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KMID : 0383820050580050473
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Tuberculosis and Respiratory Diseases
2005 Volume.58 No. 5 p.473 ~ p.479
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Immunohistochemical Study of Phosphatase and Tensin Homolog Deleted on Chromosome Ten in Gefitinib Treated Nonsmall Cell Lung Cancer Patients
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Lee Sung-Yong
Lee Ju-Han
Jung Jin-Yong
Lee Kyung-Joo
Lee Seung-Hyeun
Kim Se-Joong
Lee Eun-Joo
Hur Gyu-Young
Jung Ki-Hwan
Jeong Hye-Cheol
Lee Sang-Yeub
Kim Je-Hyeong
Shin Chol
Shim Jae-Jeong
In Kwang-Ho
Kang Kyung-Ho
Yoo Se-Hwa
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Abstract
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Background: Gefitinib targets the epidermal growth factor receptor r(EGFR), and Gefitinib has antitumor activity in patient with non-small cell lung cancer (NSCLC). However, only 10 to 20 percent of patients show a clinical response to this drug, and the molecular mechanisms underlying patient sensitivity to gefitinib are unknown. PTEN (Phosphatase and tensin homolog deleted on chromosome Ten) plays a role for the modulation of the phosphatidylinositol 3-kinase pathway (PI3K), which is involved in cell proliferation and survival, so that it can inhibit cell cycle progression and induce G1 arrest. Therefore, we analyzed the relationship between PTEN expression and gefitinib’s responsiveness in patients having advanced non small cell lung cancer that had progressed after previous chemotherapy.
Methods: The expression of PTEN was studied by immunohistochemistry in paraffin-embedded tumor blocks that were obtained from 22 patients who had been treated with gefitinib from JAN, 2001 to AUG. 2004. For the evaluation of the relationships between the PTEN expression, the clinical stage and the basal characteristics, those cases that showed the respective antigen expression in >50% of the tumor cells were considered positive.
Results: The positive rate of PTEN staining was 55% of the total of 22 patients. There was a significant relationship between the increased expression of PTEN and the response group (p=0.039). However, there was no significant relationship between the expression of PTEN and other clinicopathologic characteristics.
Conclusion: The expression of PTEN in patients with advanced non small cell lung cancer that has progressed after previous chemotherapy may play a role in gefitinib’s responsiveness.
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KEYWORD
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EGFR, Gefitinib, PTEN
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