Search

Your search keyword '"Baker, Sharyn D."' showing total 782 results
Start Over Author "Baker, Sharyn D."
782 results on '"Baker, Sharyn D."'

103. A Metabolomics Approach for Predicting OATP1B-Type Transporter-Mediated Drug–Drug Interaction Liabilities

Author

Li, Yang, primary, Jin, Yan, additional, Taheri, Hanieh, additional, Schmidt, Keith T., additional, Gibson, Alice A., additional, Buck, Stefan A. J., additional, Eisenmann, Eric D., additional, Mathijssen, Ron H. J., additional, Figg, William D., additional, Baker, Sharyn D., additional, Sparreboom, Alex, additional, and Hu, Shuiying, additional

Published
2022
Full Text
View/download PDF

107. A Metabolomics Approach for Predicting OATP1B-Type Transporter-Mediated Drug-Drug Interaction Liabilities

Author

Li, Yang, Jin, Yan, Taheri, Hanieh, Schmidt, Keith T., Gibson, Alice A., Buck, Stefan A. J., Eisenmann, Eric D., Mathijssen, Ron H. J., Figg, William D., Baker, Sharyn D., Sparreboom, Alex, Hu, Shuiying, Li, Yang, Jin, Yan, Taheri, Hanieh, Schmidt, Keith T., Gibson, Alice A., Buck, Stefan A. J., Eisenmann, Eric D., Mathijssen, Ron H. J., Figg, William D., Baker, Sharyn D., Sparreboom, Alex, and Hu, Shuiying

Abstract

In recent years, various endogenous compounds have been proposed as putative biomarkers for the hepatic uptake transporters OATP1B1 and OATP1B3 that have the potential to predict transporter-mediated drug-drug interactions (DDIs). However, these compounds have often been identified from top-down strategies and have not been fully utilized as a substitute for traditional DDI studies. In an attempt to eliminate observer bias in biomarker selection, we applied a bottom-up, untargeted metabolomics screening approach in mice and found that plasma levels of the conjugated bile acid chenodeoxycholate-24-glucuronide (CDCA-24G) are particularly sensitive to deletion of the orthologous murine transporter Oatp1b2 (31-fold increase vs. wild type) or the entire Oatp1a/1b(-/-)cluster (83-fold increased), whereas the humanized transgenic overexpression of hepatic OATP1B1 or OATP1B3 resulted in the partial restoration of transport function. Validation studies with the OATP1B1/OATP1B3 inhibitors rifampin and paclitaxel in vitro as well as in mice and human subjects confirmed that CDCA-24G is a sensitive and rapid response biomarker to dose-dependent transporter inhibition. Collectively, our study confirmed the ability of CDCA-24G to serve as a sensitive and selective endogenous biomarker of OATP1B-type transport function and suggests a template for the future development of biomarkers for other clinically important xenobiotic transporters.

Published
2022

110. Abstract 1060: Introducing a novel DHODH inhibitor with superior in vivo activity as monotherapy or in novel combination regimen with immunotherapy for hematological malignancies

Author

Elgamal, Ola A., primary, Vibhute, Sandip, additional, Fobare, Sydney, additional, Mehmood, Abeera, additional, Johnson, Mariah L., additional, Truxall, Jean, additional, Stahl, Emily, additional, Carmichael, Bridget, additional, Orwick, Shelley J., additional, Santhanam, Ramasamy, additional, Hill, Kasey, additional, Tridandapani, Susheela, additional, Coss, Christopher C., additional, Mims, Alice S., additional, Larkin, Karilyn T., additional, Phelps, Mitch A., additional, Baker, Sharyn D., additional, Sparreboom, Alex, additional, Goodwin, Thomas E., additional, Hilinski, Gerard, additional, Bennett, Chad E., additional, Hertlein, Erin, additional, and Byrd, John C., additional

Published
2022
Full Text
View/download PDF

111. A phase 1b/2 study of TP-0903 and decitabine targeting mutant TP53 and/or complex karyotype in patients with untreated acute myeloid leukemia ≥ age 60 years: Phase 1b interim results.

Author

Mims, Alice S., primary, Huang, Ying, additional, Eisenmann, Eric, additional, Buelow, Daelynn, additional, Swords, Ronan T., additional, Foster, Matthew Charles, additional, Lin, Tara L., additional, Baer, Maria R., additional, Kovacsovics, Tibor, additional, Al-Mansour, Zeina, additional, Stefanos, Mona, additional, Druggan, Franchesca, additional, Chen, Timothy, additional, Yocum, Ashley, additional, Borate, Uma, additional, Druker, Brian J., additional, Burd, Amy, additional, Levine, Ross L., additional, Baker, Sharyn D., additional, and Byrd, John C., additional

Published
2022
Full Text
View/download PDF

112. Framework of clonal mutations concurrent with WT1mutations in adults with acute myeloid leukemia: Alliance for Clinical Trials in Oncology study

Author

Bhatnagar, Bhavana, Kohlschmidt, Jessica, Orwick, Shelley J., Buelow, Daelynn R., Fobare, Sydney, Oakes, Christopher C., Kolitz, Jonathan E., Uy, Geoff, Stock, Wendy, Powell, Bayard L., Nicolet, Deedra, Hertlein, Erin K., Mrózek, Krzysztof, Blachly, James S., Eisfeld, Ann-Kathrin, Baker, Sharyn D., and Byrd, John C.

Published
2023
Full Text
View/download PDF

113. Preclinical and Pilot Study of Type I FLT3 Tyrosine Kinase Inhibitor, Crenolanib, with Sorafenib in Acute Myeloid Leukemia and FLT3-Internal Tandem Duplication

Author

Inaba, Hiroto, primary, van Oosterwijk, Jolieke G., additional, Panetta, John C., additional, Li, Lie, additional, Buelow, Daelynn R., additional, Blachly, James S., additional, Shurtleff, Sheila, additional, Pui, Ching-Hon, additional, Ribeiro, Raul C., additional, Rubnitz, Jeffrey E., additional, Pounds, Stanley, additional, and Baker, Sharyn D., additional

Published
2022
Full Text
View/download PDF

116. TP-0903 Is Active in Preclinical Models of Acute Myeloid Leukemia with TP53 Mutation/Deletion.

Author

Eisenmann, Eric D., Stromatt, Jack C., Fobare, Sydney, Huang, Kevin M., Buelow, Daelynn R., Orwick, Shelley, Jeon, Jae Yoon, Weber, Robert H., Larsen, Bill, Mims, Alice S., Hertlein, Erin, Byrd, John C., and Baker, Sharyn D.

Subjects
BIOLOGICAL models, IN vitro studies, GENETIC mutation, XENOGRAFTS, DNA, IN vivo studies, PROTEIN kinase inhibitors, PHOSPHOTRANSFERASES, ANIMAL experimentation, ANTINEOPLASTIC agents, APOPTOSIS, CELL cycle proteins, CELL survival, IMMUNOBLOTTING, DECITABINE, TUMOR suppressor genes, RESEARCH funding, CELL lines, MICE, OVERALL survival, PHARMACODYNAMICS
Abstract

Simple Summary: Acute myeloid leukemia (AML) with mutations in the tumor suppressor gene TP53 is rapidly lethal for most patients. Here, we investigated the preclinical activity of TP-0903, a multikinase inhibitor that inhibits kinases with potential synthetical lethality in TP53 mutant AML. TP-0903 inhibited cell viability and induced apoptosis in multiple TP53 mutant AML cell lines at nanomolar concentrations in vitro. TP-0903, both alone and in combination with decitabine, the current standard of care, improved survival in two xenograft models of TP53 mutant AML. These results demonstrate that TP-0903 has activity in AML with TP53 dysfunction and support the clinical evaluation of TP-0903 in combination with decitabine in TP53 mutant AML. Acute myeloid leukemia (AML) with mutations in the tumor suppressor gene TP53 confers a dismal prognosis with 3-year overall survival of <5%. While inhibition of kinases involved in cell cycle regulation induces synthetic lethality in a variety of TP53 mutant cancers, this strategy has not been evaluated in mutant TP53 AML. Previously, we demonstrated that TP-0903 is a novel multikinase inhibitor with low nM activity against AURKA/B, Chk1/2, and other cell cycle regulators. Here, we evaluated the preclinical activity of TP-0903 in TP53 mutant AML cell lines, including a single-cell clone of MV4-11 containing a TP53 mutation (R248W), Kasumi-1 (R248Q), and HL-60 (TP 53 null). TP-0903 inhibited cell viability (IC50, 12–32 nM) and induced apoptosis at 50 nM. By immunoblot, 50 nM TP-0903 upregulated pChk1/2 and pH2AX, suggesting induction of DNA damage. The combination of TP-0903 and decitabine was additive in vitro, and in vivo significantly prolonged median survival compared to single-agent treatments in mice xenografted with HL-60 (vehicle, 46 days; decitabine, 55 days; TP-0903, 63 days; combination, 75 days) or MV4-11 (R248W) (51 days; 62 days; 81 days; 89 days) (p < 0.001). Together, these results provide scientific premise for the clinical evaluation of TP-0903 in combination with decitabine in TP53 mutant AML. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

119. Human Ontogeny of Drug Transporters: Review and Recommendations of the Pediatric Transporter Working Group

Author

Brouwer, KLR, Aleksunes, LM, Brandys, B, Giacoia, GP, Knipp, G, Lukacova, V, Meibohm, B, Nigam, SK, Rieder, M, de Wildt, SN, Abdel-Rahman, Susan, Aleksunse, Lauren M., Baker, Sharyn D., Bolger, Michael B., Brandys, Barbara, Brouwer, Kim L. R., Bush, Kevin T., Clancy, Barbara, DeSesso, John M., Fisher, Jeffery, Fukuda, Tsuyoshi, Giacoia, George P., Kim, Richard, Knipp, Gregory, Koren, Gideon, Lee, Grace S., Leeder, Steven J., Lukacova, Viera, Meibohm, Bernd, Mizuno, Tomoyuki, Mooij, Miriam G., Nigam, Sanjay K., Rieder, Michael, Schwab, Matthias, van de Steeg, Evita, Thomson, Margaret M.S., Vasilyeva, Aksana, Vinks, Alexander A., de Wildt, Saskia N., and Wu, Wei

Published
2015
Full Text
View/download PDF

121. Gilteritinib Inhibits Glutamine Uptake and Utilization in FLT3-ITD–Positive AML

Author

Zavorka Thomas, Megan E., primary, Lu, Xiyuan, additional, Talebi, Zahra, additional, Jeon, Jae Yoon, additional, Buelow, Daelynn R., additional, Gibson, Alice A., additional, Uddin, Muhammad Erfan, additional, Brinton, Lindsey T., additional, Nguyen, Julie, additional, Collins, Meghan, additional, Lodi, Alessia, additional, Sweeney, Shannon R., additional, Campbell, Moray J., additional, Sweet, Douglas H., additional, Sparreboom, Alex, additional, Lapalombella, Rosa, additional, Tiziani, Stefano, additional, and Baker, Sharyn D., additional

Published
2021
Full Text
View/download PDF

122. Integrative Genomic Analysis of Pediatric Myeloid-Related Acute Leukemias Identifies Novel Subtypes and Prognostic Indicators

Author

Fornerod, Maarten, primary, Ma, Jing, additional, Noort, Sanne, additional, Liu, Yu, additional, Walsh, Michael P., additional, Shi, Lei, additional, Nance, Stephanie, additional, Liu, Yanling, additional, Wang, Yuanyuan, additional, Song, Guangchun, additional, Lamprecht, Tamara, additional, Easton, John, additional, Mulder, Heather L., additional, Yergeau, Donald, additional, Myers, Jacquelyn, additional, Kamens, Jennifer L., additional, Obeng, Esther A., additional, Pigazzi, Martina, additional, Jarosova, Marie, additional, Kelaidi, Charikleia, additional, Polychronopoulou, Sophia, additional, Lamba, Jatinder K., additional, Baker, Sharyn D., additional, Rubnitz, Jeffrey E., additional, Reinhardt, Dirk, additional, van den Heuvel-Eibrink, Marry M., additional, Locatelli, Franco, additional, Hasle, Henrik, additional, Klco, Jeffery M., additional, Downing, James R., additional, Zhang, Jinghui, additional, Pounds, Stanley, additional, Zwaan, C. Michel, additional, and Gruber, Tanja A., additional

Published
2021
Full Text
View/download PDF

123. Results of a Phase 1 Trial Testing the Novel Combination Therapy of Venetoclax and Ruxolitinib in Relapsed/Refractory Acute Myeloid Leukemia Patients

Author

Borate, Uma M., Madanat, Yazan F., Tognon, Cristina, Mishra, Shikha, Kaempf, Andy, Patel, Prapti A., Kurtz, Stephen E., Johnson, Kara, Vasu, Sumithira, Baker, Sharyn D., Robinson, Bridget A, Vu, Tania Q, Eide, Christopher A., Minnier, Jessica, Zhang, Yiqing, Clement, Peter, Avaylon, Sammantha, Jacob, Thomas, Cook, Rachel, Gandhi, Arpita, Leonard, Jessica T., Hayes-Lattin, Brandon, Newell, Laura F., Maziarz, Richard T, Traer, Elie, Swords, Ronan T., Tyner, Jeffrey W, Druker, Brian J., and Saultz, Jennifer N.

Published
2023
Full Text
View/download PDF

128. CREBBP mutations in relapsed acute lymphoblastic leukaemia

Author

Mullighan, Charles G., Zhang, Jinghui, Kasper, Lawryn H., Lerach, Stephanie, Payne-Turner, Debbie, Phillips, Letha A., Heatley, Sue L., Holmfeldt, Linda, Collins-Underwood, J. Racquel, Ma, Jing, Buetow, Kenneth H., Pui, Ching-Hon, Baker, Sharyn D., Brindle, Paul K., and Downing, James R.

Subjects
Gene mutations -- Research, Lymphocytic leukemia -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Relapsed acute lymphoblastic leukaemia (ALL) is a leading cause of death due to disease in young people, but the biological determinants of treatment failure remain poorly understood. Recent genome-wide profiling of structural DNA alterations in ALL have identified multiple submicroscopic somatic mutations targeting key cellular pathways (1,2), and have demonstrated substantial evolution in genetic alterations from diagnosis to relapse (3). However, DNA sequence mutations in ALL have not been analysed in detail. To identify novel mutations in relapsed ALL, we resequenced 300 genes in matched diagnosis and relapse samples from 23 patients with ALL. This identified 52 somatic non-synonymous mutations in 32 genes, many of which were novel, including the transcriptional coactivators CREBBP and NCOR1, the transcription factors ERG, SPI1, TCF4 and TCF7L2, components of the Ras signalling pathway, histone genes, genes involved in histone modification (CREBBP and CTCF), and genes previously shown (1,2) to be targets of recurring DNA copy number alteration in ALL. Analysis of an extended cohort of 71 diagnosis-relapse cases and 270 acute leukaemia cases that did not relapse found that 18.3% of relapse cases had sequence or deletion mutations of CREBBP, which encodes the transcriptional coactivator and histone acetyltransferase CREB-binding protein (CREBBP, also known as CBP) (4). The mutations were either present at diagnosis or acquired at relapse, and resulted in truncated alleles or deleterious substitutions in conserved residues of the histone acetyltransferase domain. Functionally, the mutations impaired histone acetylation and transcriptional regulation of CREBBP targets, including glucocorticoid responsive genes. Several mutations acquired at relapse were detected in subclones at diagnosis, suggesting that the mutations may confer resistance to therapy. These results extend the landscape of genetic alterations in leukaemia, and identify mutations targeting transcriptional and epigenetic regulation as a mechanism of resistance in ALL., Acute lymphoblastic leukaemia (ALL) is the commonest childhood malignancy (5), and is a leading cause of cancer-related death in young people. Several structural chromosomal alterations in ALL, including rearrangement of [...]

Published
2011
Full Text
View/download PDF

135. Influence of probenecid on the pharmacokinetics and pharmacodynamics of sorafenib

Author

Hussaarts, Koen G.A.M., van Doorn, Leni, Eechoute, Karel, Damman, Jeffrey, Fu, Qiang, van Doorn, Nadia, Eisenmann, Eric D., Gibson, Alice A., Hoop, Esther Oomen De, de Bruijn, Peter, Baker, Sharyn D., Koolen, Stijn L.W., van Gelder, Teun, van Leeuwen, Roelof W.F., Mathijssen, Ron H.J., Sparreboom, Alex, Bins, Sander, Hussaarts, Koen G.A.M., van Doorn, Leni, Eechoute, Karel, Damman, Jeffrey, Fu, Qiang, van Doorn, Nadia, Eisenmann, Eric D., Gibson, Alice A., Hoop, Esther Oomen De, de Bruijn, Peter, Baker, Sharyn D., Koolen, Stijn L.W., van Gelder, Teun, van Leeuwen, Roelof W.F., Mathijssen, Ron H.J., Sparreboom, Alex, and Bins, Sander

Abstract

Prior studies have demonstrated an organic anion transporter 6 (OAT6)-mediated accumulation of sorafenib in keratinocytes. The OAT6 inhibitor probenecid decreases sorafenib uptake in skin and might, therefore, decrease sorafenib-induced cutaneous adverse events. Here, the influence of probenecid on sorafenib pharmacokinetics and toxicity was investigated. Pharmacokinetic sampling was performed in 16 patients on steady-state sorafenib treatment at days 1 and 15 of the study. Patients received sorafenib (200–800 mg daily) in combination with probenecid (500 mg two times daily (b.i.d.)) on days 2–15. This study was designed to determine bioequivalence with geometric mean Area under the curve from zero to twelve hours (AUC0–12 h) as primary endpoint. During concomitant probenecid, sorafenib plasma AUC0–12 h decreased by 27% (90% CI: −38% to −14%; P < 0.01). Furthermore, peak and trough levels of sorafenib, as well as sorafenib concentrations in skin, decreased to a similar extent in the presence of probenecid. The metabolic ratio of sorafenib-glucuronide to parent drug increased (+29%) in the presence of probenecid. A decrease in systemic sorafenib concentrations during probenecid administration seems to have influenced cutaneous concentrations. Since sorafenib-glucuronide concentrations increased compared with sorafenib and sorafenib-N-oxide, probenecid may have interrupted enterohepatic circulation of sorafenib by inhibition of the organic anion transporting polypeptides 1B1 (OATP1B1). Sorafenib treatment with probenecid is, therefore, not bioequivalent to sorafenib monotherapy. A clear effect of probenecid on sorafenib toxicity could not be identified in this study.

Published
2020

137. Nephrotoxicity of the BRAF-kinase inhibitor Vemurafenib is driven by off-target Ferrochelatase inhibition

Author

Bai, Yuntao, primary, Kim, Ji Young, additional, Jayne, Laura A., additional, Gandhi, Megha, additional, Huang, Kevin M., additional, Silvaroli, Josie A., additional, Sander, Veronika, additional, Prosek, Jason, additional, Jhaveri, Kenar D., additional, Baker, Sharyn D., additional, Sparreboom, Alex, additional, Bajwa, Amandeep, additional, and Pabla, Navjot Singh, additional

Published
2021
Full Text
View/download PDF

138. Targeting OCT3 attenuates doxorubicin-induced cardiac injury

Author

Huang, Kevin M., primary, Zavorka Thomas, Megan, additional, Magdy, Tarek, additional, Eisenmann, Eric D., additional, Uddin, Muhammad Erfan, additional, DiGiacomo, Duncan F., additional, Pan, Alexander, additional, Keiser, Markus, additional, Otter, Marcus, additional, Xia, Sherry H., additional, Li, Yang, additional, Jin, Yan, additional, Fu, Qiang, additional, Gibson, Alice A., additional, Bonilla, Ingrid M., additional, Carnes, Cynthia A., additional, Corps, Kara N., additional, Coppola, Vincenzo, additional, Smith, Sakima A., additional, Addison, Daniel, additional, Nies, Anne T., additional, Bundschuh, Ralf, additional, Chen, Taosheng, additional, Lustberg, Maryam B., additional, Wang, Joanne, additional, Oswald, Stefan, additional, Campbell, Moray J., additional, Yan, Pearlly S., additional, Baker, Sharyn D., additional, Hu, Shuiying, additional, Burridge, Paul W., additional, and Sparreboom, Alex, additional

Published
2021
Full Text
View/download PDF

145. Contributors

Author

Albritton, Karen, primary, Amatruda, James F., additional, Anderson, Megan E., additional, Argani, Pedram, additional, Armstrong, Scott A., additional, Baker, Sharyn D., additional, Barfield, Raymond C., additional, Barr, Frederic G., additional, Berde, Charles B., additional, Berman, Jason N., additional, Bernstein, Mark L., additional, Bhatia, Smita, additional, Billett, Amy Louise, additional, Blackman, Samuel, additional, Branowicki, Patricia A., additional, Casey, Robert L., additional, Chi, Susan N., additional, Clark, Jennifer J., additional, Conley, Susanne B., additional, Davis, Ian J., additional, Degar, Barbara A., additional, DeSantes, Kenneth B., additional, Diller, Lisa, additional, Dome, Jeffrey S., additional, DuBois, Steven G., additional, Duncan, Janet, additional, Dunn, Ian F., additional, Evan, Elana E., additional, Evans, William E., additional, Felix, Carolyn A., additional, Ferrando, Adolfo A., additional, Fisher, David E., additional, Fleming, Mark D., additional, Fletcher, Jonathan A., additional, Folkman, Judah, additional, Frazier, A. Lindsay, additional, Gebhardt, Mark C., additional, George, Rani E., additional, Goldberg, John M., additional, Gorlick, Richard, additional, Grabowski, Eric F., additional, Grier, Holcombe E., additional, Haas-Kogan, Daphne, additional, Hahn, William C., additional, Herrington, Betsy, additional, Houlahan, Kathleen E., additional, Italiano, Joseph E., additional, Janeway, Katherine A., additional, Kenney, Lisa B., additional, Kieran, Mark W., additional, Kim, Heung Bae, additional, Kiss, Szilárd, additional, Kodish, Eric, additional, Koh, Andrew Y., additional, Lechpammer, Mirna, additional, Leiderman, Yannek I., additional, Lessnick, Stephen L., additional, Look, A. Thomas, additional, Mack, Jennifer W., additional, Marcus, Karen J., additional, Mukai, Shizuo, additional, Mullen, Elizabeth, additional, O'Sullivan, Maureen J., additional, Pappo, Alberto, additional, Perez-Atayde, Antonio R., additional, Pizzo, Philip A., additional, Prabhu, Sanjay P., additional, Recklitis, Christopher J., additional, Reiter, Alfred, additional, Roberts, Charles W.M., additional, Robison, Leslie L., additional, Rollins, Barrett J., additional, Samuel, David, additional, Schlis, Krysta D., additional, Segal, Rosalind A., additional, Sellers, William R., additional, Shamberger, Robert C., additional, Shusterman, Suzanne, additional, Silverman, Lewis B., additional, Sondel, Paul M., additional, Sparreboom, Alex, additional, Stegmaier, Kimberly, additional, Tomlinson, Gail E., additional, Turner, Christopher, additional, Ullrich, Christina K., additional, Voss, Stephan D., additional, Vrooman, Lynda M., additional, Weldon, Christopher B., additional, Whangbo, Jennifer, additional, Wolfe, Joanne, additional, Womer, Richard B., additional, and Zeltzer, Lonnie, additional

Published
2009
Full Text
View/download PDF

148. TP-0903 is active in models of drug-resistant acute myeloid leukemia

Author

Jeon, Jae Yoon, primary, Buelow, Daelynn R., additional, Garrison, Dominique A., additional, Niu, Mingshan, additional, Eisenmann, Eric D., additional, Huang, Kevin M., additional, Zavorka Thomas, Megan E., additional, Weber, Robert H., additional, Whatcott, Clifford J., additional, Warner, Steve L., additional, Orwick, Shelley J., additional, Carmichael, Bridget, additional, Stahl, Emily, additional, Brinton, Lindsey T., additional, Lapalombella, Rosa, additional, Blachly, James S., additional, Hertlein, Erin, additional, Byrd, John C., additional, Bhatnagar, Bhavana, additional, and Baker, Sharyn D., additional

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results