Gefitinib is an orally bioavailable, EGF receptor tyrosine kinase inhibitor and was the first targeted drug to be approved for non-small-cell lung cancer (NSCLC). Identification of objective tumor regressions with gefitinib in NSCLC patients has resulted in intense, worldwide clinical and basic research directed toward finding the optimal use of gefitinib in NSCLC. A recent large international Phase III study (IRESSA NSCLC Trial Evaluating Response and Survival Against Taxotere [INTEREST]) comparing gefitinib and docetaxel in unselected pretreated patients showed equivalent survival with better tolerability and quality of life. In addition, a Phase III study (WJTOG0203) evaluating gefitinib as sequential therapy after platinum-doublet chemotherapy showed the improved progression-free survival time. Furthermore, a large-scale randomized study (IRESSA Pan-Asia study [IPASS]) comparing gefitinib monotherapy with carboplatin/paclitaxel for previously untreated patients with adenocarcinoma who were never- or light-smokers showed an improved progression-free survival time in the gefitinib arm. A smaller Phase III study of pretreated Japanese patients (V-15-32) also demonstrated no difference in overall survival compared with docetaxel, with a statistically greater overall response rate. Somatic mutations in the EGFR gene, the target of gefitinib, were associated with dramatic and durable regressions in patients with NSCLC. Currently, investigators are trying to determine the optimal approach to select patients for treatment with gefitinib. This article aims to briefly summarize the profile of gefitinib, EGFR mutations, landmark trials with gefitinib and, also, ongoing trials that may herald an era of individualized therapy in at least some NSCLC patients.
Our retrospective study suggested that PCI might have a role in surgically resected patients with p-stage II/III SCLC because of their relatively high frequency of brain metastasis.
The relationship of an insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene to left-ventricular hypertrophy in individuals with essential hypertension (EH) was investigated in a large population of Japanese men and women. The ACE genotype of 762 subjects with EH (425 men and 337 women) and 1,157 healthy controls (604 men and 553 women) was determined by polymerase chain reaction analysis. The distribution of ACE genotypes did not differ significantly between patients with EH and control in both men and women. For women with EH, the DD genotype was positively associated with the thickness of the interventricular septum and inversely associated with the left ventricular end-diastolic dimension, both determined by echocardiography. In contrast, the DD genotype was not associated with any echocardiographic parameter in men with EH. These results indicate that the DD genotype is a risk factor for left-ventricular hypertrophy in Japanese women with EH, but not for Japanese men.
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