Gene expression profiling of chronic myeloid leukemia with variant t(9;22) reveals a different signature from cases with classic translocation

Molecular Cancer

Short Communication

Giorgina Specchia¹  Nicoletta Coccaro¹  Luciana Impera¹  Angela Minervini¹  Antonella Zagaria¹  Paola Casieri¹  Luisa Anelli¹  Giuseppina Tota¹  Antonella Russo Rossi¹  Francesco Albano¹  Crescenzio Francesco Minervini¹ 

[1] Department of Emergency and Organ Transplantation (D.E.T.O.), Hematology Section - University of Bari, 70124, Bari, Italy;

关键词: Chronic myeloid leukemia;    Variant t(9;    22) rearrangements;    Gene expression profiling;    Protein kinases;    Cellular pathways;   

DOI  :  10.1186/1476-4598-12-36

 received in 2013-02-13, accepted in 2013-04-29,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundThe 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.FindingsIn 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.ConclusionsOur 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.

【 授权许可】

CC BY   
© Albano et al.; licensee BioMed Central Ltd. 2013