoul National University College of Medicine
  • , Seung-Hyun JungAffiliated withDepartment of Internal Medicine, Diagnostic DNA Chip Center, Seoul National University College of Medicine
  • , Yeun-Jun ChungAffiliated withDepartment of Internal Medicine, Diagnostic DNA Chip Center, Seoul National University College of Medicine

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Abstract

Chromosomal alteration is one of the hallmarks of chronic myeloid leukemia (CML), and the Philadelphia chromosome is the most important and key example of the chromosomal changes in this disease. Indeed, the BCRABL1 fusion product is a target against which many tyrosine kinase inhibitors (TKIs) have been proven to be effective in the treatment of CML. However, the reality is that CML patients show resistance to TKIs both in an acquired and de novo manner, and the mechanism of TKI resistance is still largely unknown. This phenomenon suggests that in addition to the BCRABL mutation, further genetic alterations such as copy number aberration may be involved in unexplained TKI resistance. Although the recent array comparative genomic hybridization analyses (array-CGH) across the whole genome have detected multiple genetic aberrations in CML, the detailed feature of chromosomal alterations involved in different clinical phases of CML, such as chronic phase, accelerated phase, and blast crisis, remains unclear. Here we review the methodological aspects of array-CGH analysis for studying CML and its related data analysis.

Key words

Chronic myeloid leukemia Array comparative genomic hybridization Copy number alteration Tyrosine kinase inhibitor