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[Cancer Research 64, 7241-7244, October 15, 2004]
© 2004 American Association for Cancer Research

Advances in Brief

Gefitinib Induces Apoptosis in the EGFRL858R Non–Small-Cell Lung Cancer Cell Line H3255

Sean Tracy1, Toru Mukohara1,2,3, Mark Hansen4, Matthew Meyerson1,2,5,6,7, Bruce E. Johnson1,2,3 and Pasi A. Jänne1,2,3

1 Lowe Center for Thoracic Oncology and 2 Department of Medical Oncology, Dana Farber Cancer Institute; 3 Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School; 4 Shannon McCormack Advanced Molecular Diagnostic Laboratory, Dana Farber Cancer Institute; and Departments of 5 Pathology, 6 Biological Chemistry, and 7 Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts

Somatic mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) have recently been described in patients with non–small-cell lung cancer (NSCLC) who achieve radiographic regressions to the EGFR inhibitor gefitinib. One of these mutations, L858R (Leu->Arg), is also found in NSCLC cell line H3255, which is very sensitive to gefitinib treatment. We characterized nine NSCLC cell lines (three isolated from patients with bronchioloalveolar carcinoma and six isolated from patients with adenocarcinoma) for their in vitro sensitivity to gefitinib. Of these, only H3255 (EGFRL858R) and H1666 (EGFRWT) are sensitive to gefitinib with IC50 values of 40 nmol/L and 2 µmol/L, respectively. We examined the effects of gefitinib on H3255 and cell lines containing wild-type EGFR that are either sensitive (H1666) or resistant (A549 and H441) to gefitinib exposure in vitro. Gefitinib treatment (1 µmol/L) leads to significant apoptosis accompanied by increased poly(ADP-ribose) polymerase cleavage only in the H3255 cell line, leads to G1-S arrest in H1666, and has no effects in the A549 and H441 cell lines. Although EGFR and AKT are constitutively phosphorylated in H3255, H1666, and H441 cell lines, AKT is completely inhibited by gefitinib treatment only in the H3255 cell line. These findings further characterize a mechanism by which gefitinib treatment of NSCLC harboring EGFRL858R leads to a dramatic response to gefitinib.




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PNAS, March 8, 2005; 102(10): 3788 - 3793.
[Abstract] [Full Text] [PDF]

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H. Shigematsu, T. Takahashi, M. Nomura, K. Majmudar, M. Suzuki, H. Lee, I. I. Wistuba, K. M. Fong, S. Toyooka, N. Shimizu, et al.
Somatic Mutations of the HER2 Kinase Domain in Lung Adenocarcinomas
Cancer Res., March 1, 2005; 65(5): 1642 - 1646.
[Abstract] [Full Text] [PDF]

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H. VARMUS, W. PAO, K. POLITI, K. PODSYPANINA, and Y.-C.N. DU
Oncogenes Come of Age
Cold Spring Harb Symp Quant Biol, January 1, 2005; 70(0): 1 - 9.
[Abstract] [PDF]

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R.K. THOMAS, H. GREULICH, Y. YUZA, J.C. LEE, T. TENGS, W. FENG, T.-H. CHEN, E. NICKERSON, J. SIMONS, M. EGHOLM, et al.
Detection of Oncogenic Mutations in the EGFR Gene in Lung Adenocarcinoma with Differential Sensitivity to EGFR Tyrosine Kinase Inhibitors
Cold Spring Harb Symp Quant Biol, January 1, 2005; 70(0): 73 - 81.
[Abstract] [PDF]


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