Identification of JAK2 as a Mediator of FIP1L1-PDGFRA-Induced Eosinophil Growth and Function in CEL

Comparative Proteomic Analysis of Blood Eosinophils Reveals Redox Signaling Modifications in Patients with FIP1L1-PDGFRA-Associated Chronic Eosinophilic Leukemia

(2011) Jean-Emmanuel Kahn et al.   JOURNAL OF PROTEOME RESEARCH

ConcomitantFIP1L1–PDGFRAfusion gene and T-cell clonality in a case of chronic eosinophilic leukemia with clonal evolution and an incomplete response to imatinib

(2011) Kate Burbury et al.   LEUKEMIA & LYMPHOMA

Jak2 Is a Negative Regulator of Ubiquitin-Dependent Endocytosis of the Growth Hormone Receptor

(2011) Joyce Putters et al.   PLoS One

Icaritin Shows Potent Anti-Leukemia Activity on Chronic Myeloid Leukemia In Vitro and In Vivo by Regulating MAPK/ERK/JNK and JAK2/STAT3 /AKT Signalings

(2011) Jian feng Zhu et al.   PLoS One

JAK2 V617F-Dependent Upregulation of PU.1 Expression in the Peripheral Blood of Myeloproliferative Neoplasm Patients

(2011) Tamotsu Irino et al.   PLoS One

FIP1L1/PDGFRα-Associated Systemic Mastocytosis

(2010) Yoshiyuki Yamada et al.   INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY

Chemoattractant-Induced Signaling via the Ras-ERK and PI3K-Akt Networks, along with Leukotriene C4 Release, Is Dependent on the Tyrosine Kinase Lyn in IL-5- and IL-3-Primed Human Blood Eosinophils

(2010) Y. Zhu et al.   JOURNAL OF IMMUNOLOGY

JAK2 mutation and disease phenotype: a double L611V/V617F in cis mutation of JAK2 is associated with isolated erythrocytosis and increased activation of AKT and ERK1/2 rather than STAT5

(2010) C Cleyrat et al.   LEUKEMIA

JAK2 Exon 14 Deletion in Patients with Chronic Myeloproliferative Neoplasms

(2010) Wanlong Ma et al.   PLoS One

The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes

(2009) J. W. Vardiman et al.   BLOOD

The JAK2 Inhibitor AZD1480 Potently Blocks Stat3 Signaling and Oncogenesis in Solid Tumors

(2009) Michael Hedvat et al.   CANCER CELL

Triptolide abrogates oncogene FIP1L1-PDGFRα addiction and induces apoptosis in hypereosinophilic syndrome

(2009) Yanli Jin et al.   CANCER SCIENCE

The roles of MCP-1 and protein kinase Cδ activation in human eosinophilic leukemia EoL-1 cells

(2009) Ji-Sook Lee et al.   CYTOKINE

Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer

(2009) Sergei I. Grivennikov et al.   CYTOKINE & GROWTH FACTOR REVIEWS

FIP1L1-PDGFRα Imposes Eosinophil Lineage Commitment on Hematopoietic Stem/Progenitor Cells

(2009) Kentaro Fukushima et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

JAK pathway induction of c-Myc critical to IL-5 stimulation of cell proliferation and inhibition of apoptosis

(2009) Wei-Hwa Lee et al.   JOURNAL OF CELLULAR BIOCHEMISTRY

Leukotactin-1/CCL15 induces cell migration and differentiation of human eosinophilic leukemia EoL-1 cells through PKCδ activation

(2009) Ji-Sook Lee et al.   MOLECULAR BIOLOGY REPORTS

Jak2 inhibition deactivates Lyn kinase through the SET–PP2A–SHP1 pathway, causing apoptosis in drug-resistant cells from chronic myelogenous leukemia patients

(2009) A K Samanta et al.   ONCOGENE

The JAK-3 inhibitor CP-690550 is a potent anti-inflammatory agent in a murine model of pulmonary eosinophilia

(2008) Elizabeth Kudlacz et al.   EUROPEAN JOURNAL OF PHARMACOLOGY

Dasatinib inhibits the growth and survival of neoplastic human eosinophils (EOL-1) through targeting of FIP1L1-PDGFRα

(2008) Christian Baumgartner et al.   EXPERIMENTAL HEMATOLOGY

The molecular anatomy of the FIP1L1-PDGFRA fusion gene

(2008) C Walz et al.   LEUKEMIA

Contributions of the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways to leukemia

(2008) L S Steelman et al.   LEUKEMIA

Five years since the discovery of FIP1L1–PDGFRA: what we have learned about the fusion and other molecularly defined eosinophilias

(2008) J Gotlib et al.   LEUKEMIA

Mechanisms for the proliferation of eosinophilic leukemia cells by FIP1L1-PDGFRα

(2007) Kenji Ishihara et al.   BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS