| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
National Cancer Institute-Navy Medical Oncology Branch, National Naval Medical Center [A. M. S., E. R., R. I. L., R. M. P., A. F. G., B. E. J.], and Uniformed Services University of the Health Sciences [J. B., D. C. I.], Bethesda, Maryland 20889-5105, and the Division of Biostatistics, Yale University, New Haven, Connecticut 06510 [T. O., R. W. M.]
We studied 107 specimens (38 tumors and 69 tumor cell lines) from 90 patients with small cell lung cancer to determine the characteristics and clinical situations of patients from whom tumor cell lines could be established and the myc family DNA copy number. The proportion of extensive stage small cell lung cancer patients from whom a tumor cell line could be established prior to the initiation of therapy increased during the 10 years of the study (P < 0.001). Amplification of one of the myc family genes occurred in 3 of 40 (8%) of the untreated patient specimens compared to 19 of 67 (28%) of the treated patient specimens (P = 0.01). The myc family DNA amplification occurred in 17 of 54 (31%) of the specimens from patients treated with cyclophosphamide-based combinations and 2 of 13 (15%) of the specimens from patients treated with etoposide/cisplatin (P = 0.25). Both tumors and tumor cell lines were obtained from 17 patients with small cell lung cancer and the myc family DNA copy number was similar in 16 of the 17 patients. We conclude that: (a) myc family DNA amplification occurs more commonly in specimens from treated than untreated patients; (b) there are no prominent differences in the frequency of amplification following treatment with different chemotherapy regimens; and (c) myc family DNA amplification is similar in tumors and tumor cell lines from the same patients.
1 The opinions and assertions contained herein are the expressed views of the authors and are not to be construed as official or as reflecting the views of the Department of the Navy or the Department of Defense.
2 To whom requests for reprints should be addressed, at NCI-Navy Medical Oncology Branch, Building 8, Room 5101, National Naval Medical Center, Bethesda, MD 20889-5105.
Received 10/15/90. Accepted 1/ 8/91.
This article has been cited by other articles:
![]() |
E. T. Olejniczak, C. Van Sant, M. G. Anderson, G. Wang, S. K. Tahir, G. Sauter, R. Lesniewski, and D. Semizarov Integrative Genomic Analysis of Small-Cell Lung Carcinoma Reveals Correlates of Sensitivity to Bcl-2 Antagonists and Uncovers Novel Chromosomal Gains Mol. Cancer Res., April 1, 2007; 5(4): 331 - 339. [Abstract] [Full Text] [PDF] |
||||
![]() |
J.-C. Cutz, J. Guan, J. Bayani, M. Yoshimoto, H. Xue, M. Sutcliffe, J. English, J. Flint, J. LeRiche, J. Yee, et al. Establishment in Severe Combined Immunodeficiency Mice of Subrenal Capsule Xenografts and Transplantable Tumor Lines from a Variety of Primary Human Lung Cancers: Potential Models for Studying Tumor Progression-Related Changes. Clin. Cancer Res., July 1, 2006; 12(13): 4043 - 4054. [Abstract] [Full Text] [PDF] |
||||
![]() |
Z. Dai, W.-G. Zhu, C. D. Morrison, R. M. Brena, D. J. Smiraglia, A. Raval, Y.-Z. Wu, L. J. Rush, P. Ross, J. R. Molina, et al. A comprehensive search for DNA amplification in lung cancer identifies inhibitors of apoptosis cIAP1 and cIAP2 as candidate oncogenes Hum. Mol. Genet., April 1, 2003; 12(7): 791 - 801. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Danesi, F. De Braud, S. Fogli, T. M. De Pas, A. Di Paolo, G. Curigliano, and M. Del Tacca Pharmacogenetics of Anticancer Drug Sensitivity in Non-Small Cell Lung Cancer Pharmacol. Rev., March 1, 2003; 55(1): 57 - 103. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Lin, X. Jin, C. Page, V. K. Sondak, G. Jiang, and R. K. Reynolds A Modified p53 Overcomes mdm2-mediated Oncogenic Transformation: A Potential Cancer Therapeutic Agent Cancer Res., October 1, 2000; 60(20): 5895 - 5901. [Abstract] [Full Text] |
||||
![]() |
L. F. Barr, S. E. Campbell, G. B. Diette, E. W. Gabrielson, S. Kim, H. Shim, and C. V. Dang c-Myc Suppresses the Tumorigenicity of Lung Cancer Cells and Down-Regulates Vascular Endothelial Growth Factor Expression Cancer Res., January 1, 2000; 60(1): 143 - 149. [Abstract] [Full Text] |
||||
![]() |
A. K. Walch, H. F. Zitzelsberger, M. M. Aubele, A. E. Mattis, M. Bauchinger, S. Candidus, H. W. Prauer, M. Werner, and H. Hofler Typical and Atypical Carcinoid Tumors of the Lung Are Characterized by 11q Deletions as Detected by Comparative Genomic Hybridization Am. J. Pathol., October 1, 1998; 153(4): 1089 - 1098. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Butterfield, B. Storey, L. Maas, and L. E. Heasley c-Jun NH2-terminal Kinase Regulation of the Apoptotic Response of Small Cell Lung Cancer Cells to Ultraviolet Radiation J. Biol. Chem., April 11, 1997; 272(15): 10110 - 10116. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |