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[Title] Extramedullary hematopoiesis in the axillary lymph node in a patient with an accelerated phase of chronic myeloid leukemia.

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(PMID = 27265110.001).

[ISSN] 1300-7777

[Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology

[ISO-abbreviation] Turk J Haematol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Turkey

   

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[Title] A comparison of donor lymphocyte infusions or imatinib mesylate for patients with chronic myelogenous leukemia who have relapsed after allogeneic stem cell transplantation.

Imatinib mesylate is highly effective in relapsed chronic myelogenous leukemia (CML) after allogeneic hematopoetic stem cell transplantation (HSCT).

The outcome of CML patients transplanted at our center who had received only imatinib for relapse after HSCT was compared with that of patients treated with donor lymphocyte infusions (DLI).

Imatinib therapy resulted in a higher incidence of relapse and inferior leukemia-free survival (p=0.006 and p=0.016, respectively).

[MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Salvage Therapy

[MeSH-minor] Adult. Benzamides. Biomarkers, Tumor / biosynthesis. Disease-Free Survival. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / biosynthesis. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase / surgery. Leukemia, Myeloid, Chronic-Phase / surgery. Living Donors. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Transplantation, Homologous. Treatment Outcome

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(PMID = 16627251.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Comparative Study; Evaluation Studies; Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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The chimeric BCR-ABL gene, originated by the Philadelphia chromosome, encodes a fusion protein, BCR-ABL, bearing unregulated tyrosine kinase activity, the pivotal pathogenetic step of chronic myeloid leukemia (CML).

Imatinib, an inhibitor of the BCR-ABL tyrosine kinase, significantly improves the outcome of patients with CML.

Although the majority of CML patients are responsive to imatinib, a subset of patients loses the response and some progress to accelerated- or blast-phase CML.

The understanding of mechanisms of imatinib resistance has led to the development of novel BCR-ABL inhibitors; among these, dasatinib emerged as the most promising, being approximately 300-fold more potent than imatinib; it also inhibits SRC family kinases.

Preliminary data, after the introduction of dasatinib in clinical trials, in patients with CML, suggest that this drug is safe and well tolerated; furthermore, the majority of patients with imatinib-resistant disease achieved objective responses, although the durability of responses remains to be defined.

The preclinical data concerning its activity on several human solid tumor lines widen new opportunities for their use outside CML.

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(PMID = 17591830.001).

[ISSN] 0923-7534

[Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology

[ISO-abbreviation] Ann. Oncol.

[Language] ENG

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib

[Number-of-references] 30

   

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[Title] Nilotinib is superior to imatinib as first-line therapy of chronic myeloid leukemia: the ENESTnd study.

Nilotinib (Tasigna(®)) is a more potent BCR-ABL inhibitor than imatinib and was designed to overcome imatinib's deficiencies.

Nilotinib has significant efficacy in patients with chronic myeloid leukemia (CML) in chronic phase, accelerated phase and blastic phase, following imatinib failure.

Based on the results of the Evaluating Nilotinib Efficacy and Safety in Clinical Trials-Newly Diagnosed Patients (ENESTnd) study, the US FDA has granted accelerated approval of nilotinib for the treatment of adult patients with newly diagnosed Philadelphia chromosome-positive CML in chronic phase.

Nilotinib, a designer agent built on the imatinib scaffold, has proven superior to its template agent by every significant surrogate marker we use in monitoring CML.

Nilotinib's clinical superiority over imatinib, as demonstrated by the ENESTnd study, has established it as an agent that we believe is a significant further step towards the cure of CML.

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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(PMID = 21091142.001).

[ISSN] 1747-4094

[Journal-full-title] Expert review of hematology

[ISO-abbreviation] Expert Rev Hematol

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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[Title] Hematopoietic cell transplantation from HLA-identical sibling donors after low-dose radiation-based conditioning for treatment of CML.

A total of 24 patients (median age 58; range, 27-71 years) with chronic myeloid leukemia (CML) in first chronic (CP1) (n=14), second chronic (n=4), or accelerated phase (n=6) who were not candidates for conventional hematopoietic cell transplantation (HCT), received nonmyeloablative HCT from HLA-matched siblings a median of 28.5 (range, 11-271) months after diagnosis.

The 2-year estimate of chronic GVHD was 32%.

This study shows encouraging remission rates for patients with CML not eligible for conventional allografting.

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(PMID = 15800667.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / CA78902; United States / NCI NIH HHS / CA / CA49605; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / P01 CA078902

[Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine

   

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[Title] Safety and efficacy of an indigenous recombinant interferon-alpha-2b in patients with chronic myelogenous leukaemia: results of a multicentre trial from India.

BACKGROUND: Compared to hydroxyurea, treatment with interferon-alpha (IFN-alpha) is known to prolong survival in patients with chronic phase of chronic myelogenous leukaemia (CML) and was considered as first-line therapy till recently.

We conducted a multicentre trial using an indigenous recombinant IFN-alpha-2b to evaluate its efficacy and toxicity in chronic phase CML.

METHODS: Between September 2000 and August 2001, patients with chronic phase CML were recruited within 8 weeks of diagnosis at 7 centres in India.

All patients were given the study drug in a dose of 5 million units daily subcutaneously.

Nineteen patients had progression (blast crisis n=15, accelerated phase n=4) while on treatment.

Currently, 95 patients are alive, 91 in the chronic phase and 4 in the accelerated phase.

Four patients were lost to follow up and all 15 patients with blast crisis died of progressive disease at a median Interval of 6.5 months (range 1-15 months).

CONCLUSION: This study confirms the efficacy of the indigenous recombinant IFN-alpha-2b in chronic phase CML.

[MeSH-major] Antineoplastic Agents / therapeutic use. Interferon-alpha / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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[ErratumIn] Natl Med J India. 2005 May-Jun;18(3):130

(PMID = 15981440.001).

[ISSN] 0970-258X

[Journal-full-title] The National medical journal of India

[ISO-abbreviation] Natl Med J India

[Language] eng

[Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] India

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b

   

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[Title] Early intervention during imatinib therapy in patients with newly diagnosed chronic-phase chronic myeloid leukemia: a study of the Spanish PETHEMA group.

BACKGROUND: Despite the favorable results of imatinib front line in chronic-phase chronic myeloid leukemia there is room for improvement.

DESIGN AND METHODS: Early intervention during imatinib therapy was undertaken in 210 adults with chronic-phase chronic myeloid leukemia less than three months from diagnosis (Sokal high risk: 16%).

RESULTS: Seventy-two percent of patients started imatinib within one month from diagnosis.

At five years, survival was 97.5%, survival free from accelerated/blastic phase 94.3%, failure free survival 82.5%, and event free survival (including permanent imatinib discontinuation) 71.5%.

[MeSH-major] Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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[Cites] Eur J Haematol. 2004 Oct;73(4):243-50 [15347310.001]

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(PMID = 20220063.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00390897

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] Italy

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

[Other-IDs] NLM/ PMC2913080

   

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[Title] Chronic myeloid leukemia blast crisis arises from progenitors.

Chronic myeloid leukemia (CML) progresses through three distinct clinical stages: chronic phase, accelerated phase, and blast crisis.

The progression to accelerated phase and blast crisis is driven by activation of oncogenes, inactivation of tumor suppressor genes, and/or amplification of the BCR-ABL fusion gene, which causes the chronic phase of the disease.

Here, I develop a simple mathematical model of CML blast crisis to investigate whether blasts arise from leukemic stem cells or more differentiated leukemic cells.

Therefore, CML blasts are likely to arise from leukemic progenitors.

[MeSH-major] Blast Crisis / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplastic Stem Cells / pathology

[MeSH-minor] Benzamides. Disease Progression. Humans. Imatinib Mesylate. Models, Immunological. Mutation. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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(PMID = 17218393.001).

[ISSN] 1066-5099

[Journal-full-title] Stem cells (Dayton, Ohio)

[ISO-abbreviation] Stem Cells

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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Diagnoses included myelodysplastic syndrome (MDS; n = 35), chronic myeloid leukemia (CML; n = 8), acute myeloid leukemia (AML; n = 6), and other (n = 3).

Grade 3 to 4 acute graft-versus-host disease (GVHD) occurred in 20% of patients, and chronic extensive GVHD was described in 53% of patients.

Four of six patients with CML in chronic or accelerated phase are alive at a median of 6.9 years (range, 4.1 to 9.1 years) after transplantation.

None of the patients with AML, CML in blast crisis, or other diagnoses have survived.

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(PMID = 15824415.001).

[ISSN] 0732-183X

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA78902; United States / NHLBI NIH HHS / HL / HL 36444; United States / NCI NIH HHS / CA / T32 CA009515-20; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / T32 CA009515; United States / NCI NIH HHS / CA / P01 CA1802; United States / NCI NIH HHS / CA / P01 CA078902

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

   

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[Title] Summary of 615 patients of chronic myeloid leukemia in Shanghai from 2001 to 2006.

BACKGROUND: To retrospectively review the incidence, treatment efficacy, we followed up newly diagnosed chronic myelogenous leukemia (CML) patients residing in Shanghai during 2001-2006.

CML mainly afflicted those aged 40-60 years old and was slightly more frequent in males than females.

More than 85% of the patients were in chronic phase (CP) when diagnosed.

With the median follow-up of 18 months, imatinib treatment induced 92.2% complete hematologic responses, and 64.3% complete cytogenetic responses among CML-CP patients.

Meanwhile, in the imatinib group, all response rates of patients in CP were significantly greater than that in accelerated or blastic crisis phase.

As the first-line regime for CML, imatinib was less administered in Shanghai before, but has received considerable development and great responses since 2003.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. China. Disease-Free Survival. Female. Humans. Imatinib Mesylate. Incidence. Male. Middle Aged. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Retrospective Studies. Treatment Outcome

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(PMID = 20199658.001).

[ISSN] 1756-9966

[Journal-full-title] Journal of experimental & clinical cancer research : CR

[ISO-abbreviation] J. Exp. Clin. Cancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

[Other-IDs] NLM/ PMC2844373

   

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[Title] Clinical outcomes and direct hospital costs of reduced-intensity allogeneic transplantation in chronic myeloid leukemia.

A reduced-intensity conditioning allogeneic stem cell transplantation was given to 19 patients (aged 15-59 years) in the first chronic phase and one patient in the accelerated phase with chronic myeloid leukemia (CML) after a regimen consisting of fludarabine (Flu), busulfan (Bu) and ATG Fresenius.

The incidence of acute and chronic graft-versus-host disease (GvHD) was 55 and 75%, respectively.

Flu+Bu+ATG is a low-toxicity regimen for patients with CML.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / economics. Hospital Costs / statistics & numerical data. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Transplantation Conditioning

[MeSH-minor] Adolescent. Adult. Antilymphocyte Serum / administration & dosage. Busulfan / administration & dosage. Czech Republic. Female. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Myeloablative Agonists / administration & dosage. Philadelphia Chromosome. Retrospective Studies. Survival Analysis. Transplantation, Homologous / economics. Transplantation, Homologous / methods. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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(PMID = 16980996.001).

[ISSN] 0268-3369

[Journal-full-title] Bone marrow transplantation

[ISO-abbreviation] Bone Marrow Transplant.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Myeloablative Agonists; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine

   

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[Title] Decreased expression level of SH2 domain-containing protein tyrosine phosphatase-1 (Shp1) is associated with progression of chronic myeloid leukaemia.

Chronic myeloid leukaemia (CML) is characterized by t(9;22)(q34;q11) and the aberrant expression of the fusion protein Bcr-Abl that leads to constitutive activation of c-Abl kinase.

Bcr-Abl plays a major role in the development and progression of CML through chronic, accelerated, and blast phases.

The interaction between Bcr-Abl and other oncogenic molecules has been extensively documented.

Nonetheless, negative regulatory mechanisms of Bcr-Abl are not completely defined.

In the present study, we demonstrate that Shp1 levels are markedly decreased in advanced stage CML patients compared with those in chronic phase.

Furthermore, we did not detect mutations in the Shp1 gene in CML cell lines or patient samples.

These data suggest that the decrease in Shp1 in advanced stage CML patients is due to post-transcriptional modifications.

Our findings suggest that the decrease in Shp1 expression levels plays a role in the progression of CML.

Also, the decrease in Shp1 and subsequently its inhibitory effect on Bcr-Abl could provide an explanation for imatinib resistance seen in advanced stage CML patients.

[MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Neoplasm Proteins / metabolism. Protein Tyrosine Phosphatase, Non-Receptor Type 6 / metabolism

[MeSH-minor] Adult. Aged. DNA Methylation. DNA Mutational Analysis / methods. DNA, Complementary / genetics. DNA, Neoplasm / genetics. Disease Progression. Female. Humans. Male. Middle Aged. Protein Phosphatase 1. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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[Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

(PMID = 17503411.001).

[ISSN] 0022-3417

[Journal-full-title] The Journal of pathology

[ISO-abbreviation] J. Pathol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA100067; United States / NCI NIH HHS / CA / CA105771; United States / NCI NIH HHS / CA / CA114395

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6

   

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[Title] Complex chromosomal rearrangements in patients with chronic myeloid leukemia.

During progression of chronic myeloid leukemia (CML) from the chronic to the accelerated phase and/or blast crisis, clonal evolution with nonrandom secondary aberrations such as +8, +Ph, i(17q), +19, -Y, +21, +17, and -7 is frequently observed.

The aim of this study was to determine the chromosomes and chromosomal regions which are involved in CCR during progression of the disease and the frequency of nonrandom changes.

Conventional cytogenetics, FISH, and multicolor FISH (mFISH) were used to study karyotypes of 18 CML patients with CCR ascertained by G-banding.

Precise determination of breakpoints involved in CCR can give new dimension to the understanding of genetic mechanisms which play role in progression of malignant disease.

[MeSH-major] Chromosome Aberrations. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

[MeSH-minor] Adult. Chromosome Banding. Chromosome Breakage / genetics. Chromosomes, Human, Pair 2 / genetics. Female. Fusion Proteins, bcr-abl / genetics. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Philadelphia Chromosome. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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(PMID = 16772117.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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[Title] [Kinetics of proliferation, differentiation and transcription of genes regulating apoptosis in cultured human BCR/ABL+ Ph+-cells].

Ph+, bcr/abl+ cells arise due to t(9,22) chromosome translocation and Ph+ chromosome formation in hematopoietic stem cells.

Ph chromosome, bcr/abl oncogene and Ph+, bcr/abl+ cells themselves are the hallmark of chronic myeloid leukemia.

Under leukemia progression differentiating Ph+, bcr/abl+ cells transform into leukemic malignant cells with differentiation block.

This work was performed to develop a proper cell model allowing us to study functioning of differentiating Ph+, bcr/abl+ cells and their real transformation into malignant cells with block of differentiation.

For this purpose we have investigated kinetics of Ph+, bcr/abl+ cells proliferation, differentiation, cell death and transcription of antiapoptotic genes in cultured 14-day of Ph+ mononuclear cells isolated from peripheral blood of a patient in chronic phase of chronic myeloid leukemia before treatment.

The results obtained revealed that Ph+ cell differentiation proceeded in accord with characteristic scheme of chronic myeloid leukemia in vivo.

Myeloid cells of hematopoietic cell lineage amounted to 3/4 of live Ph+ mononuclear cells undergoing accumulation and subsequent consumption in the course of differentiation.

95% myeloid cells were differentiating Ph+ granulocytes.

The peaks of antiapoptotic bcr/abl gene transcription activity coincided with the observed active proliferation at the beginning and at the end of cultivation.

Cell proliferation, differentiation and apoptosis were noticeably accelerated by growth factor treatment.

Thus, the study of the Ph+ cells cultivation kinetics is rather informative approach to investigation of continuous regulation of cellular and molecular processes in vitro in the case of chronic myeloid leukemia and allows more complete consideration of Ph+, bcr/abl+ cells hematopoiesis.

[MeSH-major] Apoptosis / genetics. Cell Differentiation / genetics. Cell Proliferation. Fusion Proteins, bcr-abl / genetics. Hematopoietic Stem Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Philadelphia Chromosome

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(PMID = 18074781.001).

[ISSN] 0041-3771

[Journal-full-title] Tsitologiia

[ISO-abbreviation] Tsitologiia

[Language] rus

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Russia (Federation)

[Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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[Title] Dasatinib: in chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia.

Dasatinib is a small-molecule inhibitor of multiple tyrosine kinases, including BCR-ABL, SRC, c-KIT, ephrin A receptor and platelet-derived growth factor-beta receptor kinases, at nanomolar concentrations.

In vitro, dasatinib is 325-fold more potent than imatinib against cells expressing wild-type BCR-ABL.

The efficacy and tolerability of oral dasatinib has been established in the START phase II trials in adults with chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph-positive ALL) who were intolerant or resistant to imatinib, and optimal dasatinib dosage regimens were identified in phase III randomized trials.

In patients with chronic phase CML, the major cytogenetic response rate in the START-C trial (median follow-up 15.2 months) was 59% with dasatinib, and in the randomized START-R trial (median follow-up 15 months), was greater with dasatinib than with high-dose imatinib (52% vs 33%).

Major hematologic response rates with dasatinib were 63% in patients with accelerated phase CML (follow-up > or =9 months; START-A trial), 34% in patients with myeloid blast phase CML and 35% in those with lymphoid blast phase CML (follow-up > or =12 months; START-B and START-L trials), and 41% in patients with Ph-positive ALL (follow-up > or =12 months; START-L trial).

Based on phase III results, a once-daily dasatinib regimen is considered optimal in chronic phase CML (starting dosage 100 mg once daily), while a twice-daily regimen continues to be recommended in accelerated phase, myeloid blast phase or lymphoid blast phase CML and Ph-positive ALL (starting dosage 70 mg twice daily).

[MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage

[MeSH-minor] Animals. Controlled Clinical Trials as Topic. Dasatinib. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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(PMID = 18215092.001).

[ISSN] 1173-8804

[Journal-full-title] BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy

[ISO-abbreviation] BioDrugs

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] New Zealand

[Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib

[Number-of-references] 57

   

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[Title] Failure to achieve a major cytogenetic response by 12 months defines inadequate response in patients receiving nilotinib or dasatinib as second or subsequent line therapy for chronic myeloid leukemia.

Projected 1-year progression to hematologic failure, accelerated phase, or blast phase was also significantly different (3% vs 17%, P = .003).

[MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Pyrimidines / administration & dosage. Thiazoles / administration & dosage

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[Cites] Blood. 2001 Nov 15;98(10):3074-81 [11698293.001]

[Cites] Blood. 2003 Jan 15;101(2):441-5 [12393604.001]

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(PMID = 18492956.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA016672

[Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib

[Other-IDs] NLM/ PMC4082324

   

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[Title] Phase II study of all-trans retinoic acid in the accelerated phase or early blastic phase of chronic myeloid leukemia: a study of the Eastern Cooperative Oncology Group (E1993).

The aims of this study were to evaluate the safety and efficacy of all-trans retinoic acid (ATRA) in the treatment of the accelerated and blastic phase of chronic myeloid leukemia (CML) and to evaluate in vitro correlates of biological activity.

ATRA was administered in an intermittent schedule to patients with CML in the accelerated or blastic phases for a 6 week induction period, which was continued if there was evidence of clinical response or stable disease.

Laboratory correlative studies were performed prior to treatment and at intervals during treatment to evaluate effects on maturation and differentiation, and on CML progenitor cell growth by assessment of colony-forming cells (CFC).

ATRA demonstrated clinical and hematological activity in 5 of 18 patients with the accelerated phase of CML, and there was evidence of a biological effect in laboratory studies of 3 of the 5 patients' progenitor cells.

Combination therapy with other differentiating agents may be useful in this disease.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Tretinoin / administration & dosage

[MeSH-minor] Adult. Aged. Blast Crisis. Combined Modality Therapy. Cytogenetic Analysis. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Interferon-alpha / administration & dosage. Interferon-alpha / adverse effects. Male. Middle Aged. Recombinant Proteins. Survival Analysis. Time Factors

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(PMID = 15621827.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA 11083; United States / NCI NIH HHS / CA / CA 14548; United States / NCI NIH HHS / CA / CA 14958; United States / NCI NIH HHS / CA / CA 23318; United States / NCI NIH HHS / CA / CA 66636; United States / NCI NIH HHS / CA / CA21115

[Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.

[Publication-country] England

[Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 5688UTC01R / Tretinoin; 76543-88-9 / interferon alfa-2a

   

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[Title] Circulating heat shock protein 70 and progression in patients with chronic myeloid leukemia.

We evaluated the association of circulating levels of heat shock protein 70 (Hsp70) in plasma with clinical behavior and progression in 139 chronic myeloid leukemia (CML) patients.

Circulating Hsp70 levels did not differ significantly between CML patients in the chronic phase (n=93; median 33.24 ng/mL, range 3.89-128.2 ng/mL) and those in the accelerated/blast phase (n=46; median 26.57 ng/mL, range 4.5-114.7 ng/mL).

However, overall CML patients had significantly higher levels of Hsp70 than healthy subjects (n=95, median 4.17 ng/mL, range 1.75-24.7 ng/mL) (P<0.001).

In chronic phase CML patients, Hsp70 levels above the median were associated with a higher rate of progression to the accelerated/blast phase and a tendency toward shorter survival.

Plasma Hsp70 thus could be a potential marker for predicting disease progression in patients with chronic phase CML.

[MeSH-major] HSP70 Heat-Shock Proteins / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis

[MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Biomarkers / blood. Disease Progression. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase / diagnosis. Leukemia, Myeloid, Chronic-Phase / diagnosis. Middle Aged. Piperazines / therapeutic use. Prognosis. Pyrimidines / therapeutic use. Young Adult

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[CommentIn] Leuk Res. 2009 Feb;33(2):205-6 [18752847.001]

(PMID = 18715642.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA016672

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Benzamides; 0 / Biomarkers; 0 / HSP70 Heat-Shock Proteins; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

[Other-IDs] NLM/ NIHMS593155; NLM/ PMC4163801

   

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[Title] Stem cell regulation and the development of blast crisis in chronic myeloid leukemia: Implications for the outcome of Imatinib treatment and discontinuation.

Chronic myeloid leukemia (CML) is a cancer of the hematopoietic system that is initiated by a single genetic alteration (the BCR-ABL fusion gene or Philadelphia chromosome) and progresses in several phases: during the chronic phase the number of cells grows slowly and the fraction of immature cells is low.

During the accelerated phase and blast crisis, the population of CML cells and the fraction of immature cells rises sharply.

The mechanisms that drive the transition from the chronic phase to blast crisis are not understood, and the requirement of genetic instability and further mutations has been suggested.

Using mathematical models, I describe a theory that can account for the transition from the chronic phase to blast crisis without the need to invoke further mutations.

According to the model, treatment can lead to the low level persistence of CML stem cells without assuming that these cells are less susceptible to drug-mediated activity, and this might explain why disease tends to relapse after treatment discontinuation even in the absence of acquired drug resistance.

Further, the model defines conditions when Imatinib treatment might lead to the eradication of CML, which is relevant in the context of recent data that show absence of relapse as long as two years after treatment cessation.

[MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use

[MeSH-minor] Benzamides. Cell Division / drug effects. Disease Progression. Drug Administration Schedule. Humans. Imatinib Mesylate. Models, Biological. Stem Cells / pathology

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(PMID = 17566666.001).

[ISSN] 0306-9877

[Journal-full-title] Medical hypotheses

[ISO-abbreviation] Med. Hypotheses

[Language] eng

[Publication-type] Journal Article

[Publication-country] Scotland

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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[Title] [Analysis of long-term treatment outcome and related factors in 95 chronic myeloid leukemia patients treated with imatinib].

OBJECTIVE: To investigate the efficacy of imatinib in the treatment of chronic myeloid leukemia (CML) and analyse the treatment outcome and related factors.

METHODS: Ninety five CML patients were treated with imatinib in our hospital from May 2002 to May 2006.

(1) One year after therapy, there were 95.5% of chronic phase (CP) patients achieved complete hematologic response (CHR).

The expected survival at 12-, 24-, 36- and 50-month after imatinib treatment for CP group was (98.1 +/-1.9)%, (87.8 +/- 7.1)%, (81.9 +/- 8.7)% and (81.9 +/- 8.7)%, respectively. (2) Twelve month after therapy, there are 70% of accelerated phase (AP) patients achieve CHR and 10% get MCyR.

Conclusion (1) Imatinib as a primary treatment for CP CML can significantly improve the survival time as compared with that AP or BC patients or with that used in previously treated patients. (2) Imatinib could induce hematologic, even cytogenetic response to a certain extent, in CP or BC patients and prolong the survival time.

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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(PMID = 18512310.001).

[ISSN] 0253-2727

[Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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[Title] Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia.

BACKGROUND: Nilotinib has been shown to be a more potent inhibitor of BCR-ABL than imatinib.

We evaluated the efficacy and safety of nilotinib, as compared with imatinib, in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia (CML) in the chronic phase.

METHODS: In this phase 3, randomized, open-label, multicenter study, we assigned 846 patients with chronic-phase Philadelphia chromosome-positive CML in a 1:1:1 ratio to receive nilotinib (at a dose of either 300 mg or 400 mg twice daily) or imatinib (at a dose of 400 mg once daily).

Patients receiving either the 300-mg dose or the 400-mg dose of nilotinib twice daily had a significant improvement in the time to progression to the accelerated phase or blast crisis, as compared with those receiving imatinib (P=0.01 and P=0.004, respectively).

No patient with progression to the accelerated phase or blast crisis had a major molecular response.

CONCLUSIONS: Nilotinib at a dose of either 300 mg or 400 mg twice daily was superior to imatinib in patients with newly diagnosed chronic-phase Philadelphia chromosome-positive CML. (ClinicalTrials.gov number, NCT00471497. )

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Blast Crisis / prevention & control. Disease Progression. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Kaplan-Meier Estimate. Male. Middle Aged. Young Adult

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[Copyright] 2010 Massachusetts Medical Society

[CommentIn] N Engl J Med. 2010 Jun 17;362(24):2314-5 [20525994.001]

[CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672; author reply 1673-5 [20961253.001]

[CommentIn] Expert Opin Pharmacother. 2011 Jan;12(1):157-63 [21108601.001]

[CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973146.001]

[CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973145.001]

[CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672-3; author reply 1673-5 [20973144.001]

(PMID = 20525993.001).

[ISSN] 1533-4406

[Journal-full-title] The New England journal of medicine

[ISO-abbreviation] N. Engl. J. Med.

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00471497

[Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl

[Investigator] Moiraghi B; Perez M; Greil R; Valent P; Bosly A; Martiat P; Noens L; André M; Verhoef G; Conchon M; Souza C; Nonino A; Hungria V; Zanichelli MA; Colturato V; Forrest D; Lipton JH; Savoie ML; Delage R; Lalancette M; Quintero G; Gomez M; Klamova H; Faber E; Bjerrum OW; Fredriksen H; Vestergaard H; Marcher C; Kamel H; Elzawam H; Porkka K; Remes K; Reiffers J; Guilhot F; Facon T; Tulliez M; Guerci-Bresler AP; Nicolini FE; Charbonnier A; Rea D; Johnson-Ansah A; Legros L; Harousseau JL; Rigal-Huguet F; Escoffre M; Gardembas M; Guyotat D; Cahn JY; Gattermann N; Ottmann O; Niederwieser D; Stegelmann F; Schafhausen P; Brümmendorf T; Duyster J; Blumenstengel K; Scheid C; Kneba M; Kwong YL; Masszi T; Petrini M; Alimena G; Di Raimondo F; Rosti G; Rotoli B; Pane F; Pungolino E; Amadori S; Abruzzese E; Fioritoni G; Lauria F; Bosi A; Martelli M; Rambaldi A; Ferrara F; Nobile F; Gobbi M; Carella AM; Orlandi EM; Leoni P; Tiribelli M; Levis A; Imamura M; Takahashi N; Tsukamoto N; Chiba S; Nagai T; Okamoto S; Miura O; Kurokawa M; Ohnishi K; Toba K; Nakao S; Tomita A; Miyamura K; Hino M; Maeda Y; Kimura A; Kawaguchi T; Miyazaki Y; Nakaseko C; Jinnai I; Matsuda A; Matsumura I; Ishikawa J; Ohyashiki K; Okada M; Usuki K; Kobayashi Y; Ohishi K; Imai K; Miyawaki S; Kanda Y; Park SY; Kim HJ; Sohn SK; Lee KH; Jung CW; Ong TC; Gómez Almaguer D; Kassack J; Ossenkoppele GJ; Gedde-Dahl T; Hjorth-Hansen H; Jedrzejczak W; Dmoszynska A; Starzak-Dwozdz J; Holowiecki J; Kyrcz-Krzemieñ S; Kuliczkowski K; Zaritsky A; Turkina A; Pospelova T; Goh YT; Koh LP; Demitrovicova L; Mistrik M; Ruff P; Louw V; Dreosti LM; Novitzky N; Cohen G; Cervantes F; Cañizo C; de Paz R; del Castillo S; Perez Encinas M; Sanz Alonso M; Marin F; Pérez-López R; Hernandez Boluda J; Echeveste Gutierrez MA; Odriozola J; Herrera P; Steegman JL; Conde E; Lopez P; Giraldo P; Boque C; Heredia B; Font AJ; Rodriguez RF; Rodriguez MJ; Batlle J; Stenke L; Lehmann S; Wadenvik H; Simonsson B; Markevärn B; Själander A; Richter J; Bjoreman M; Eriksson KM; Chalandon Y; Shih LY; Yao M; Wang MC; Jootar S; Bunworasate U; Ulkü B; Haznedar R; Undar B; Sahin B; Marin D; Smith G; Byrne J; Holyoake T; Kalaycio M; Akard L; Heaney M; Al-Janadi A; Goldberg S; Powell B; Harker WG; Shea T; Gingrich R; Glass J; Paquette R; Siegrist C; Woodson M; Fehrenbacher L; Koh H; Flinn I; Arrowsmith E; Ervin T; Guerra M; Wallach H; Berry W; Burke J; Edenfield W; Guzley G; Davis J; Richards D; Schlossman D; Kolibaba K; Alemany C; Savin M; Robbins G; Lopez J; Goldman JM; Camm J; Schiffer CA; Sargent DJ

   

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[Title] [Quantification of prame gene transcript in chronic myeloid leukemia].

This study was purposed to analyze the expression level of preferentially expressed antigen of melanoma (prame) transcript in the patients with chronic myeloid leukemia (CML) and explore its clinical significance.

Real-time quantitative PCR (RQ-PCR) assay was used to detect the level of prame gene transcript in the bone marrow samples from 30 patients with CML and 15 patients with iron deficiency anemia (IDA).

The results showed that CML patients had significantly higher prame mRNA level (0% - 772.25%, median 8.28%) than IDA cases (0% - 1.46%, median 0.19%) (p < 0.001).

The level of prame gene transcript was significantly correlated with that of bcr-abl fusion gene transcript (r = 0.708, p < 0.001) in CML patients.

Furthermore, 6 patients in blastic crisis (BC) and accelerated phase (AP) had significantly higher prame gene transcript than that of 24 cases in chronic phase (CP) (p = 0.007).

In 2 CML patients with sequential samples, prame gene transcript increased in AP and BC, compared with in CP, and was consistent with the altering tendency of bcr-abl transcript.

It is concluded that the level of prame gene transcript increases in CML which associates with the progression of the disease, prame gene transcript level can be used for monitoring the disease state.

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(PMID = 20723287.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / PRAME protein, human

   

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[Title] A report of early cytogenetic response to imatinib in two patients with chronic myeloid leukemia at accelerated phase and carrying the e19a2 BCR-ABL transcript.

The development of imatinib is a milestone in the treatment of chronic myeloid leukemia (CML), and its therapeutic effect has been extensively investigated in CML patients carrying M-bcr and m-bcr BCR/ABL fusion transcripts.

However, our knowledge about its therapeutic effect on CML patients with rare BCR/ABL fusion transcripts e19a2(u-bcr) remains sparse.

Here, we report on two CML patients with e19a2 transcripts who rapidly progressed into the accelerated phase, further confirming the possibility that 19a2 might be associated with an unfavorable prognosis in CML.

[MeSH-major] Gene Expression Regulation, Leukemic / drug effects. Genes, abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

[MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Benzamides. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Cytogenetic Analysis. Disease Progression. Exons. Female. Humans. Imatinib Mesylate. Male. Middle Aged. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Time Factors. Translocation, Genetic. Treatment Outcome

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(PMID = 17656262.001).

[ISSN] 1873-4456

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate

   

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[Title] Characterization of cancer stem cells in chronic myeloid leukaemia.

CML (chronic myeloid leukaemia) is a myeloproliferative disease that originates in an HSC (haemopoietic stem cell) as a result of the t(9;22) translocation, giving rise to the Ph (Philadelphia chromosome) and bcr-abl oncoprotein.

The disease starts in CP (chronic phase), but as a result of genomic instability, it progresses over time to accelerated phase and then to BC (blast crisis), becoming increasingly resistant to therapy. bcr-abl is a constitutively active tyrosine kinase that has been targeted by TKIs (tyrosine kinase inhibitors), including IM (imatinib mesylate), nilotinib and dasatinib.

We have developed various flow cytometry techniques to enable us to isolate candidate CML stem cells from CP patients at diagnosis that efflux Hoechst dye, express CD34, lack CD38 and are cytokine-non-responsive in culture over periods of up to 12 days in growth factors.

These stem cells have been shown to regenerate bcr-abl-positive haemopoiesis in immunocompromised mice upon transplantation.

We previously demonstrated that IM was antiproliferative for CML stem cells but did not induce apoptosis.

Clinical experience now confirms that IM may not target CML stem cells in vivo with few patients achieving complete molecular remission and relapse occurring rapidly upon drug withdrawal.

Our recent efforts have focused on understanding why CML stem cells are resistant to IM and on trying to find novel ways to induce apoptosis of this population.

We have shown that CML stem cells express very high levels of functional wild-type bcr-abl; no kinase domain mutations have been detected in the stem cell population.

Dasatinib, a more potent multitargeted TKI than IM, inhibits bcr-abl activity more efficiently than IM but still does not induce apoptosis of the stem cell population.

Most recently, we have tested a number of novel drug combinations and found that FTIs (farnesyl transferase inhibitors) have activity against CML.

BMS-214662 is the most effective of these and induces apoptosis of phenotypically and functionally defined CML stem cells in vitro, as a single agent and in combination with IM or dasatinib.

The effect against CML stem cells is selective with little effect on normal stem cells.

The drug is also effective against BC CML stem cells and equally effective against wild-type and mutant bcr-abl, including the most resistant mutant T315I.

Our intentions are now to explore the activity of BMS-214662 in other cancer stem cell disorders and to move this preclinical work to a clinical trial combining dasatinib with BMS-214662 in CML.

[MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplastic Stem Cells / cytology

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(PMID = 17956348.001).

[ISSN] 0300-5127

[Journal-full-title] Biochemical Society transactions

[ISO-abbreviation] Biochem. Soc. Trans.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / 7-cyano-2,3,4,5-tetrahydro-1-(1H-imidazol-4-ylmethyl)-3-(phenylmethyl)-4-(2-thienylsulfonyl)-1H-1,4-benzodiazepine; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Imidazoles; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 12794-10-4 / Benzodiazepines; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib

[Number-of-references] 16

   

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[Title] Myeloperoxidase cytochemical negativity: an unexpected but intrinsic property of blasts of all phases of chronic myeloid leukemia.

Myeloperoxidase (MPO) cytochemical activity, recognized as a very important hallmark of myeloblasts, is generally negative in chronic myeloid leukemia (CML) blast crisis (BC).

Because this finding is unexpected, being not in keeping with the myeloproliferative nature of CML, we tried to ascertain if MPO cytochemical negativity could be an intrinsic property of blasts of CML and hence present in the preblastic phases as well.

Myeloperoxidase cytochemistry of peripheral blood blasts in 161 cases of CML, including 103 in chronic phase (CP) and 29 each in accelerated phase (AP) and BC, was assessed and compared with that of 30 cases of acute myeloid leukemia, AML-M2.

Blasts of 97 (94.2%) of 103 cases of CP, 28 (96.6%) of 29 cases of AP, and 22 (75.9%) of 29 cases of BC were negative for MPO (<3% MPO-positive blasts).

Compared with the strong MPO positivity, both in terms of intensity and proportion, in the AML-M2 cases, the positivity in the CML cases was generally weak and was seen in a small number of blasts (5-15%), except in one case of BC with 20% positive blasts.

Absence or, at times, weak MPO cytochemical activity is an intrinsic property of blasts of all phases of CML, and use of the term myeloblast in CML should be understood to refer to a cell with this property.

This also explains why MPO cytochemistry, despite its high reputation as a myeloid-lineage marker, generally does not help in CML BC.

CML BC should therefore be considered as a possible diagnosis along with acute lymphoblastic leukemia, AML-M0, AML-M7, etc., in the setting of MPO-negative blasts.

Similarity between MPO expression pattern in CML, i.e., negative in blasts and positive in the more mature cells, and that during maturation of normal myeloid series of cells shows the deranged myelopoiesis of CML to be undisturbed at least with respect to MPO expression.

[MeSH-major] Biomarkers, Tumor / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Neoplasm Proteins / biosynthesis. Peroxidase / biosynthesis

[MeSH-minor] Female. Gene Expression Regulation, Enzymologic. Histocytochemistry. Humans. Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / pathology. Leukocytes / enzymology. Leukocytes / pathology. Male. Predictive Value of Tests

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(PMID = 15990995.001).

[ISSN] 0939-5555

[Journal-full-title] Annals of hematology

[ISO-abbreviation] Ann. Hematol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 1.11.1.7 / Peroxidase

   

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[Title] [Successful induction of complete cytogenetic response with low-dose imatinib mesylate in an accelerated phase chronic myelogenous leukemia patient who developed severe bone marrow aplasia following standard-dose imatinib mesylate therapy].

Bone marrow appearance was consistent with CML-AP, and t (9;22) (q34;q11) was detected on karyotyping.

Bone marrow biopsy showed severe bone marrow aplasia with no morphological evidence of disease progression.

This case also suggests that low-dose imatinib would be tolerable and effective for some CML patients who are intolerant of a standard dose of imatinib.

[MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Bone Marrow / drug effects. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / administration & dosage. Piperazines / adverse effects. Pyrimidines / administration & dosage. Pyrimidines / adverse effects

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(PMID = 20332700.001).

[ISSN] 0385-0684

[Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy

[ISO-abbreviation] Gan To Kagaku Ryoho

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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[Title] [Methylation status of id4 gene promoter in patients with chronic myeloid leukemia].

This study was purposed to investigate the methylation status of id4 gene promoter in patients with chronic myeloid leukemia (CML) and explore the relationship between methylation of the id4 gene and progress of CML.

The methylation status of id4 gene in 48 chronic myeloid leukemia patients and 10 healthy individuals was detected by using methylation-specific polymerase chain reaction (MS-PCR).

The results showed that id4 gene was unmethylated in bone marrow samples from both healthy individuals and CML patients in chronic phase (CP).

The rate of id4 gene methylation in both CML patients in accelerated phase (AP) and blast crisis (BC) was 66%, and was higher than those of CML patients in CP phase.

In one CML patient who received a serial observations, the status of id4 was unmethylated in CP, but it was methylated in AP and BC phase.

It is concluded that the id4 gene in CML patients is unmethylated in CP, while it is methylated in AP or BC.

The detection of id4 gene methylation status may be useful for monitoring disease advance in CML and may be used as a marker of disease progression in CML.

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(PMID = 21176338.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / DNA Primers; 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Proteins

   

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[Title] Correlation between trough imatinib plasma concentration and clinical response in chronic myeloid leukemia.

[MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacokinetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Piperazines / pharmacokinetics. Pyrimidines / administration & dosage. Pyrimidines / pharmacokinetics

[MeSH-minor] Benzamides. Cytogenetic Analysis. Drug Monitoring. Female. Fusion Proteins, bcr-abl / analysis. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Accelerated Phase. Leukemia, Myeloid, Chronic-Phase. Male. Middle Aged. Polymerase Chain Reaction. Risk Assessment

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[CommentOn] Leuk Res. 2009 Feb;33(2):271-5 [18762338.001]

(PMID = 19395027.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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[Title] Current role of stem cell transplantation in chronic myeloid leukaemia.

Haematopoietic stem cell transplantation (HSCT) has seen considerable ups and downs in its role for patients with chronic myeloid leukaemia (CML).

It has provided the first proof of the principle for cure and has confirmed the concept of successful immunotherapy of leukaemia.

CML became the most frequent indication for an allogeneic HSCT worldwide.

The frequency of HSCT declined rapidly when the specific BCR/ABL tyrosine kinase inhibitor (TKI) imatinib appeared.

Risk assessment of both, disease risk and transplant risk, has become standard.

Allogeneic HSCT remains the first-line approach for patients with CML in accelerated phase or blast crisis.

It is the best option for all patients with failed second-line TKIs, with mutations T315I or with progressive disease.

[MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Protein Kinase Inhibitors / therapeutic use

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(PMID = 19959092.001).

[ISSN] 1532-1924

[Journal-full-title] Best practice & research. Clinical haematology

[ISO-abbreviation] Best Pract Res Clin Haematol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Protein Kinase Inhibitors

[Number-of-references] 74

   

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[Title] Novel treatment strategies for chronic myeloid leukemia.

PURPOSE: Despite dramatic advances in the treatment of chronic myeloid leukemia (CML), resistance to therapeutic agents has emerged as a significant treatment dilemma.

Mutations of the BCR-ABL kinase domain, a common mechanism of resistance to imatinib in CML, are discussed.

SUMMARY: Several new targeted kinase inhibitors have reached clinical trials and have proved to be efficacious in halting the oncogenic activity of most BCR-ABL mutants.

Dasatinib is 300 times more potent than imatinib at BCR-ABL inhibition, has few side effects, and inhibits the SRC family kinases.

Nilotinib inhibits BCR-ABL at 20-50 times more potency than imatinib.

Both agents were highly effective in treating chronic phase CML but were less effective at treating accelerated phase CML in early phase clinical trials.

CONCLUSION: The new kinase inhibitors, dasatinib and nilotinib, are emerging as plausible therapeutic options for the treatment of imatinib-refractory CML.

[MeSH-major] Drug Therapy / methods. Immunotherapy, Active / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy

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(PMID = 17106016.001).

[ISSN] 1079-2082

[Journal-full-title] American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists

[ISO-abbreviation] Am J Health Syst Pharm

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Protein Kinase Inhibitors

[Number-of-references] 23

   

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[Title] Epigenetic heterochromatin markers distinguish terminally differentiated leukocytes from incompletely differentiated leukemia cells in human blood.

In order to identify the chromatin regulatory factors associated with incomplete cell differentiation and impaired chromatin condensation in hematological malignancies, we examined expression levels of major heterochromatin proteins in normal blood cells and cells derived from a number of chronic and acute myeloid leukemia patients exhibiting different degrees of differentiation.

RESULTS: While the major epigenetic heterochromatin factor, histone H3 methylated at lysine 9, is present in all cell types, its main counterparts, nonhistone proteins, heterochromatin proteins 1 (HP1) alpha, beta, and gamma, are dramatically reduced in peripheral blood leukocytes of normal donors and chronic myeloid leukemia patients, but are substantially increased in the blood of accelerated phase and blast crisis patients.

HP1 and MNEI levels inversely correlate in a number of normal and leukemia myeloid cells and show strikingly opposite coordinated changes during differentiation of U937 cell line induced by retinoic acid.

CONCLUSIONS: Our results suggest that repression of HP1 and accumulation of MNEI are linked to terminal cell differentiation and that their levels may be monitored in blood cell populations to detect transitions in cell differentiation associated with leukemia progression and treatment.

[MeSH-major] Cell Differentiation. Epigenesis, Genetic. Heterochromatin / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukocytes / metabolism

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(PMID = 16569592.001).

[ISSN] 0301-472X

[Journal-full-title] Experimental hematology

[ISO-abbreviation] Exp. Hematol.

[Language] eng

[Grant] United States / NIGMS NIH HHS / GM / GM-59118

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Chromosomal Proteins, Non-Histone; 0 / Heterochromatin; 0 / Histones; 0 / Neoplasm Proteins; 0 / Proteins; 0 / Serpins; 147416-07-7 / SERPINB1 protein, human; 5688UTC01R / Tretinoin

   

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[Title] Targeted chronic myeloid leukemia therapy: seeking a cure.

BACKGROUND: Chronic myeloid leukemia (CML) is a hematopoietic stem cell cancer driven by the BCR-ABL fusion protein that arises from the translocation of chromosomes 9 and 22.

The disease begins with an indolent chronic phase (CP) that can last for 3 to 5 years.

If untreated, it progresses into accelerated phase (AP) and within a year, blast phase (BP).

Survival at this point is less than 1 year. during disease progression, mutations and the Philadelphia chromosome (Ph) appear (a process called clonal evolution).

The only known curative therapy for CML is allogeneic bone marrow transplant (BMT).

Thus, effective therapy that maintains the patient with CML in CP with minimal toxicity is the goal for treatment of modern therapies.

Because the preeminent mutation driving CML is BCr-ABL, therapies targeting BCR-ABL are the logical choice for disease-specific therapy.

BCR-ABL inhibitors, such as imatinib, are proof that targeting specific genetic mutations associated with cancer yields a high degree of efficacy with minimal toxicity.

OBJECTIVE: This review will outline the evolution of therapy in CML.

SUMMARY: The discovery of the Ph and, subsequently, the identification of BCr-ABL revolutionized the treatment of CML.

Cytoreductive chemotherapy, such as busulfan and hydroxyurea, was a mainstay of therapy to control white blood cell (WBC) counts; however, it did not modify the progression of the disease to AP and BP.

The overall survival with CML ranges from 45 to 58 months in patients treated with cytoreductive therapy only.

Allogeneic BMT is the only known curative therapy for CML; however, treatment-related mortality from infection, bleeding, and graft versus host disease, age, and the availability of suitable donors limits its widespread use.

Imatinib functions by competing with adenosine triphosphate (ATP) for binding to the BCr-ABL tyrosine kinase.

In the absence of ATP, BCR-ABL is not able to activate downstream effector tyrosine kinase molecules that drive wBC proliferation.

Toxicities associated with this therapy are low. response in patients with advanced CML is less pronounced than in CP and is shorter lived, with less than 30% of patients achieving a CHR.

For patients with CML in BP, the only viable therapy is to attempt a temporary reduction in disease burden with a salvage chemotherapy regimen, such as VAC (etoposide, cytarabine, and carboplatin).

Imatinib resistance may develop at any time and inevitably leads to disease progression. resistance is usually caused by mutations within BCr-ABL, decreasing the affinity of imatinib binding. next-generation kinase inhibitors are focused on the ability to inhibit these mutated forms of BCR-ABL.

CONCLUSION: For the majority of patients with CML in CP, the standard of care is to maintain the patient in CP with imatinib therapy.

Allogeneic BMT continues to be an option for those who cannot tolerate imatinib or when CML progresses on imatinib therapy.

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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(PMID = 17970609.001).

[ISSN] 1083-4087

[Journal-full-title] Journal of managed care pharmacy : JMCP

[ISO-abbreviation] J Manag Care Pharm

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

[Number-of-references] 14

   

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[Title] BCR-ABL mutation testing to predict response to tyrosine kinase inhibitors in patients with chronic myeloid leukemia.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of chronic myeloid leukemia (CML).

Although randomized evidence demonstrates that imatinib (a commercially available TKI) prolongs event-free survival in patients with CML, some patients develop imatinib intolerance or resistance.

In addition, imatinib is less effective in patients who have progressed to more advanced disease stages, such as accelerated phase and blastic phase CML.

For these reasons, 2nd generation TKIs that can inhibit the BCR-ABL protein more effectively or target additional disease mechanisms have been developed.

Resistance to TKI treatment is thought to be mediated through various mechanisms, the most common of which is BCR-ABL1 mutations.

Testing for mutations in BCR-ABL1 may predict lack of response to imatinib or may inform the choice between alternative TKIs.

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(PMID = 21188137.001).

[ISSN] 2157-3999

[Journal-full-title] PLoS currents

[ISO-abbreviation] PLoS Curr

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Other-IDs] NLM/ PMC3001986.1

   

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[Title] Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia.

Patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia (CML-AP) have very limited therapeutic options.

Nilotinib is a highly selective BCR-ABL tyrosine kinase inhibitor.

This phase 2 trial was designed to characterize the efficacy and safety of nilotinib (400 mg twice daily) in this patient population with hematologic response (HR) as primary efficacy endpoint.

In conclusion, nilotinib is an effective and well-tolerated treatment in imatinib-resistant and -intolerant CML-AP.

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use

[MeSH-minor] Adult. Aged. Benzamides. Blood Cell Count. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Resistance. Female. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Male. Middle Aged. Mutation. Safety

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(PMID = 18048643.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00384228

[Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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[Title] [A clinical study of treating 120 cases of adult chronic myelocytic leukemia with imatinib mesylate].

OBJECTIVE: To analyze and evaluate the clinical efficacy and safety of imatinib mesylate (IM) as a tyrosine kinase inhibitor on Ph-positive or BCR/ABL positive chronic myelogenous leukemia (CML).

METHODS: 120 patients diagnosed as CML with positive Ph chromosome were treated with IM 400 mg/d for CML in chronic phase (CP) (n = 90) or 600 mg/d for CML in accelerated or blastic phase (AP or BP) (n = 30) once daily.

Hematological, cytogenetic and molecular effects of IM on the disease process of these patients were evaluated with blood and marrow cells morphology examination, G-band conventional cytogenetics analysis for Ph chromosome and PCR assay for BCR/ABL gene.

(1) In CML-CP patients, after a follow-up of 9 ( range 3-42) months, cumulative complete hematological response (CHR), complete cytogenetic response (CCyR) and complete molecular response (CMR) rates were 73.3%, 66.7% and 54.4%, which was not influenced by prior treatment of interferon.

CMR was better when time from diagnosis to treatment with IM was < or = 6 months (P < 0.05).

It is significant that the time to first CHR and time to first CCyR were related with the time to first CCyR and the time to first negative BCR/ ABL, respectively (both P < 0.05), while there was no relation between the time to first CHR and the time to first negative BCR/ABL (P > 0.05). (2) CHR, CCyR and CMR rates of the patients with progressive course (AP and BP) were 43.3%, 25.9% and 25.0%, respectively.

CONCLUSION: IM can lead to considerable hematological, cytogenetic and molecular response rates in CML, especially CML-CP patients, with minor tolerable side effects.

[MeSH-major] Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

[MeSH-minor] Adolescent. Adult. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Benzamides. Female. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Philadelphia Chromosome. Retrospective Studies. Treatment Outcome

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(PMID = 18478917.001).

[ISSN] 0578-1426

[Journal-full-title] Zhonghua nei ke za zhi

[ISO-abbreviation] Zhonghua Nei Ke Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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[Title] The derivation of diagnostic markers of chronic myeloid leukemia progression from microarray data.

Currently, limited molecular markers exist that can determine where in the spectrum of chronic myeloid leukemia (CML) progression an individual patient falls at diagnosis.

Gene expression profiles can predict disease and prognosis, but most widely used microarray analytical methods yield lengthy gene candidate lists that are difficult to apply clinically.

Consequently, we applied a probabilistic method called Bayesian model averaging (BMA) to a large CML microarray dataset.

BMA identified 6 genes (NOB1, DDX47, IGSF2, LTB4R, SCARB1, and SLC25A3) that discriminated chronic phase (CP) from blast crisis (BC) CML.

In CML, phase labels divide disease progression into discrete states.

In validation studies of 88 patients, the 6-gene signature discriminated early CP from late CP, accelerated phase, and BC.

This distinction between early and late CP is not possible with current classifications, which are based on known duration of disease.

Because therapeutic outcomes are so closely tied to disease phase, these probabilities can be used to determine a risk-based treatment strategy at diagnosis.

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(PMID = 19654405.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NICHD NIH HHS / HD / R01 HD054511; United States / NCI NIH HHS / CA / K25 CA106988-05; United States / NIAID NIH HHS / AI / U54 AI057141; United States / NCI NIH HHS / CA / CA18029; United States / NHLBI NIH HHS / HL / P50HL073996; United States / NCI NIH HHS / CA / R01 CA140371; United States / NCRR NIH HHS / RR / R24 RR021863; United States / NCI NIH HHS / CA / K25CA106988; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCRR NIH HHS / RR / R24RR021863-01A1; United States / NIGMS NIH HHS / GM / R01 GM084163-01A1; United States / PHS HHS / / R01HDO54511-01A1; United States / NIGMS NIH HHS / GM / GM084163-01A1; United States / NIGMS NIH HHS / GM / R01 GM084163; United States / NIDCR NIH HHS / DE / R01DE012212-06; United States / NHLBI NIH HHS / HL / P50 HL073996; United States / NIAID NIH HHS / AI / U54AI057141; United States / NIGMS NIH HHS / GM / R01 GM084163-02; None / None / / K25 CA106988-05; United States / NCRR NIH HHS / RR / UL1 RR025014; None / None / / R01 GM084163-02; United States / NIDCR NIH HHS / DE / R01 DE012212; United States / NCRR NIH HHS / RR / UL1RR025014-01; United States / NIGMS NIH HHS / GM / R01GM084163-01A1; United States / NICHD NIH HHS / HD / R24 HD042828; United States / NCI NIH HHS / CA / K25 CA106988

[Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins

[Other-IDs] NLM/ PMC2759651

   

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[Title] [Chronic myeloid leukemia onset with marked thrombocythemia].

This study was aimed to investigate the clinical, pathological and biological features of a special case of chronic myeloid leukemia (CML) with marked thrombocythemic onset.

The morphological changes of cells were analyzed by using bone marrow smear and biopsy; Ph chromosome, a specific marker of CML, was assayed by conventional chromosomal analysis and fluorescence in situ hybridization, bcr/abl fusion gene was detected by reverse transcription-polymerase chain reaction.

The results indicated that CML mimicked essential thrombocythemia (ET) at presentation was relatively rare and might be misdiagnosed as ET, bone marrow smear and biopsy revealed, marked thrombocytosis and moderate leukocytosis; RT-PCR, FISH and conventional chromosomal analysis demonstrated the existence of Ph chromosome and bcr/abl fusion gene.

This special CML could progress into accelerated phase or blast crisis.

Patients diagnosed as Ph+ ET might progress into CML and showed a high tendency to myelofibrosis and blastic transformation.

It is concluded that the value of routine cytogenetical and molecular biological analysis in diagnosis for potential CML cases, which mimicked ET as in this presentation, is very distinctive, and the importance is magnified by the recent availability of imatinib, a specific inhibitor of the bcr/abl tyrosine kinase produced by the Philadelphia chromosome.

Every case of "ET" should be tested for the Philadelphia chromosome and bcr/abl transcript.

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(PMID = 16638190.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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[Title] Outcomes of reduced-intensity transplantation for chronic myeloid leukemia: an analysis of prognostic factors from the Chronic Leukemia Working Party of the EBMT.

This study reports outcomes of allogeneic hematopoietic stem cell transplantation with reduced-intensity conditioning (RIC) in 186 patients with chronic myeloid leukemia (CML) from the European Group for Blood and Marrow Transplantation (EBMT).

The median age was 50 years, and 64% were in first chronic phase (CP1), CP2 13%, accelerated phase 17%, and blast crises 6%.

Acute graft-versus-host disease (GvHD) grade II to IV occurred in 32% and chronic GvHD in 43% (extensive in 24%).

ATG was associated with a lower incidence of chronic GvHD (cGvHD).

Adverse OS was associated with advanced disease (relative risk [RR], 3.4).

PFS was inferior in advanced disease (RR, 2.7) and a trend to improved outcomes with Fd/Bu/ATG (RR, 0.58).

RIC allografts are feasible in CML in first or second CP.

[MeSH-major] Bone Marrow Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery

[MeSH-minor] Adolescent. Adult. Aged. Benzamides. Disease Progression. Europe. Female. Graft vs Host Disease. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / therapeutic use. Prognosis. Pyrimidines / therapeutic use. Risk Factors. Societies, Scientific. Survival Rate. Transplantation Conditioning. Treatment Outcome

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(PMID = 15998838.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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[Title] Global target profile of the kinase inhibitor bosutinib in primary chronic myeloid leukemia cells.

The detailed molecular mechanism of action of second-generation BCR-ABL tyrosine kinase inhibitors, including perturbed targets and pathways, should contribute to rationalized therapy in chronic myeloid leukemia (CML) or in other affected diseases.

Here, we characterized the target profile of the dual SRC/ABL inhibitor bosutinib employing a two-tiered approach using chemical proteomics to identify natural binders in whole cell lysates of primary CML and K562 cells in parallel to in vitro kinase assays against a large recombinant kinase panel.

The combined strategy resulted in a global survey of bosutinib targets comprised of over 45 novel tyrosine and serine/threonine kinases.

We have found clear differences in the target patterns of bosutinib in primary CML cells versus the K562 cell line.

Finally, bosutinib is the first kinase inhibitor shown to target CAMK2G, recently implicated in myeloid leukemia cell proliferation.

[MeSH-major] Aniline Compounds / pharmacology. Antineoplastic Agents / pharmacology. K562 Cells / drug effects. Leukemia, Myeloid, Accelerated Phase / enzymology. Neoplasm Proteins / antagonists & inhibitors. Nitriles / pharmacology. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Quinolines / pharmacology

[MeSH-minor] Calcium-Calmodulin-Dependent Protein Kinase Type 2 / antagonists & inhibitors. Dasatinib. Drug Delivery Systems. Drug Screening Assays, Antitumor. Fusion Proteins, bcr-abl / antagonists & inhibitors. Gene Expression Profiling. Humans. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / enzymology. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Nerve Tissue Proteins / antagonists & inhibitors. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-abl / antagonists & inhibitors. Pyrimidines / pharmacology. Signal Transduction / drug effects. Substrate Specificity. Thiazoles / pharmacology. src-Family Kinases / antagonists & inhibitors

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(PMID = 19039322.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Aniline Compounds; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / Nitriles; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Quinolines; 0 / Thiazoles; 5018V4AEZ0 / bosutinib; EC 2.7.1.- / STK24 protein, human; EC 2.7.1.- / Tec protein-tyrosine kinase; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.17 / CAMK2G protein, human; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; RBZ1571X5H / Dasatinib

   

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[Title] Synergy between proteasome inhibitors and imatinib mesylate in chronic myeloid leukemia.

BACKGROUND: Resistance developed by leukemic cells, unsatisfactory efficacy on patients with chronic myeloid leukemia (CML) at accelerated and blastic phases, and potential cardiotoxity, have been limitations for imatinib mesylate (IM) in treating CML.

METHODS AND FINDINGS: We tested the therapeutic efficacies as well as adverse effects of low dose IM in combination with proteasome inhibitor, Bortezomib (BOR) or proteasome inhibitor I (PSI), in two CML murine models, and investigated possible mechanisms of action on CML cells.

Consistently, BOR and PSI enhanced IM-induced inhibition of long-term clonogenic activity and short-term cell growth of CML stem/progenitor cells, and potentiated IM-caused inhibition of proliferation and induction of apoptosis of BCR-ABL+ cells.

While exerting suppressive effects on BCR-ABL, E2F1, and beta-catenin, IM/BOR and IM/PSI inhibited proteasomal degradation of protein phosphatase 2A (PP2A), leading to a re-activation of this important negative regulator of BCR-ABL.

CONCLUSION: These data suggest that combined use of tyrosine kinase inhibitor and proteasome inhibitor might be helpful for optimizing CML treatment.

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protease Inhibitors / therapeutic use. Proteasome Inhibitors. Pyrimidines / therapeutic use

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(PMID = 19606213.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

[Other-IDs] NLM/ PMC2705802

   

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[Title] Dasatinib and nilotinib in imatinib-resistant Philadelphia-positive chronic myelogenous leukemia: a 'head-to-head comparison'.

Imatinib has revolutionized the treatment of patients with chronic myeloid leukemia (CML).

Dasatinib, approved in 2006 for the treatment of patients with CML in all phases who experience imatinib resistance or intolerance, has displayed significant efficacy, with a 2-year follow-up showing durable hematologic and cytogenetic responses, as well as prolonged progression-free and overall survival.

Nilotinib was approved in 2007 for the treatment of patients with CML in chronic phase or CML in accelerated phase, resistant or intolerant to prior therapy including imatinib, based on strong efficacy as well as a favorable safety profile.

[MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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(PMID = 20302388.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib

[Number-of-references] 30

   

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[Title] Grading of marrow fibrosis in chronic myeloid leukemia--a comprehensive approach.

In the course of Chronic myeloid leukemia (CML), appearance of increased number of blasts may herald evolution of accelerated phase as well as onset of marrow fibrosis (MF) thereby necessitating the need to perform trephine biopsy for correct diagnosis and appropriate treatment.

We performed 50 bone marrow (BM) trephine biopsies in patients of CML in order to assess the incidence and degree of MF.

A positive correlation was found between increasing grades of MF and number of megakaryocytes in the BM.

[MeSH-major] Bone Marrow Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Primary Myelofibrosis / pathology

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(PMID = 16761746.001).

[ISSN] 0377-4929

[Journal-full-title] Indian journal of pathology & microbiology

[ISO-abbreviation] Indian J Pathol Microbiol

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

   

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[Title] Association of the GSTP1 gene (Ile105Val) polymorphism with chronic myeloid leukemia.

We here assessed the impact of the GSTP1 codon 105 polymorphism in chronic myeloid leukemia (CML) development and therapy response.

Two hundred and sixty patients with CML and 248 healthy, age and sex matched controls were included in the study of associations with patient characteristics and treatment outcome.

The GSTP1 Ile105Val polymorphism was significantly associated with CML development (?2 = 9.57; df = 2; p = 0.0084).

With respect to clinical phase, CML patients in advanced phase (accelerated and blast crisis) had higher frequency of heterozygous (Ile/Val) genotype (47.62%) compared to chronic phase (36.5%).

Further 54.5% of patients in blast crisis carried valine allele as compared to those in chronic phase (36.5%).

Hence the present study suggests that GSTP1 Ile105Val polymorphism with reduced GSTP1 enzyme activity might influence CML development, progression and response rates.

[MeSH-major] Glutathione S-Transferase pi / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Polymorphism, Single Nucleotide / genetics

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(PMID = 20843134.001).

[ISSN] 2476-762X

[Journal-full-title] Asian Pacific journal of cancer prevention : APJCP

[ISO-abbreviation] Asian Pac. J. Cancer Prev.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Thailand

[Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.7.10.1 / Protein-Tyrosine Kinases

   

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[Title] Dasatinib in chronic myeloid leukemia: a review.

Deregulated BCR-ABL tyrosine kinase (TK) activity is the molecular marker for chronic myeloid leukemia (CML), which provides an identifiable target for developing therapeutic agents.

Imatinib mesylate, a BCR-ABL TK inhibitor, is the frontline therapy for CML.

In newly diagnosed patients with chronic phase CML, the rate of resistance to imatinib at 4 years was up to 20%, increasing to 70% to 90% for patients in the accelerated/blastic phase.

Dasatinib is well tolerated and has broad efficacy, resulting in durable responses in patients with any BCR-ABL mutation except for T3151 and mutations in codon 317 - most commonly F317L - including mutations that were highly resistant to imatinib, such as L248, Y253, E255, F359, and H396.

Dasatinib is recommended for CML in chronic, blastic or accelerated phase that is resistant or intolerant to imatinib.

Dasatinib was approved by the FDA at 100 mg once daily as the starting dose in patients with chronic phase CML and at 70 mg twice daily in patients with accelerated or blastic phase CML.

Other second-generation TKIs with activity in CML include nilotinib, bosutinib and INNO 406.

New molecules, such as the inhibitor of Aurora family serine-threonine kinases, MK0457, which has antileukemic activity in CML associated with a T315I mutation, are being investigated.

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(PMID = 19536317.001).

[ISSN] 1176-6336

[Journal-full-title] Therapeutics and clinical risk management

[ISO-abbreviation] Ther Clin Risk Manag

[Language] eng

[Publication-type] Journal Article

[Publication-country] New Zealand

[Other-IDs] NLM/ PMC2697539

[Keywords] NOTNLM ; BCR-ABL / chronic myeloid leukemia / dasatininb / tyrosine kinase inhibitor

   

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[Title] Favorable long-term follow-up results over 6 years for response, survival, and safety with imatinib mesylate therapy in chronic-phase chronic myeloid leukemia after failure of interferon-alpha treatment.

Imatinib mesylate, a targeted inhibitor of BCR-ABL tyrosine kinase, is the standard of care for chronic myeloid leukemia (CML).

A phase 2 trial of imatinib in late chronic-phase (CP) CML after interferon-alpha (IFNalpha) failure enrolled 532 patients, 454 with a confirmed diagnosis of CP CML.

Median time from diagnosis was 34 months; median duration of imatinib treatment was 65 months.

Estimated rates of freedom from progression to accelerated phase (AP) and blastic phase (BP) and overall survival at 6 years were 61% and 76%, respectively.

Imatinib continues to be an effective and safe therapy for patients with CP CML after failure of IFN.

[MeSH-major] Drug-Related Side Effects and Adverse Reactions. Interferon-alpha / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / pathology. Piperazines / adverse effects. Piperazines / therapeutic use. Pyrimidines / adverse effects. Pyrimidines / therapeutic use. Salvage Therapy

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Disease Progression. Follow-Up Studies. Humans. Imatinib Mesylate. Middle Aged. Survival Rate. Time Factors. Treatment Outcome

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[ErratumIn] Blood. 2008 Jul 15;112(2):452. Gambacorti, Carlo [corrected to Gambacorti-Passerini, Carlo]

(PMID = 17932248.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study

[Publication-country] United States

[Chemical-registry-number] 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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[Title] HLA-matched unrelated donor hematopoietic cell transplantation after nonmyeloablative conditioning for patients with chronic myeloid leukemia.

We evaluated 10/10 HLA antigen-matched unrelated hematopoietic cell transplantation (HCT) after nonmyeloablative conditioning with fludarabine 3 x 30 mg/m2 and 2 Gy of total body irradiation as treatment for patients with chronic myeloid leukemia who were ineligible for conventional HCT.

Data from 21 consecutive patients in first chronic phase (CP1; n = 12), accelerated phase (AP; n = 5), second CP (CP2; n = 3), and blast crisis (n = 1) were analyzed.

The patient who underwent transplantation in blast crisis died on day 21 (too early to be evaluated for engraftment) from progressive disease.

Graft rejections were nonfatal in all cases and were followed by autologous reconstitution with persistence or recurrence of chronic myeloid leukemia.

Two of the remaining 4 patients died of nonrelapse causes in complete (n = 1) or major (n = 1) cytogenetic remissions, and 2 died of progressive disease.

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(PMID = 15812392.001).

[ISSN] 1083-8791

[Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

[ISO-abbreviation] Biol. Blood Marrow Transplant.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / CA78902; United States / NCI NIH HHS / CA / CA92058; United States / NCI NIH HHS / CA / CA49605; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / P01 CA078902

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / HLA Antigens

   

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[Title] Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy.

Due to the end replication problem, each cell division results in a loss of telomeric repeats in normal somatic cells.

However, elevated telomerase activity has also been reported in the majority of solid tumours as well as in acute and chronic leukaemia.

Chronic myeloid leukaemia (CML) serves as a model disease to study telomere biology in clonal myeloproliferative disorders.

In CML, telomere shortening correlates with disease stage, duration of chronic phase (CP), prognosis measured by the Hasford risk score and the response to disease-modifying therapeutics such as the tyrosine kinase inhibitor Imatinib.

In addition, telomerase activity (TA) is already increased in CP CML and further upregulated with disease progression to accelerated phase and blast crisis (BC).

Here, we review the current state of knowledge of the role of telomere and telomerase biology in CML and discuss the possible impact of novel treatment approaches.

[MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Telomerase / antagonists & inhibitors. Telomerase / metabolism. Telomere / pathology

[MeSH-minor] Animals. Disease Progression. Humans

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(PMID = 19569255.001).

[ISSN] 1099-1069

[Journal-full-title] Hematological oncology

[ISO-abbreviation] Hematol Oncol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] EC 2.7.7.49 / Telomerase

[Number-of-references] 67

   

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[Title] Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice.

The BCR-ABL inhibitor imatinib revolutionized the treatment of chronic myeloid leukemia (CML).

The mechanisms underlying resistance are multifactorial and may include mutations in the kinase domain of BCR-ABL, increased production of BCR-ABL, or activation of BCR-ABL-independent pathways.

Two second-line BCR-ABL inhibitors are now approved for treatment of patients with resistance or intolerance to imatinib.

Dasatinib is a dual BCR-ABL/Src-family kinase (SFK) inhibitor approved for patients with imatinib-resistant and -intolerant CML in any phase and Ph+ ALL.

Nilotinib, an analogue of imatinib, is approved for the treatment of imatinib-resistant or -intolerant patients with chronic or accelerated phase CML.

Both agents have shown significant clinical activity in patients with imatinib-resistant or -intolerant CML, and their approval represents a major advancement in the treatment options available.

The presence of certain disease characteristics (e.g. specific BCR-ABL mutations) or patient comorbidities may facilitate more effective treatment.

[MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mutation. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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(PMID = 20038231.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / src-Family Kinases; RBZ1571X5H / Dasatinib

   

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[Title] HLA-mismatched/haploidentical hematopoietic stem cell transplantation without in vitro T cell depletion for chronic myeloid leukemia: improved outcomes in patients in accelerated phase and blast crisis phase.

BACKGROUND: Allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains the only proven curative therapy for chronic myeloid leukemia (CML), but lack of human leukocyte antigen (HLA)-matched sibling or unrelated donors has restricted its application.

AIM: To evaluate the outcomes of CML patients who underwent haploidentical allo-HSCT.

RESULTS: Our data showed that the cumulative incidence of acute graft-versus-host disease (GVHD) was 64.52%, and grade III-IV was 26.45%, 61.79% had chronic GVHD, and 28.93% had extensive chronic GVHD.

Probability of 1-year and 4-year leukemia-free survival was similar in chronic phase (CP) 1, CP2/CR2, accelerated phase, and blast crisis patients.

Probability of 4-year overall survival varied as 76.5% (CP1), 85.7% (CP2/CR2), 73.3% (accelerated phase), and 61.5% (blast crisis).

Multivariate analysis indicated that factors affecting transplantation outcomes were HLA-B+DR mismatches versus others for II-III acute GVHD and III-IV acute GVHD, the stage of disease at transplantation for relapse, and the time from diagnosis to transplantation for leukemia-free survival, overall survival, and transplantation-related mortality.

In our protocol, survival of HSCT for advanced CML was similar to stable stage.

[MeSH-major] Blast Crisis / therapy. Hematopoietic Stem Cell Transplantation / methods. Histocompatibility Testing. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy

[MeSH-minor] Adolescent. Adult. Child. Directed Tissue Donation. Female. Graft Survival. Graft vs Host Disease. Humans. Male. Middle Aged. Opportunistic Infections. Survival Analysis. Transplantation Conditioning. Transplantation, Homologous. Young Adult

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(PMID = 18608121.001).

[ISSN] 0785-3890

[Journal-full-title] Annals of medicine

[ISO-abbreviation] Ann. Med.

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Sweden

   

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[Title] Intermittent exposure of primitive quiescent chronic myeloid leukemia cells to granulocyte-colony stimulating factor in vitro promotes their elimination by imatinib mesylate.

PURPOSE: Primitive quiescent chronic myeloid leukemia (CML) cells are biologically resistant to imatinib mesylate, an inhibitor of the p210(BCR-ABL) kinase.

EXPERIMENTAL DESIGN: CD34(+) leukemic cells were isolated from six newly diagnosed chronic phase CML patients and cultured for 12 days in serum-free medium with or without G-CSF and/or imatinib mesylate present either continuously or intermittently (three cycles of G-CSF for 0, 1, or 4 days +/- imatinib mesylate for 0, 3, or 4 days).

RESULTS: Intermittent but not continuous exposure to G-CSF significantly accelerated the disappearance in vitro of initially quiescent CD34(+) CML cells.

CONCLUSION: Intermittent exposure to G-CSF can enhance the effect of imatinib mesylate on CML cells by specifically targeting the primitive quiescent leukemic elements.

A protocol for treating chronic-phase CML patients with imatinib mesylate that incorporates intermittent G-CSF exposure may offer a novel strategy for obtaining improved responses in vivo.

[MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow Cells / drug effects. Granulocyte Colony-Stimulating Factor / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

[MeSH-minor] Benzamides. Blast Crisis. Culture Media, Serum-Free / pharmacology. Drug Combinations. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. In Vitro Techniques. Protein-Tyrosine Kinases / antagonists & inhibitors. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Granulocyte Colony-Stimulating Factor / genetics. Receptors, Granulocyte Colony-Stimulating Factor / metabolism. Tumor Cells, Cultured

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(PMID = 16428509.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] eng

[Grant] United Kingdom / Medical Research Council / / G84/6317; United Kingdom / Chief Scientist Office / / SCD/04

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Culture Media, Serum-Free; 0 / Drug Combinations; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl