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Jonathan A. Fletcher

Researcher at Brigham and Women's Hospital

Publications -  426
Citations -  57627

Jonathan A. Fletcher is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: GiST & PDGFRA. The author has an hindex of 109, co-authored 413 publications receiving 53642 citations. Previous affiliations of Jonathan A. Fletcher include Albany Medical College & Oregon Health & Science University.

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Journal Article

Constitutive activation of insulin receptor substrate 1 is a frequent event in human tumors: therapeutic implications.

TL;DR: It is found that IRS-1 is constitutively activated in a variety of solid tumors, including breast cancers, leiomyomas, Wilms' tumors, rhabdomyosarcomas, liposar comas,LeiomyosarComas, and adrenal cortical carcinomas, and that activated IRS- 1 may present an attractive therapeutic target.
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BAL is a novel risk-related gene in diffuse large B-cell lymphomas that enhances cellular migration.

TL;DR: Differential display was used to identify a novel gene, termed BAL (B-aggressivelymphoma), which is expressed at significantly higher levels in fatal high-risk DLB-CLs than in cured low-risk tumors, indicating that the risk-related BAL gene promotes malignant B-cell migration.
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Protein Kinase C θ (PKCθ) Expression and Constitutive Activation in Gastrointestinal Stromal Tumors (GISTs)

TL;DR: The signaling intermediate protein kinase C θ (PKCθ) is a diagnostic marker in GISTs, including those that lack KIT expression and/or contain PDGFRA mutations and may serve, along with KIT/PDGFRA, as a novel therapeutic target.
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Targeting human gastrointestinal stromal tumor cells with a quadruplex-binding small molecule.

TL;DR: It is shown here that the naphthalene diimide derivative is a potent inducer of growth arrest in a patient-derived GIST cell line at a concentration that also results in effective inhibition of telomerase activity and almost complete suppression of KIT mRNA and KIT protein expression.
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Response markers and the molecular mechanisms of action of Gleevec in gastrointestinal stromal tumors.

TL;DR: The potential value of an in vitro cell model to investigate GIST response to imatinib in vivo is emphasized, for the purpose of identifying important genetic markers of clinical response, mechanisms of drug action, and possible therapeutic targets.