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Albano et al. Molecular Cancer 2013, 12:36 http://www.molecularcancer.com/content/12/1/SHORT COMMUNICATIONOpen AccessGene expression profiling of chronic myeloid leukemia with variant t(9;22) reveals a distinctive signature from circumstances with classic translocationFrancesco Albano, Antonella Zagaria, Luisa Anelli, Nicoletta Coccaro, Luciana Impera, Crescenzio Francesco Minervini, Angela Minervini, Antonella Russo Rossi, Giuseppina Tota, Paola Casieri and Giorgina SpecchiaAbstractBackground: The t(9;22)(q34;q11) producing the BCR/ABL1 fusion gene represents the cytogenetic hallmark of chronic myeloid leukemia (CML).Price of 4,6-Dichloro-5-nitropicolinic acid About 50 of CML cases show variant translocations with the involvement of other chromosomes as well as chromosomes 9 and 22.PMID:33438294 The molecular bases of biological variations in 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 related together with the two analyzed groups. The role of precise candidate genes for example TRIB1 (tribbles homolog 1), PTK2B (protein tyrosine kinase 2 beta), and C5AR1 (complement component 5a receptor 1) is discussed. Conclusions: Our final results reveal that in CML instances with variant t(9;22) there is an enhancement on the MAPK pathway deregulation and show that kinases are a common target of molecular alterations in hematological issues. Key phrases: Chronic myeloid leukemia, Variant t(9;22) rearrangem.
