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Phase II Trial of Decitabine in Patients With Chronic Myelogenous Leukemia Chronic Phase Who Are Refractory to Imatinib Mesylate (Gleevec)

2014-08-27 03:55:54 | BioPortfolio

Summary

To determine the safety and efficacy of decitabine in patients with Philadelphia chromosome-positive chronic myelogenous leukemia chronic phase that were previously treated with imatinib mesylate (STI 571) and became resistant/refractory or were found to be intolerant to the drug.

Study Design

Allocation: Non-Randomized, Control: Uncontrolled, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment

Conditions

Chronic Myelogenous Leukemia

Intervention

decitabine (5-aza-2'deoxycytidine)

Location

City of Hope Medical Center
Duarte
California
United States
77030

Status

Completed

Source

SuperGen

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:55:54-0400

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Phase II Trial of Decitabine in Patients With Chronic Myelogenous Leukemia Blast Phase Who Are Refractory to Imatinib Mesylate (Gleevec)

To determine the safety and efficacy of decitabine in patients with Philadelphia chromosome-positive chronic myelogenous leukemia blastic phase that were previously treated with imatinib m...

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PubMed Articles [7229 Associated PubMed Articles listed on BioPortfolio]

ZNF224 is a transcriptional repressor of AXL in chronic myeloid leukemia cells.

ZNF224 is a KRAB-zinc finger transcription factor that exerts a key tumor suppressive role in chronic myelogenous leukemia. In this study, we identify the receptor tyrosine kinase Axl as a novel targe...

Novel benzobfurans with anti-microtubule activity upregulate expression of apoptotic genes and arrest leukemia cells in G2/M phase.

Novel derivatives of benzo[b]furan were found to be highly toxic towards human chronic myelogenous (K562), acute myelogenous (HL-60) and acute lymphoblastic (MOLT-4) leukemia cells.

Interferon-α Based Individualized Treatment of a High Risk Chronic Myelogenous Leukemia Patient Harboring T315I Mutation.

T315I mutation is the most common BCR-ABL mutation and confers resistance to all the first and second generation BCR-ABL tyrosine kinases, including nilotinib and dasatinib. We report a high risk chro...

Successful Decitabine Treatment in Unfit, Elderly Patients with Acute Myeloid Leukemia following Chronic Myeloproliferative Neoplasm.

Chronic Myelogenous Leukemia.

The advent of tyrosine kinase inhibitors (TKI) has improved prognosis and outcome of patients with chronic myelogenous leukemia (CML) considerably. In comparison to imatinib, first line use of second ...

Medical and Biotech [MESH] Definitions

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).

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.

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.

An advanced phase of chronic myelogenous leukemia, characterized by a rapid increase in the proportion of immature white blood cells (blasts) in the blood and bone marrow to greater than 30%.

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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