KIT mutations and dose selection for imatinib in patients with advanced gastrointestinal stromal tumours.

By M. Debiec-Rychter, R. Sciot, A. Le Cesne, M. Schlemmer, P. Hohenberger, A. V. van Oosterom, J. Blay, S. Leyvraz, M. Stul, P. Casali and 5 more. European Journal of Cancer, 2006

864 citations recorded by the source corpus.

Subfields: Gastroenterology, Pulmonary and Respiratory Medicine, Surgery

View Paper: https://www.semanticscholar.org/paper/fa483f986f583df906a3166dce5f778c08644fed

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Gastroenterology

1. Christopher Corless
2. Heikki Joensuu
3. M. Heinrich
4. J. Fletcher
5. C. Fletcher

In Pulmonary and Respiratory Medicine

1. Heikki Joensuu
2. Christopher Corless
3. M. Heinrich

In Surgery

1. Heikki Joensuu
2. Christopher Corless
3. M. Heinrich

Citations in the corpus

• Long-term results from a randomized phase II trial of standard- versus higher-dose imatinib mesylate for patients with unresectable or metastatic gastrointestinal stromal tumors expressing KIT. (2008, result): “These findings are consistent with reported data from at least one other study that examined the relationship of KIT and PDGFRA mutations to response to imatinib, though that trial did detail a 23% response rate in patients who lack detectable mutations.(17,21) The phase III European Organisation fo”
• 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 kinase: S0033. (2008, background): “The EORTC phase III trial showed patients with exon 9 mutations had superior progression-free survival when initially treated with a higher dose of imatinib (800 v 400 mg daily).(22) These data, as well as a combined mutational meta-analysis of S0033 and EORTC information, were strong enough for the”
• Gastrointestinal stromal tumours: origin and molecular oncology (2011, background): “One of the interesting observations that has emerged from the Phase II trials, and which was confirmed in the Phase III trials, is that tumour response to imatinib correlates with the underlying kinase genotyp”