Evolution to eosinophilic leukemia with a t(5:11) translocation in a patient with idiopathic hypereosinophilic syndrome

Yoo, T. J.; Orman, S.; Patil, Shivanand R.; Dorminey, C.; Needleman, Samuel W.; Rajtora, D.; Graves, N.; Ackerman, Laurie L.; Taylor, W. W.

doi:10.1016/0165-4608(84)90018-9

Cited by 33 publications

(14 citation statements)

References 14 publications

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“…For example, eosinophil monoclonality has been demonstrated in some cases of HES 10,11 and progression into WHO-defined myeloid neoplasm in other cases. [12][13][14][15] Additionally, patients with FIP1L1-PDGFRA-positive clonal eosinophilia were often diagnosed as having HES before the mutation was discovered in 2003. 16 …”

Section: Classification Of Clonal and Idiopathic Eosinophiliamentioning

confidence: 99%

Hypereosinophilic Syndrome and Clonal Eosinophilia: Point-of-Care Diagnostic Algorithm and Treatment Update

Tefferi

Gotlib²,

Pardanani

2010

Mayo Clinic Proceedings

138

136

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Section: Classification Of Clonal and Idiopathic Eosinophiliamentioning

confidence: 99%

Hypereosinophilic Syndrome and Clonal Eosinophilia: Point-of-Care Diagnostic Algorithm and Treatment Update

Tefferi

Gotlib²,

Pardanani

2010

Mayo Clinic Proceedings

138

136

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“…For example, there are well-documented cases of ‘HES’ that on either close scrutiny of bone marrow pathology or performance of additional molecular studies were reclassified as clonal eosinophilia [12, 16, 17]. There are also reported cases of HES that had evolved into either acute leukemia or an aggressive disease phenotype that is indistinguishable from an MPD [18,19,20,21]. Similarly, X-linked DNA analysis has suggested eosinophil monoclonality in some cases of HES [22, 23].…”

Section: Introductionmentioning

confidence: 99%

Modern Diagnosis and Treatment of Primary Eosinophilia

Tefferi

2005

Acta Haematol

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The recent discovery of an eosinophilia-specific, imatinib-sensitive, karyotypically occult but fluorescence in situ hybridization-apparent molecular lesion in a subset of patients with blood eosinophilia has transformed the diagnostic as well as treatment approach to eosinophilic disorders. Primary (i.e. nonreactive) eosinophilia is considered either ‘clonal’ or ‘idiopathic’ based on the presence or absence, respectively, of either a molecular or bone marrow histological evidence for a myeloid neoplasm. Clonal eosinophilia might accompany a spectrum of clinicopathological entities, the minority of whom are molecularly characterized; Fip1-like-1-platelet-derived growth factor receptor α (FIP1L1-PDGFRA⁺) systemic mastocytosis, platelet-derived growth factor receptor β (PDGFRB)-rearranged atypical myeloproliferative disorder, chronic myeloid leukemia, and the 8p11 syndrome that is associated with fibroblast growth factor receptor 1 (FGFR1) rearrangement. Hypereosinophilic syndrome (HES) is a subcategory of idiopathic eosinophilia and is characterized by an absolute eosinophil count of ≧1.5 × 10⁹/l for at least 6 months as well as eosinophil-mediated tissue damage. At present, a working diagnosis of primary eosinophilia mandates a bone marrow examination, karyotype analysis, and additional molecular studies in order to provide the patient with accurate prognostic information as well as select appropriate therapy. For example, the presence of either PDGFRA or PDGFRB mutations warrants the use of imatinib in clonal eosinophilia. In HES, prednisone, hydroxyurea, and interferon-α constitute first-line therapy, whereas imatinib, cladribine, and monoclonal antibodies to either interleukin-5 (mepolizumab) or CD52 (alemtuzumab) are considered investigational. Allogeneic transplantation offers a viable treatment option for drug-refractory cases.

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“…Although there has been a report of a case of cosinoblastic leukemia evolved in HES, in which the eosinoblasts were identified ultrastructurally by the presence of specif ic granules in blasts [5], the possibility of eosinoblastic transformation in the present case was excluded by the positive reaction for an antimyeloperoxidase antibody.…”

Section: Hyperéosinophilie Syndrome Terminating In Acute Myelogenous mentioning

confidence: 91%

“…In the majority of patients with HES the proliferation of eosinophils is thought to be due to a reaction to an unknown agent rather than to a clo nal expansion, although this syndrome often results in marked morbidity and mortality due to eosinophilic infil tration into various organs, especially the heart. Only a few cases of HES have been reported to terminate in acute myeloid leukemia (AML) [2][3][4][5][6][7], although the diagnosis of acute lymphoid leukemia has recently been noted to be preceded or masked by HES in some patients [8]. In this paper we describe a patient with typical HES who suffered from cardiac symptoms due to hypereosinophilia and thromboembolic complications for nearly 5 years; the dis ease terminated in AML.…”

Section: Hyperéosinophilie Syndrome Terminating In Acute Myelogenous mentioning

confidence: 99%

Hypereosinophilic Syndrome Terminating in Acute Myelogenous Leukemia

et al. 1993

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Evolution to eosinophilic leukemia with a t(5:11) translocation in a patient with idiopathic hypereosinophilic syndrome

Cited by 33 publications

References 14 publications

Hypereosinophilic Syndrome and Clonal Eosinophilia: Point-of-Care Diagnostic Algorithm and Treatment Update

Hypereosinophilic Syndrome and Clonal Eosinophilia: Point-of-Care Diagnostic Algorithm and Treatment Update

Modern Diagnosis and Treatment of Primary Eosinophilia

Hypereosinophilic Syndrome Terminating in Acute Myelogenous Leukemia

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