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Journal articles on the topic 'Tanespimycine'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Flint, Oliver P., Jae Kwagh, Faye Wang, et al. "Tanespimycin Prevents Bortezomib Toxicity and Preserves Neuronal Morphology in Primary Rat Dorsal Root Ganglion Cultures." Blood 114, no. 22 (2009): 2847. http://dx.doi.org/10.1182/blood.v114.22.2847.2847.

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Abstract Abstract 2847 Poster Board II-823 INTRODUCTION: Tanespimycin, an inhibitor of Hsp90, is in phase 3 clinical trials in combination with bortezomib in patients with relapsed/refractory multiple myeloma (MM). The combination of tanespimycin and bortezomib produces synergistic antitumor activity and enhanced proteasome inhibition in primary MM cells (Mitsiades, Blood, 2006). In a phase 1/2 study in 72 patients with relapsed/refractory myeloma, tanespimycin + bortezomib produced durable responses in patients including bortezomib-refractory patients. Bortezomib-induced peripheral neuropathy

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2

Car, Bruce D., Oliver P. Flint, Jan Oberdoerster, et al. "Tanespimycin Reverses Bortezomib-Induced Inhibition of Granulopoiesis." Blood 114, no. 22 (2009): 3846. http://dx.doi.org/10.1182/blood.v114.22.3846.3846.

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Abstract Abstract 3846 Poster Board III-782 INTRODUCTION Tanespimycin, an Hsp90 inhibitor, is in phase 3 clinical trials with bortezomib for the treatment of multiple myeloma (MM). Neutropenia and thrombocytopenia are commonly observed during bortezomib treatment in patients with MM. However, in a phase 1/2 study of tanespimycin + bortezomib in patients with MM, the incidence and severity of neutropenia was low (Richardson ASCO 2009). Here we present the in vitro effects of tanespimycin and bortezomib on hematopoiesis and granulopoiesis in cell culture systems using mononuclear cells from heal

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3

Mitsiades, Constantine S., Michele Agler, YingJie Zhu, et al. "Effects of Tanespimycin On Glucocorticoid Receptor Translocation." Blood 114, no. 22 (2009): 4921. http://dx.doi.org/10.1182/blood.v114.22.4921.4921.

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Abstract Abstract 4921 INTRODUCTION Tanespimycin (BMS-722782) exhibits antitumor activity in diverse models of hematologic malignancies and solid tumors by suppressing the chaperoning activity of heat shock protein 90 (Hsp90) including its ability to preserve the proper three-dimensional structure and intracellular trafficking of its client proteins. However, not all potential client proteins are affected to the same degree by Hsp90 inhibitors. Tanespimycin is in phase 3 clinical development with bortezomib for the treatment of multiple myeloma (MM). Because glucocorticoids form the backbone o

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4

Badros, Ashraf Z., Paul G. Richardson, Maher Albitar, et al. "Tanespimycin + Bortezomib in Relapsed/Refractory Myeloma Patients: Results From the Time-2 Study." Blood 114, no. 22 (2009): 1871. http://dx.doi.org/10.1182/blood.v114.22.1871.1871.

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Abstract Abstract 1871 Poster Board I-896 Introduction: Tanespimycin is an inhibitor of Hsp90, a molecular chaperone for proteins critical to growth, survival, and drug resistance of multiple myeloma (MM) cells. Increased Hsp70 expression is a pharmacodynamic (PD) marker of Hsp90 inhibition (Modi et al, J Clin Oncol, 2007). In primary MM cells, tanespimycin synergizes with bortezomib resulting in increased antitumor activity and enhanced proteasome inhibition. Tanespimycin + bortezomib has demonstrated durable responses in patients with relapsed/refractory MM with low rates of neutropenia and

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5

Dimopoulos, Meletios-Athanassios, Constantine S. Mitsiades, Kenneth C. Anderson, and Paul G. Richardson. "Tanespimycin as Antitumor Therapy." Clinical Lymphoma Myeloma and Leukemia 11, no. 1 (2011): 17–22. http://dx.doi.org/10.3816/clml.2011.n.002.

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6

Richardson, Paul G., Asher A. Chanan-Khan, Sagar Lonial, et al. "Tanespimycin + Bortezomib Demonstrates Safety, Activity, and Effective Target Inhibition in Relapsed/Refractory Myeloma Patients: Updated Results of a Phase 1/2 Study." Blood 114, no. 22 (2009): 2890. http://dx.doi.org/10.1182/blood.v114.22.2890.2890.

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Abstract Abstract 2890 Poster Board II-866 INTRODUCTION: Tanespimycin disrupts Hsp90, a key molecular chaperone for signal transduction proteins critical to myeloma growth, survival, and drug resistance. Increased Hsp70 expression is a pharmacodynamic (PD) marker for Hsp90 inhibition (Modi et al, J Clin Oncol, 2007). Tanespimycin + bortezomib has synergistic antitumor activity and enhanced proteasome inhibition in primary multiple myeloma (MM) cells. Tanespimycin + bortezomib has demonstrated durable responses in patients with relapsed/refractory MM with low rates of neutropenia and peripheral

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7

Modi, Shanu, Alison T. Stopeck, Michael S. Gordon, et al. "Combination of Trastuzumab and Tanespimycin (17-AAG, KOS-953) Is Safe and Active in Trastuzumab-Refractory HER-2–Overexpressing Breast Cancer: A Phase I Dose-Escalation Study." Journal of Clinical Oncology 25, no. 34 (2007): 5410–17. http://dx.doi.org/10.1200/jco.2007.11.7960.

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Purpose This phase I study examined whether a heat shock protein (Hsp) 90 inhibitor tanespimycin (17-AAG; KOS-953) could be administered safely in combination with trastuzumab at a dose that inhibits Hsp90 function in vivo in lymphocytes. Patients and Methods Patients with an advanced solid tumor progressing during standard therapy were eligible. Patients were treated with weekly trastuzumab followed by intravenous tanespimycin, assessed in escalating dose levels. Results Twenty-five patients were enrolled onto four tanespimycin dose levels: 225 (n = 4), 300 (n = 3), 375 (n = 8), and 450 mg/m2

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8

Kefford, R., M. Millward, P. Hersey, et al. "Phase II trial of tanespimycin (KOS-953), a heat shock protein-90 (Hsp90) inhibitor in patients with metastatic melanoma." Journal of Clinical Oncology 25, no. 18_suppl (2007): 8558. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.8558.

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8558 Background: Tanespimycin binds to and inhibits the activity of Heat Shock Protein 90 (Hsp90). Hsp90 inhibition results in the degradation of a variety of RAF family proteins, including mutant BRAF. As the majority of melanomas have activation of the BRAF-MAPK pathway, we postulate that tanespimycin will interrupt the MAPK pathway and may lead to clinically significant anti-melanoma effects. Methods: This is a multi-center two-stage Simon design study; continuation to the second stage required at least 1 pt with progression free survival (PFS) of at least 24 weeks (the primary endpoint of

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9

Megill, J., O. Flint, J. Kwagh, et al. "Tanespimycin Protects Cultured Rat Dorsal Root Ganglia from Bortezmib Toxicity." Microscopy and Microanalysis 16, S2 (2010): 646–47. http://dx.doi.org/10.1017/s1431927610055248.

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10

Krzykowska-Petitjean, Katarzyna, Jędrzej Małecki, Anna Bentke, Barbara Ostrowska, and Piotr Laidler. "Tipifarnib and tanespimycin show synergic proapoptotic activity in U937 cells." Journal of Cancer Research and Clinical Oncology 138, no. 3 (2011): 537–44. http://dx.doi.org/10.1007/s00432-011-1131-9.

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11

Erlichman, Charles. "Tanespimycin: the opportunities and challenges of targeting heat shock protein 90." Expert Opinion on Investigational Drugs 18, no. 6 (2009): 861–68. http://dx.doi.org/10.1517/13543780902953699.

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12

Vaishampayan, Ulka N., Angelika M. Burger, Edward A. Sausville, et al. "Safety, Efficacy, Pharmacokinetics, and Pharmacodynamics of the Combination of Sorafenib and Tanespimycin." Clinical Cancer Research 16, no. 14 (2010): 3795–804. http://dx.doi.org/10.1158/1078-0432.ccr-10-0503.

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13

Gaspar, Nathalie, Swee Y. Sharp, Simon Pacey, et al. "Acquired Resistance to 17-Allylamino-17-Demethoxygeldanamycin (17-AAG, Tanespimycin) in Glioblastoma Cells." Cancer Research 69, no. 5 (2009): 1966–75. http://dx.doi.org/10.1158/0008-5472.can-08-3131.

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14

Burris, Howard A., David Berman, Bindu Murthy, and Suzanne Jones. "Tanespimycin pharmacokinetics: a randomized dose-escalation crossover phase 1 study of two formulations." Cancer Chemotherapy and Pharmacology 67, no. 5 (2010): 1045–54. http://dx.doi.org/10.1007/s00280-010-1398-6.

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15

Katragadda, Usha, Wei Fan, Yingzhe Wang, Quincy Teng, and Chalet Tan. "Combined Delivery of Paclitaxel and Tanespimycin via Micellar Nanocarriers: Pharmacokinetics, Efficacy and Metabolomic Analysis." PLoS ONE 8, no. 3 (2013): e58619. http://dx.doi.org/10.1371/journal.pone.0058619.

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16

McWilliams, Robert R., Nathan R. Foster, Andrea Wang-Gillam, Charles Erlichman, and George P. Kim. "Phase II consortium (P2C) study of gemcitabine and tanespimycin (17AAG) for metastatic pancreatic cancer." Journal of Clinical Oncology 31, no. 4_suppl (2013): 245. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.245.

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245 Background: Gemcitabine (GEM) monotherapy for PDA has modest activity. 17-N-Allylamino-17-demthoxygeldanamycin (Tanespimycin/17AAG), is an HSP90 inhibitor, which results in degradation of a number of client proteins such as RAF and Akt. Arlander et al (J Biol Chem. 2003 278:52572-7) have demonstrated that 17AAG targeting of HSP90 leads to Chk1 degradation. Chk1 is upregulated with GEM treatment which affects cell survival (Karnitz et al. Mol Pharmacol. 2005 68:1636-44). In vitro, the combination demonstrated in vitro synergy. Thus the potential clinical activity in pancreatic cancer of the

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17

Gupta, Biki, Shiva Pathak, Bijay Kumar Poudel, et al. "Folate receptor-targeted hybrid lipid-core nanocapsules for sequential delivery of doxorubicin and tanespimycin." Colloids and Surfaces B: Biointerfaces 155 (July 2017): 83–92. http://dx.doi.org/10.1016/j.colsurfb.2017.04.010.

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18

Kaufmann, S. H., J. E. Karp, M. R. Litzow, et al. "Phase I and pharmacological study of cytarabine and tanespimycin in relapsed and refractory acute leukemia." Haematologica 96, no. 11 (2011): 1619–26. http://dx.doi.org/10.3324/haematol.2011.049551.

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19

Oki, Yasuhiro, Amanda Copeland, Jorge Romaguera, et al. "Clinical experience with the heat shock protein-90 inhibitor, tanespimycin, in patients with relapsed lymphoma." Leukemia & Lymphoma 53, no. 5 (2012): 990–92. http://dx.doi.org/10.3109/10428194.2011.631236.

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20

Schenk, Erin, Andrea E. Wahner Hendrickson, Donald Northfelt, et al. "Phase I study of tanespimycin in combination with bortezomib in patients with advanced solid malignancies." Investigational New Drugs 31, no. 5 (2013): 1251–56. http://dx.doi.org/10.1007/s10637-013-9946-7.

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21

Yu, Kyoung Hyun, Hyewon Youn, Myung Geun Song, Dong Soo Lee, and June-Key Chung. "The Effect of Tanespimycin (17-AAG) on Radioiodine Accumulation in Sodium-Iodide Symporter Expressing Cells." Nuclear Medicine and Molecular Imaging 46, no. 4 (2012): 239–46. http://dx.doi.org/10.1007/s13139-012-0158-4.

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22

Pradhan, Roshan, Thiruganesh Ramasamy, Ju Yeon Choi, et al. "Hyaluronic acid-decorated poly(lactic-co-glycolic acid) nanoparticles for combined delivery of docetaxel and tanespimycin." Carbohydrate Polymers 123 (June 2015): 313–23. http://dx.doi.org/10.1016/j.carbpol.2015.01.064.

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23

Larson, Nate, Khaled Greish, Hillevi Bauer, Hiroshi Maeda, and Hamidreza Ghandehari. "Synthesis and evaluation of poly(styrene-co-maleic acid) micellar nanocarriers for the delivery of tanespimycin." International Journal of Pharmaceutics 420, no. 1 (2011): 111–17. http://dx.doi.org/10.1016/j.ijpharm.2011.08.011.

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24

Wang, Qilin, та Xiangguo Liu. "VDAC upregulation and αTAT1‑mediated α‑tubulin acetylation contribute to tanespimycin‑induced apoptosis in Calu‑1 cells". Oncology Reports 44, № 6 (2020): 2725–34. http://dx.doi.org/10.3892/or.2020.7789.

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25

Pacey, Simon, Martin Gore, David Chao, et al. "A Phase II trial of 17-allylamino, 17-demethoxygeldanamycin (17-AAG, tanespimycin) in patients with metastatic melanoma." Investigational New Drugs 30, no. 1 (2010): 341–49. http://dx.doi.org/10.1007/s10637-010-9493-4.

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26

Richardson, Paul G., Asher Chanan-Khan, Sagar Lonial, et al. "Tanespimycin (T) + Bortezomib (BZ) in Multiple Myeloma (MM): Confirmation of the Recommended Dose Using a Novel Formulation." Blood 110, no. 11 (2007): 1165. http://dx.doi.org/10.1182/blood.v110.11.1165.1165.

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Abstract Introduction: Tanespimycin (17-AAG/KOS-953) disrupts Hsp90, a molecular chaperone of client proteins including IL-6 and IGF-1R, key to MM growth, survival and drug resistance. Single agent T is well tolerated with modest anti-MM activity in Phase 1; preclinical studies suggest synergy with BZ. Methods: To date, 63 patients (pts) received BZ followed by 1-hr infusion of T on D1,4,8,11 q 21d. Dose escalating phase: 36 pts were enrolled in 7 cohorts (T 100–340 mg/m2; BZ 0.7–1.3 mg/m2). Confirmation of the phase 2 dose occurred in 27 pts across 2 groups: 1 group received a Cremophor formu

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Bentke, Anna, Jędrzej Małecki, Barbara Ostrowska, Katarzyna Krzykowska-Petitjean, and Piotr Laidler. "Tanespimycin and Tipifarnib Exhibit Synergism in Inducing Apoptosis in Melanoma Cell Lines From Later Stages of Tumor Progression." Cancer Investigation 31, no. 8 (2013): 545–49. http://dx.doi.org/10.3109/07357907.2013.830736.

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28

Wahner Hendrickson, Andrea E., Ann L. Oberg, Gretchen Glaser, et al. "A phase II study of gemcitabine in combination with tanespimycin in advanced epithelial ovarian and primary peritoneal carcinoma." Gynecologic Oncology 124, no. 2 (2012): 210–15. http://dx.doi.org/10.1016/j.ygyno.2011.10.002.

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29

Xiong, May P., Jaime A. Yáñez, Glen S. Kwon, Neal M. Davies, and M. Laird Forrest. "A Cremophor-Free Formulation for Tanespimycin (17-AAG) Using PEO-b-PDLLA Micelles: Characterization and Pharmacokinetics in Rats." Journal of Pharmaceutical Sciences 98, no. 4 (2009): 1577–86. http://dx.doi.org/10.1002/jps.21509.

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30

Pedersen, Katrina S., George P. Kim, Nathan R. Foster, Andrea Wang-Gillam, Charles Erlichman, and Robert R. McWilliams. "Phase II trial of gemcitabine and tanespimycin (17AAG) in metastatic pancreatic cancer: a Mayo Clinic Phase II Consortium study." Investigational New Drugs 33, no. 4 (2015): 963–68. http://dx.doi.org/10.1007/s10637-015-0246-2.

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31

Richardson, P. G., A. Chanan-Khan, S. Lonial, et al. "Tanespimycin plus bortezomib in patients with relapsed and refractory multiple myeloma: Final results of a phase I/II study." Journal of Clinical Oncology 27, no. 15_suppl (2009): 8503. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.8503.

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8503 Background: Tanespimycin (Tan) disrupts HSP90, a key molecular chaperone for signal transduction proteins critical to myeloma (MM) growth, survival and drug resistance. Preclinical data show anti-tumor synergy between Tan and bortezomib (Bz) and suggest Tan may be neuroprotective, including reversibility of Bz-induced peripheral neuropathy (PN). A phase I study of single agent Tan in advanced MM showed favorable tolerability and modest activity. Methods: 72 patients (pts) with relapsed/refractory MM received 0.7 - 1.3 mg/m2 Bz as IVB followed by 1-hr infusion of 100 -340 mg/m2 Tan on days

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32

Richardson, P. G., A. Chanan-Khan, S. Lonial, et al. "Tanespimycin (T) + bortezomib (BZ) in multiple myeloma (MM): Pharmacology, safety and activity in relapsed/refractory (rel/ref) patients (Pts)." Journal of Clinical Oncology 25, no. 18_suppl (2007): 3532. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.3532.

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3532 Background: Tanespimycin (17-AAG/KOS 953) disrupts Hsp90, a molecular chaperone of MM client proteins including IL-6 and IGF-1R that are key to MM growth, survival and drug resistance. Single agent T was well tolerated with modest anti- MM activity. Preclinical studies suggest potential synergy with BZ. Methods: Pts received BZ as IVB followed by 1-hr infusion of T on D1,4,8,11 q 21d. Results: 49 pts were enrolled in 7 cohorts (T 100- 340 mg/m2; BZ 0.7 - 1.3 mg/m2). PK of T was similar with or without BZ. Inhibition of 20S proteasome with T+BZ was not different vs. historical BZ single ag

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33

Ma, Liang, Dawei Yang, Zhaoxin Li, Xin Zhang, and Lei Pu. "Co-delivery of paclitaxel and tanespimycin in lipid nanoparticles enhanced anti-gastric-tumor effect in vitro and in vivo." Artificial Cells, Nanomedicine, and Biotechnology 46, sup2 (2018): 904–11. http://dx.doi.org/10.1080/21691401.2018.1472101.

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34

Pastvova, Nikola, Petr Dolezel, and Petr Mlejnek. "Heat Shock Protein Inhibitor 17-Allyamino-17-Demethoxygeldanamycin, a Potent Inductor of Apoptosis in Human Glioma Tumor Cell Lines, Is a Weak Substrate for ABCB1 and ABCG2 Transporters." Pharmaceuticals 14, no. 2 (2021): 107. http://dx.doi.org/10.3390/ph14020107.

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Glioblastoma multiforme (GBM) is the most common primary brain tumor in adults and has a poor prognosis. Complex genetic alterations and the protective effect of the blood–brain barrier (BBB) have so far hampered effective treatment. Here, we investigated the cytotoxic effects of heat shock protein 90 (HSP90) inhibitors, geldanamycin (GDN) and 17-allylamino-17-demethoxygeldanamycin (17-AAG, tanespimycin), in a panel of glioma tumor cell lines with various genetic alterations. We also assessed the ability of the main drug transporters, ABCB1 and ABCG2, to efflux GDN and 17-AAG. We found that GD

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35

Zhong, Z., J. Simmons, and P. Timmermans. "152 POSTER Prevention and treatment of bortezomib-induced peripheral neuropathy by the Hsp90 inhibitor tanespimycin (KOS-953) in the rat." European Journal of Cancer Supplements 6, no. 12 (2008): 49. http://dx.doi.org/10.1016/s1359-6349(08)72084-6.

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36

Pires, Vinícius Couto, Carla Pires Magalhães, Marcos Ferrante, et al. "Solid lipid nanoparticles as a novel formulation approach for tanespimycin (17-AAG) against leishmania infections: Preparation, characterization and macrophage uptake." Acta Tropica 211 (November 2020): 105595. http://dx.doi.org/10.1016/j.actatropica.2020.105595.

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37

Gan, Jinping, Peggy Liu-Kreyche, and W. Griffith Humphreys. "In vitro assessment of cytochrome P450 inhibition and induction potential of tanespimycin and its major metabolite, 17-amino-17-demethoxygeldanamycin." Cancer Chemotherapy and Pharmacology 69, no. 1 (2011): 51–56. http://dx.doi.org/10.1007/s00280-011-1672-2.

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38

Powers, Marissa V., Melanie Valenti, Susana Miranda, et al. "Mode of cell death induced by the HSP90 inhibitor 17-AAG (tanespimycin) is dependent on the expression of pro-apoptotic BAX." Oncotarget 4, no. 11 (2013): 1963–75. http://dx.doi.org/10.18632/oncotarget.1419.

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39

&NA;. "Tanespimycin,* a heat shock protein 90 inhibitor, in combination with trastuzumab is effective for patients with HER 2+ metastatic breast cancer." Inpharma Weekly &NA;, no. 1619 (2008): 11. http://dx.doi.org/10.2165/00128413-200816190-00024.

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40

Modi, S., S. Sugarman, A. Stopeck, et al. "Phase II trial of the Hsp90 inhibitor tanespimycin (Tan) + trastuzumab (T) in patients (pts) with HER2-positive metastatic breast cancer (MBC)." Journal of Clinical Oncology 26, no. 15_suppl (2008): 1027. http://dx.doi.org/10.1200/jco.2008.26.15_suppl.1027.

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41

Richardson, Paul G., Asher A. Chanan-Khan, Sagar Lonial, et al. "Tanespimycin and bortezomib combination treatment in patients with relapsed or relapsed and refractory multiple myeloma: results of a phase 1/2 study." British Journal of Haematology 153, no. 6 (2011): 729–40. http://dx.doi.org/10.1111/j.1365-2141.2011.08664.x.

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42

Thomas, Brian M., Scott H. Kaufmann, Jacqueline M. Greer, et al. "Phase I Dose-Escalation Study of SCH 900776 in Combination with Cytarabine (Ara-C) in Patients with Acute Leukemia." Blood 118, no. 21 (2011): 1531. http://dx.doi.org/10.1182/blood.v118.21.1531.1531.

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Abstract Abstract 1531 Checkpoint kinase (Chk1) is a serine-threonine kinase that is activated via phosphorylation in response to DNA damage and is critical to the regulation of cell cycle progression. Ara-C triggers sequential activation of ATR kinase and Chk1 ex vivo to induce the S phase slowing that accompanies Ara-C treatment. Inhibition of Chk1 may abrogate S phase slowing, thereby preventing repair of Ara-C-induced DNA damage and potentiating the antitumor activity of Ara-C. The Hsp90 inhibitor tanespimycin (17-AAG) has been shown to enhance the cytotoxicity of Ara-C in part through Chk

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43

Spector, Neil L., and Kimberly L. Blackwell. "Understanding the Mechanisms Behind Trastuzumab Therapy for Human Epidermal Growth Factor Receptor 2–Positive Breast Cancer." Journal of Clinical Oncology 27, no. 34 (2009): 5838–47. http://dx.doi.org/10.1200/jco.2009.22.1507.

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PurposeTargeted therapy with the humanized monoclonal antibody trastuzumab has become a mainstay for human epidermal growth factor receptor 2 (HER2) –positive breast cancer (BC). The mechanisms of action of trastuzumab have not been fully elucidated, and data available to date are reviewed here. The impact of the mechanisms of action on clinical benefit also is discussed.MethodsAn extensive literature review of trastuzumab and proposed mechanisms of action was performed.ResultsAt least five potential extracellular and intracellular antitumor mechanisms of trastuzumab have been identified in th

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44

He, Yi, Yihong Chen, Yuxin Tong, Wenyong Long, and Qing Liu. "Identification of a circRNA-miRNA-mRNA regulatory network for exploring novel therapeutic options for glioma." PeerJ 9 (August 6, 2021): e11894. http://dx.doi.org/10.7717/peerj.11894.

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Background Glioma is the most common brain neoplasm with a poor prognosis. Circular RNA (circRNA) and their associated competing endogenous RNA (ceRNA) network play critical roles in the pathogenesis of glioma. However, the alteration of the circRNA-miRNA-mRNA regulatory network and its correlation with glioma therapy haven’t been systematically analyzed. Methods With GEO, GEPIA2, circBank, CSCD, CircInteractome, mirWalk 2.0, and mirDIP 4.1, we constructed a circRNA–miRNA–mRNA network in glioma. LASSO regression and multivariate Cox regression analysis established a hub mRNA signature to asses

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45

Zhong, Danli, Chanyuan Wu, Jingjing Bai, Dong Xu, Xiaofeng Zeng, and Qian Wang. "Co-expression network analysis reveals the pivotal role of mitochondrial dysfunction and interferon signature in juvenile dermatomyositis." PeerJ 8 (February 18, 2020): e8611. http://dx.doi.org/10.7717/peerj.8611.

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Background Juvenile dermatomyositis (JDM) is an immune-mediated disease characterized by chronic organ inflammation. The pathogenic mechanisms remain ill-defined. Methods Raw microarray data of JDM were obtained from the gene expression omnibus (GEO) database. Based on the GSE3307 dataset with 39 samples, weighted correlation network analysis (WGCNA) was performed to identify key modules associated with pathological state. Functional enrichment analyses were conducted to identify potential mechanisms. Based on the criteria of high connectivity and module membership, candidate hub genes were se

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46

Faria, Morse, Omnia Ismaiel, James Waltrip, et al. "LC-MS/MS Method for the Quantitative Determination of Tanespimycin and its Active Metabolite in Human Plasma: Method Validation and Overcoming an Insidious APCI Source Phenomenon." Journal of Applied Bioanalysis 6, no. 3 (2020): 145–63. http://dx.doi.org/10.17145/jab.20.015.

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47

Richardson, Paul, Asher Alban Chanan-Khan, Sagar Lonial, et al. "A Multicenter Phase 1 Clinical Trial of Tanespimycin (KOS-953) + Bortezomib (BZ): Encouraging Activity and Manageable Toxicity in Heavily Pre-Treated Patients with Relapsed Refractory Multiple Myeloma (MM)." Blood 108, no. 11 (2006): 406. http://dx.doi.org/10.1182/blood.v108.11.406.406.

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Abstract Background: Tanespimycin (KOS-953, 17-AAG) disrupts the function of Hsp90, a molecular chaperone of MM client proteins such as IL-6, IGF-1R that are key to growth, survival and drug resistance. In vitro, BZ + KOS-953 show additive cytotoxicity against MM cells. Single-agent KOS-953 produced durable MR and SD (ASH 2005 A#361) in relapsed and refractory MM pts with an MTD ≥ 420 mg/m2. Objectives: Define a phase 2 dose of BZ+KOS-953 in pts with relapsed, refractory MM. Determine PK of KOS-953 and its active metabolite. Evaluate proteasome inhibition in whole blood lysates. Explore change

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Modi, Shanu, Alison Stopeck, Hannah Linden, et al. "HSP90 Inhibition Is Effective in Breast Cancer: A Phase II Trial of Tanespimycin (17-AAG) Plus Trastuzumab in Patients with HER2-Positive Metastatic Breast Cancer Progressing on Trastuzumab." Clinical Cancer Research 17, no. 15 (2011): 5132–39. http://dx.doi.org/10.1158/1078-0432.ccr-11-0072.

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McMillin, Douglas W., Joseph Negri, Jake Delmore, et al. "Activity of New Heat Shock Protein 90 (hsp90) Inhibitor NVP-AUY922 Against Myeloma Cells Sensitive and Resistant to Conventional Agents." Blood 110, no. 11 (2007): 1587. http://dx.doi.org/10.1182/blood.v110.11.1587.1587.

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Abstract Context: The molecular chaperone hsp90 is a major anti-cancer therapeutic target because it regulates the function of proteins with pivotal roles in tumor cell proliferation, survival and drug resistance, including mutated/chimeric oncoproteins or oncogenic kinases/receptors. Our preclinical studies on the ansamycin hsp90 inhibitor tanespimycin (17-AAG) provided the rationale for clinical trials, either alone or in combination with the proteasome inhibitor bortezomib, for treatment of relapsed/refractory MM. In this study, we report preclinical studies of the new, non-ansamycin, hsp90

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Kivioja, Jarno, Angeliki Thanasopoulou, Mika Kontro, et al. "Identification of Optimized Compound Combinations for the Treatment of NUP98-NSD1+ AML." Blood 128, no. 22 (2016): 4711. http://dx.doi.org/10.1182/blood.v128.22.4711.4711.

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Abstract Introduction The t(5;11)(q35;p15.4) translocation joining the nucleoporin-98 kD (NUP98) and nuclear receptor binding SET domain protein 1 (NSD1) genes is a recurrent chromosomal aberration in pediatric acute myeloid leukemia (AML). The NUP98-NSD1 frequently co-occurs with FLT3-ITD and with high-rates of induction failure. Analyzing primary samples and cell models by high-throughput drug testing, we aimed to identify alternative therapeutic approaches and better understand the impact of the NUP98-NSD1 and FLT3-ITDalterations on drug response. Methods Bone marrow mononuclear cells (BM M

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