Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms. - Wikidata - wikimedia - TriplyDB

Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.

Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.

http://www.wikidata.org/entity/Q36553791

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Insights into the pathogenesis of Langerhans cell histiocytosis: the development of targeted therapies Phospho-proteomic analyses of B-Raf protein complexes reveal new regulatory principles.Revised classification of histiocytoses and neoplasms of the macrophage-dendritic cell lineages.3D clusters of somatic mutations in cancer reveal numerous rare mutations as functional targets.Real-time genomic profiling of histiocytoses identifies early-kinase domain BRAF alterations while improving treatment outcomes.Alectinib (CH5424802) antagonizes ABCB1- and ABCG2-mediated multidrug resistance in vitro, in vivo and ex vivo Genetic evaluation of juvenile xanthogranuloma: genomic abnormalities are uncommon in solitary lesions, advanced cases may show more complexity.A somatic mutation in erythro-myeloid progenitors causes neurodegenerative disease.High prevalence of myeloid neoplasms in adults with non-Langerhans cell histiocytosis.Mutually exclusive recurrent KRAS and MAP2K1 mutations in Rosai-Dorfman disease.Review of Rosai-Dorfman Disease: New Insights into the Pathogenesis of This Rare Disorder.Functional evidence for derivation of systemic histiocytic neoplasms from hematopoietic stem/progenitor cells.Activating MAPK1 (ERK2) mutation in an aggressive case of disseminated juvenile xanthogranuloma.Histiocytic neoplasms in the era of personalized genomic medicine.Langerhans cell histiocytosis is a neoplasm and consequently its recurrence is a relapse: In memory of Bob Arceci.Lymphoma classification update: T-cell lymphomas, Hodgkin lymphomas, and histiocytic/dendritic cell neoplasms.Diagnosis and classification of hematologic malignancies on the basis of genetics.Identification and Targeting of Kinase Alterations in Histiocytic Neoplasms.Assessment of BRAF(V600E) mutation in pulmonary Langerhans cell histiocytosis in tissue biopsies and bronchoalveolar lavages by droplet digital polymerase chain reaction.Molecular profiling of metastatic colorectal tumors using next-generation sequencing: a single-institution experience.Rosai-Dorfman Disease Harboring an Activating KRAS K117N Missense Mutation.New somatic BRAF splicing mutation in Langerhans cell histiocytosis.Diffuse reduction of cerebral grey matter volumes in Erdheim-Chester disease.Anakinra as efficacious therapy for 2 cases of intracranial Erdheim-Chester disease Alternative genetic mechanisms of BRAF activation in Langerhans cell histiocytosis.ALK Fusions in a Wide Variety of Tumor Types Respond to Anti-ALK Targeted Therapy.The histopathology of Erdheim-Chester disease: a comprehensive review of a molecularly characterized cohort.Efficacy of biological agents in the treatment of Erdheim-Chester disease.Novel activating BRAF fusion identifies a recurrent alternative mechanism for ERK activation in pediatric Langerhans cell histiocytosis.Clinical and radiological responses to oral methotrexate alone or in combination with other agents in Erdheim-Chester disease.Langerhans Cells: Sensing the Environment in Health and Disease.Hematopoietic origin of Langerhans cell histiocytosis and Erdheim-Chester disease in adults.Trametinib for the treatment of IGHV4-34, MAP2K1-mutant variant hairy cell leukemia.Outcome After Radiation Therapy for Langerhans Cell Histiocytosis Is Dependent on Site of Involvement.Histiocytic and dendritic cell neoplasms: what have we learnt by studying 67 cases.Allele-Specific Mechanisms of Activation of MEK1 Mutants Determine Their Properties.Consensus recommendations for the diagnosis and clinical management of Rosai-Dorfman-Destombes disease.Tocilizumab in patients with multisystem Erdheim-Chester disease.Efficacy of the MEK inhibitor cobimetinib for wild-type BRAF Erdheim-Chester disease.Trametinib in Histiocytic Sarcoma with an Activating MAP2K1 (MEK1) Mutation.

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Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.

http://www.wikidata.org/entity/Q36553791

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2015 nî lūn-bûn

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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2015年论文

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2015年论文

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Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.

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Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.

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Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.

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Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.

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Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.

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Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.

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Cancer Discovery

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Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms

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Adriana Heguy

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Ahmet Dogan

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Barry S Taylor

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David W Ellison

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Filip Janku

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P2860

Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.

Recurrent BRAF mutations in Langerhans cell histiocytosis

The genetic basis of early T-cell precursor acute lymphoblastic leukaemia.

Melanoma genome sequencing reveals frequent PREX2 mutations

Transcript assembly and quantification by RNA-Seq reveals unannotated transcripts and isoform switching during cell differentiation

BRAF fusions define a distinct molecular subset of melanomas with potential sensitivity to MEK inhibition

Oncogenic and sorafenib-sensitive ARAF mutations in lung adenocarcinoma

Safety and activity of alectinib against systemic disease and brain metastases in patients with crizotinib-resistant ALK-rearranged non-small-cell lung cancer (AF-002JG): results from the dose-finding portion of a phase 1/2 study.

First-line crizotinib versus chemotherapy in ALK-positive lung cancer.

Vemurafenib in Multiple Nonmelanoma Cancers with BRAF V600 Mutations.

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Benjamin Durham

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Sébastien Héritier

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