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1. A new genomic framework to categorize pediatric acute myeloid leukemia

Author

Umeda, Masayuki, Ma, Jing, Westover, Tamara, Ni, Yonghui, Song, Guangchun, Maciaszek, Jamie L., Rusch, Michael, Rahbarinia, Delaram, Foy, Scott, Huang, Benjamin J., Walsh, Michael P., Kumar, Priyadarshini, Liu, Yanling, Yang, Wenjian, Fan, Yiping, Wu, Gang, Baker, Sharyn D., Ma, Xiaotu, Wang, Lu, Alonzo, Todd A., Rubnitz, Jeffrey E., Pounds, Stanley, and Klco, Jeffery M.

Published
2024
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6. Pyrimidine depletion enhances targeted and immune therapy combinations in acute myeloid leukemia

Author

Elgamal, Ola A., primary, Fobare, Sydney, additional, Vibhute, Sandip, additional, Mehmood, Abeera, additional, Vroom, Dennis C., additional, Johnson, Mariah L., additional, Stearns, Blaise, additional, Lerma, James R., additional, Truxall, Jean, additional, Stahl, Emily, additional, Carmichael, Bridget, additional, Orwick, Shelley J., additional, Mims, Alice S., additional, Curran, Emily, additional, Santhanam, Ramasamy, additional, Tridandapani, Susheela, additional, Phelps, Mitch A., additional, Xie, Zhiliang, additional, Coss, Christopher C., additional, Baker, Sharyn D., additional, Patrick, Jeffrey, additional, Ezzell, Janel K., additional, Rai, Jayesh, additional, Pan, Jianmin, additional, Rai, Shesh N., additional, Stillwell, Cody, additional, Wunderlich, Mark, additional, Abdulrahim, Mouad, additional, Goodwin, Thomas E., additional, Hilinski, Gerard, additional, Bennett, Chad E., additional, Hertlein, Erin, additional, and Byrd, John C., additional

Published
2024
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9. Vincristine Disposition and Neurotoxicity Are Unchanged in Humanized CYP3A5 Mice

Author

Li, Y, Kazuki, Y, Drabison, T, Kobayashi, K, Fujita, K, Xu, Y, Jin, Y, Ahmed, E, Li, J, Eisenmann, E, Baker, S, Cavaletti, G, Sparreboom, A, Hu, S, Li, Yang, Kazuki, Yasuhiro, Drabison, Thomas, Kobayashi, Kaoru, Fujita, Ken-Ichi, Xu, Yue, Jin, Yan, Ahmed, Eman, Li, Junan, Eisenmann, Eric D, Baker, Sharyn D, Cavaletti, Guido, Sparreboom, Alex, Hu, Shuiying, Li, Y, Kazuki, Y, Drabison, T, Kobayashi, K, Fujita, K, Xu, Y, Jin, Y, Ahmed, E, Li, J, Eisenmann, E, Baker, S, Cavaletti, G, Sparreboom, A, Hu, S, Li, Yang, Kazuki, Yasuhiro, Drabison, Thomas, Kobayashi, Kaoru, Fujita, Ken-Ichi, Xu, Yue, Jin, Yan, Ahmed, Eman, Li, Junan, Eisenmann, Eric D, Baker, Sharyn D, Cavaletti, Guido, Sparreboom, Alex, and Hu, Shuiying

Abstract

Previous studies have suggested that the incidence of vincristine-induced peripheral neuropathy (VIPN) is potentially linked with cytochrome P450 (CYP)3A5, a polymorphic enzyme that metabolizes vincristine in vitro, and with concurrent use of azole antifungals such as ketoconazole. The assumed mechanism for these interactions is through modulation of CYP3A-mediated metabolism, leading to decreased vincristine clearance and increased susceptibility to VIPN. Given the controversy surrounding the contribution of these mechanisms, we directly tested these hypotheses in genetically engineered mouse models with a deficiency of the entire murine Cyp3a locus [Cyp3a(2/2) mice] and in humanized transgenic animals with hepatic expression of functional and nonfunctional human CYP3A5 variants. Compared with wild-type mice, the systemic exposure to vincristine was increased by only 1.15-fold (95% confidence interval, 0.84–1.58) in Cyp3a(2/2) mice, suggesting that the clearance of vincristine in mice is largely independent of hepatic Cyp3a function. In line with these observations, we found that Cyp3a deficiency or pretreatment with the CYP3A inhibitors ketoconazole or nilotinib did not influence the severity and time course of VIPN and that exposure to vincristine was not substantially altered in humanized CYP3A5*3 mice or humanized CYP3A5*1 mice compared with Cyp3a(2/2) mice. Our study suggests that the contribution of CYP3A5-mediated metabolism to vincristine elimination and the associated drug–drug interaction potential is limited and that plasma levels of vincristine are unlikely to be strongly predictive of VIPN. SIGNIFICANCE STATEMENT The current study suggests that CYP3A5 genotype status does not substantially influence vincristine disposition and neurotoxicity in translationally relevant murine models. These findings raise concerns about the causality of previously reported relationships between variant CYP3A5 genotypes or concomitant azole use with the incidence of vincr

Published
2024

12. A phosphotyrosine switch regulates organic cation transporters.

Author

Sprowl, Jason A, Ong, Su Sien, Gibson, Alice A, Hu, Shuiying, Du, Guoqing, Lin, Wenwei, Li, Lie, Bharill, Shashank, Ness, Rachel A, Stecula, Adrian, Offer, Steven M, Diasio, Robert B, Nies, Anne T, Schwab, Matthias, Cavaletti, Guido, Schlatter, Eberhard, Ciarimboli, Giuliano, Schellens, Jan HM, Isacoff, Ehud Y, Sali, Andrej, Chen, Taosheng, Baker, Sharyn D, Sparreboom, Alex, and Pabla, Navjotsingh

Subjects
Ganglia, Spinal, Hela Cells, Animals, Humans, Mice, Organoplatinum Compounds, Phosphotyrosine, Organic Anion Transporters, Organic Cation Transport Proteins, Organic Cation Transporter 1, Antineoplastic Agents, Protein Kinase Inhibitors, Models, Molecular, Proto-Oncogene Proteins c-yes, Protein-Tyrosine Kinases, HEK293 Cells, Organic Cation Transporter 2, Oxaliplatin, Liver-Specific Organic Anion Transporter 1, HeLa Cells
Abstract

Membrane transporters are key determinants of therapeutic outcomes. They regulate systemic and cellular drug levels influencing efficacy as well as toxicities. Here we report a unique phosphorylation-dependent interaction between drug transporters and tyrosine kinase inhibitors (TKIs), which has uncovered widespread phosphotyrosine-mediated regulation of drug transporters. We initially found that organic cation transporters (OCTs), uptake carriers of metformin and oxaliplatin, were inhibited by several clinically used TKIs. Mechanistic studies showed that these TKIs inhibit the Src family kinase Yes1, which was found to be essential for OCT2 tyrosine phosphorylation and function. Yes1 inhibition in vivo diminished OCT2 activity, significantly mitigating oxaliplatin-induced acute sensory neuropathy. Along with OCT2, other SLC-family drug transporters are potentially part of an extensive 'transporter-phosphoproteome' with unique susceptibility to TKIs. On the basis of these findings we propose that TKIs, an important and rapidly expanding class of therapeutics, can functionally modulate pharmacologically important proteins by inhibiting protein kinases essential for their post-translational regulation.

Published
2016

15. Vincristine Disposition and Neurotoxicity are Unchanged in Humanized CYP3A5 Mice

Author

Li, Yang, primary, Kazuki, Yasuhiro, additional, Drabison, Thomas, additional, Kobayashi, Kaoru, additional, Fujita, Ken-ichi, additional, Xu, Yue, additional, Jin, Yan, additional, Ahmed, Eman, additional, Li, Junan, additional, Eisenmann, Eric D, additional, Baker, Sharyn D., additional, Cavaletti, Guido, additional, Sparreboom, Alex, additional, and Hu, Shuiying, additional

Published
2023
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17. Differentiation therapy in poor risk myeloid malignancies: Results of a dose finding study of the combination bryostatin-1 and GM-CSF

Author

Smith, B Douglas, Jones, Richard J, Cho, Eunpi, Kowalski, Jeanne, Karp, Judith E, Gore, Steven D, Vala, Milada, Meade, Brooke, Baker, Sharyn D, Zhao, Ming, Piantadosi, Steven, Zhang, Zhe, Blumenthal, Gideon, Warlick, Erica D, Brodsky, Robert A, Murgo, Anthony, Rudek, Michelle A, and Matsui, William H

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Clinical Research, Rare Diseases, Hematology, Clinical Trials and Supportive Activities, Cancer, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Adult, Aged, Antineoplastic Agents, Bryostatins, Cell Differentiation, Dose-Response Relationship, Drug, Female, Granulocyte-Macrophage Colony-Stimulating Factor, Humans, Male, Middle Aged, Prognosis, Leukemia, Differentiation therapy, Myelodysplastic syndrome, Growth factors, Bryostatin, Drug resistance, Immunology, Cardiovascular medicine and haematology
Abstract

PurposePharmacologic differentiating agents have had relatively limited clinical success outside of the use of ATRA in acute promyelocytic leukemia and DNA methyltransferase inhibitors in myelodysplastic syndromes. The differentiating effects of such agents can be enhanced in combination with lineage-specific growth factors. We developed a dose finding trial to assess toxicity, differentiating activity, and clinical impact of the combination of bryostatin-1 and GM-CSF.Experimental designPatients with poor risk myeloid malignancies were eligible to enroll in a dose finding study of continuous infusion bryostatin-1 combined with a fixed dose of daily GM-CSF. Toxicities were graded per NCI CTC version 2.0 and pharmacokinetic and correlative study samples were obtained to assess the combination's clinical and biologic differentiating effects.ResultsThirty-two patients were treated with the combination therapy and the dose determined to be most suitable for study in a larger trial was continuous infusion broystatin-1 at 16μg/m(2) for 14 days and subcutaneous GM-CSF at 125μg/m(2) daily for 14 days every 28 days. Arthralgias and myalgias limited further dose escalation. Clinically, the combination impacted differentiation with improvement of absolute neutrophil counts (p=0.0001) in the majority of patients. Interestingly, there were two objective clinical responses, including a CR after a single cycle. Both the bryostatin-1 plasma concentrations and the correlative studies supported biologic activity of the combination at the doses where clinical responses were observed.ConclusionsCombining growth factors with pharmacologic differentiating agents may increase their clinical effectiveness and further studies should focus on such combinations.

Published
2011

18. Phase II, Randomized, Placebo-Controlled Trial of Neoadjuvant Celecoxib in Men With Clinically Localized Prostate Cancer: Evaluation of Drug-Specific Biomarkers

Author

Antonarakis, Emmanuel S, Heath, Elisabeth I, Walczak, Janet R, Nelson, William G, Fedor, Helen, De Marzo, Angelo M, Zahurak, Marianna L, Piantadosi, Steven, Dannenberg, Andrew J, Gurganus, Robin T, Baker, Sharyn D, Parnes, Howard L, DeWeese, Theodore L, Partin, Alan W, and Carducci, Michael A

Subjects
Clinical Research, Prevention, Aging, Clinical Trials and Supportive Activities, Cancer, Urologic Diseases, Prostate Cancer, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Aged, Biomarkers, Tumor, Celecoxib, Cyclooxygenase Inhibitors, Double-Blind Method, Humans, Male, Middle Aged, Neoadjuvant Therapy, Prostate, Prostatic Neoplasms, Pyrazoles, Sulfonamides, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeCyclooxygenase-2 (COX-2) is a potential pharmacologic target for the prevention of various malignancies, including prostate cancer. We conducted a randomized, double-blind trial to examine the effect of celecoxib on drug-specific biomarkers from prostate tissue obtained at prostatectomy.Patients and methodsPatients with localized prostate cancer and Gleason sum > or = 7, prostate-specific antigen (PSA) > or = 15 ng/mL, clinical stage T2b or greater, or any combination with greater than 45% risk of capsular penetration were randomly assigned to celecoxib 400 mg by mouth twice daily or placebo for 4 to 6 weeks before prostatectomy. The primary end point was the difference in prostatic prostaglandin levels between the two groups. Secondary end points were differences in COX-1 and -2 expressions; oxidized DNA bases; and markers of proliferation, apoptosis and angiogenesis. Tissue celecoxib concentrations also were measured. Tertiary end points were drug safety and compliance.ResultsSeventy-three patients consented, and 64 were randomly assigned and included in the intention-to-treat analysis. There were no treatment differences in any of the primary or secondary outcomes. Multivariable regression revealed that tumor tissue had significantly lower COX-2 expression than benign prostatic tissue (P = .01) and significantly higher levels of the proliferation marker Ki-67 (P < .0001). Celecoxib was measurable in prostate tissue of patients on treatment, demonstrating that celecoxib reached its target. Celecoxib was safe and resulted in only grade 1 toxicities.ConclusionTreatment with 4 to 6 weeks of celecoxib had no effect on intermediate biomarkers of prostate carcinogenesis, despite the achievement of measurable tissue levels. We caution against using celecoxib 400 mg twice daily as a preventive agent for prostate cancer in additional studies.

Published
2009

19. Targeting a xenobiotic transporter to ameliorate vincristine-induced sensory neuropathy

Author

Li, Yang, primary, Drabison, Thomas, additional, Nepal, Mahesh, additional, Ho, Richard H., additional, Leblanc, Alix F., additional, Gibson, Alice A., additional, Jin, Yan, additional, Yang, Wenjian, additional, Huang, Kevin M., additional, Uddin, Muhammad Erfan, additional, Chen, Mingqing, additional, DiGiacomo, Duncan F., additional, Chen, Xihui, additional, Razzaq, Sobia, additional, Tonniges, Jeffrey R., additional, McTigue, Dana M., additional, Mims, Alice S., additional, Lustberg, Maryam B., additional, Wang, Yijia, additional, Hummon, Amanda B., additional, Evans, William E., additional, Baker, Sharyn D., additional, Cavaletti, Guido, additional, Sparreboom, Alex, additional, and Hu, Shuiying, additional

Published
2023
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20. A kinome-wide screen identifies a CDKL5-SOX9 regulatory axis in epithelial cell death and kidney injury

Author

Kim, Ji Young, Bai, Yuntao, Jayne, Laura A., Hector, Ralph D., Persaud, Avinash K., Ong, Su Sien, Rojesh, Shreshtha, Raj, Radhika, Feng, Mei Ji He Ho, Chung, Sangwoon, Cianciolo, Rachel E., Christman, John W., Campbell, Moray J., Gardner, David S., Baker, Sharyn D., Sparreboom, Alex, Govindarajan, Rajgopal, Singh, Harpreet, Chen, Taosheng, Poi, Ming, Susztak, Katalin, Cobb, Stuart R., and Pabla, Navjot Singh

Published
2020
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22. Hypoxia-induced upregulation of BMX kinase mediates therapeutic resistance in acute myeloid leukemia

Author

van Oosterwijk, Jolieke G., Buelow, Daelynn R., Drenberg, Christina D., Vasilyeva, Aksana, Li, Lie, Shi, Lei, Wang, Yong -Dong, Finkelstein, David, Shurtleff, Sheila A., Janke, Laura J., Pounds, Stanley, Rubnitz, Jeffrey E., Inaba, Hiroto, Pabla, Navjotsingh, and Baker, Sharyn D.

Subjects
Tyrosine -- Health aspects, Drug resistance -- Development and progression -- Health aspects, RNA sequencing -- Health aspects -- Analysis, Acute myelocytic leukemia -- Development and progression -- Health aspects, Health care industry
Abstract

Oncogenic addiction to the Fms-like tyrosine kinase 3 (FLT3) is a hallmark of acute myeloid leukemia (AML) that harbors the FLT3-internal tandem duplication (FLT3-ITD) mutation. While FLT3 inhibitors like sorafenib show initial therapeutic efficacy, resistance rapidly develops through mechanisms that are incompletely understood. Here, we used RNA-Seq-based analysis of patient leukemic cells and found that upregulation of the Tec family kinase BMX occurs during sorafenib resistance. This upregulation was recapitulated in an in vivo murine FLT3-ITD-positive ([FLT3-ITD.sup.+]) model of sorafenib resistance. Mechanistically, the antiangiogenic effects of sorafenib led to increased bone marrow hypoxia, which contributed to HIF-dependent BMX upregulation. In in vitro experiments, hypoxia-dependent BMX upregulation was observed in both AML and non-AML cell lines. Functional studies in human [FLT3-ITD.sup.+] cell lines showed that BMX is part of a compensatory signaling mechanism that promotes AML cell survival during FLT3 inhibition. Taken together, our results demonstrate that hypoxia-dependent upregulation of BMX contributes to therapeutic resistance through a compensatory prosurvival signaling mechanism. These results also reveal the role of off-target drug effects on tumor microenvironment and development of acquired drug resistance. We propose that the bone marrow niche can be altered by anticancer therapeutics, resulting in drug resistance through cell-nonautonomous microenvironment-dependent effects., Introduction Advances in genomics, as well as the development of molecularly targeted drugs, have transformed cancer therapy (1). Identification of genomic alterations and oncogenic addictions in specific cancer subtypes has [...]

Published
2018
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26. Supplementary Excel Tables from Integrative Genomic Analysis of Pediatric Myeloid-Related Acute Leukemias Identifies Novel Subtypes and Prognostic Indicators

Author

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

Published
2023
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27. Supplementary Tables and Figures from Integrative Genomic Analysis of Pediatric Myeloid-Related Acute Leukemias Identifies Novel Subtypes and Prognostic Indicators

Author

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

Published
2023
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28. Data from Integrative Genomic Analysis of Pediatric Myeloid-Related Acute Leukemias Identifies Novel Subtypes and Prognostic Indicators

Author

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

Published
2023
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36. Vincristine Disposition and Neurotoxicity Are Unchanged in Humanized CYP3A5 Mice

Author

Li, Yang, Kazuki, Yasuhiro, Drabison, Thomas, Kobayashi, Kaoru, Fujita, Ken-ichi, Xu, Yue, Jin, Yan, Ahmed, Eman, Li, Junan, Eisenmann, Eric D., Baker, Sharyn D., Cavaletti, Guido, Sparreboom, Alex, and Hu, Shuiying

Abstract

Previous studies have suggested that the incidence of vincristine-induced peripheral neuropathy (VIPN) is potentially linked with cytochrome P450 (CYP)3A5, a polymorphic enzyme that metabolizes vincristine in vitro, and with concurrent use of azole antifungals such as ketoconazole. The assumed mechanism for these interactions is through modulation of CYP3A-mediated metabolism, leading to decreased vincristine clearance and increased susceptibility to VIPN. Given the controversy surrounding the contribution of these mechanisms, we directly tested these hypotheses in genetically engineered mouse models with a deficiency of the entire murine Cyp3alocus [Cyp3a(−/−) mice] and in humanized transgenic animals with hepatic expression of functional and nonfunctional human CYP3A5 variants. Compared with wild-type mice, the systemic exposure to vincristine was increased by only 1.15-fold (95% confidence interval, 0.84–1.58) in Cyp3a(−/−) mice, suggesting that the clearance of vincristine in mice is largely independent of hepatic Cyp3a function. In line with these observations, we found that Cyp3a deficiency or pretreatment with the CYP3A inhibitors ketoconazole or nilotinib did not influence the severity and time course of VIPN and that exposure to vincristine was not substantially altered in humanized CYP3A5*3 mice or humanized CYP3A5*1 mice compared with Cyp3a(−/−) mice. Our study suggests that the contribution of CYP3A5-mediated metabolism to vincristine elimination and the associated drug–drug interaction potential is limited and that plasma levels of vincristine are unlikely to be strongly predictive of VIPN.SIGNIFICANCE STATEMENTThe current study suggests that CYP3A5 genotype status does not substantially influence vincristine disposition and neurotoxicity in translationally relevant murine models. These findings raise concerns about the causality of previously reported relationships between variant CYP3A5 genotypes or concomitant azole use with the incidence of vincristine neurotoxicity.

Published
2024
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37. Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms

Author

Zhang, Haijiao, Savage, Samantha, Schultz, Anna Reister, Bottomly, Daniel, White, Libbey, Segerdell, Erik, Wilmot, Beth, McWeeney, Shannon K., Eide, Christopher A., Nechiporuk, Tamilla, Carlos, Amy, Henson, Rachel, Lin, Chenwei, Searles, Robert, Ho, Hoang, Lam, Yee Ling, Sweat, Richard, Follit, Courtney, Jain, Vinay, Lind, Evan, Borthakur, Gautam, Garcia-Manero, Guillermo, Ravandi, Farhad, Kantarjian, Hagop M., Cortes, Jorge, Collins, Robert, Buelow, Daelynn R., Baker, Sharyn D., Druker, Brian J., and Tyner, Jeffrey W.

Published
2019
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41. Supplementary Tables from Cellular Uptake of Imatinib into Leukemic Cells Is Independent of Human Organic Cation Transporter 1 (OCT1)

Author

Nies, Anne T., primary, Schaeffeler, Elke, primary, van der Kuip, Heiko, primary, Cascorbi, Ingolf, primary, Bruhn, Oliver, primary, Kneba, Michael, primary, Pott, Christiane, primary, Hofmann, Ute, primary, Volk, Christopher, primary, Hu, Shuiying, primary, Baker, Sharyn D., primary, Sparreboom, Alex, primary, Ruth, Peter, primary, Koepsell, Hermann, primary, and Schwab, Matthias, primary

Published
2023
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43. Supplementary Methods from Phase I Trial, Pharmacokinetics, and Pharmacodynamics of Vandetanib and Dasatinib in Children with Newly Diagnosed Diffuse Intrinsic Pontine Glioma

Author

Broniscer, Alberto, primary, Baker, Sharyn D., primary, Wetmore, Cynthia, primary, Pai Panandiker, Atmaram S., primary, Huang, Jie, primary, Davidoff, Andrew M., primary, Onar-Thomas, Arzu, primary, Panetta, John C., primary, Chin, Thomas K., primary, Merchant, Thomas E., primary, Baker, Justin N., primary, Kaste, Sue C., primary, Gajjar, Amar, primary, and Stewart, Clinton F., primary

Published
2023
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44. Supplementary Figures from Cellular Uptake of Imatinib into Leukemic Cells Is Independent of Human Organic Cation Transporter 1 (OCT1)

Author

Nies, Anne T., primary, Schaeffeler, Elke, primary, van der Kuip, Heiko, primary, Cascorbi, Ingolf, primary, Bruhn, Oliver, primary, Kneba, Michael, primary, Pott, Christiane, primary, Hofmann, Ute, primary, Volk, Christopher, primary, Hu, Shuiying, primary, Baker, Sharyn D., primary, Sparreboom, Alex, primary, Ruth, Peter, primary, Koepsell, Hermann, primary, and Schwab, Matthias, primary

Published
2023
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46. Data from OCTN1 Is a High-Affinity Carrier of Nucleoside Analogues

Author

Drenberg, Christina D., primary, Gibson, Alice A., primary, Pounds, Stanley B., primary, Shi, Lei, primary, Rhinehart, Dena P., primary, Li, Lie, primary, Hu, Shuiying, primary, Du, Guoqing, primary, Nies, Anne T., primary, Schwab, Matthias, primary, Pabla, Navjotsingh, primary, Blum, William, primary, Gruber, Tanja A., primary, Baker, Sharyn D., primary, and Sparreboom, Alex, primary

Published
2023
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47. Supplementary Figures and Tables from OCTN1 Is a High-Affinity Carrier of Nucleoside Analogues

Author

Drenberg, Christina D., primary, Gibson, Alice A., primary, Pounds, Stanley B., primary, Shi, Lei, primary, Rhinehart, Dena P., primary, Li, Lie, primary, Hu, Shuiying, primary, Du, Guoqing, primary, Nies, Anne T., primary, Schwab, Matthias, primary, Pabla, Navjotsingh, primary, Blum, William, primary, Gruber, Tanja A., primary, Baker, Sharyn D., primary, and Sparreboom, Alex, primary

Published
2023
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48. Supplementary Figure 2 from Emergence of Polyclonal FLT3 Tyrosine Kinase Domain Mutations during Sequential Therapy with Sorafenib and Sunitinib in FLT3-ITD–Positive Acute Myeloid Leukemia

Author

Baker, Sharyn D., primary, Zimmerman, Eric I., primary, Wang, Yong-Dong, primary, Orwick, Shelley, primary, Zatechka, Douglas S., primary, Buaboonnam, Jassada, primary, Neale, Geoffrey A., primary, Olsen, Scott R., primary, Enemark, Eric J., primary, Shurtleff, Sheila, primary, Rubnitz, Jeffrey E., primary, Mullighan, Charles G., primary, and Inaba, Hiroto, primary

Published
2023
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