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Imatinib Mesylate and Decitabine in Treating Patients With Chronic Myelogenous Leukemia

2014-08-27 03:55:28 | BioPortfolio

Summary

RATIONALE: Imatinib mesylate may stop the growth of cancer cells by blocking the enzymes necessary for cancer cell growth. Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Giving imatinib mesylate together with decitabine may kill more cancer cells.

PURPOSE: This phase II trial is studying how well giving imatinib mesylate together with decitabine works in treating patients with accelerated or blast phase chronic myelogenous leukemia.

Description

OBJECTIVES:

- Determine the duration of response and response rate in patients with accelerated or blastic phase chronic myelogenous leukemia treated with imatinib mesylate and decitabine.

- Determine the survival rate of patients treated with this regimen.

- Determine the toxicity of this regimen in these patients.

- Determine the effects of this regimen on gene methylation in the leukemic cells of these patients.

OUTLINE: Patients are stratified according to prior exposure to imatinib mesylate (yes vs no).

Patients receive oral imatinib mesylate daily and decitabine IV over 1 hour daily, 5 days per week, for 2 consecutive weeks. Courses repeat every 4-6 weeks in the absence of disease progression or unacceptable toxicity.

PROJECTED ACCRUAL: A total of 20-80 patients (10-40 per stratum) will be accrued for this study within 20 months.

Study Design

Masking: Open Label, Primary Purpose: Treatment

Conditions

Leukemia

Intervention

decitabine, imatinib mesylate

Location

M.D. Anderson Cancer Center at University of Texas
Houston
Texas
United States
77030-4009

Status

Completed

Source

National Cancer Institute (NCI)

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:55:28-0400

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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...

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

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An Extension Study of the Safety and Anti-leukemic Effects of Imatinib Mesylate in Adult Patients With Ph + Leukemia

This extension study will allow for further follow-up of the disease under treatment with imatinib mesylate and allow patients to continue to receive imatinib mesylate.

Study of Hyper-CVAD Plus Imatinib Mesylate for Philadelphia-Positive Acute Lymphocytic Leukemia

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PubMed Articles [1101 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...

Overexpression of Tpl2 is linked to imatinib resistance and activation of MEK-ERK and NF-κB pathways in a model of Chronic Myeloid Leukemia.

The introduction of tyrosine kinase inhibitors (TKI) has transformed chronic myeloid leukemia (CML) into a chronic disease with long-term survival exceeding 85%. However, resistance of CML stem cells ...

PARP1 inhibitor eliminated imatinib-refractory chronic myeloid leukemia cells in bone marrow microenvironment conditions.

Imatinib resistance due to a novel and rare class of mutation at position S348 (1043nt C→A) of Bcr/Abl gene in a chronic myeloid leukemia patient.

Hyaluronated Imatinib Liposomes with Hybrid approach to Target CD44 and P-gp Overexpressing MDR Cancer: An In-vitro, In-vivo and Mechanistic Investigation.

Multi Drug Resistance (MDR) of cancer cells is a constant threat to the clinically used drugs as well as new drug development. In present, work we aimed to assess in-vitro as well as in-vivo efficacy ...

Medical and Biotech [MESH] Definitions

A tyrosine kinase inhibitor and ANTINEOPLASTIC AGENT that inhibits the BCR-ABL kinase created by chromosome rearrangements in CHRONIC MYELOID LEUKEMIA and ACUTE LYMPHOBLASTIC LEUKEMIA, as well as PDG-derived tyrosine kinases that are overexpressed in gastrointestinal stromal tumors.

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.

A replication-defective strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) capable of transforming lymphoid cells and producing a rapidly progressing lymphoid leukemia after superinfection with FRIEND MURINE LEUKEMIA VIRUS; MOLONEY MURINE LEUKEMIA VIRUS; or RAUSCHER VIRUS.

A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) producing leukemia of the reticulum-cell type with massive infiltration of liver, spleen, and bone marrow. It infects DBA/2 and Swiss mice.

A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. It also infects rats and newborn hamsters. It is apparently transmitted to embryos in utero and to newborns through mother's milk.

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