Estrogen Receptor-Positive Proliferating Cells in the Normal and Precancerous Breast
| Autor: | Balvinder S. Shoker, Michael P.A. Davies, Christine Jarvis, Joanne Hewlett, John P. Sloane, Elizabeth Anderson, D. Ross Sibson, Robert Clarke |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 1999 |
| Předmět: |
medicine.medical_specialty
medicine.drug_class Mammary gland Short Communications Estrogen receptor Down-Regulation Fluorescent Antibody Technique Breast Neoplasms Biology medicine.disease_cause Pathology and Forensic Medicine Breast cancer Internal medicine medicine Humans Neoplastic transformation Breast Hyperplasia Carcinoma Ductal Breast Cell Cycle Cell cycle medicine.disease Postmenopause Endocrinology medicine.anatomical_structure Cell Transformation Neoplastic Ki-67 Antigen Premenopause Receptors Estrogen Estrogen Female Carcinogenesis Precancerous Conditions Carcinoma in Situ Cell Division |
| Popis: | Recently it has been shown that epithelial cell expression of the estrogen receptor (ER) and that of the proliferation-associated marker Ki-67 are almost mutually exclusive in the normal premenopausal human breast but that coexpression frequently occurs in estrogen receptor-positive (ER+) breast cancers. This coexpression may indicate disordered expression of ER in the cell cycle or failure to suppress division of ER+ cells and could be important in neoplastic transformation. The purpose of this study was to determine whether in situ proliferations known to be associated with different levels of risk for developing breast cancer contain these coexpressing cells and, if so, the stage at which they occur. We found that ER+ proliferating cells were rare in premenopausal lobules but increased with age in the normal breast. There was no difference in nonlesional tissue between cancerous and noncancerous breasts. The percentage of dual-expressing cells was significantly increased, however, in all of the in situ proliferations and correlated positively with the level of risk of developing breast cancer. We suggest that development of at least some human breast cancers is associated with increasing failure to down-regulate ER as cells enter the cycle or to suppress division of ER+ cells. The mechanism may involve the loss of a tumor suppresser gene. |
| Databáze: | OpenAIRE |
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