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Your search keyword '"Bates, Susan"' showing total 41 results
Start Over Author "Bates, Susan" Journal cancer research
41 results on '"Bates, Susan"'

1. Abstract PR05: CheMo4METPANC: Combination Chemotherapy (gemcitabine and nab-paclitaxel), chemokine (C-X-C) Motif receptor 4 inhibitor (motixafortide), and immune checkpoint blockade (cemiplimab) in METastatic treatment-naïve PANCreatic adenocarcinoma

Author

Manji, Gulam A., primary, May, Michael, additional, Chalabi, Morteza Hajkarim, additional, Pellicciotta, Ilenia, additional, Sta Ana, Sarah I., additional, Sender, Naomi, additional, Pan, Samuel S., additional, Ross, Isabelle V., additional, Olive, Kenneth P., additional, Wang, Shikun, additional, Izar, Benjamin, additional, White, Ruth A., additional, Bates, Susan E., additional, and Raufi, Alexander G., additional

Published
2024
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2. Abstract CT084: Targeted intra-arterial gemcitabine vs. continuation of IV gemcitabine plus nab-paclitaxel following Induction with sequential IV gemcitabine plus nab-paclitaxel and radiotherapy for unresectable locally advanced pancreatic cancer (TIGeR-PaC) - phase III trial interim analysis

Author

Pishvaian, Michael, primary, Zureikat, Amer, additional, Lopez, Charles, additional, Meredith, Kenneth, additional, Zervos, Emmanuel, additional, Hatoum, Hassan, additional, Chung, Ki, additional, Berg, Daniel J., additional, Ucar, Antonio, additional, Gandhi, Ripal, additional, Nazemzadeh, Reza, additional, Nainesh, Parikh, additional, Novelli, Paula, additional, Kouri, Brian, additional, Laing, Christopher, additional, Boone, Brian, additional, Johnson, Thor, additional, Bates, Susan, additional, Goodman, Karyn, additional, and Agah, Ramtin, additional

Published
2023
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8. Abstract 5480: Effects of UGT1A1 genotype on pharmacokinetics and toxicities of belinostat administered by continuous infusion in two clinical trials

Author

Goey, Andrew K.L., primary, Sissung, Tristan M., additional, Peer, Cody J., additional, Ehrlich, Sheryl, additional, Bryla, Christina, additional, Berman, Arlene W., additional, Balasubramaniam, Sanjeeve, additional, Rajan, Arun, additional, Giaccone, Giuseppe, additional, Bates, Susan E., additional, and Figg, William D., additional

Published
2015
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9. Abstract 5536: Short-term romidepsin treatment combined with MAPK pathway inhibition results in decreased mitochondrial hexokinase 2, increased mitochondrial Bim and apoptosis in BRAF mutant cancers

Author

Bates, Susan E., primary, Luchenko, Victoria, additional, Basseville, Agnes, additional, Bahr, Julian, additional, Chakraborty, Arup R., additional, McDonald, Andrew, additional, Zimmer, Alexandra, additional, Piekarz, Richard L., additional, and Robey, Robert W., additional

Published
2014
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11. Abstract 3399: Resistance to the histone deacetylase inhibitor romidepsin is associated with degradation of Bim following MAPK pathway activation.

Author

Chakraborty, Arup R., primary, Robey, Rob, additional, Zhan, Zhirong, additional, Luchenko, Victoria, additional, Gottesman, Michael, additional, Collie, Nathan, additional, Gillet, Jean-Pierre, additional, Piekarz, Richard, additional, Kossenkov, Andrew, additional, Showe, Louise, additional, and Bates, Susan, additional

Published
2013
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14. Mithramycin Represses Basal and Cigarette Smoke–Induced Expression of ABCG2 and Inhibits Stem Cell Signaling in Lung and Esophageal Cancer Cells

Author

Zhang, Mary, primary, Mathur, Aarti, additional, Zhang, Yuwei, additional, Xi, Sichuan, additional, Atay, Scott, additional, Hong, Julie A., additional, Datrice, Nicole, additional, Upham, Trevor, additional, Kemp, Clinton D., additional, Ripley, R. Taylor, additional, Wiegand, Gordon, additional, Avital, Itzak, additional, Fetsch, Patricia, additional, Mani, Haresh, additional, Zlott, Daniel, additional, Robey, Robert, additional, Bates, Susan E., additional, Li, Xinmin, additional, Rao, Mahadev, additional, and Schrump, David S., additional

Published
2012
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20. Sildenafil Reverses ABCB1- and ABCG2-Mediated Chemotherapeutic Drug Resistance

Author

Shi, Zhi, primary, Tiwari, Amit K., additional, Shukla, Suneet, additional, Robey, Robert W., additional, Singh, Satyakam, additional, Kim, In-Wha, additional, Bates, Susan E., additional, Peng, Xingxiang, additional, Abraham, Ioana, additional, Ambudkar, Suresh V., additional, Talele, Tanaji T., additional, Fu, Li-Wu, additional, and Chen, Zhe-Sheng, additional

Published
2011
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23. Abstract 2620: Identification of cell context specific and pleiotropic effects of the histone deacetylase inhibitors romidepsin (depsipeptide) and vorinostat (SAHA)

Author

Luchenko, Victoria L., primary, Litman, Thomas, additional, Devor, Christopher, additional, Heffner, Aaron, additional, Robey, Robert W., additional, Wilkerson, Julia, additional, Chakraborty, Arup R., additional, Bangiolo, Lois, additional, Levens, David, additional, and Bates, Susan E., additional

Published
2011
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25. Abstract 1739: Reversal of ABCB1- and ABCG2-mediated drug resistance by sildenafil

Author

Tiwari, Amit K., primary, Shi, Zhi, additional, Shukla, Suneet, additional, Robey, Robert W., additional, Singh, Satyakam, additional, Kim, In-Wha, additional, Bates, Susan E., additional, Peng, Xing-xiang, additional, Abraham, Ioana, additional, Ambudkar, Suresh V., additional, Talele, Tanaji T., additional, Fu, Li-wu, additional, and Chen, Zhe-Sheng, additional

Published
2011
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27. Abstract 5372: Mechanisms of synergy of histone deacetylase inhibitors, belinostat and depsipeptide, with DNA damaging agents, etoposide and cisplatin in small cell lung cancer cell lines

Author

Luchenko, Victoria, primary, Salcido, Crystal D., additional, Zhang, Yongwei W., additional, Mumau, Melanie D., additional, Agama, Kelli, additional, Giaccone, Giuseppe, additional, Pommier, Yves, additional, Bates, Susan E., additional, and Varticovski, Lyuba, additional

Published
2010
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28. Abstract 3527: A pharmacodynamic study of docetaxel in combination with the p-glycoprotein antagonist, tariquidar (XR9576) in patients with lung, ovarian, and cervical cancer

Author

Kelly, Ronan J., primary, Robey, Robert, additional, Draper, Deborah, additional, Chen, Clara, additional, Venkatesan, Aradhana M., additional, Figg, William D., additional, Gardner, Erin, additional, Piekarz, Richard, additional, Balis, Frank, additional, Fojo, Tito, additional, and Bates, Susan E., additional

Published
2010
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29. Abstract 3528: Mutational analysis of threonine 402 adjacent to the GXXXG dimerization motif in TM1 of ABCG2

Author

Bates Susan E, Robert W. Robey, Caterina Ieranò, Nadya I. Tarasova, Di Xia, Yvona Ward, Orsolya Polgar, Akina Tamaki, and Bradford J. Stanley

Subjects
chemistry.chemical_classification, Cancer Research, animal structures, Glycosylation, biology, Endoplasmic reticulum, Mutant, Wild type, Endoglycosidase H, chemistry.chemical_compound, Oncology, chemistry, Biochemistry, biology.protein, Threonine, Leucine, Glycoprotein
Abstract

ABCG2 is an ATP-binding cassette half-transporter important in normal tissue protection, drug distribution and excretion. ABCG2 requires homodimerization for function, though the mechanism for dimerization has not been worked out. We carried out mutational analysis of threonine 402, three residues away from the GXXXG motif in TM1, to study its potential role in ABCG2 dimerization (TXXXGXXXG). Single mutations to leucine (T402L) or arginine (T402R) did not have significant impact on the ABCG2 protein. On the other hand, combining the T402 mutations with the GXXXG glycine to leucine mutations (T402L/G406L/G410L and T402R/G406L/G410L) resulted in substantially reduced expression, altered glycosylation, degradation by a proteosome independent pathway and partial retention in the endoplasmic reticulum as suggested by immunostaining, Endoglycosidase H sensitivity and MG132 and bafilomycin failed effect. The T402L/G406L/G410L mutant when incubated with the ABCG2-substrate mitoxantrone showed a shift on immunoblot analysis to the band representing the fully matured glycoprotein. The T402R/G406L/G410L mutant carrying the more drastic substitution failed to shift to the surface with mitoxantrone. The same set of mutations also displayed impaired dimerization in the TOXCAT assay for TM1 compared to the wild type. Homology modeling of ABCG2 places the TXXXGXXXG motif at the dimer interface. These studies are consistent with a role for the extended TXXXGXXXG motif in ABCG2 folding, processing, and/or dimerization. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3528.

Published
2010

30. Erlotinib (Tarceva, OSI-774) Antagonizes ATP-Binding Cassette Subfamily B Member 1 and ATP-Binding Cassette Subfamily G Member 2–Mediated Drug Resistance

Author

Shi, Zhi, primary, Peng, Xing-Xiang, additional, Kim, In-Wha, additional, Shukla, Suneet, additional, Si, Qiu-Sheng, additional, Robey, Robert W., additional, Bates, Susan E., additional, Shen, Tong, additional, Ashby, Charles R., additional, Fu, Li-Wu, additional, Ambudkar, Suresh V., additional, and Chen, Zhe-Sheng, additional

Published
2007
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31. Autoantibody Cancer Biomarker: Extracellular Protein Kinase A

Author

Nesterova, Maria V., primary, Johnson, Natalie, additional, Cheadle, Christopher, additional, Bates, Susan E., additional, Mani, Sridhar, additional, Stratakis, Constantine A., additional, Kahn, Islam, additional, Gupta, Rishab K., additional, and Cho-Chung, Yoon S., additional

Published
2006
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38. Effects of Anticancer Drugs on Chromosome Instability and New Clinical Implications for Tumor-Suppressing Therapies.

Author

Hee-Sheung Lee, Lee, Nicholas C. O., Kouprina, Natalay, Jung-Hyun Kim, Kagansky, Alex, Bates, Susan, Trepel, Jane B., Pommier, Yves, Sackett, Dan, and Larionov, Vladimir

Subjects
*ANTINEOPLASTIC agents, *CHROMOSOME abnormalities, *TUMOR suppressor genes, *CELL division, *ARTIFICIAL chromosomes, *DNA replication
Abstract

Whole chromosomal instability (CIN), manifested as unequal chromosome distribution during cell division, is a distinguishing feature of most cancer types. CIN is generally considered to drive tumorigenesis, but a threshold level exists whereby further increases in CIN frequency in fact hinder tumor growth. While this attribute is appealing for therapeutic exploitation, drugs that increase CIN beyond this therapeutic threshold are currently limited. In our previous work, we developed a quantitative assay for measuring CIN based on the use of a nonessential human artificial chromosome (HAC) carrying a constitutively expressed EGFP transgene. Here, we used this assay to rank 62 different anticancer drugs with respect to their effects on chromosome transmission fidelity. Drugs with various mechanisms of action, such as antimicrotubule activity, histone deacetylase inhibition, mitotic checkpoint inhibition, and targeting of DNA replication and damage responses, were included in the analysis. Ranking of the drugs based on their ability to induce HAC loss revealed that paclitaxel, gemcitabine, dactylolide, LMP400, talazoparib, olaparib, peloruside A, GW843682, VX-680, and cisplatin were the top 10 drugs demonstrating HAC loss at a high frequency. Therefore, identification of currently used compounds that greatly increase chromosome mis-segregation rates should expedite the development of new therapeutic strategies to target and leverage the CIN phenotype in cancer cells. [ABSTRACT FROM AUTHOR]

Published
2016
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39. Transport of methotrexate, methotrexate polyglutamates, and 17beta-estradiol 17-(beta-D-glucuronide) by ABCG2: effects of acquired mutations at R482 on methotrexate transport.

Author

Chen ZS, Robey RW, Belinsky MG, Shchaveleva I, Ren XQ, Sugimoto Y, Ross DD, Bates SE, and Kruh GD

Subjects
ATP Binding Cassette Transporter, Subfamily G, Member 2, ATP-Binding Cassette Transporters genetics, Biological Transport drug effects, Carrier Proteins genetics, Carrier Proteins metabolism, Humans, Indoles pharmacology, Transfection, ATP-Binding Cassette Transporters metabolism, Estradiol analogs & derivatives, Estradiol pharmacokinetics, Methotrexate analogs & derivatives, Methotrexate pharmacokinetics, Mutation, Neoplasm Proteins, Polyglutamic Acid analogs & derivatives, Polyglutamic Acid pharmacokinetics
Abstract

ABCG2 is a plasma membrane efflux pump that is able to confer resistance to several anticancer agents, including mitoxantrone, camptothecins, anthracyclines, and flavopiridol. The antimetabolite methotrexate (MTX) was inferred recently to be an additional substrate of the pump based on the analysis of ABCG2-overexpressing cell lines. However, the transport characteristics of the pump with regard to this agent have not been determined. In addition, physiological substrates of ABCG2 have not been identified. Here we examine the in vitro transport properties of the pump using membrane vesicles prepared from HEK293 cells transfected with ABCG2 expression vector. In so doing it is shown that MTX is a high capacity low affinity substrate of the pump, with K(m) and V(max) values of 1.34 +/- 0.18 mM and 687 +/- 87 pmol/mg/min, respectively. Unlike previously characterized multidrug resistance protein family members, ABCG2 is also able to transport MTX diglutamate and MTX triglutamate. However, addition of even one more glutamyl residue is sufficient to completely abrogate ABCG2-mediated transport. By contrast with the wild-type protein (ABCG2-R482), two ABCG2 variants that have been identified in drug selected cell lines, R482T and R482G, were unable to transport MTX to any extent. Similarly, folic acid was subject to efflux by the wild-type protein but not by the two mutants. However, transport of the reduced folate leucovorin was not detected for either the wild-type or the mutant proteins. Finally, it is shown that ABCG2 is capable of transporting E(2)17betaG with K(m) and V(max) values of 44.2 +/- 4.3 micro M and 103 +/- 17 pmol/mg/min, respectively. These results indicate that ABCG2 is a component of the energy-dependent efflux system for certain folates and antifolates, but that its transport characteristics with respect to polyglutamates and reduced folates are not identical to those of multidrug resistance protein family members. In addition, it is demonstrated that R482 mutations observed in drug-resistant cell lines have profound effects on the in vitro transport properties of the pump.

Published
2003

40. Differential effects of the breast cancer resistance protein on the cellular accumulation and cytotoxicity of 9-aminocamptothecin and 9-nitrocamptothecin.

Author

Rajendra R, Gounder MK, Saleem A, Schellens JH, Ross DD, Bates SE, Sinko P, and Rubin EH

Subjects
ATP Binding Cassette Transporter, Subfamily B, Member 1 genetics, ATP Binding Cassette Transporter, Subfamily B, Member 1 metabolism, ATP Binding Cassette Transporter, Subfamily G, Member 2, ATP-Binding Cassette Transporters genetics, Animals, Cell Division drug effects, Dogs, Humans, Multidrug Resistance-Associated Protein 2, Multidrug Resistance-Associated Proteins genetics, Multidrug Resistance-Associated Proteins metabolism, Neoplasm Proteins genetics, Recombinant Fusion Proteins physiology, Selection, Genetic, Transfection, Tumor Cells, Cultured drug effects, Tumor Cells, Cultured metabolism, ATP-Binding Cassette Transporters physiology, Antineoplastic Agents, Phytogenic metabolism, Camptothecin analogs & derivatives, Camptothecin metabolism, Drug Resistance, Neoplasm physiology, Membrane Transport Proteins, Neoplasm Proteins physiology
Abstract

Breast cancer resistance protein (BCRP)/MXR/ABCG2 is a new member of the family of ATP-dependent drug efflux proteins. Whereas overexpression of another member of this family, P-glycoprotein, minimally affects the cytotoxicity of camptothecins (CPTs), overexpression of wild-type as well as certain mutant BCRPs confers resistance to CPT analogues that are used clinically, including topotecan and irinotecan. Relatively little is known regarding the effects of BCRP on other CPT analogues. We now report studies of 9-aminocamptothecin (9-AC) and 9-nitrocamptothecin (9-NC) using mammalian cells stably transfected with constructs expressing a variety of efflux proteins, including wild-type BCRP and a mutant BCRP that contains a threonine rather than an arginine at position 482 (R482T). The results indicate that overexpression of either P-glycoprotein, multidrug resistance protein type 1, or multidrug resistance protein type 2 has little effect on the cytotoxicity of 9-NC or 9-AC. By contrast, overexpression of either wild-type or R482T BCRP confers resistance to 9-AC, but not to 9-NC. Furthermore, overexpression of wild-type or mutant BCRP is associated with reduced intracellular accumulation of 9-AC, but not 9-NC. In addition, immunoblotting studies indicate that whereas increased BCRP expression is evident in cells selected for resistance to irinotecan, BCRP expression is not detectable in two different cell lines selected for resistance to 9-NC. Taken together, these findings suggest that wild-type as well as R482T BCRP mediates cellular efflux of 9-AC but not 9-NC. Furthermore, the results suggest that polar groups at the 9 or 10 position of the CPT A ring facilitate interaction with BCRP and have implications for the clinical development of new CPT analogues.

Published
2003

41. MS-27-275, an inhibitor of histone deacetylase, has marked in vitro and in vivo antitumor activity against pediatric solid tumors.

Author

Jaboin J, Wild J, Hamidi H, Khanna C, Kim CJ, Robey R, Bates SE, and Thiele CJ

Subjects
Acetylation drug effects, Animals, Cell Cycle drug effects, Child, DNA, Neoplasm biosynthesis, Dose-Response Relationship, Drug, Drug Screening Assays, Antitumor, Gene Expression Regulation, Neoplastic drug effects, Histones metabolism, Humans, Mice, Mice, Nude, Mice, SCID, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Antineoplastic Agents pharmacology, Benzamides pharmacology, Enzyme Inhibitors pharmacology, Histone Deacetylase Inhibitors, Pyridines pharmacology
Abstract

The antitumor efficacy of the synthetic benzamide derivative MS-27-275 (MS-275), an inhibitor of histone deacetylation [T. Suzuki et al., J. Med. Chem., 42: 3001-3003, 1999], was evaluated in a series of pediatric solid tumor cell lines, including neuroblastoma, rhabdomyosarcoma, Ewing's sarcoma (EWS), retinoblastoma, medulloblastoma, undifferentiated sarcoma (US), osteosarcoma, and malignant rhabdoid tumors. Treatment with MS-275 results in an increase in acetylation of histones within 4 h of drug exposure. The cell lines were treated with various concentrations of MS-275 for 3 days and incubated with [(3)H]thymidine for 20 h before cell harvest. MS-275 inhibited [(3)H]thymidine uptake in a dose-dependent manner in all tumor cell lines examined. The IC(50) ranged from 50 nm in the D283 medulloblastoma cell line to 1.3 micro M in the US. A common feature of MS-275 treatment of pediatric tumor cell lines was induction of p21mRNA. However, the effects on cell cycle were diverse because in some cases MS-275 induced an increase in G(1) or G(2), whereas in others, there was an induction of apoptosis. In EWS, the EWS/fli chimeric transcription factor created by the t(11;22) suppresses transforming growth factor (TGF) betaRII transcription, however, MS-275 was able to induce an increase in TGF-betaRII mRNA and restore TGF-beta signaling. Using xenograft orthotopic models of US, EWS, and neuroblastoma, we find that the growth of established tumors is inhibited in mice treated with MS-275.

Published
2002

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