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Rollover Study of BMS-354825 in Patients With CML and Ph+ALL

2014-08-27 03:17:19 | BioPortfolio

Summary

To assess the safety of BMS-354825 in subjects with Imatinib resistant or intolerant chronic myelogenous leukemia (CML) and Ph+ acute lymphoblastic leukemia (AL) who are resistant or intolerant to treatment and will continue study drug after completing the previous Phase I/II study (CA180031)

Study Design

Endpoint Classification: Safety Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment

Conditions

Chronic Myelogenous Leukemia

Intervention

dasatinib

Status

Completed

Source

Bristol-Myers Squibb

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:17:19-0400

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Study of BMS-354825 in Subjects With CML Who Are Resistant to or Intolerant of Imatinib or Ph+All in Japan

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Medical and Biotech [MESH] Definitions

Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.

An aberrant form of human CHROMOSOME 22 characterized by translocation of the distal end of chromosome 9 from 9q34, to the long arm of chromosome 22 at 22q11. It is present in the bone marrow cells of 80 to 90 per cent of patients with chronic myelocytic leukemia (LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE).

A pyrimidine and thiazole derived ANTINEOPLASTIC AGENT and PROTEIN KINASE INHIBITOR of BCR-ABL KINASE. It is used in the treatment of patients with CHRONIC MYELOID LEUKEMIA who are resistant or intolerant to IMATINIB.

Retrovirus-associated DNA sequences (abl) originally isolated from the Abelson murine leukemia virus (Ab-MuLV). The proto-oncogene abl (c-abl) codes for a protein that is a member of the tyrosine kinase family. The human c-abl gene is located at 9q34.1 on the long arm of chromosome 9. It is activated by translocation to bcr on chromosome 22 in chronic myelogenous leukemia.

A chronic leukemia characterized by a large number of circulating prolymphocytes. It can arise spontaneously or as a consequence of transformation of CHRONIC LYMPHOCYTIC LEUKEMIA.

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