| Project/Area Number |
15590149
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Medical pharmacy
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| Research Institution | Japanese Foundation for Cancer Research |
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Principal Investigator |
NISHIO Makoto Japanese Foundation for Cancer Research, The Cancer Institute of JFCR, Researcher, 癌研究所, 研究員 (00281593)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIKAWA Yuichi Japanese Foundation for Cancer Research, The Cancer Institute of JFCR, Pathology, Chief, 癌研究所・病理部, 部長 (80222975)
SATOH Yukitoshi Japanese Foundation for Cancer ResearchThe Cancer Institute of JFCR, The Cancer Institute of JFCR, Researcher, 癌研究所, 研究員 (90321637)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2004: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | gefitinib / epidermal growth factor receptor / lung cancer / 肺がん / 化学療法感受性 / EGFR / Her family受容体 / 免疫染色 / 再発症例 / 手術材料 |
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| Research Abstract |
PURPOSE : Gefitinib is an inhibitor of the epidermal growth factor receptor (EGFR, HER1/ErbB1) tyrosine kinase that has shown clinical activity against non-small-cell lung cancer (NSCLC). The aim of the present study was to compare the relationship between expression status of HER family(EGFR, HER2,HER3,HER4) and EGFR gene mutations and clinical response to gefitinib.
PATIENTS AND METHODS : Lung carcinoma tissues of advanced or recurrent NSCLC patients treated with monotherapy of gefitinib were analyzed. Expressions of HER family in 31 tumors were exmined by immunohistochemistry (IHC) and EGFR gene mutations were examined in 17 frozen tissues by PCR single-strand conformation polymorphism (SSCP) analysis. The medical records were reviewed for clinical variables.
RESULTS : Total positivity rates were 21 for EGFR (68%), 24 for HER2 (77%), 17 for HER3 (55%) and 4 for HER4 (13%). Fourteen of 31 (45%) demonstrated triple expression of EGFR and HER2, as well as HER3 or HER4. A significantly better response rate (RR) and time to progression (TTP) were observed for the group with the triple expression than for the other groups (RR 50 vs 11% ; P<0.05, median TTP 4.29 vs 1.2 months ; P<0.05), although no difference was found with the expression status of individual HER family members. Six EGFR mutations were found in 17 frozen tumor tissues (48%). Triple expression of HER family were present in all 6 cases with EGFR mutations and in 4 of 11 cases without mutations ; P=.011.
Conclusion : Gefitinib may act on EFGR and HER2 and other HER family members in combination, providing a means for selection of patients most likely to respond to therapy.
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