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ArtikelGastrointestinal stromal tumour  
Oleh: Rubin, Brian P ; Heinrich, Michael C. ; Corless, Christopher L
Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The Lancet (keterangan: ada di Proquest) vol. 369 no. 9574 (May 2007), page 1731.
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  • Perpustakaan FK
    • Nomor Panggil: L01.K.2007.03
    • Non-tandon: 1 (dapat dipinjam: 0)
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Isi artikelGastrointestinal stromal tumours are the most common mesenchymal neoplasm of the gastrointestinal tract and are highly resistant to conventional chemotherapy and radiotherapy. Such tumours usually have activating mutations in either KIT (75–80%) or PDGFRA (5–10%), two closely related receptor tyrosine kinases. These mutations lead to ligand-independent activation and signal transduction mediated by constitutively activated KIT or PDGFRA. Targeting these activated proteins with imatinib mesylate, a small-molecule kinase inhibitor, has proven useful in the treatment of recurrent or metastatic gastrointestinal stromal tumours and is now being tested as an adjuvant or neoadjuvant. However, resistance to imatinib is a growing problem and other targeted therapeutics such as sunitinib are available. The important interplay between the molecular genetics of gastrontestinal stromal tumour and responses to targeted therapeutics serves as a model for the study of targeted therapies in other solid tumours.
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