help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Journal of Clinical Endocrinology & Metabolism Vol. 49, No. 2 272-277
doi:10.1210/jcem-49-2-272
Copyright © 1979 by the Endocrine Society.
This Article
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Reprints, Permissions and Rights
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by MACINDOE, J. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by MACINDOE, J. H.

Estradiol Formation from Testosterone by Continuously Cultured Human Breast Cancer Cells*

JOHN H. MACINDOE{dagger}

Department of Internal Medicine, University of Iowa, College of Medicine Iowa City, Iowa, 52242

Two human breast cancer cell lines (MCF-7 and MDA-MB-231) and one cell line derived from normal human breast (HBL-100) were examined for the presence of aromatase activity by determining the amounts of [3H]estradiol ([3(H]E2formed by cell cultures incubated with [3H]testosterone. Aro-matase activity was demonstrable in both breast cancer cell lines, but estradiol synthesis was not observed in HBL-100 cultures. The [3H]E2 content of MCF-7 cultures rose as a function of incubation time and substrate concentration. Furthermore, [3H[E2 formation by this cell line was suppressed by several known inhibitors of human placental aromatase.

These observations represent the first evidence that some lines of continuously cultured human breast cancer cells, like some human breast tumors, are capable of forming estrogen from an extracellular precursor steroid. Cultured breast cells may provide model systems for investigating the relative importance of intracellular estrogen formation in the regulation of human breast cancer cell growth.

* These studies were supported by NIH Grant CA-17649.

{dagger} To whom requests for reprints should be addresd.

Received January 12, 1979.




This article has been cited by other articles:


Home page
Cancer Res.Home page
T. W. Miller, M. Perez-Torres, A. Narasanna, M. Guix, O. Stal, G. Perez-Tenorio, A. M. Gonzalez-Angulo, B. T. Hennessy, G. B. Mills, J. P. Kennedy, et al.
Loss of Phosphatase and Tensin Homologue Deleted on Chromosome 10 Engages ErbB3 and Insulin-Like Growth Factor-I Receptor Signaling to Promote Antiestrogen Resistance in Breast Cancer
Cancer Res., May 15, 2009; 69(10): 4192 - 4201.
[Abstract] [Full Text] [PDF]


Home page
Clin. Cancer Res.Home page
M. H. Cohen, J. R. Johnson, N. Li, G. Chen, and R. Pazdur
Approval Summary: Letrozole in the Treatment of Postmenopausal Women with Advanced Breast Cancer
Clin. Cancer Res., March 1, 2002; 8(3): 665 - 669.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1979 by The Endocrine Society