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10.1016/j.clml.2013.11.001 http://scihub22266oqcxt.onion/10.1016/j.clml.2013.11.001 C4096861!4096861!24355079     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Lymphoma+Myeloma+Leuk 2014 ; 14 (3): 223-30 Nephropedia Template TP {{tp|p=24355079|t=2014. A Phase I and pharmacodynamic study of AT9283, a small molecule inhibitor of aurora kinases in patients with relapsed/refractory leukemia or myelofibrosis |pdf=|usr=}}{{24355079}} gab.com Text A Phase I and pharmacodynamic study of AT9283, a small molecule inhibitor of aurora kinases in patients with relapsed/refractory leukemia or myelofibrosis JO: Clin Lymphoma Myeloma Leuk http://www.kidney.de/pget.php?&tw=1&pmid=24355079 #FOAvip Purpose: To identify the MTD of AT9283, an inhibitor of Aurora kinases A and B, in patients with relapsed or refractory leukemias. Other endpoints included pharmacokinetics, safety and tolerability, pharmacodynamics and preliminary evidence of efficacy. Patients and Methods: AT9283 was administered as a continuous 72h infusion every 21 days. Doses were escalated by a standard 3+3 design. After the MTD for the 72h infusion was identified, infusion duration was increased incrementally to 96h and 120h. In total, 48 patients received ?1 cycle of AT9283. Median age was 61 years (range 22?86 years), with 56% men, 75% diagnosed with AML, and 89% having received ?3 (up to 16) prior lines of therapy. Results: 324 mg/m2/72h AT9283 was determined to be the MTD. DLTs were myocardial infarction, hypertension, cardiomyopathy, tumor lysis syndrome, pneumonia and multiorgan failure. Other AT9283-related toxicities (non-DLT) included myelosuppression, predominantly leucopenia and mucositis. Bone marrow blasts decreased ?38% after AT9283 treatment in approximately one-third of patients with relapsed/refractory AML; however, this effect was transient and no objective responses were achieved, despite evidence of aurora kinase B inhibition. Two patients with accelerated phase CML showed evidence of benefit, manifest as a cytogenetic response in one case; one patient completed 6 cycles of treatment. Exposure to AT9283 was generally dose proportional. Conclusion: AT9283 tolerability was strongly dose dependent with reversible myelosuppression predominating at lower doses and events such as cardiovascular toxicities manifesting at higher doses. Clinical trials with AT9283 are ongoing in alternative patient populations. Twit Text FOAVip A Phase I and pharmacodynamic study of AT9283, a small molecule inhibitor of aurora kinases in patients with relapsed/refractory leukemia or myelofibrosis ????Clin Lymphoma Myeloma Leuk http://www.kidney.de/pget.php?&tw=1&pmid=24355079 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24355079 #FOAvip English Wikipedia <ref>{{Cite pmid|24355079}}</ref> A Phase I and pharmacodynamic study of AT9283, a small molecule inhibitor of aurora kinases in patients with relapsed/refractory leukemia or myelofibrosis #MMPMID24355079 Foran J; Ravandi F; Wierda W; Garcia-Manero G; Verstovsek S; Kadia T; Burger J; Yule M; Langford G; Lyons J; Ayrton J; Lock V; Borthakur G; Cortes J; Kantarjian H Clin Lymphoma Myeloma Leuk 2014[Jun]; 14 (3): 223-30 PMID24355079show ga Purpose: To identify the MTD of AT9283, an inhibitor of Aurora kinases A and B, in patients with relapsed or refractory leukemias. Other endpoints included pharmacokinetics, safety and tolerability, pharmacodynamics and preliminary evidence of efficacy. Patients and Methods: AT9283 was administered as a continuous 72h infusion every 21 days. Doses were escalated by a standard 3+3 design. After the MTD for the 72h infusion was identified, infusion duration was increased incrementally to 96h and 120h. In total, 48 patients received ?1 cycle of AT9283. Median age was 61 years (range 22?86 years), with 56% men, 75% diagnosed with AML, and 89% having received ?3 (up to 16) prior lines of therapy. Results: 324 mg/m2/72h AT9283 was determined to be the MTD. DLTs were myocardial infarction, hypertension, cardiomyopathy, tumor lysis syndrome, pneumonia and multiorgan failure. Other AT9283-related toxicities (non-DLT) included myelosuppression, predominantly leucopenia and mucositis. Bone marrow blasts decreased ?38% after AT9283 treatment in approximately one-third of patients with relapsed/refractory AML; however, this effect was transient and no objective responses were achieved, despite evidence of aurora kinase B inhibition. Two patients with accelerated phase CML showed evidence of benefit, manifest as a cytogenetic response in one case; one patient completed 6 cycles of treatment. Exposure to AT9283 was generally dose proportional. Conclusion: AT9283 tolerability was strongly dose dependent with reversible myelosuppression predominating at lower doses and events such as cardiovascular toxicities manifesting at higher doses. Clinical trials with AT9283 are ongoing in alternative patient populations. äA Phase I and pharmacodynamic study of AT9283, a small molecule inhibi(epmc).pdf DeepDyve Pubget Overpricing