about
Type 5 acid phosphatase. Sequence, expression and chromosomal localization of a differentiation-associated protein of the human macrophageSomatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2A new aldolase B variant, N334K, is a common cause of hereditary fructose intolerance in YugoslaviaDosage analysis of cancer predisposition genes by multiplex ligation-dependent probe amplificationKIT mutation analysis in mast cell neoplasms: recommendations of the European Competence Network on MastocytosisA tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.Durable responses to imatinib in patients with PDGFRB fusion gene-positive and BCR-ABL-negative chronic myeloproliferative disorders.The clinical significance of NOTCH1 and SF3B1 mutations in the UK LRF CLL4 trial.Isolation and characterization of the genes encoding mouse and human type-5 acid phosphataseCHIC2 deletion, a surrogate for FIP1L1-PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib mesylate therapyThe 8p11 myeloproliferative syndrome: a distinct clinical entity caused by constitutive activation of FGFR1Myeloproliferative disorders with translocations of chromosome 5q31-35: role of the platelet-derived growth factor receptor BetaMolecular analysis of aldolase B genes in hereditary fructose intoleranceNIN, a gene encoding a CEP110-like centrosomal protein, is fused to PDGFRB in a patient with a t(5;14)(q33;q24) and an imatinib-responsive myeloproliferative disorderTFG, a target of chromosome translocations in lymphoma and soft tissue tumors, fuses to GPR128 in healthy individualsThe genomic structure of ZNF198 and location of breakpoints in the t(8;13) myeloproliferative syndromeProfound parental bias associated with chromosome 14 acquired uniparental disomy indicates targeting of an imprinted locusThe t(8;22) in chronic myeloid leukemia fuses BCR to FGFR1: transforming activity and specific inhibition of FGFR1 fusion proteinsDistinct stem cell myeloproliferative/T lymphoma syndromes induced by ZNF198-FGFR1 and BCR-FGFR1 fusion genes from 8p11 translocationsCombining gene mutation with gene expression data improves outcome prediction in myelodysplastic syndromes.Megalencephaly syndromes: exome pipeline strategies for detecting low-level mosaic mutationsThe t(8;17)(p11;q23) in the 8p11 myeloproliferative syndrome fuses MYO18A to FGFR1.Nilotinib first-line therapy in patients with Philadelphia chromosome-negative/BCR-ABL-positive chronic myeloid leukemia in chronic phase: ENEST1st sub-analysis.A polymorphism associated with STAT3 expression and response of chronic myeloid leukemia to interferon α.Null alleles of the aldolase B gene in patients with hereditary fructose intolerance.Patients with myeloid malignancies bearing PDGFRB fusion genes achieve durable long-term remissions with imatinib.Detection and quantification of residual disease in chronic myelogenous leukemia.The t(14;20) is a poor prognostic factor in myeloma but is associated with long-term stable disease in monoclonal gammopathies of undetermined significanceAberrations of EZH2 in cancer.Cytogenetics of chronic myeloid leukaemia.KIT D816V and JAK2 V617F mutations are seen recurrently in hypereosinophilia of unknown significance.Tyrosine kinase fusion genes in chronic myeloproliferative diseases.A certified plasmid reference material for the standardisation of BCR-ABL1 mRNA quantification by real-time quantitative PCRThe JAK2 46/1 haplotype predisposes to MPL-mutated myeloproliferative neoplasmsLaboratory recommendations for scoring deep molecular responses following treatment for chronic myeloid leukemia.Serial measurement of BCR-ABL transcripts in the peripheral blood after allogeneic stem cell transplantation for chronic myeloid leukemia: an attempt to define patients who may not require further therapyDecrease in JAK2 V617F allele burden is not a prerequisite to clinical response in patients with polycythemia vera.Oncogenic derivatives of platelet-derived growth factor receptors.Comparison of mutated ABL1 and JAK2 as oncogenes and drug targets in myeloproliferative disordersExon-centric regulation of ATM expression is population-dependent and amenable to antisense modification by pseudoexon targeting
P50
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P50
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hulumtues
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հետազոտող
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name
Nicholas Cross
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Nicholas Cross
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Nicholas Cross
@es
Nicholas Cross
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Nicholas Cross
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Николас Кросс
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type
label
Nicholas Cross
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Nicholas Cross
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Nicholas Cross
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Nicholas Cross
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Nicholas Cross
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Николас Кросс
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prefLabel
Nicholas Cross
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Nicholas Cross
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Nicholas Cross
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Nicholas Cross
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Nicholas Cross
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Николас Кросс
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P1053
B-4817-2009
P106
P21
P214
19150999496429870565
P31
P3829
P496
0000-0001-5481-2555
P734
P735
P7859
viaf-19150999496429870565