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108 results on '"Glisson, B. S."'

2. Adenovirus-Mediated p53 Gene Transfer in Sequence With Cisplatin to Tumors of Patients With Non–Small-Cell Lung Cancer

Author

Nemunaitis, J., Swisher, S. G., Timmons, T., Connors, D., Mack, M., Doerksen, L., Weill, D., Wait, J., Lawrence, D. D., Kemp, B. L., Fossella, F., Glisson, B. S., Hong, W. K., Khuri, F. R., Kurie, J. M., Lee, J. J., Lee, J. S., Nguyen, D. M., Nesbitt, J. C., Perez-Soler, R., Pisters, K. M. W., Putnam, J. B., Richli, W. R., Shin, D. M., Walsh, G. L., Merritt, J., and Roth, J.

Published
2000

17. Phase II trial of irinotecan plus cisplatin (IP) and etoposide plus cisplatin (EP) given weekly on alternating weeks with granulocyte colony-stimulating factor support in the treatment of extensive-stage small cell lung cancer

Author

Uyeki, J., primary, Johnson, F. M., additional, Feng, L., additional, Peeples, B. O., additional, Blumenschein, G. J., additional, Fossella, F. V., additional, Karp, D. D., additional, Pisters, K. M., additional, Stewart, D. J., additional, and Glisson, B. S., additional

Published
2007
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27. Adenovirus-Mediated p53 Gene Transfer in Advanced Non-Small-Cell Lung Cancer

Author

Swisher, S. G., primary, Roth, J. A., additional, Nemunaitis, J., additional, Lawrence, D. D., additional, Kemp, B. L., additional, Carrasco, C. H., additional, Connors, D. G., additional, El-Naggar, A. K., additional, Fossella, F., additional, Glisson, B. S., additional, Hong, W. K., additional, Khuri, F. R., additional, Kurie, J. M., additional, Lee, J. J., additional, Lee, J. S., additional, Mack, M., additional, Merritt, J. A., additional, Nguyen, D. M., additional, Nesbitt, J. C., additional, Perez-Soler, R., additional, Pisters, K. M. W., additional, Putnam, J. B., additional, Richli, W. R., additional, Savin, M., additional, Schrump, D. S., additional, Shin, D. M., additional, Shulkin, A., additional, Walsh, G. L., additional, Wait, J., additional, Weill, D., additional, and Waugh, M. K. A., additional

Published
1999
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28. Phase II trial of paclitaxel, ifosfamide, and cisplatin in patients with recurrent head and neck squamous cell carcinoma.

Author

Shin, D M, primary, Glisson, B S, additional, Khuri, F R, additional, Ginsberg, L, additional, Papadimitrakopoulou, V, additional, Lee, J J, additional, Lawhorn, K, additional, Gillenwater, A M, additional, Ang, K K, additional, Clayman, G L, additional, Callender, D L, additional, Hong, W K, additional, and Lippman, S M, additional

Published
1998
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32. Phase II study of topotecan in patients with advanced non-small-cell lung cancer previously untreated with chemotherapy.

Author

Perez-Soler, R, primary, Fossella, F V, additional, Glisson, B S, additional, Lee, J S, additional, Murphy, W K, additional, Shin, D M, additional, Kemp, B L, additional, Lee, J J, additional, Kane, J, additional, Robinson, R A, additional, Lippman, S M, additional, Kurie, J M, additional, Huber, M H, additional, Raber, M N, additional, and Hong, W K, additional

Published
1996
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35. Phase II study of the antiangiogenesis agent thalidomide in recurrent or metastatic squamous cell carcinoma of the head and neck.

Author

Tseng, Jennifer E., Glisson, Bonnie S., Khuri, Fadlo R., Shin, Dong M., Myers, Jeffrey N., El-Naggar, Adel K., Roach, Jennifer S., Ginsberg, Lawrence E., Thall, Peter F., Wang, Xuemei, Teddy, Stephanie, Lawhorn, Kristie N., Zentgraf, Rebecca E., Steinhaus, Ganene D., Pluda, James M., Abbruzzese, James L., Hong, Waun Ki, Herbst, Roy S., Tseng, J E, and Glisson, B S

Published
2001
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36. Phase II study of paclitaxel, ifosfamide, and carboplatin in patients with recurrent or metastatic head and neck squamous cell carcinoma.

Author

Shin, Dong M., Khuri, Fadlo R., Glisson, Bonnie S., Ginsberg, Lawrence, Papadimitrakopoulou, Vali M., Clayman, Gary, Lee, J. Jack, Ang, K. Kian, Lippman, Scott M., Hong, Waun Ki, Shin, D M, Khuri, F R, Glisson, B S, Ginsberg, L, Papadimitrakopoulou, V M, Clayman, G, Lee, J J, Ang, K K, Lippman, S M, and Hong, W K

Published
2001
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37. Dissociation of cytotoxicity and DNA cleavage activity induced by topoisomerase II-reactive intercalating agents in hamster-human somatic cell hybrids.

Author

Glisson, Bonnie, Killary, Ann, Merta, Philip, Ross, Warren, Siciliano, Jeanette, Siciliano, Michael, Glisson, B S, Killary, A M, Merta, P, Ross, W E, Siciliano, J, and Siciliano, M J

Abstract

Previous studies using the mutant Chinese hamster ovary cell line VpmR-5 indicate that its resistance to epipodophyllotoxins and intercalating agents is likely to be mediated through a qualitative change in type II topoisomerase that confers resistance to drug-stimulated DNA cleavage activity. In a further investigation of the genetic basis of drug resistance in VpmR-5 cells, we fused a hypoxanthine-guanine phosphoribosyl transferase-deficient subline of VpmR-5 (Vtgm-6) with normal human lymphocytes and analyzed the resultant hybrid lines (HL) for altered drug sensitivity. In all, 3 of 16 hybrid clones exhibited partial reconstitution of sensitivity to etoposide, mitoxantrone, doxorubicin, and 5-iminodaunorubicin while retaining complete resistance to m-AMSA. However, enhanced sensitivity to drug-induced DNA cleavage activity was observed only for etoposide. Biochemical and molecular-marker analysis of the hybrids failed to identify human chromosome 17 (the provisional location of TOP2) or any other human chromosome that is consistently and uniquely associated with drug sensitivity. We therefore sought to verify the chromosomal assignment of TOP2 by Southern blot hybridization of TOP2 cDNA on a human hybrid mapping panel and confirmed its location on chromosome 17. However, no hybridizing sequence to the TOP2 cDNA was found in any of the 16 Vtgm-6 hybrid lines. Efforts to select more directly for human chromosome 17 VpmR-5 hybrids using microcell fusion of mouse A9 cells carrying human 17 linked to pSV2neo were unsuccessful. None of the five hybrid clones thus obtained had 17q markers, including the gene for TOP2. Although the mechanism underlying partial reversion to a drug-sensitive phenotype in the original Vtgm-6 hybrid lines has yet to be defined, the data obtained in these lines indicate that anthracycline- and anthracenedione-induced cytotoxic effects can be dissociated from DNA cleavage activity. This suggests that pathways distal to cleavable-complex formation or, alternatively, independent of interactions with topoisomerase II that involve other intracellular targets are important in mediating the cytotoxicity produced by these drugs. [ABSTRACT FROM AUTHOR]

Published
1992
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38. Etoposide-induced DNA cleavage in human leukemia cells.

Author

Edwards, Catherine, Glisson, Bonnie, King, Charles, Smallwood-Kentro, Sherin, Ross, Warren, Edwards, C M, Glisson, B S, King, C K, Smallwood-Kentro, S, and Ross, W E

Abstract

The nuclear enzyme, topoisomerase II, is the major site of action for cancer chemotherapy agents such as etoposide, teniposide, and a variety of intercalating agents. These compounds cause the enzyme to cleave DNA, forming a DNA-protein complex that may be a key step leading to cell death. It is apparently unique as a chemotherapy target, since drug potency diminishes with decreasing enzyme activity. It was thus of interest to examine the topoisomerase content and drug-induced DNA cleavage in freshly obtained human leukemia cells and to compare the obtained data with the results of similar studies performed in well-characterized human leukemia cell lines. The human T-lymphoblast line, CCRF-CEM, was more than 100-fold more sensitive to the DNA-cleavage effect of etoposide than the cells of the 13 leukemic patients examined. One of the leukemia lines (HL-60) and a lymphoblastoid line (RPMI-7666) were somewhat less sensitive than cells of the CCRF-CEM cells, but were still 10-fold more sensitive than the patients studied. The relative insensitivity of the freshly obtained cells could not be accounted for by differences with respect to drug uptake but were associated with markedly reduced topoisomerase-II content as assayed by immunoblotting using a mouse polyclonal serum against topoisomerase II. Heterogeneity was observed in the sensitivities of patients' cells with respect to both drug-induced DNA cleavage and enzyme content. The observed differences between cultured cell lines and patients' cells may have been related to their proliferative status. Etoposide potency in normal resting lymphocytes resembles that observed in circulating leukemia cells. However, following mitogenesis with phytohemagglutinin and interleukin-2, proliferating lymphocytes become as sensitive to etoposide as cultured cell lines with regard to DNA cleavage. This effect was accompanied by an increase in topoisomerase-II content. Our data thus support the hypothesis that topoisomerase-II content may be an important determinant of cell sensitivity to certain classes of chemotherapy agents. Efforts to stimulate topoisomerase-II content may improve the therapeutic efficacy of these drugs. [ABSTRACT FROM AUTHOR]

Published
1987
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39. Induction chemotherapy followed by radiotherapy versus radiotherapy alone in patients with advanced nasopharyngeal carcinoma: results of a matched cohort study.

Author

Geara, Fady B., Glisson, Bonnie S., Sanguineti, Giuseppe, Tucker, Susan L., Garden, Adam S., Ang, K. Kian, Lippman, Scott M., Clayman, Gary L., Goepfert, Helmuth, Peters, Lester J., Hong, Waun K., Geara, F B, Glisson, B S, Sanguineti, G, Tucker, S L, Garden, A S, Ang, K K, Lippman, S M, Clayman, G L, and Goepfert, H

Published
1997
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