• Publications
  • Influence
Diagnosis of gastrointestinal stromal tumors: A consensus approach.
TLDR
Key elements of the consensus are the defining role of KIT immunopositivity in diagnosis and a proposed scheme for estimating metastatic risk in these lesions, based on tumor size and mitotic count, recognizing that it is probably unwise to use the definitive term "benign" for any GIST, at least at the present time.
Pathology and genetics of tumours of soft tissue and bone
TLDR
This list includes tumours of undefined neoplastic nature, which are of uncertain differentiation Bone Tumours, Ewing sarcoma/Primitive neuroedtodermal tumour, Myogenic, lipogenic, neural and epithelial tumours, and others.
WHO classification of tumours of soft tissue and bone
TLDR
The mechanisms of human cancer the causes 500 referencesThese issues facilitate future progress and related genetic alterations are described in a unified method and provide an international standard for use.
Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors.
TLDR
Imatinib induced a sustained objective response in more than half of patients with an advanced unresectable or metastatic gastrointestinal stromal tumor, indicating that inhibition of the KIT signal-transduction pathway is a promising treatment for advanced gastrointestinalStromal tumors, which resist conventional chemotherapy.
PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors
TLDR
Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression, suggesting KIT and PDGFra mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs.
Soft Tissue Tumors
  • C. Fletcher
  • Medicine
    Current Topics in Pathology
  • 1 May 1998
Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor.
TLDR
Activating mutations of KIT or PDGFRA are found in the vast majority of GISTs, and the mutational status of these oncoproteins is predictive of clinical response to imatinib.
Inflammatory Myofibroblastic Tumor: Comparison of Clinicopathologic, Histologic, and Immunohistochemical Features Including ALK Expression in Atypical and Aggressive Cases
TLDR
A subset of IMTs with histologic atypia and/or clinical aggressiveness that were analyzed for clinicopathologic features, outcome, and immunohistochemical expression of anaplastic lymphoma kinase (ALK) and other markers to identify potential pathologic prognostic features found ALK reactivity may be a favorable prognostic indicator in IMT and abdominopelvic IMTs recur more frequently.
tp53 mutant zebrafish develop malignant peripheral nerve sheath tumors.
TLDR
These mutant zebrafish lines provide a unique platform for modifier screens to identify genetic mutations or small molecules that affect tp53-related pathways, including apoptosis, cell-cycle delay, and tumor suppression.
Phase III randomized, intergroup trial assessing imatinib mesylate at two dose levels in patients with unresectable or metastatic gastrointestinal stromal tumors expressing the kit receptor tyrosine
TLDR
This trial confirms the effectiveness of imatinib as primary systemic therapy for patients with incurable GIST but did not show any advantage to higher dose treatment.
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