Surgical treatment of gastrointestinal stromal tumors in the imatinib (STI-571) era

Peter C. Wu, Alex Langerman, Christopher Ryan, John Hart, Susan Swiger, Mitchell C. Posner, Gerard V. Aranha, Mark S. Talamonti, Raymond P. Onders, Raymond Pollak

Research output: Contribution to journalArticle

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Abstract

Background. Gastrointestinal stromal tumors (GIST) are rare mesenchymal tumors that are characterized by constitutive overexpression of the tyrosine kinase receptor KIT (CD117). Imatinib mesylate is a selective inhibitor of tyrosine kinase-mediated activity. This study reports a single-institution experience of surgical resection and the use of imatinib in the treatment of GIST. Methods. A retrospective review from 1995 to 2002 identified 57 patients (M:F, 29:28; median age, 61 years) with GIST who were treated at the University of Chicago. Twenty-eight patients underwent exploratory surgery with curative intent; 29 patients were referred for treatment ofmetastatic disease after surgery at outside institutions. Twenty-nine patients were treated with oral imatinib for either metastatic disease (n = 26 patients) or in the adjuvant setting after complete resection (n = 3 patients). Results. Resections were performed in 53 patients, and metastatic disease was identified in 17 patients at the time of exploratory surgery. Immunohistochemical staining for CD117 was positive in 96% of patients. A size larger than 5 cm, a mitotic rate larger than 1/10 high-power field, and tumor necrosis predicted recurrence in patients after resection. The median follow-up period was 18 months (range, 4-81 months). Twenty-three patients (40%) are alive without disease; 22 patients (39%) are alive with disease; 7 patients died, and 5 patients are lost to follow-up. Among the 26 patients with metastatic disease who were treated with imatinib, 5 deaths have occurred, and disease stabilization or tumor regression was observed initially in 22 patients, with a median duration of response of 19 months. Conclusions. Complete surgical extirpation remains the only curative treatment of GIST. Imatinib-targeted therapy of metastatic disease yields encouraging clinical responses. The true efficacy of imatinib in this setting, as induction therapy or as an adjuvant treatment in patients with GIST, is unknown pending the completion of ongoing prospective trials.

Original languageEnglish (US)
Pages (from-to)656-666
Number of pages11
JournalSurgery
Volume134
Issue number4
DOIs
StatePublished - Oct 2003
Externally publishedYes

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Gastrointestinal Stromal Tumors
Therapeutics
Imatinib Mesylate
Neoplasms
Lost to Follow-Up
Receptor Protein-Tyrosine Kinases

ASJC Scopus subject areas

  • Surgery

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Wu, P. C., Langerman, A., Ryan, C., Hart, J., Swiger, S., Posner, M. C., ... Pollak, R. (2003). Surgical treatment of gastrointestinal stromal tumors in the imatinib (STI-571) era. Surgery, 134(4), 656-666. https://doi.org/10.1016/S0039-6060(03)00314-3

Surgical treatment of gastrointestinal stromal tumors in the imatinib (STI-571) era. / Wu, Peter C.; Langerman, Alex; Ryan, Christopher; Hart, John; Swiger, Susan; Posner, Mitchell C.; Aranha, Gerard V.; Talamonti, Mark S.; Onders, Raymond P.; Pollak, Raymond.

In: Surgery, Vol. 134, No. 4, 10.2003, p. 656-666.

Research output: Contribution to journalArticle

Wu, PC, Langerman, A, Ryan, C, Hart, J, Swiger, S, Posner, MC, Aranha, GV, Talamonti, MS, Onders, RP & Pollak, R 2003, 'Surgical treatment of gastrointestinal stromal tumors in the imatinib (STI-571) era', Surgery, vol. 134, no. 4, pp. 656-666. https://doi.org/10.1016/S0039-6060(03)00314-3
Wu, Peter C. ; Langerman, Alex ; Ryan, Christopher ; Hart, John ; Swiger, Susan ; Posner, Mitchell C. ; Aranha, Gerard V. ; Talamonti, Mark S. ; Onders, Raymond P. ; Pollak, Raymond. / Surgical treatment of gastrointestinal stromal tumors in the imatinib (STI-571) era. In: Surgery. 2003 ; Vol. 134, No. 4. pp. 656-666.
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abstract = "Background. Gastrointestinal stromal tumors (GIST) are rare mesenchymal tumors that are characterized by constitutive overexpression of the tyrosine kinase receptor KIT (CD117). Imatinib mesylate is a selective inhibitor of tyrosine kinase-mediated activity. This study reports a single-institution experience of surgical resection and the use of imatinib in the treatment of GIST. Methods. A retrospective review from 1995 to 2002 identified 57 patients (M:F, 29:28; median age, 61 years) with GIST who were treated at the University of Chicago. Twenty-eight patients underwent exploratory surgery with curative intent; 29 patients were referred for treatment ofmetastatic disease after surgery at outside institutions. Twenty-nine patients were treated with oral imatinib for either metastatic disease (n = 26 patients) or in the adjuvant setting after complete resection (n = 3 patients). Results. Resections were performed in 53 patients, and metastatic disease was identified in 17 patients at the time of exploratory surgery. Immunohistochemical staining for CD117 was positive in 96{\%} of patients. A size larger than 5 cm, a mitotic rate larger than 1/10 high-power field, and tumor necrosis predicted recurrence in patients after resection. The median follow-up period was 18 months (range, 4-81 months). Twenty-three patients (40{\%}) are alive without disease; 22 patients (39{\%}) are alive with disease; 7 patients died, and 5 patients are lost to follow-up. Among the 26 patients with metastatic disease who were treated with imatinib, 5 deaths have occurred, and disease stabilization or tumor regression was observed initially in 22 patients, with a median duration of response of 19 months. Conclusions. Complete surgical extirpation remains the only curative treatment of GIST. Imatinib-targeted therapy of metastatic disease yields encouraging clinical responses. The true efficacy of imatinib in this setting, as induction therapy or as an adjuvant treatment in patients with GIST, is unknown pending the completion of ongoing prospective trials.",
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AU - Langerman, Alex

AU - Ryan, Christopher

AU - Hart, John

AU - Swiger, Susan

AU - Posner, Mitchell C.

AU - Aranha, Gerard V.

AU - Talamonti, Mark S.

AU - Onders, Raymond P.

AU - Pollak, Raymond

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N2 - Background. Gastrointestinal stromal tumors (GIST) are rare mesenchymal tumors that are characterized by constitutive overexpression of the tyrosine kinase receptor KIT (CD117). Imatinib mesylate is a selective inhibitor of tyrosine kinase-mediated activity. This study reports a single-institution experience of surgical resection and the use of imatinib in the treatment of GIST. Methods. A retrospective review from 1995 to 2002 identified 57 patients (M:F, 29:28; median age, 61 years) with GIST who were treated at the University of Chicago. Twenty-eight patients underwent exploratory surgery with curative intent; 29 patients were referred for treatment ofmetastatic disease after surgery at outside institutions. Twenty-nine patients were treated with oral imatinib for either metastatic disease (n = 26 patients) or in the adjuvant setting after complete resection (n = 3 patients). Results. Resections were performed in 53 patients, and metastatic disease was identified in 17 patients at the time of exploratory surgery. Immunohistochemical staining for CD117 was positive in 96% of patients. A size larger than 5 cm, a mitotic rate larger than 1/10 high-power field, and tumor necrosis predicted recurrence in patients after resection. The median follow-up period was 18 months (range, 4-81 months). Twenty-three patients (40%) are alive without disease; 22 patients (39%) are alive with disease; 7 patients died, and 5 patients are lost to follow-up. Among the 26 patients with metastatic disease who were treated with imatinib, 5 deaths have occurred, and disease stabilization or tumor regression was observed initially in 22 patients, with a median duration of response of 19 months. Conclusions. Complete surgical extirpation remains the only curative treatment of GIST. Imatinib-targeted therapy of metastatic disease yields encouraging clinical responses. The true efficacy of imatinib in this setting, as induction therapy or as an adjuvant treatment in patients with GIST, is unknown pending the completion of ongoing prospective trials.

AB - Background. Gastrointestinal stromal tumors (GIST) are rare mesenchymal tumors that are characterized by constitutive overexpression of the tyrosine kinase receptor KIT (CD117). Imatinib mesylate is a selective inhibitor of tyrosine kinase-mediated activity. This study reports a single-institution experience of surgical resection and the use of imatinib in the treatment of GIST. Methods. A retrospective review from 1995 to 2002 identified 57 patients (M:F, 29:28; median age, 61 years) with GIST who were treated at the University of Chicago. Twenty-eight patients underwent exploratory surgery with curative intent; 29 patients were referred for treatment ofmetastatic disease after surgery at outside institutions. Twenty-nine patients were treated with oral imatinib for either metastatic disease (n = 26 patients) or in the adjuvant setting after complete resection (n = 3 patients). Results. Resections were performed in 53 patients, and metastatic disease was identified in 17 patients at the time of exploratory surgery. Immunohistochemical staining for CD117 was positive in 96% of patients. A size larger than 5 cm, a mitotic rate larger than 1/10 high-power field, and tumor necrosis predicted recurrence in patients after resection. The median follow-up period was 18 months (range, 4-81 months). Twenty-three patients (40%) are alive without disease; 22 patients (39%) are alive with disease; 7 patients died, and 5 patients are lost to follow-up. Among the 26 patients with metastatic disease who were treated with imatinib, 5 deaths have occurred, and disease stabilization or tumor regression was observed initially in 22 patients, with a median duration of response of 19 months. Conclusions. Complete surgical extirpation remains the only curative treatment of GIST. Imatinib-targeted therapy of metastatic disease yields encouraging clinical responses. The true efficacy of imatinib in this setting, as induction therapy or as an adjuvant treatment in patients with GIST, is unknown pending the completion of ongoing prospective trials.

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