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136. Chen LL, Trent JC, Wu EF, et al.: A missense mutation in KIT kinase domain 1 correlates with imatinib resistance in gastro- intestinal stromal tumors. Cancer Res 2004;64:5913–5919. 137. Tamborini E, Bonadiman L, Greco A, et al.: A new mutation in the KIT ATP pocket causes acquired resistance to imatinib in a gastrointestinal stromal tumor patient. Gastroenterology 2004; 127:294–299. 138. Fletcher JA, Corless CL, Dimitrijevic S, et al.: for the GIST working group. Mechanisms of resistance to imatinib mesylate (IM) in advanced gastrointestinal stromal tumor (GIST). Proc ASCO 2003;22:815 (abstract). 139. Desai J, Shankar S, Heinrich MC, et al.: Clonal evolution of resistance to imatinib (IM) in patients (pts) with gastrointestinal stromal tumor (GIST): Molecular and radiologic evaluation of new lesions. Proc Am Soc Clin Oncol 2004;22:197 (abstract). 140. Demetri GD, Desai J, Fletcher JA, et al.: SU11248, a multi- targeted tyrosine kinase inhibitor, can overcome imatinib (IM) resistance caused by diverse genomic mechanisms in patients (pts) with metastatic gastrointestinal stromal tumor (GIST). Proc Am Soc Clin Oncol 2004;23:195 (abstract). 141. https://www.acosog.org/studies/closed.jsp. 2005. Internet com- munication. 142. https://www.acosog.org/studies/synopses/Z9001_Synopsis.pdf. 2005. Internet communication. 143. Bumming P, Andersson J, Meis-Kindblom JM, et al.: Neoadju- vant, adjuvant and palliative treatment of gastrointestinal stromal tumours (GIST) with imatinib: A centre-based study of 17 pati- ents. Br J Cancer 2003;89:460–464. 144. Scaife CL, Hunt KK, Patel SR, et al.: Is there a role for surgery in patients with ‘‘unresectable’’ cKITþ gastrointestinal stromal tumors treated with imatinib mesylate? Am J Surg 2003;186: 665–669. 145. http://www.rtog.org/. 2005. Internet communication. 146. Verweij J, Van Oosterom A, Blay JY, et al.: Imatinib mesylate (STI-571 Glivec(R), Gleevec) is an active agent for gastro- intestinal stromal tumours, but does not yield responses in other soft-tissue sarcomas that are unselected for a molecular target. Results from an EORTC Soft Tissue and Bone Sarcoma Group Phase II Study. Eur J Cancer 2003;39:2006–2011. 147. von Mehren M, Blanke CD, Joensuu H, et al.: High incidence of durable responses induced by imatinib mesylate (Gleevec) in patients with unresectable and metastatic gastrointestinal stro- mal tumors (GISTs). Proc Am Soc Clin Oncol 2002;21:403a (abstract). 148. Rankin C, von Mehren M, Blanke C, et al.: Dose effect of imatinib (IM) in patients (pts) with metastatic GIST—Phase III Sarcoma Group Study S0033. Proc Am Soc Clin Oncol 2004;23: 815 (abstract). COMMENT These authors are from the oncology group in Oregon who have pioneered tyrosine kinase inhibition, an exciting therapeutic advance in the management of GISTs. The future implications of such targeted therapy for the control of other cancers is really exciting. Walter Lawrence, Jr., MD Guest Editor DOI 10.1002/jso.20231 Published online in Wiley InterScience (www.interscience.wiley.com). Gastric GI Stromal Tumors 207 ß 2005 Wiley-Liss, Inc.

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136. Chen LL, Trent JC, Wu EF, et al.: A missense mutation in KITkinase domain 1 correlates with imatinib resistance in gastro-intestinal stromal tumors. Cancer Res 2004;64:5913–5919.

137. Tamborini E, Bonadiman L, Greco A, et al.: A new mutation inthe KIT ATP pocket causes acquired resistance to imatinib in agastrointestinal stromal tumor patient. Gastroenterology 2004;127:294–299.

138. Fletcher JA, Corless CL, Dimitrijevic S, et al.: for the GISTworking group. Mechanisms of resistance to imatinib mesylate(IM) in advanced gastrointestinal stromal tumor (GIST). ProcASCO 2003;22:815 (abstract).

139. Desai J, Shankar S, Heinrich MC, et al.: Clonal evolution ofresistance to imatinib (IM) in patients (pts) with gastrointestinalstromal tumor (GIST): Molecular and radiologic evaluation ofnew lesions. Proc Am Soc Clin Oncol 2004;22:197 (abstract).

140. Demetri GD, Desai J, Fletcher JA, et al.: SU11248, a multi-targeted tyrosine kinase inhibitor, can overcome imatinib (IM)resistance caused by diverse genomic mechanisms in patients(pts) with metastatic gastrointestinal stromal tumor (GIST). ProcAm Soc Clin Oncol 2004;23:195 (abstract).

141. https://www.acosog.org/studies/closed.jsp. 2005. Internet com-munication.

142. https://www.acosog.org/studies/synopses/Z9001_Synopsis.pdf.2005. Internet communication.

143. Bumming P, Andersson J, Meis-Kindblom JM, et al.: Neoadju-vant, adjuvant and palliative treatment of gastrointestinal stromaltumours (GIST) with imatinib: A centre-based study of 17 pati-ents. Br J Cancer 2003;89:460–464.

144. Scaife CL, Hunt KK, Patel SR, et al.: Is there a role for surgery inpatients with ‘‘unresectable’’ cKITþ gastrointestinal stromaltumors treated with imatinib mesylate? Am J Surg 2003;186:665–669.

145. http://www.rtog.org/. 2005. Internet communication.146. Verweij J, Van Oosterom A, Blay JY, et al.: Imatinib mesylate

(STI-571 Glivec(R), Gleevec) is an active agent for gastro-intestinal stromal tumours, but does not yield responses in othersoft-tissue sarcomas that are unselected for a molecular target.Results from an EORTC Soft Tissue and Bone Sarcoma GroupPhase II Study. Eur J Cancer 2003;39:2006–2011.

147. von Mehren M, Blanke CD, Joensuu H, et al.: High incidence ofdurable responses induced by imatinib mesylate (Gleevec) inpatients with unresectable and metastatic gastrointestinal stro-mal tumors (GISTs). Proc Am Soc Clin Oncol 2002;21:403a(abstract).

148. Rankin C, von Mehren M, Blanke C, et al.: Dose effect ofimatinib (IM) in patients (pts) with metastatic GIST—Phase IIISarcoma Group Study S0033. Proc Am Soc Clin Oncol 2004;23:815 (abstract).

COMMENT

These authors are from the oncology group in Oregon who have pioneered tyrosinekinase inhibition, an exciting therapeutic advance in the management of GISTs. Thefuture implications of such targeted therapy for the control of other cancers is reallyexciting.

Walter Lawrence, Jr., MD

Guest Editor

DOI 10.1002/jso.20231

Published online in Wiley InterScience (www.interscience.wiley.com).

Gastric GI Stromal Tumors 207

� 2005 Wiley-Liss, Inc.