MLL2/KMT2D and MLL3/KMT2C expression correlates with disease progression and response to imatinib mesylate in chronic myeloid leukemia

Cancer Cell International
Doralina do Amaral RabelloFabio Pittella-Silva

Abstract

Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm whose pathogenesis is linked to the Philadelphia chromosome presence that generates the BCR-ABL1 fusion oncogene. Tyrosine kinase inhibitors (TKI) such as imatinib mesylate (IM) dramatically improved the treatment efficiency and survival of CML patients by targeting BCR-ABL tyrosine kinase. The disease shows three distinct clinical-laboratory stages: chronic phase, accelerated phase and blast crisis. Although patients in the chronic phase respond well to treatment, patients in the accelerated phase or blast crisis usually show therapy resistance and CML relapse. It is crucial, therefore, to identify biomarkers to predict CML genetic evolution and resistance to TKI therapy, considering not only the effects of genetic aberrations but also the role of epigenetic alterations during the disease. Although dysregulations in epigenetic modulators such as histone methyltrasnferases have already been described for some hematologic malignancies, to date very limited data is available for CML, especially when considering the lysine methyltransferase MLL2/KMT2D and MLL3/KMT2C. Here we investigated the expression profile of both genes in CML patients in different stages o...Continue Reading

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Citations

Jan 23, 2019·EMBO Reports·Theodoros RampiasApostolos Klinakis
Sep 18, 2020·Global Medical Genetics·Darja Kanduc, Yehuda Shoenfeld
Jan 2, 2019·The Journal of Venomous Animals and Toxins Including Tropical Diseases·Rogério Bodini BenatiSandra Mara Burin
Apr 4, 2021·International Journal of Molecular Sciences·Oriol de Barrios, Maribel Parra

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Methods Mentioned

BETA
flow cytometry
FACS
PCR

Software Mentioned

Diva
GraphPad
Prism

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