PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors

By M. Heinrich, Christopher Corless, A. Duensing, Laura S. McGreevey, Chang-jie Chen, Nora E. Joseph, S. Singer, D. Griffith, Andrea Haley, Ajia Town and 3 more. Science, 2003

2,423 citations recorded by the source corpus.

Subfields: Gastroenterology, Pulmonary and Respiratory Medicine, Surgery

View Paper: https://www.semanticscholar.org/paper/9a36c8a828e63fe0d867743090524be2f903f303

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Citations in the corpus

Molecular correlates of imatinib resistance in gastrointestinal stromal tumors. (2006, methodology): “Several of the secondary KIT mutations identified in our series have been previously identified in human cancers: D816H, D820A, N822H/K, and Y823D.4,17,18,26-30 In contrast, there are no reports of V654A, T670I, or C809G mutations occurring as a primary mutation.”
The novel marker, DOG1, is expressed ubiquitously in gastrointestinal stromal tumors irrespective of KIT or PDGFRA mutation status. (2004, methodology): “Recently, a subset of GISTs have been found to have PDGFRA mutations rather than KIT mutations.(13,14) Patients with GISTs containing mutations in PDGFRA may still benefit from imatinib therapy, but these tumors often fail to react with antibodies against KIT and hence may remain undiagnosed as GIST”
The Epidemiology of Malignant Gastrointestinal Stromal Tumors: An Analysis of 1,458 Cases from 1992 to 2000 (2005, background): “Specifically, all patients diagnosed with the following histologies were included: stromal sarcoma (8,930), leiomyosarcoma (8,890), epithelioid leiomyosarcoma (8,891), cellular leiomyosarcoma (8,892), bizarre leiomyosarcoma (8,893), myxoid leiomyosarcoma (8,896), smooth muscle cell tumor (8,897), sa”
Bronchioloalveolar pathologic subtype and smoking history predict sensitivity to gefitinib in advanced non-small-cell lung cancer. (2004, background): “This could explain why gefitinib seems to induce tumor regression so rapidly in those patients that do respond, a mechanism that could be seen as analogous to inhibition by imatinib of specific activated tyrosine kinases in patients with gastrointestinal stromal tumors [27,28].”
Defects in succinate dehydrogenase in gastrointestinal stromal tumors lacking KIT and PDGFRA mutations (2010, background): “9084–9088. 5. Corless CL, Fletcher JA, Heinrich MC (2004) Biology of gastrointestinal stromal tumors.”
Efficacy of gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, in symptomatic patients with non-small cell lung cancer: a randomized trial. (2003, neutral): “Symptom improvement rate [95% CI] 44 (43) [33-53] 40 (35) [26-45] 84 (39) [32-45] .”
Gastrointestinal Stromal Tumors of the Stomach: A Clinicopathologic, Immunohistochemical, and Molecular Genetic Study of 1765 Cases With Long-term Follow-up (2005, neutral): “Fundus* 124 71:53 (59) 61 (19–86) 2-16-15-5 2-15-23-24 Spindle malignant 49% 26/72 (36) 42/44 (95) 41/45 (91) 4/47 (9) 0/44 (0) 1/46 (2)”
Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. (2003, methodology): “KIT and PDGFRA mutations were cloned by site-directed mutagenesis of the respective wild-type cDNA.(11,22) All mutations were confirmed by bidirectional sequencing.”
Roles of PDGF in animal development (2003, background): “A recent study also identified Pdgfra-activating mutations in a subset of human gastrointestinal stromal tumors, for which Pdgfra may prove to be a useful molecular marker and therapeutic target (Heinrich et al., 2003).”