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Your search keyword '"Bast, Robert C."' showing total 42 results
Start Over Author "Bast, Robert C." Journal gynecologic oncology
42 results on '"Bast, Robert C."'

2. Perifosine plus docetaxel in patients with platinum and taxane resistant or refractory high-grade epithelial ovarian cancer

Author

Fu, Siqing, Hennessy, Bryan T., Ng, Chaan S., Ju, Zhenlin, Coombes, Kevin R., Wolf, Judith K., Sood, Anil K., Levenback, Charles F., Coleman, Robert L., Kavanagh, John J., Gershenson, David M., Markman, Maurie, Dice, Kristine, Howard, Adrienne, Li, Jane, Li, Yang, Stemke-Hale, Katherine, Dyer, Mary, Atkinson, Edward, Jackson, Ed, Kundra, Vikas, Kurzrock, Razelle, Bast, Robert C., Jr., and Mills, Gordon B.

Published
2012
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6. Specific Keynote: Molecular Therapeutics in Ovarian Cancer

Author

Mills, Gordon B., Fang, Xianjun, Lu, Yiling, Hasegawa, Yutaka, Eder, Astrid, Tanyi, Janos, Tabassam, Fazad Haq, Mao, Muling, Wang, Hongwei, Cheng, Kwai Wa, Nakayama, Yasuhisa, Kuo, Wenlin, Erickson, Jim, Gershenson, David, Kohn, Elise C., Jaffe, Robert, Bast, Robert C., Jr., and Gray, Joe

Published
2003
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22. Combining multiple serum tumor markers improves detection of stage I epithelial ovarian cancer

Author

Zhang, Zhen, primary, Yu, Yinhua, additional, Xu, Fengji, additional, Berchuck, Andrew, additional, van Haaften-Day, Carolien, additional, Havrilesky, Laura J., additional, de Bruijn, Henk W.A., additional, van der Zee, Ate G.J., additional, Woolas, Robert P., additional, Jacobs, Ian J., additional, Skates, Steven, additional, Chan, Daniel W., additional, and Bast, Robert C., additional

Published
2007
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23. Urinary mesothelin provides greater sensitivity for early stage ovarian cancer than serum mesothelin, urinary hCG free beta subunit and urinary hCG beta core fragment

Author

Badgwell, Donna, primary, Lu, Zhen, additional, Cole, Laurence, additional, Fritsche, Herbert, additional, Atkinson, Edward N., additional, Somers, Elizabeth, additional, Allard, Jeffrey, additional, Moore, Richard G., additional, Lu, Karen H., additional, and Bast, Robert C., additional

Published
2007
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30. Combinations of Multiple Serum Markers Are Superior to Individual Assays for Discriminating Malignant from Benign Pelvic Masses

Author

Woolas, Robert P., primary, Conaway, Mark R., additional, Xu, Fengji, additional, Jacobs, Ian J., additional, Yu, Yinhua, additional, Daly, Lee, additional, Davies, Ann Prys, additional, O'Briant, Kathy, additional, Berchuck, Andrew, additional, Soper, John T., additional, Clarke-Pearson, Daniel L., additional, Rodriguez, Gustavo, additional, Oram, David H., additional, and Bast, Robert C., additional

Published
1995
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33. Clinical trial endpoints in ovarian cancer: Report of an FDA/ASCO/AACR Public Workshop

Author

Bast, Robert C., Thigpen, J. Tate, Arbuck, Susan G., Basen-Engquist, Karen, Burke, Laurie B., Freedman, Ralph, Horning, Sandra J., Ozols, Robert, Rustin, Gordon J., Spriggs, David, Wenzel, Lari B., and Pazdur, Richard

Subjects
*CANCER treatment, *MEDICAL research, *MEDICAL experimentation on humans, *TUMORS
Abstract

Abstract: Objective: The unique characteristics of cancer, particularly issues involving the use of surrogate endpoints in clinical trials, present special challenges in the development of cancer drugs. In response, the U.S. Food and Drug Administration (FDA) has partnered with the American Society of Clinical Oncology, the American Association for Cancer Research, and the American Society of Hematology to conduct public workshops evaluating potential endpoints for drug approvals for the most common tumor types. Methods: A workshop evaluating potential endpoints in ovarian cancer drug research was held in Bethesda, Maryland, in April 2006. Invited experts presented research findings and discussed endpoints in trials of drugs for treatment of Stage III and IV ovarian cancer. Results: The panel responded to specific questions from FDA, discussing use of progression-free survival as a surrogate for overall survival and use of CA-125 levels as an indicator of response. Panel members also addressed endpoints in first-line therapy, second-line and subsequent therapy, and maintenance therapy. Conclusion: Expert commentary provided by panel members will inform FDA''s draft guidance on clinical endpoints for cancer drug approvals and will be discussed at meetings of the FDA''s Oncologic Drugs Advisory Committee. FDA intends to develop a set of principles that can be used to define efficacy standards for drugs used to treat ovarian and other cancers. [Copyright &y& Elsevier]

Published
2007
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34. High-dose alkylating agent chemotherapy with autologous bone marrow support in patients with stage III/IV epithelial ovarian cancer

Author

Shpall, Elizabeth J., primary, Clarke-Pearson, Daniel, additional, Soper, John T., additional, Berchuck, Andrew, additional, Jones, Roy B., additional, Bast, Robert C., additional, Ross, Maureen, additional, Lidor, Yaron, additional, Vanacek, Karen, additional, Tyler, Terry, additional, and Peters, William P., additional

Published
1990
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36. Prospective evaluation of serum CA 125 levels in a normal population, phase I: The specificities of single and serial determinations in testing for ovarian cancer

Author

Zurawski, Vincent R., primary, Sjovall, Kerstin, additional, Schoenfeld, David A., additional, Broderick, Susan F., additional, Hall, Paul, additional, Bast, Robert C., additional, Eklund, Gunnar, additional, Mattsson, Britta, additional, Connor, Robert J., additional, Prorok, Philip C., additional, Knapp, Robert C., additional, and Einhorn, Nina, additional

Published
1990
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37. Synergistic Interaction between an Anti-p185HER-2Pseudomonas Exotoxin Fusion Protein [scFv(FRP5)–ETA] and Ionizing Radiation for Inhibiting Growth of Ovarian Cancer Cells That Overexpress HER-2

Author

Schmidt, Mathias, McWatters, Amanda, White, R.Allen, Groner, Bernd, Wels, Winfried, Fan, Zhen, and Bast, Robert C.

Abstract

Objectives.The HER-2 proto-oncogene is overexpressed in 15–30% of ovarian cancers, providing a target for therapy in a fraction of patients. We previously described the ability of a recombinant single-chain anti-p185HER-2–Pseudomonas exotoxin A fusion protein, scFv(FRP5)–ETA, to inhibit growth of cancer cells in culture and tumor xenografts in vivo.We have also described synergistic interaction between an anti-p185HER-2-ricin A chain immunotoxin and ionizing radiation for inhibiting growth of ovarian and breast cancer cells that overexpress HER-2. Our objective in this report was to evaluate the in vitroand in vivoeffects of scFv(FRP5)–ETA against SKOv3 ovarian cancer cells that have been transfected to express >106p185HER-2receptors per cell (clone-9002-18).

Published
2001
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38. Transfection of Human Ovarian Cancer Cells with the HER-2/neuReceptor Tyrosine Kinase Induces a Selective Increase in PTP-H1, PTP-1B, and PTP-α Expression

Author

Wiener, Jon R., Kassim, Samar K., Yu, Yinhua, Mills, Gordon B., and Bast, Robert C.

Abstract

Protein tyrosine phosphorylation is a key regulator of cell growth regulation and, when aberrant, is linked with the process of oncogenic transformation. Since tyrosine phosphatases (PTP) reverse phosphorylation mediated by tyrosine kinases (PTK), it has been hypothesized, but insufficiently studied to date, that PTPs function as tumor suppressors. Alternatively, PTPs may augment signal transduction by repriming substrates. To begin to assess the role of PTPs in ovarian cancer cell growth regulation, PTP partial cDNAs were cloned from the OVCA 433 ovarian cancer cell line using RT/PCR and degenerate oligonucleotide primers for the PTP consensus domain. Thirteen partial cDNAs were isolated, the sequences of which, when compared to GenBank, suggested that they were derived from PTP family members. These included PTP-α, PTP-γ, LAR, PTP-δ, T-cell PTP, PTP-2A(1D), PTP-1B, PTP-1C, PTP-H1, PTP-PEST, PTP-Gallus, and two isolates which potentially represent novel PTPs. Steady-state expression analyses revealed that PTP-1B expression was undetectable in normal epithelium but was expressed in four of five ovarian cancer cell lines. In contrast, the expression of two SH2-containing PTPs, PTP-1C and PTP-2A, was detected in the normal ovarian epithelium but lost from one or more ovarian cancer cell lines. Finally, PTP-1B, PTP-α, and PTP-H1 expression was increased following HER-2/neutransfection of ovarian cancer cell lines. These results suggest that both normal ovarian epithelial cells and ovarian cancer cells express multiple PTPs. Further, some PTPs are differentially expressed between normal ovarian epithelium and ovarian cancer cells. Intriguingly, the transfection and increased expression of the prognostically significant HER-2/neuPTK induced a selective increase in the expression of the PTP-α, PTP-1B, and PTP-H1 tyrosine phosphatases.

Published
1996
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39. Characterization of Gelatinases Linked to Extracellular Matrix Invasion in Ovarian Adenocarcinoma: Purification of Matrix Metalloproteinase 2

Author

Young, Timothy N., Rodriguez, Gustavo C., Rinehart, Alex R., Bast, Robert C., Pizzo, Salvatore V., and Stack, M.Sharon

Abstract

Substantial evidence indicates that proteolytic degradation of the extracellular matrix is necessary for invasion and metastasis by cancer cells. Our previous work has demonstrated elevated secretion by cultured ovarian adenocarcinoma cells of two gelatinolytic metalloproteinases, a 72-kDa enzyme resembling matrix metalloproteinase 2 (MMP-2) and a 92-kDa enzyme resembling MMP-9 (Moseret al., Int. J. Cancer56, 552–559, 1994). To assess the potentialin vivorelevance of these enzymes, we have examined ovarian carcinoma ascites using gelatin substrate zymography. MMP species identical to those secreted from several well-characterized ovarian adenocarcinoma cell lines were found in the majority of ascites: MMP-2-like gelatinase (23 of 23 cases) and MMP-9-like gelatinase (18 of 23 cases), suggesting a prevalence of these species in the ovarian carcinoma microenvironment and their availability for tumor-associated proteolysis. The contribution of these proteinases to ovarian cancer invasion was further demonstrated by experiments measuring tumor cell-mediated proteolysis of native endothelial cell extracellular matrix (ECM) and tumor cell invasion of reconstituted basement membrane (Matrigel). These data showed that secretion of type IV collagenase activity by a series of independently isolated ovarian adenocarcinoma cell lines correlated well with the ability of these cells to proteolyze the ECM and invade the basement membrane. Furthermore, we have identified and characterized an ovarian carcinoma-associated gelatinase, the 72-kDa MMP found in conditioned media of the DOV 13 cell line, as MMP-2. This enzyme was identical to the previously described MMP-2 from other sources by Western blot, amino terminal sequence, and substrate specificity. Additionally, a large portion of the MMP-2 activity found in DOV 13 conditioned media is active without organomercurial treatment, suggesting that ovarian cancer cells have an endogenous activator of the zymogen. Together, these data suggest that ECM proteolysis mediated by tumor-associated proteinases plays an important role in the invasion and/or metastasis of ovarian carcinoma.

Published
1996
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