ERC
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Endocrine-Related Cancer 5 (1) 45-48    DOI: 10.1677/erc.0.0050045
Copyright © 1998 by the Society for Endocrinology.
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via ISI Web of Science (6)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Waldum, H L
Right arrow Articles by Falkmer, S
Right arrow Search for Related Content
PubMed
Right arrow Articles by Waldum, H L
Right arrow Articles by Falkmer, S

Hormones and carcinogenesis

H L Waldum 1, E Brenna 1, A K Sandvik 1, U Syversen 1, and S Falkmer 1

1 Departments of Medicine and Pathology, University Hospital, and Institutes of Physiology and Biomedical Engineering, and Morphology, Norwegian University of Science and Technology, N-7006 Trondheim, Norway

Hormones are important regulators of growth. By stimulating proliferation, hormones may increase the risk of mutation and at the same time stimulate the replication of the mutated cell. Thus, hormones are complete carcinogens. A direct carcinogenic effect of oestrogen in man is known from the occurrence of vaginal carcinomas in girls born of mothers who were treated with oestrogen during pregnancy. There are also experimental animal studies indicating that even peptide hormones may induce malignant tumours.

An excellent example is the so-called enterochromaffin-like cell (ECL-cell) carcinoid of the stomach, which is caused by hypergastrinaemia and where the pathogenesis is diffuse hyperplasia, linear and nodular hyperplasia, dysplasia (with micronodules), intramucosal carcinoid, and invasive carcinoid. This sequence of events can be followed not only histopathologically but also by means of image DNA cytometry of the nuclei of the ECL-cells. As soon asclear-cut neoplasia is present, the cytometric DNA distribution pattern switches from the normal diploid type to an aneuploid one. The hyperplastic lesions are all reversible, as soon as the hypergastrinaemia is eliminated.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1998 by the Society for Endocrinology.