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18 results on '"Buhler, Kent R."'

3. A Quantitative Model for the Dynamics of Serum Prostate-Specific Antigen as a Marker for Cancerous Growth : An Explanation for a Medical Anomaly

Author

Swanson, Kristin R., True, Lawrence D., Lin, Daniel W., Buhler, Kent R., Vessella, Robert, and Murray, James D.

Subjects
Male, Transplantation, Heterologous, Prostatic Neoplasms, Regular Article, Mice, SCID, Adenocarcinoma, Middle Aged, Models, Theoretical, Prostate-Specific Antigen, urologic and male genital diseases, Mice, Animals, Humans, Cell Division, Neoplasm Transplantation
Abstract

Prostate-specific antigen (PSA) is an enzyme produced by both normal and cancerous prostate epithelial cells. Although PSA is the most widely used serum marker to detect and follow patients with prostatic adenocarcinoma, there are certain anomalies in the values of serum levels of PSA that are not understood. We developed a mathematical model for the dynamics of serum levels of PSA as a function of the tumor volume. Our model results show good agreement with experimental observations and provide an explanation for the existence of significant prostatic tumor mass despite a low-serum PSA. This result can be very useful in enhancing the use of serum PSA levels as a marker for cancer growth.

Published
2001

7. THE LuCaP SERIES OF HUMAN PROSTATE CANCER XENOGRAFTS

Author

Buhler, Kent R., primary, Quinn, Janna E., additional, Whitney, Sarah C., additional, Lin, Daniel W., additional, Ellis, William J., additional, Corey, Eva, additional, Liu, Alvin Y., additional, True, Lawrence D., additional, Lange, Paul H., additional, Vessella, Robert L., additional, Macoska, Jill A., additional, and Bruchovsky, Nicholas, additional

Published
1999
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15. Synthesis and nca-Radioiodination of Arylstannyl−Cobalamin Conjugates. Evaluation of Aryliodo−Cobalamin Conjugate Binding to Transcobalamin II and Biodistribution in Mice

Author

Wilbur, D. Scott, primary, Hamlin, Donald K., additional, Pathare, Pradip M., additional, Heusser, Shannon, additional, Vessella, Robert L., additional, Buhler, Kent R., additional, Stray, James E., additional, Daniel, Janna, additional, Quadros, Edward V., additional, McLoughlin, Patricia, additional, and Morgan, A. Charles, additional

Published
1996
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18. Inhibition of androgen-independent growth of prostate cancer xenografts by 17beta-estradiol.

Author

Corey E, Quinn JE, Emond MJ, Buhler KR, Brown LG, and Vessella RL

Subjects
Animals, Cell Division physiology, Estradiol therapeutic use, Estrogen Receptor beta, Female, Gene Expression Regulation, Neoplastic, Humans, Male, Mice, Mice, Inbred BALB C, Mice, Nude, Neoplasm Transplantation, Ovariectomy, Prostatic Neoplasms genetics, Prostatic Neoplasms pathology, RNA, Neoplasm genetics, RNA, Neoplasm metabolism, Receptors, Estrogen genetics, Reverse Transcriptase Polymerase Chain Reaction, Time Factors, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Androgens physiology, Estradiol pharmacology, Prostatic Neoplasms prevention & control
Abstract

Purpose: Estrogen treatment has long been known to be of benefit in prostate cancer (CaP), but its mechanism was thought to involve merely a reduction in androgen levels. However, new evidence indicates that estrogen may exert effects on CaP cells in the absence of androgens., Experimental Design: Implantation of CaP xenografts (LuCaP 35, LuCaP 49, LuCaP 58, LuCaP 73, PC-3, and LNCaP) into intact and ovariectomized female mice was done to characterize growth and take rates in the absence of androgens. Ovariectomized female mice were supplemented with 17beta-estradiol, and LuCaP 35 CaP xenograft take and growth rates were determined. Reverse transcription-PCR was used to evaluate the presence of the estrogen receptor messages in CaP xenografts., Results: We have observed significant inhibition of CaP growth in intact versus ovariectomized female animals in five of six CaP xenograft lines. 17beta-Estradiol supplements given to ovariectomized female mice led to inhibition of tumor establishment and diminished growth of LuCaP 35 similar to that observed in intact female mice. Using reverse transcription-PCR, we have shown that these xenografts express the estrogen receptor beta message., Conclusions: We have determined that 17beta-estradiol supplementation causes inhibition of CaP growth in an animal model by mechanisms that are independent of androgen action. This gives rise to the possibility that estrogen therapy may be of potential use with hormone-refractory cancers. The xenograft models we describe herein may be useful as well in elucidating the pathways mediating the androgen-independent effects of estrogen on CaP.

Published
2002

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