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[Cancer Research 48, 4045-4048, July 15, 1988]
© 1988 American Association for Cancer Research

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Multiple Restriction Fragment Length Polymorphisms of the Human Epidermal Growth Factor Receptor Gene1

Jin S. Lee2, Jung S. Ro, Avraham Eisbruch3, Mordechai Shtalrid, Robert E. Ferrell, Jordan U. Gutterman and Mark Blick

Departments of Medical Oncology in the Division of Medicine [J. S. L., J. S. R., A. E.] and Clinical Immunology and Biological Therapy [M. S., M. B., J. U. G.], The University of Texas M. D. Anderson Hospital and Tumor Institute at Houston, Houston, Texas 77030, and Department of Biostatistics, The University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania 15261 [R. E. F.]

We have examined the epidermal growth factor (EGF) receptor gene for structural alterations in fresh human tumors. DNA samples from 92 patients with solid tumors (lung cancer, 37; breast cancer, 24; head and neck cancer, 17; other tumors, 14) were analyzed and compared with those from 22 leukemia patients and 14 individuals without malignant neoplasms. When DNA samples were digested with HindIII restriction endonuclease, Southern blot analysis demonstrated 3 distinct polymorphic bands (9.8, 11, and 12 kilobases) after hybridization to the HER-A64-1 probe and another 2 distinct polymorphic bands (4.9 and 5.2 kilobases) after hybridization to the HER-A64-3 probe. Pedigree analysis of 43 members of a single family and comparative analysis of tumor and normal DNA samples from the same patients demonstrated that the variations in fragment size observed were due to 2 independent restriction fragment length polymorphisms in the region of the EGF receptor gene. Amplification of the EGF receptor gene was detected in 3 cases of breast cancer, but not in other tumors studied. We conclude that the human EGF receptor gene has multiple restriction fragment length polymorphisms and that in fresh human tumor samples rearrangement and amplification of the gene occur infrequently, if ever, within the region encompassed by the 2 complementary DNA probes used.

1 This work was presented in part at the Annual Meeting of the American Association for the Advancement of Science in Chicago, IL, February 1987.

2 To whom requests for reprints should be addressed, at Department of Clinical Immunology and Biological Therapy, Box 41, The University of Texas M. D. Anderson Hospital and Tumor Institute at Houston, 1515 Holcombe Blvd., Houston, TX 77030.

3 Present address: P. O. Box 3099, Bat-Yam 59130, Israel.

Received 10/ 7/87. Revised 4/19/88. Accepted 4/20/88.







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
Copyright © 1988 by the American Association for Cancer Research.