BCR-ABL and JAK2V617F Mutation Co-existence, Rare or Just Unexplored

Coexistance of JAK2V617F mutation and BCR/ABL translocation in one patient Aynı hastada JAK2V617F mutasyonu ve BCR/ABL translokasyonu birlikteliği

1Sema Hospital, Department of Hematology, İstanbul; 2Erciyes University Department of Hematology, Kayseri; 3Fatih University Department of Hematology, Ankara, 4Hacettepe University Department of Hematology, Ankara; 5Dışkapı Yıldırım Beyazıt Education and Research Hospital, Department of Hematology, Ankara, Turkey Yazışma Adresi /Correspondence: Burak Uz MD Hacettepe University Medical School, D...

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

The concomitant occurrence of JAK2V617F mutation and BCR/ABL transcript with phenotypic expression – an overlapping myeloproliferative disorder or two distinct diseases? - case report

The concomitant occurrence of JAK2617F mutation and BCR/ABL translocation is a rare event. It is unclear if this is a result of the clonal evolution or a separately emergence of two clones and if it could lead to the progression to a more aggressive phase of the disease. We present the case of a 61-year-old man diagnosed and treated for polycythaemia vera for 7 years, which evolved into chronic...

Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification.

Clinical studies with the Abl tyrosine kinase inhibitor STI-571 in chronic myeloid leukemia demonstrate that many patients with advanced stage disease respond initially but then relapse. Through biochemical and molecular analysis of clinical material, we find that drug resistance is associated with the reactivation of BCR-ABL signal transduction in all cases examined. In six of nine patients, r...

Molecular pathways: BCR-ABL.

Aberrant tyrosine kinase activity plays a critical role in many hematologic disorders, including chronic myeloid leukemia characterized by the constitutive activity of BCR-ABL. ABL therefore represents a crucial target for new therapeutic strategies. Here, we summarize the molecular pathways that are abnormally activated by the oncoprotein. Such pathways may provide additional opportunities to ...