CLINICAL TRIALS AND OBSERVATIONS A pharmacodynamic study of the FLT3 inhibitor KW-2449 yields insight into the basis for clinical response

نویسندگان

  • Keith W. Pratz
  • Jorge Cortes
  • Gail J. Roboz
  • Niranjan Rao
  • Omotayo Arowojolu
  • Adam Stine
  • Yukimasa Shiotsu
  • Aiko Shudo
  • Shiro Akinaga
  • Donald Small
  • Judith E. Karp
  • Mark Levis
چکیده

1Department of Oncology, Division of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD; 2Department of Leukemia, University of Texas M. D. Anderson Cancer Center, Houston; 3Division of Hematology/Oncology, Weill Medical College of Cornell Medical University and New York Presbyterian Hospital, NY; 4Kyowa Pharmaceutical, Princeton, NJ; and 5Clinical Development Department, Kyowa Hakko Kirin, Tokyo, Japan

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS Single-agent CEP-701, a novel FLT3 inhibitor, shows biologic and clinical activity in patients with relapsed or refractory acute myeloid leukemia

Activating mutations of FMS-like tyrosine kinase 3 (FLT3) are present in approximately 30% of patients with de novo acute myeloid leukemia (AML) and are associated with lower cure rates from standard chemotherapy-based treatment. Targeting the mutation by inhibiting the tyrosine kinase activity of FLT3 is cytotoxic to cell lines and primary AML cells harboring FLT3 mutations. Successful FLT3 in...

متن کامل

CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412

Leukemic cells from 30% of patients with acute myeloid leukemia (AML) have an activating mutation in the FLT3 (fms-like tyrosine kinase) gene, which represents a target for drug therapy. We treated 20 patients, each with mutant FLT3 relapsed/ refractory AML or high-grade myelodysplastic syndrome and not believed to be candidates for chemotherapy, with an FLT3 tyrosine kinase inhibitor, PKC412 (...

متن کامل

CLINICAL TRIALS AND OBSERVATIONS A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy

Activating mutations of FMS-like tyrosine kinase 3 (FLT3) are present in approximately one third of patients with acute myeloid leukemia (AML) and are associated with adverse prognosis. The important role played by FLT3 in the survival and proliferation of blasts, and its overexpression in most patients with AML, make FLT3 an attractive therapeutic target. We undertook a phase 2 trial of the FL...

متن کامل

Clinical and Ultrasonographic Findings of Collagenase Induced Tendinitis in the Horse

Objective- The aim of this study was to assess the clinical and ultrasonographic alterations in the superficial digital flexor tendon (SDFT) of  horses with collagenase-induced tendinitis. Design- Experimental study.   Animals- Five clinically normal adult horse.   Procedures- Two thousand units of collagenase were injected in the center of the SDFT of forelimbs of each horse under ultrasou...

متن کامل

CLINICAL TRIALS AND OBSERVATIONS Mutant nucleophosmin (NPM1) predicts favorable prognosis in younger adults with acute myeloid leukemia and normal cytogenetics: interaction with other gene mutations

To assess the prognostic relevance of mutations in the NPM1 gene encoding a nucleocytoplasmic shuttle protein in younger adults with acute myeloid leukemia (AML) and normal cytogenetics, sequencing of NPM1 exon 12 was performed in diagnostic samples from 300 patients entered into 2 consecutive multicenter trials of the AML Study Group (AMLSG). Treatment included intensive double-induction thera...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2009