Correlation of immunophenotype with progression-free survival in patients with gastrointestinal stromal tumors treated with imatinib mesylate

Lucian R. Chirieac, Jonathan Trent, Dejka M. Steinert, Haesun Choi, Ying Yang, Jiexin Zhang, Shreyaskumar R. Patel, Robert S. Benjamin, A. Kevin Raymond

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Abstract

BACKGROUND. The therapy for gastrointestinal stromal tumor (GIST) has been revolutionized by imatinib mesylate (IM). It is unknown whether the levels of KIT expression or the presence of CD34, smooth muscle actin (SMA), desmin, or S-100 protein predicts patient outcome from IM therapy. In the current study, the prognostic effects for KIT and other proteins (CD34, SMA, desmin, S-100) were analyzed in a series of GISTs in which protein expression was evaluated by immunohistochemical analysis (IHC). METHODS. The cases of 106 patients with GIST who were uniformly treated with IM at the study institution between December 15, 2000, and January 13, 2002 were evaluated retrospectively. The association between KIT intensity, CD34, desmin, SMA, S-100 protein, and progression-free survival (PFS) was studied. Kaplan-Meier analysis and the Cox proportional hazards regression model were used for statistical analysis. RESULTS. The majority of tumors arose from the stomach (37%), small intestine (35%), and colorectum (14%). KIT expression as determined by IHC was categorized as weak (10%), intermediate (32%), or strong (58%). Patient tumors expressed CD34 (75%), SMA (56%), desmin (1%), and S-100 protein (32%). Patients whose GIST had weak intermediate, or strong KIT expression were found to have an 18-month PFS rate of 80%, 84%, and 69%, respectively (P = .30). The presence or absence of CD34, SMA, desmin, or S-100 protein did not appear to correlate with PFS after IM. CONCLUSIONS. Patients with the appropriate clinical presentation and KIT-positive GIST tumors appear to benefit from IM independent of the level of KIT or the expression of CD34, SMA, desmin, or S-100 protein by IHC.

Original languageEnglish
Pages (from-to)2237-2244
Number of pages8
JournalCancer
Volume107
Issue number9
DOIs
StatePublished - Nov 1 2006
Externally publishedYes

Fingerprint

Gastrointestinal Stromal Tumors
Desmin
S100 Proteins
Disease-Free Survival
Smooth Muscle
Actins
Neoplasms
Kaplan-Meier Estimate
Proportional Hazards Models
Small Intestine
Imatinib Mesylate
Stomach
Proteins
Survival Rate
Therapeutics

Keywords

  • Gastrointestinal stromal tumor
  • Imatinib mesylate
  • Immunohistochemistry
  • Outcome

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Chirieac, L. R., Trent, J., Steinert, D. M., Choi, H., Yang, Y., Zhang, J., ... Raymond, A. K. (2006). Correlation of immunophenotype with progression-free survival in patients with gastrointestinal stromal tumors treated with imatinib mesylate. Cancer, 107(9), 2237-2244. https://doi.org/10.1002/cncr.22226

Correlation of immunophenotype with progression-free survival in patients with gastrointestinal stromal tumors treated with imatinib mesylate. / Chirieac, Lucian R.; Trent, Jonathan; Steinert, Dejka M.; Choi, Haesun; Yang, Ying; Zhang, Jiexin; Patel, Shreyaskumar R.; Benjamin, Robert S.; Raymond, A. Kevin.

In: Cancer, Vol. 107, No. 9, 01.11.2006, p. 2237-2244.

Research output: Contribution to journalArticle

Chirieac, LR, Trent, J, Steinert, DM, Choi, H, Yang, Y, Zhang, J, Patel, SR, Benjamin, RS & Raymond, AK 2006, 'Correlation of immunophenotype with progression-free survival in patients with gastrointestinal stromal tumors treated with imatinib mesylate', Cancer, vol. 107, no. 9, pp. 2237-2244. https://doi.org/10.1002/cncr.22226
Chirieac, Lucian R. ; Trent, Jonathan ; Steinert, Dejka M. ; Choi, Haesun ; Yang, Ying ; Zhang, Jiexin ; Patel, Shreyaskumar R. ; Benjamin, Robert S. ; Raymond, A. Kevin. / Correlation of immunophenotype with progression-free survival in patients with gastrointestinal stromal tumors treated with imatinib mesylate. In: Cancer. 2006 ; Vol. 107, No. 9. pp. 2237-2244.
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title = "Correlation of immunophenotype with progression-free survival in patients with gastrointestinal stromal tumors treated with imatinib mesylate",
abstract = "BACKGROUND. The therapy for gastrointestinal stromal tumor (GIST) has been revolutionized by imatinib mesylate (IM). It is unknown whether the levels of KIT expression or the presence of CD34, smooth muscle actin (SMA), desmin, or S-100 protein predicts patient outcome from IM therapy. In the current study, the prognostic effects for KIT and other proteins (CD34, SMA, desmin, S-100) were analyzed in a series of GISTs in which protein expression was evaluated by immunohistochemical analysis (IHC). METHODS. The cases of 106 patients with GIST who were uniformly treated with IM at the study institution between December 15, 2000, and January 13, 2002 were evaluated retrospectively. The association between KIT intensity, CD34, desmin, SMA, S-100 protein, and progression-free survival (PFS) was studied. Kaplan-Meier analysis and the Cox proportional hazards regression model were used for statistical analysis. RESULTS. The majority of tumors arose from the stomach (37{\%}), small intestine (35{\%}), and colorectum (14{\%}). KIT expression as determined by IHC was categorized as weak (10{\%}), intermediate (32{\%}), or strong (58{\%}). Patient tumors expressed CD34 (75{\%}), SMA (56{\%}), desmin (1{\%}), and S-100 protein (32{\%}). Patients whose GIST had weak intermediate, or strong KIT expression were found to have an 18-month PFS rate of 80{\%}, 84{\%}, and 69{\%}, respectively (P = .30). The presence or absence of CD34, SMA, desmin, or S-100 protein did not appear to correlate with PFS after IM. CONCLUSIONS. Patients with the appropriate clinical presentation and KIT-positive GIST tumors appear to benefit from IM independent of the level of KIT or the expression of CD34, SMA, desmin, or S-100 protein by IHC.",
keywords = "Gastrointestinal stromal tumor, Imatinib mesylate, Immunohistochemistry, Outcome",
author = "Chirieac, {Lucian R.} and Jonathan Trent and Steinert, {Dejka M.} and Haesun Choi and Ying Yang and Jiexin Zhang and Patel, {Shreyaskumar R.} and Benjamin, {Robert S.} and Raymond, {A. Kevin}",
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T1 - Correlation of immunophenotype with progression-free survival in patients with gastrointestinal stromal tumors treated with imatinib mesylate

AU - Chirieac, Lucian R.

AU - Trent, Jonathan

AU - Steinert, Dejka M.

AU - Choi, Haesun

AU - Yang, Ying

AU - Zhang, Jiexin

AU - Patel, Shreyaskumar R.

AU - Benjamin, Robert S.

AU - Raymond, A. Kevin

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N2 - BACKGROUND. The therapy for gastrointestinal stromal tumor (GIST) has been revolutionized by imatinib mesylate (IM). It is unknown whether the levels of KIT expression or the presence of CD34, smooth muscle actin (SMA), desmin, or S-100 protein predicts patient outcome from IM therapy. In the current study, the prognostic effects for KIT and other proteins (CD34, SMA, desmin, S-100) were analyzed in a series of GISTs in which protein expression was evaluated by immunohistochemical analysis (IHC). METHODS. The cases of 106 patients with GIST who were uniformly treated with IM at the study institution between December 15, 2000, and January 13, 2002 were evaluated retrospectively. The association between KIT intensity, CD34, desmin, SMA, S-100 protein, and progression-free survival (PFS) was studied. Kaplan-Meier analysis and the Cox proportional hazards regression model were used for statistical analysis. RESULTS. The majority of tumors arose from the stomach (37%), small intestine (35%), and colorectum (14%). KIT expression as determined by IHC was categorized as weak (10%), intermediate (32%), or strong (58%). Patient tumors expressed CD34 (75%), SMA (56%), desmin (1%), and S-100 protein (32%). Patients whose GIST had weak intermediate, or strong KIT expression were found to have an 18-month PFS rate of 80%, 84%, and 69%, respectively (P = .30). The presence or absence of CD34, SMA, desmin, or S-100 protein did not appear to correlate with PFS after IM. CONCLUSIONS. Patients with the appropriate clinical presentation and KIT-positive GIST tumors appear to benefit from IM independent of the level of KIT or the expression of CD34, SMA, desmin, or S-100 protein by IHC.

AB - BACKGROUND. The therapy for gastrointestinal stromal tumor (GIST) has been revolutionized by imatinib mesylate (IM). It is unknown whether the levels of KIT expression or the presence of CD34, smooth muscle actin (SMA), desmin, or S-100 protein predicts patient outcome from IM therapy. In the current study, the prognostic effects for KIT and other proteins (CD34, SMA, desmin, S-100) were analyzed in a series of GISTs in which protein expression was evaluated by immunohistochemical analysis (IHC). METHODS. The cases of 106 patients with GIST who were uniformly treated with IM at the study institution between December 15, 2000, and January 13, 2002 were evaluated retrospectively. The association between KIT intensity, CD34, desmin, SMA, S-100 protein, and progression-free survival (PFS) was studied. Kaplan-Meier analysis and the Cox proportional hazards regression model were used for statistical analysis. RESULTS. The majority of tumors arose from the stomach (37%), small intestine (35%), and colorectum (14%). KIT expression as determined by IHC was categorized as weak (10%), intermediate (32%), or strong (58%). Patient tumors expressed CD34 (75%), SMA (56%), desmin (1%), and S-100 protein (32%). Patients whose GIST had weak intermediate, or strong KIT expression were found to have an 18-month PFS rate of 80%, 84%, and 69%, respectively (P = .30). The presence or absence of CD34, SMA, desmin, or S-100 protein did not appear to correlate with PFS after IM. CONCLUSIONS. Patients with the appropriate clinical presentation and KIT-positive GIST tumors appear to benefit from IM independent of the level of KIT or the expression of CD34, SMA, desmin, or S-100 protein by IHC.

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KW - Outcome

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