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Expression of High-Affinity Laminin Receptor mRNA Correlates with Cell Proliferation Rather Than Invasion in Human Papillomavirus-associated Cervical Neoplasms¹

Department of Medicine/Infectious Diseases Unit [L. M. D.], Department of Biochemistry [T. R. B., L. T. C.], University of Rochester School of Medicine and Dentistry, Rochester, New York 14642; Department of Pathology, The Cleveland Clinic Foundation, Cleveland, Ohio 44195 [M. H. S.]; and Laboratory of Pathology, Division of Cancer Biology and Diagnosis, National Cancer Institute, NIH, Bethesda, Maryland 20892 [M. E. S.]

Induction of the expression of the M_r 67,000 high-affinity laminin receptor gene has been postulated as playing a role in the progression of human tumors to invasive cancers. We tested this hypothesis by examining histopathological sections of a large number of epithelial lesions of the genital tract associated with human papillomaviruses. In situ hybridization was performed with a riboprobe generated from a laminin receptor complementary DNA. Laminin receptor mRNA was expressed primarily in the less differentiated cells in normal squamous tissues and in a spectrum of squamous neoplasms. There was no net induction of mRNA per cell in intraepithelial or invasive squamous neoplasms relative to normal tissue. In contrast, laminin receptor mRNA was not expressed at a detectable level in normal glands of the uterine cervix but was dramatically induced in morphologically abnormal, human papillomavirus-positive glands, irrespective of the genotype of human papillomaviruses present. The induction occurred before any evidence of invasion, and there was no further increase during the transition from adenocarcinoma in situ to invasive carcinoma. We conclude that induction of high-affinity laminin receptor gene expression is associated with the development of malignancies of cervical glandular epithelia, but the increased expression appears to correlate with the proliferative rather than the invasive properties of these cells.

¹ This project was supported by USPHS Grant CA36200 (T. R. B. and L. T. C.) and by USPHS Grant CA43629 (M. H. S.). L. M. D. was supported in part by National Institute of Allergy and Infectious Diseases Training Grant AI-07169 and by a Wilmot Cancer Research Fellowship.

² To whom requests for reprints should be addressed, at Department of Biochemistry, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642.

Received 7/ 9/91. Accepted 1/ 6/92.