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[Cancer Research 49, 1130-1137, March 1, 1989]
© 1989 American Association for Cancer Research

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Epidermal Growth Factor Receptor Protein-Tyrosine Kinase Activity in Human Cell Lines Established from Squamous Carcinomas of the Head and Neck1

Steve A. Maxwell, Peter G. Sacks, Jordan U. Gutterman and Gary E. Gallick2

Departments of Tumor Biology [S. A. M., P. G. S., G. E. G.], Clinical Immunology [S. A. M., J. U. G.], and Head and Neck Surgery [P. G. S.], The University of Texas M. D. Anderson Hospital and Tumor Institute at Houston, Houston, Texas 77030

Two cell lines established from tumors of the head and neck area at different clinical stages were found to differ in the expression and in the tyrosine kinase activity of the epidermal growth factor (EGF) receptor. Cell line 183A was derived from an early-stage tumor and cell line 1483 was derived from a tumor that had metastasized to lymph nodes. The 1483 cells displayed a higher plating efficiency and clonogenicity in soft agar, suggesting a more tumorigenic phenotype over the 183A cells. Analyses of EGF receptor levels by using R1 anti-EGF receptor serum indicated that the 1483 cells expressed 5-fold more receptor than did the 183A cells. EGF receptors isolated from each cell line were active for kinase activity in an immune complex kinase assay, using monoclonal R1 anti-EGF receptor antibody. The autophosphorylation activity of both receptors was stimulated by addition of EGF to isolated membrane preparations and intact cells, although the EGF receptor of the 1483 cells was much less responsive to EGF than the receptor from 183A cells. In addition, the 1483 receptor consistently incorporated about twice as much phosphate as did the 183A receptor in an immune complex kinase assay. These data suggest that the basal tyrosine kinase activity of the EGF receptor from 1483 cells may be more active than the EGF receptor kinase from 183 cells.

1 This work was supported in part by the Clayton Foundation for Research to J. U. G., a Senior Clayton Foundation Investigator. This work was also aided by Grant RR5511-23 to S. A. M. and Grant CA39803 to G. E. G. from the NIH.

2 To whom reprints should be addressed, at Department of Tumor Biology, Box 79, M. D. Anderson Hospital and Tumor Institute, 1515 Holcombe Boulevard, Houston, TX 77030.

Received 5/16/88. Revised 11/ 1/88. Accepted 11/22/88.




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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 © 1989 by the American Association for Cancer Research.