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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 distinct signature from situations 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) creating the BCR/ABL1 fusion gene represents the cytogenetic hallmark of chronic myeloid leukemia (CML).Price of 2-(4-Ethynylphenyl)acetic acid About 50 of CML cases show variant translocations with the involvement of other chromosomes as well as chromosomes 9 and 22.Formula of 922718-57-8 The molecular bases of biological variations between CML sufferers with classic and variant t(9;22) have never been clarified.PMID:34856019 Findings: In this study, we performed gene expression microarray evaluation to compare CML individuals bearing variant rearrangements and these with classic t(9;22)(q34;q11). We identified 59 differentially expressed genes significantly related with all the two analyzed groups. The function of particular candidate genes such as TRIB1 (tribbles homolog 1), PTK2B (protein tyrosine kinase two beta), and C5AR1 (complement element 5a receptor 1) is discussed. Conclusions: Our results reveal that in CML instances with variant t(9;22) there’s an enhancement of your MAPK pathway deregulation and show that kinases are a typical target of molecular alterations in hematological problems. Keywords and phrases: Chronic myeloid leukemia, Variant t(9;22) rearrangem.
