Absence of the JAK2 mutation V617F in CD34+ hematopoietic stem and progenitor cells from patients with BCR-ABL-positive CML in chronic phase and blast crisis

Kronenwett, Ralf; Graf, Thorsten; Neumann, Frank; Pechtel, Sabrina; Steidl, Ulrich; Diaz-Blanco, Elena; Haas, Rainer

doi:10.1016/j.leukres.2005.12.006

Cited by 7 publications

(3 citation statements)

References 10 publications

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“…35,36 Expansion of a JAK-2-mutated clone (V617F) as a possible mechanism of emerging MF during imatinib therapy of CML has recently been reported. 37 However, a JAK-2 V617F mutation is uncommon in CML 38 and none of the patients from our study who suffered from FFI or MF showed a JAK-2 mutation (V617F) in their bone marrow cells. A loss of the inhibitory effect on platelet-derived growth factor receptor protein kinase activity 5,6 might explain the emergence of foci with fiber increase during a cytogenetic and molecular response.…”

Section: Discussionmentioning

confidence: 58%

Marrow fibrosis and its relevance during imatinib treatment of chronic myeloid leukemia

et al. 2007

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In chronic myeloid leukemia (CML), imatinib may reverse bone marrow fibrosis (MF). Whether the unfavorable prognosis of MF is also reversed and whether imatinib guarantees against evolution of MF are unclear as yet. Fifty-nine patients with Ph þ CML treated with X400 mg imatinib/day were examined for MF in 6-to 12-month intervals. Imatinib effectively reversed initial MF (Po0.0005). However, during a follow-up period of up to 4.8 years, small foci with abnormal fiber increase (FFI) emerged in 8 of 30 pretreated and 6 of 29 non-pretreated patients. Patients with FFI showed a significantly lower probability of achieving a complete cytogenetic or major molecular response (36 versus 81%; Po0.007). During the further follow up, 57% of patients with FFI but none of the other patients suffered from full-blown MF (P ¼ 0.00005). None of the patients with FFI or MF showed a Janus kinase-2 mutation (V617F). Evolutions of FFI and MF were independent significant predictors of imatinib failure (P ¼ 0.0031), accelerated phase and death of patients (P ¼ 0.0001; multivariate analyses). Imatinib effectively reverses initial MF in CML, but neither eliminates its unfavorable prognosis nor guarantees completely against new evolution of MF.

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Section: Discussionmentioning

confidence: 58%

Marrow fibrosis and its relevance during imatinib treatment of chronic myeloid leukemia

et al. 2007

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“…Classically, BCR-ABL1 and JAK2 were considered mutually exclusive driver genetic lesions [3,4]. Here we describe a case of emergence of BCR-ABL1 CML in the setting of JAK2-V617F PV.…”

Section: Introductionmentioning

confidence: 91%

Emergence of BCR-ABL1 Chronic Myeloid Leukemia in a JAK2-V617F Polycythemia Vera

2020

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Emergence of a new chronic myeloid neoplasm in the setting of a previous one, or their concomitant appearance seems to be a rare event, but plenty of cases have been reported. We describe the case of a patient with JAK2-V617F polycythemia vera, which looses JAK2 clone and develops overt BCR-ABL1 chronic myeloid leukemia after 6 years. Once treatment with tyrosine kinase inhibitors controls BCR-ABL1 clone, JAK2 clone arises again. In this report, we review the literature and discuss the clonal relationship of this event in light of the new molecular data.

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“…1,2 Recently, several novel mutations as well as deletion in exon 12 of the JAK2 gene in JAK2 V617F -negative polycythemia vera 3 and JAK2 K607N mutation in acute myeloid leukemia 4 were reported. Because the JAK-STAT pathway plays an important role in the initiation and progression of Ph þ leukemia, 5,6 we analyzed these novel mutations and deletion of the JAK2 gene among Ph þ CML patients and Ph þ acute leukemia (Ph þ AL).…”

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confidence: 99%

Analysis of the exon 12 and 14 mutations of the JAK2 gene in Philadelphia chromosome-positive leukemia

Inami

Yamaguchi

Hasegawa³

et al. 2007

Leukemia

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Absence of the JAK2 mutation V617F in CD34+ hematopoietic stem and progenitor cells from patients with BCR-ABL-positive CML in chronic phase and blast crisis

Cited by 7 publications

References 10 publications

Marrow fibrosis and its relevance during imatinib treatment of chronic myeloid leukemia

Marrow fibrosis and its relevance during imatinib treatment of chronic myeloid leukemia

Emergence of BCR-ABL1 Chronic Myeloid Leukemia in a JAK2-V617F Polycythemia Vera

Analysis of the exon 12 and 14 mutations of the JAK2 gene in Philadelphia chromosome-positive leukemia

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