MolDX: Genetic Testing for BCR-ABL Negative Myeloproliferative Disease LCD

The Importance of Jak2v617f and Bcr-abl Testing in the Diagnosis of Chronic Myeloproliferative Neoplasms: a Single Centre Experience

This article reports the molecular diagnosis findings regarding chronic myeloproliferative neoplasms made in a Molecular Biology Laboratory over a seven years’ experience (between 2009 and 2015). Ritus Biotec ltd is an ELN (European Leukemia Net) certified diagnostic laboratory for quantification of BCR-ABL. 1373 patients were subjected to Jak2 V617F testing in this time frame. The patients wer...

Diagnosing myelodysplastic/myeloproliferative neoplasms: laboratory testing strategies to exclude other disorders.

INTRODUCTION The 2008 World Health Organization classification of myeloid neoplasms includes the diagnostic category, myelodysplastic/myeloproliferative neoplasms (MDS/MPN), which encompasses those rare clonal myeloid proliferations that at initial presentation, show overlapping myeloproliferative and myelodysplastic features, making classification as either a myelodysplastic syndrome (MDS) or ...

Methylation status of SOCS1 and SOCS3 in BCR-ABL negative and JAK2V617F negative chronic myeloproliferative disorders

Bcr-Abl with an SH3 deletion retains the ability To induce a myeloproliferative disease in mice, yet c-Abl activated by an SH3 deletion induces only lymphoid malignancy.

The bcr-abl oncogene plays a critical role in the pathogenesis of chronic myelogenous leukemia (CML). The fusion of Bcr sequences to Abl constitutively activates the Abl protein tyrosine kinase. We have recently shown that expression of Bcr-Abl in bone marrow cells by retroviral transduction efficiently induces in mice a myeloproliferative disease resembling human CML and that Abl kinase activi...

Dissecting the role of aberrant DNA methylation in human leukemia

Chronic myeloid leukaemia (CML) is a myeloproliferative disorder characterized by the genetic translocation t(9;22)(q34;q11.2) encoding for the BCR-ABL fusion oncogene. However, many molecular mechanisms of the disease progression still remain poorly understood. A growing body of evidence suggests that the epigenetic abnormalities are involved in tyrosine kinase resistance in CML, leading to le...