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10. Experimental Models and Methods in Antibody Targeting of Renal Cell Carcinoma.

Author

Walker, John M., Mydlo, Jack H., Vessella, Robert L., Wilbur, D. Scott, Buhler, Kent, and Lange, Paul H.

Abstract

Metastatic renal cell carcinoma (RCC) is incurable and there are few treatment options that assure even a short prolongation in survival. It is the most common malignancy of the adult kidney and accounts for approximately 12,000 deaths per year (1). Due to a lack of diagnostic markers for early detection and the infrequency of notable symptoms early in the disease process, about one third of patients present with known metastatic disease. However, the staging of RCC is an inaccurate science and in 40% of those patients where a nephrectomy is the treatment choice for presumed organ-confined disease, metastases become evident within about 1 yr (2). For reasons that are poorly understood, metastatic RCC has remained relatively resistant to chemotherapy, biological response modifiers and cellular immunotherapy—although, glimpses of encouragement have appeared in numerous studies. These are discussed in great depth throughout the accompanying chapters. [ABSTRACT FROM AUTHOR]

Published
2001
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11. 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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19. 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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23. APC/CTNNB1 (beta-catenin) pathway alterations in human prostate cancers.

Author

Gerstein AV, Almeida TA, Zhao G, Chess E, Shih IeM, Buhler K, Pienta K, Rubin MA, Vessella R, and Papadopoulos N

Subjects
Animals, DNA Mutational Analysis methods, Exons genetics, GTP-Binding Proteins genetics, Humans, Male, Mice, Signal Transduction genetics, Tumor Cells, Cultured, beta Catenin, beta-Transducin Repeat-Containing Proteins, Cytoskeletal Proteins genetics, Genes, APC, Mutation genetics, Prostatic Neoplasms genetics, Trans-Activators
Abstract

Genetic alterations serve as beacons for the involvement of specific pathways in tumorigenesis. It was previously shown that 5% of prostate tumors harbor CTNNB1 mutations, suggesting that this tumor type may involve a deregulated APC/CTNNB1 pathway. To explore this possibility further, we searched for mutations in genes implicated in this pathway in 22 samples that included cell lines, xenografts, and primary tumors. We identified seven alterations: two in CTNNB1, three in APC, and two in hTRCP1 (also known as BTRC) which controls the degradation of CTNNB1. Alterations in the CTNNB1 regulatory domain, APC, and hTRCP1 were mutually exclusive, consistent with their equivalent effects on CTNNB1 stability. These results suggest that CTNNB1 signaling plays a critical role in the development of a significant fraction of prostate cancers. Moreover, they provide the first evidence that hTRCP1 plays a role in human neoplasia., (Copyright 2002 Wiley-Liss, Inc.)

Published
2002
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24. 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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