alexa Digital PCR (Dpcr) a Step Forward to Detection and Quantification of Minimal Residual Disease (MRD) in Ph+/BCR-ABL1 Chronic Myeloid Leukemia (CML)
ISSN-2155-9929

Journal of Molecular Biomarkers & Diagnosis
Open Access

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Short Communication

Digital PCR (Dpcr) a Step Forward to Detection and Quantification of Minimal Residual Disease (MRD) in Ph+/BCR-ABL1 Chronic Myeloid Leukemia (CML)

Simona Bernardi1,2, Giuseppina Ruggieri3, Michele Malagola1*, Valeria Cancelli1, Federica Cattina1, Nicola Polverelli1, Camilla Zanaglio1,2, Simone Perucca1,2, Federica Re1,2, Alessandro Montanelli3, and Domenico Russo1

1Bone Marrow Transplant Unit, Clinical and Experimental Sciences Department, University of Brescia, Italy

2Deep Sequencing and Molecular Biology Unit, Chair of Hematology, CREA Laboratory, ASST-Spedali Civili of Brescia, Italy

3Department of Laboratory, ASST-Spedali Civili of Brescia, Brescia, Italy

*Corresponding Author:
Michele Malagola
Chair of Hematology, Bone Marrow Transplant Unit
Clinical and Experimental Sciences, Department, University of Brescia
P.le Spedali Civili 1, 25123 Brescia, Italy
Tel: +39/30/3996811
Fax: +39/30/3996021
E-mail: [email protected]

Received Date: April 22, 2017; Accepted Date: May 25, 2017; Published Date: May 27, 2017

Citation: Bernardi S, Ruggieri G, Malagola M, Cancelli V, Cattina F, et al. (2017) Digital PCR (Dpcr) a Step Forward to Detection and Quantification of Minimal Residual Disease (MRD) in Ph+/BCR-ABL1 Chronic Myeloid Leukemia (CML). J Mol Biomark Diagn 8:330. doi: 10.4172/2155-9929.1000330

Copyright: © 2017 Bernardi S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Philadelphia-positive (Ph+), BCR-ABL1, chronic myeloid leukemia (CML) is a model of leukemia driven by a single, specific, chromosome translocation, the t (9;22) (q22;q11). This translocation, leading to a new, hybrid, leukemia-specific gene (BCR-ABL1) encoding for a deregulated tyrosine-kinase protein (p210), drives the leukemic transformation of hematopoietic stem cells [1-6] and induces the progression of the disease from the early chronic phase (CP) to the late blastic phase BP) which close the natural history of the disease. In the 2000s, the introduction of Imatinib, the first tyrosinekinase inhibitor (TKI) able to target the protein p210, significantly changed the fate of CML to fatal disease in real chronic disease.

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