eosinophilia/tyrosine

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Response of ETV6-FLT3-positive myeloid/lymphoid neoplasm with eosinophilia to inhibitors of FMS-like tyrosine kinase 3.

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Imatinib-resistant tyrosine kinase (TK) fusions involving FGFR1, JAK2, or FLT3 are rare but recurrent in patients with eosinophilia-associated neoplasms. We report here 2 male patients with ETV6-FLT3(+) myeloid/lymphoid neoplasms with eosinophilia who were treated with the multitargeted TK

Myeloproliferative disorder with eosinophilia and ETV6-ABL gene rearrangement: efficacy of second-generation tyrosine kinase inhibitors.

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ETV6/ABL is a rare gene rearrangement that has rarely been detected in Philadelphia-negative chronic myeloproliferative disorders (C-MPD) and found to have tyrosine kinase activity similar to the BCR/ABL fusion protein. We describe a case of a 61-year-old female with a C-MPD associated with an

[FIP1L1-PDGFRА-positive myeloproliferative disease with eosinophilia: A rare case with multiple organ dysfunction and a response to tyrosine kinase inhibitor therapy].

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The described case of FIP1L1-PDGFRА-positive myeloproliferative disease is characterized by an atypical aggressive course to develop severe specific complications as injuries to the brain, heart, lung, and intestine. Pathogenetic therapy with imatinib could stabilize a patient's state, but failed to

Myeloid/lymphoid neoplasms with eosinophilia/ basophilia and ETV6-ABL1 fusion: cell-of-origin and response to tyrosine kinase inhibition.

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The myeloproliferative neoplasms including the eosinophilia-related myeloproliferations associated with tyrosine kinase mutations: changes and issues in classification and diagnosis criteria.

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The classification and diagnostic criteria of the myeloproliferative neoplasms have changed significantly in the 2008 World Health Organization monograph on the classification of hematologic malignancies. Many of the changes arose from the findings that the different malignancies are associated with

T-lymphoblastic lymphoma and acute myeloid leukaemia transformed from myeloid neoplasm with eosinophilia: a divergent evolution of myeloid neoplasm with monosomy 7 but no detectable tyrosine kinase gene rearrangements designated by the WHO Classification

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NDEL1-PDGFRB fusion gene in a myeloid malignancy with eosinophilia associated with resistance to tyrosine kinase inhibitors.

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Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders.

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Eosinophilia is a recurrent feature and diagnostic clue in several hematologic malignancies. In stem cell- and myelopoietic neoplasms, eosinophils are derived from the malignant clone, whereas in lymphoid neoplasms and reactive states, eosinophilia is usually triggered by eosinopoietic cytokines.

[A man with oral ulcers caused by hypereosinophilic syndrome and a good response to the tyrosine-kinase inhibitor imatinib].

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For the last 2 years, a 55-year-old man had painful, recurrent oral ulcers. Histological examination showed non-specific inflammation. Eosinophilia in the blood and bone marrow raised the suspicion of hypereosinophilic syndrome. No other specific organ involvement was observed. The diagnosis was

Protein tyrosine phosphatases regulate asthma development in a murine asthma model.

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Allergic asthma is a chronic inflammatory disease characterized by Th2-type inflammation. Although the cellular interactions are now well studied, the intracellular signaling involved in asthma development is still a developing field. Protein tyrosine kinases are one focus of such research and their

Recurrent CEP85L-PDGFRB fusion in patient with t(5;6) and imatinib-responsive myeloproliferative neoplasm with eosinophilia.

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Fusion genes involving the catalytic domain of tyrosine kinases (TKs) play an important role in the pathogenesis of hematological malignancies and solid tumors. In BCR-ABL1-negative myeloproliferative neoplasms (MPNs) several different tyrosine kinase fusion events have been described, most commonly

Application of tyrosine kinase inhibitors as a promising targeting treatment for myeloproliferative neoplasms --- review.

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As well as playing vital roles in main cellular processes, such as abnormal proliferation, differentiation, survival, apoptosis, and a lot of tyrosine kinases (TK) are involved in oncogenesis. TK or components of their signal pathways have been found abnormal in many hematological malignancies.

A critical appraisal of conventional and investigational drug therapy in patients with hypereosinophilic syndrome and clonal eosinophilia.

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Hypereosinophilic syndrome (HES) is a rare disorder characterized by persistent and marked eosinophilia, leading to end-organ damage. Over the last decade, great progress has been made in unraveling the molecular basis of HES that has resulted in the characterization of specific genetic alterations

[Hematological side effects of tyrosine kinase inhibition using imatinib].

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Imatinib (STI571, Gleevec/Glivec) and other small-molecule tyrosine kinase inhibitors are highly effective in the treatment of chronic myeloid leukemia (CML), gastrointestinal stromal tumors and, for example, eosinophilia-associated chronic myeloproliferative disorders. This molecularly targeted

Review of current classification, molecular alterations, and tyrosine kinase inhibitor therapies in myeloproliferative disorders with hypereosinophilia.

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Recent advances in our understanding of the molecular mechanisms underlying hypereosinophilia have led to the development of a 'molecular' classification of myeloproliferative disorders with eosinophilia. The revised 2008 World Health Organization classification of myeloid neoplasms included a new

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