Prediction of Response to Docetaxel by Immunohistochemical Analysis of CYP3A4 Expression in Human Breast Cancers
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- Miyoshi Yasuo
- Department of Surgical Oncology, Osaka University Graduate School of Medicine
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- Taguchi Tetsuya
- Department of Surgical Oncology, Osaka University Graduate School of Medicine
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- Kim Seung Jin
- Department of Surgical Oncology, Osaka University Graduate School of Medicine
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- Tamaki Yasuhiro
- Department of Surgical Oncology, Osaka University Graduate School of Medicine
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- Noguchi Shinzaburo
- Department of Surgical Oncology, Osaka University Graduate School of Medicine
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Abstract
Background: Docetaxel (DOC) is inactivated by CYP3A4, high expression of which in tumor tissue might serve as a resistance mechanism. In the present study, the CYP3A4 protein level in breast cancers was determined by immunohistochemistry, and its relationship with the response to DOC treatment was studied.<br>Materials and Methods: Thirty-one patients with locally advanced (n = 21) or recurrent (n = 10) breast cancers underwent tumor biopsy, followed by DOC treatment (60 mg/m2 q3w). Expression of CYP3A4 was studied by immunohistochemistry.<br>Results: Patients with CYP3A4 negative tumors (n = 15) by immunohistochemistry showed a significantly (P < 0.01) higher response rate (67%) to DOC treatment than those with CYP3A4 positive tumors (n = 16, 19%). The positive predictive value, negative predictive value, and diagnostic accuracy of CYP3A4 expression by immunohistochemistry in the prediction of response to DOC were 67%, 81%, and 74%, respectively.<br>Conclusion: Immunohistochemical analysis of CYP3A4 expression in tumor cells might be clinically useful in the prediction of tumor response to DOC.
Journal
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- Breast Cancer
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Breast Cancer 12 (1), 11-15, 2005
The Japanese Breast Cancer Society
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Details 詳細情報について
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- CRID
- 1390001204480450816
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- NII Article ID
- 130004467367
- 10014316422
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- NII Book ID
- AA1103354X
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- COI
- 1:STN:280:DC%2BD2M%2FjtVSjsw%3D%3D
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- ISSN
- 18804233
- 13406868
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- PubMed
- 15657517
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- Text Lang
- en
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- Data Source
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- Abstract License Flag
- Disallowed