Reseña de Second-Line Treatment Options in Gist (Gastrointestinal Stromal Tumours ) (Case Study)

Second-Line Treatment Options in Gist (Gastrointestinal Stromal Tumours ) (Case Study) de Advances in Oncology Resumen del Libro

Introduction Gastrointestinal stromal tumours (GIST), the most common mesenchymal tumour of the gastrointestinal tract, are generally associated with activating KIT or platelet-derived growth factor receptor-alpha (PDGFRA) gene mutations. KIT mutations are found in approximately 85-90% of patients and PDGFRA mutations are found in another 4-7%. The remaining patients with GIST do not have detectable KIT or PDGFRA mutations, and are often referred to as wild-type even though they are likely to have other genotypic changes that have not yet been recognised. The KIT and PDGFRA genes encode the type III receptor tyrosine kinases, KIT (CD117) and PDGFRA, respectively. Under normal conditions, activation of downstream signalling cascades depends on ligand binding (stem-cell factor to KIT, and PDGF to PDGFR?) to initiate receptor dimerisation and tyrosine autophosphorylation [1]. However, activating KIT and PDGFRA mutations cause constitutive phosphorylation of key tyrosine residues in the kinase domain, thereby allowing ligand-independent activation of signalling pathways that promote cell proliferation and tumorigenesis [2]. Primary KIT mutations occur predominantly in exon 11, occasionally in exon 9, and only rarely in exons 13 and 17. In several recent series, exon 11 mutations were identified in 65% of GIST and accounted for about three-quarters of all tumours with KIT mutations. Exon 9 mutations were identified in 15-18% of GIST tumours, exon 13 mutations in approximately 2%, and exon 17 mutations in about 1%. PDGFRA mutations most frequently occur in exon 18 (kinase activation loop), occasionally in exon 12 (juxtamembrane domain) and rarely in exon 14 (kinase 1 domain) [3-5].

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