Molecular cancer · 2013
Gene expression profiling of chronic myeloid leukemia with variant t(9;22) reveals a different signature from cases with classic translocation.
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Albano Francesco, Zagaria Antonella, Anelli Luisa, Coccaro Nicoletta, Impera Luciana, Minervini Crescenzio Francesco, Minervini Angela, Rossi Antonella Russo, Tota Giuseppina, Casieri Paola, Specchia Giorgina
Аннотация
BACKGROUND: The t(9;22)(q34;q11) generating the BCR/ABL1 fusion gene represents the cytogenetic hallmark of chronic myeloid leukemia (CML). About 5-10% of CML cases show variant translocations with the involvement of other chromosomes in addition to chromosomes 9 and 22. The molecular bases of biological differences between CML patients with classic and variant t(9;22) have never been clarified.
FINDINGS: In this study, we performed gene expression microarray analysis to compare CML patients bearing variant rearrangements and those with classic t(9;22)(q34;q11). We identified 59 differentially expressed genes significantly associated with the two analyzed groups. The role of specific candidate genes such as TRIB1 (tribbles homolog 1), PTK2B (protein tyrosine kinase 2 beta), and C5AR1 (complement component 5a receptor 1) is discussed.
CONCLUSIONS: Our results reveal that in CML cases with variant t(9;22) there is an enhancement of the MAPK pathway deregulation and show that kinases are a common target of molecular alterations in hematological disorders.
FINDINGS: In this study, we performed gene expression microarray analysis to compare CML patients bearing variant rearrangements and those with classic t(9;22)(q34;q11). We identified 59 differentially expressed genes significantly associated with the two analyzed groups. The role of specific candidate genes such as TRIB1 (tribbles homolog 1), PTK2B (protein tyrosine kinase 2 beta), and C5AR1 (complement component 5a receptor 1) is discussed.
CONCLUSIONS: Our results reveal that in CML cases with variant t(9;22) there is an enhancement of the MAPK pathway deregulation and show that kinases are a common target of molecular alterations in hematological disorders.
Предметные рубрики MeSH
Chromosomes, Human, Pair 22Chromosomes, Human, Pair 9Cluster AnalysisGene Expression ProfilingGene Expression Regulation, LeukemicGene Regulatory NetworksHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMitogen-Activated Protein KinasesPhosphotransferasesProto-Oncogene Proteins p21(ras)Signal TransductionTranslocation, Genetic