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


     


CA Cancer J Clin 1972; 22:232-240
doi: 10.3322/canjclin.22.4.232
© 1972 American Cancer Society
This Article
Right arrow Full Text (PDF) Freely available
Right arrow Submit a 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
Right arrow Citation Map
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Huggins, C.
Right arrow Articles by Hodges, C. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Huggins, C.
Right arrow Articles by Hodges, C. V.

CA: A Cancer Journal for Clinicians, Vol 22, 232-240, Copyright © 1972 by American Cancer Society


Studies on Prostatic Cancer

I. The Effect of Castration, Of Estrogen and of Androgen Injection on Serum Phosphatases in Metastatic Carcinoma of the Prostate

Charles Huggins M.D. and Clarence V. Hodges M.D.

1. The content in serum of phosphatase with activity maximum at pH 5 in normal men and in men with benign prostatic hypertrophy was 3.25±1.37 King and Armstrong units in 100 cc. Serum phosphatase with activity maximum at pH 9.3 in this control group was 7.9±2.1 units in 100 cc.

2. In a group of 25 men with roentgenologic evidence of metastatic carcinoma to the bony pelvis, both acid and alkaline phosphatases were increased above normal in 19 cases, only alkaline phosphatase was increased in 2 cases, and both values were within normal limits in 4 cases. Metastatic carcinoma of the prostate may be present in bones when the phosphatases of serum are normal, but when acid phosphatase is present in activity greater than 10 units in 100 cc., disseminated prostatic cancer is present.

3. In prostatic cancer with marked elevation of acid phosphatase, castration or injection of large amounts of estrogen caused a sharp reduction of this enzyme to or towards the normal range. Alkaline phosphatase values rose following castration and then decreased, but more slowly than acid phosphatase. In certain cases, these values reached and were maintained in a normal range during the period of observation, 180 days, while in other patients the values were slightly above normal.

4. In 3 patients with prostatic cancer, androgen injection caused a sharp rise of serum acid phosphatase. In 1 case following cessation of androgen there was a decrease of the acid phosphatase followed by a secondary spontaneous rise.

5. Acid phosphatase does not readily cross membranes from the blood, since it was present only in traces in cerebrospinal and spermatocele fluids when concurrent serum level was high.

6. Prostatic cancer is influenced by androgenic activity in the body. At least with respect to serum phosphatases, disseminated carcinoma of the prostate is inhibited by eliminating androgens, through castration or neutralization of their activity by estrogen injection. Cancer of the prostate is activated by androgen injections.




This article has been cited by other articles:


Home page
Clin. Cancer Res.Home page
R. Bedolla, T. J. Prihoda, J. I. Kreisberg, S. N. Malik, N. K. Krishnegowda, D. A. Troyer, and P. M. Ghosh
Determining Risk of Biochemical Recurrence in Prostate Cancer by Immunohistochemical Detection of PTEN Expression and Akt Activation
Clin. Cancer Res., July 1, 2007; 13(13): 3860 - 3867.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
J. I. Kreisberg, S. N. Malik, T. J. Prihoda, R. G. Bedolla, D. A. Troyer, S. Kreisberg, and P. M. Ghosh
Phosphorylation of Akt (Ser473) is an Excellent Predictor of Poor Clinical Outcome in Prostate Cancer
Cancer Res., August 1, 2004; 64(15): 5232 - 5236.
[Abstract] [Full Text] [PDF]


Home page
Mol. Endocrinol.Home page
M. E. Wright, M.-J. Tsai, and R. Aebersold
Androgen Receptor Represses the Neuroendocrine Transdifferentiation Process in Prostate Cancer Cells
Mol. Endocrinol., September 1, 2003; 17(9): 1726 - 1737.
[Abstract] [Full Text] [PDF]


Home page
J. Nutr.Home page
V. M. Adhami, N. Ahmad, and H. Mukhtar
Molecular Targets for Green Tea in Prostate Cancer Prevention
J. Nutr., July 1, 2003; 133(7): 2417S - 2424.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
H. Murillo, H. Huang, L. J. Schmidt, D. I. Smith, and D. J. Tindall
Role of PI3K Signaling in Survival and Progression of LNCaP Prostate Cancer Cells to the Androgen Refractory State
Endocrinology, November 1, 2001; 142(11): 4795 - 4805.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Pathol.Home page
I. Leav, K.-M. Lau, J. Y. Adams, J. E. McNeal, M.-E. Taplin, J. Wang, H. Singh, and S.-M. Ho
Comparative Studies of the Estrogen Receptors {beta} and {{alpha}} and the Androgen Receptor in Normal Human Prostate Glands, Dysplasia, and in Primary and Metastatic Carcinoma
Am. J. Pathol., July 1, 2001; 159(1): 79 - 92.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
M. Stanbrough, I. Leav, P. W. L. Kwan, G. J. Bubley, and S. P. Balk
Prostatic intraepithelial neoplasia in mice expressing an androgen receptor transgene in prostate epithelium
PNAS, September 11, 2001; 98(19): 10823 - 10828.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVECOVER ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1972 by American Cancer Society.