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1
accelerated phase chronic myeloid leukemia 2005:2010[pubdate] *count=100
247 results
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Items 1 to 100 of about 247
1.
Quintás-Cardama A, Kantarjian H, Garcia-Manero G, O'Brien S, Faderl S, Estrov Z, Giles F, Murgo A, Ladie N, Verstovsek S, Cortes J:
Phase I/II study of subcutaneous homoharringtonine in patients with chronic myeloid leukemia who have failed prior therapy.
Cancer
; 2007 Jan 15;109(2):248-55
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[Title]
Phase
I/II study of subcutaneous homoharringtonine in patients with
chronic myeloid leukemia
who have failed prior therapy.
Intravenous HHT has demonstrated activity in patients with
chronic myeloid leukemia
(
CML
) after failure with interferon.
METHODS: A
Phase
I study was completed of subcutaneous (s.c.
) HHT in patients with
CML in
accelerated
or blast phases and demonstrated efficacy and good tolerance at the same doses used by intravenous (i.v.) administration.
The cohort was then expanded to treated at the MTD to include patients in late
chronic phase
CML
after imatinib failure.
The 2 patients with
BCR
-ABL kinase domain mutations at the start of therapy with HHT had a CG response and in both instances the mutations became undetectable.
CONCLUSIONS: Subcutaneous HHT is well tolerated and may have clinical activity in patients with
CML
after imatinib failure.
[MeSH-major]
Harringtonines / therapeutic use.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy
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[ErratumIn]
Cancer. 2007 Jun 15;109(12):2625. Dosage error in article text
(PMID = 17154172.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; 0 / Benzamides; 0 / Harringtonines; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 6FG8041S5B / homoharringtonine; 8A1O1M485B / Imatinib Mesylate
2.
Huang M, Hu Z, Chang W, Ou D, Zhou J, Zhang Y:
The growth factor independence-1 (Gfi1) is overexpressed in chronic myelogenous leukemia.
Acta Haematol
; 2010;123(1):1-5
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[Title]
The growth factor independence-1 (Gfi1) is overexpressed in
chronic
myelogenous
leukemia
.
The activation of ABL tyrosine kinase
in BCR
/ABL-
positive
chronic
myelogenous
leukemia
(
CML
) leads to a diversity of biological changes related to the pathogenesis of the
disease
.
In CML
patients, we determined the expression of growth factor independence-1 (Gfi1), a transcription repressor with weak oncogenic activity.
Our data demonstrated that the Gfi1 mRNA level in both the mononuclear cells and purified CD34(+) cells from
CML
were significantly higher as measured by quantitative real-time PCR.
Using flow cytometry and Western blot, we also showed that the Gfi1 protein content was increased
in CML
CD34(+) cells.
The expression of Gfi1 was correlated with
BCR
/ABL significantly.
Gfi1 may be implicated in the pathogenesis of
CML
and can serve as a potential target for the management of the
disease
.
[MeSH-major]
DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ metabolism. Transcription Factors / genetics. Transcription Factors / metabolism
[MeSH-minor]
Antigens, CD34 / metabolism. Base Sequence. Benzamides. Blast Crisis / genetics. Blast Crisis / metabolism. DNA Primers / genetics. Gene Expression. Genes, abl. Hematopoietic Stem Cells / immunology. Hematopoietic Stem Cells / metabolism. Humans. Imatinib Mesylate.
Leukemia
,
Myeloid
,
Accelerated Phase
/ genetics.
Leukemia
,
Myeloid
,
Accelerated Phase
/ metabolism.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ genetics.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ metabolism. Neoplastic Stem Cells / immunology. Neoplastic Stem Cells / metabolism. Piperazines / therapeutic use. Pyrimidines / therapeutic use. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Stem Cell Transplantation
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[Copyright]
Copyright (c) 2009 S. Karger AG, Basel.
(PMID = 19887785.001).
[ISSN]
1421-9662
[Journal-full-title]
Acta haematologica
[ISO-abbreviation]
Acta Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Benzamides; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / GFI1 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate
3.
Irfan SM, Bhurgri Y:
Clinico-pathological features and outcomes in chronic phase chronic myeloid leukemia patients treated with hydroxyurea.
Asian Pac J Cancer Prev
; 2009 Oct-Dec;10(4):591-4
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[Title]
Clinico-pathological features and outcomes in
chronic phase chronic myeloid leukemia
patients treated with hydroxyurea.
OBJECTIVE: To study the clinico-pathological features and major outcomes in patients with
chronic myeloid leukemia
,
chronic phase
, treated with hydroxyurea.
The median age at
diagnosis
was 39 years (range 11 to 66 years).
The median delay
in diagnosis
was 156 days (range 30 to 360 days).
LDH values above 1,000 ug/l were observed in 38 (21.5%) cases and creatinine above 1.5 ug/
l in
21 (12%) cases.
All patients tested, were
positive
for Philadelphia chromosome and
bcr
-abl transcripts.
At the close of the study,
disease
advancement was observed in 76 (43.2%) cases, of which 35 (20%) transformed to acute
leukemia
.
One hundred and two (58.4%) patients were in
chronic phase
, 22 (12.5%) in
accelerated phase
and 19 (10.7%) in blast crisis.
Disease
progression remained the major cause of death and was seen in 29 (16.4%) patients.
CONCLUSION: In the study population,
CML
was observed
in a
younger age group with significant delay in definitive
diagnosis
.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Hydroxyurea / therapeutic use.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ drug therapy.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ pathology
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(PMID = 19827875.001).
[ISSN]
2476-762X
[Journal-full-title]
Asian Pacific journal of cancer prevention : APJCP
[ISO-abbreviation]
Asian Pac. J. Cancer Prev.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
Thailand
[Chemical-registry-number]
0 / Antineoplastic Agents; X6Q56QN5QC / Hydroxyurea
Advertisement
4.
Breccia M, Muscaritoli M, Cannella L, Stefanizzi C, Frustaci A, Alimena G:
Fasting glucose improvement under dasatinib treatment in an accelerated phase chronic myeloid leukemia patient unresponsive to imatinib and nilotinib.
Leuk Res
; 2008 Oct;32(10):1626-8
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[Title]
Fasting glucose improvement under dasatinib treatment in an
accelerated phase chronic myeloid leukemia
patient unresponsive to imatinib and nilotinib.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Blood Glucose / analysis. Diabetes Complications / drug therapy.
Leukemia
,
Myeloid
,
Accelerated Phase
/ drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
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(PMID = 18321570.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Letter
[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 / Blood Glucose; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
5.
Ahmed R, Naqi N, Hussain I, Khattak BK, Nadeem M, Iqbal J:
Presentating phases of chronic myeloid leukaemia.
J Coll Physicians Surg Pak
; 2009 Aug;19(8):469-72
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[Title]
Presentating phases of
chronic myeloid
leukaemia
.
OBJECTIVE: To determine the frequency of three phases of
chronic myeloid
leukaemia
at first presentation.
METHODOLOGY: Forty-five patients of either gender with
Chronic Myeloid
Leukaemia
(
CML
) at their first presentation in outpatient department were included in the study by consecutive sampling technique.
Each
phase
was defined on the basis of World Health Organization (WHO) criteria.
The pattern of presentation revealed 35 (77.8%) in
Chronic Phase
(CP), 7 (15.5%) in
Accelerated Phase
(AP) and 3 (6.7%) in Blast Crisis (BC).
CONCLUSION:
CML
presented at a younger age in the
chronic phase
.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/
diagnosis
.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Philadelphia Chromosome
[MeSH-minor]
Adolescent. Adult. Age Factors. Aged. Blast Crisis /
diagnosis
. Blast Crisis / epidemiology. Blast Crisis / genetics. Blast Crisis / pathology. Female. Humans.
Leukemia
,
Myeloid
,
Accelerated Phase
/
diagnosis
.
Leukemia
,
Myeloid
,
Accelerated Phase
/ epidemiology.
Leukemia
,
Myeloid
,
Accelerated Phase
/ genetics.
Leukemia
,
Myeloid
,
Accelerated Phase
/ pathology.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/
diagnosis
.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ epidemiology.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ genetics.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ pathology. Male. Middle Aged. Pakistan / epidemiology. Risk Assessment. Risk Factors. Sex Factors. Young Adult
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(PMID = 19651006.001).
[ISSN]
1022-386X
[Journal-full-title]
Journal of the College of Physicians and Surgeons--Pakistan : JCPSP
[ISO-abbreviation]
J Coll Physicians Surg Pak
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Pakistan
6.
Kaygusuz G, Kuzu I, Akpınar E, Uysal A:
Extramedullary hematopoiesis in the axillary lymph node in a patient with an accelerated phase of chronic myeloid leukemia.
Turk J Haematol
; 2009 Mar 5;26(1):40-1
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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
7.
Weisser M, Tischer J, Schnittger S, Schoch C, Ledderose G, Kolb HJ:
A comparison of donor lymphocyte infusions or imatinib mesylate for patients with chronic myelogenous leukemia who have relapsed after allogeneic stem cell transplantation.
Haematologica
; 2006 May;91(5):663-6
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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
8.
Olivieri A, Manzione L:
Dasatinib: a new step in molecular target therapy.
Ann Oncol
; 2007 Jun;18 Suppl 6:vi42-6
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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
9.
Giles FJ, Rosti G, Beris P, Clark RE, le Coutre P, Mahon FX, Steegmann JL, Valent P, Saglio G:
Nilotinib is superior to imatinib as first-line therapy of chronic myeloid leukemia: the ENESTnd study.
Expert Rev Hematol
; 2010 Dec;3(6):665-73
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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
10.
Kerbauy FR, Storb R, Hegenbart U, Gooley T, Shizuru J, Al-Ali HK, Radich JP, Maloney DG, Agura E, Bruno B, Epner EM, Chauncey TR, Blume KG, Niederwieser D, Sandmaier BM:
Hematopoietic cell transplantation from HLA-identical sibling donors after low-dose radiation-based conditioning for treatment of CML.
Leukemia
; 2005 Jun;19(6):990-7
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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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.
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VIDARABINE
.
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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
11.
Kumar L, Gangadharan VP, Rao DR, Saikia T, Shah S, Malhotra H, Bapsy PP, Singh K, Rao R:
Safety and efficacy of an indigenous recombinant interferon-alpha-2b in patients with chronic myelogenous leukaemia: results of a multicentre trial from India.
Natl Med J India
; 2005 Mar-Apr;18(2):66-70
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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
12.
Cervantes F, López-Garrido P, Montero MI, Jonte F, Martínez J, Hernández-Boluda JC, Calbacho M, Sureda A, Pérez-Rus G, Nieto JB, Pérez-López C, Román-Gómez J, González M, Pereira A, Colomer D:
Early intervention during imatinib therapy in patients with newly diagnosed chronic-phase chronic myeloid leukemia: a study of the Spanish PETHEMA group.
Haematologica
; 2010 Aug;95(8):1317-24
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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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(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
13.
Michor F:
Chronic myeloid leukemia blast crisis arises from progenitors.
Stem Cells
; 2007 May;25(5):1114-8
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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
14.
Wallen H, Gooley TA, Deeg HJ, Pagel JM, Press OW, Appelbaum FR, Storb R, Gopal AK:
Ablative allogeneic hematopoietic cell transplantation in adults 60 years of age and older.
J Clin Oncol
; 2005 May 20;23(15):3439-46
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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
15.
Wang AH, Wang YY, Yao Y, Xu ZZ, Zhou L, Wang L, Zhang L, Chen Y, Shen ZX, Hu J, Li JM:
Summary of 615 patients of chronic myeloid leukemia in Shanghai from 2001 to 2006.
J Exp Clin Cancer Res
; 2010;29:20
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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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[Cites]
N Engl J Med. 2006 Dec 7;355(23):2408-17
[
17151364.001
]
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Science. 2001 Aug 3;293(5531):876-80
[
11423618.001
]
[Cites]
N Engl J Med. 2002 Feb 28;346(9):645-52
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Blood. 2002 Sep 1;100(5):1628-33
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Nature. 1973 Jun 1;243(5405):290-3
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Biochem Biophys Res Commun. 2004 Oct 22;323(3):728-30
[
15381060.001
]
(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
16.
Krejci M, Mayer J, Doubek M, Brychtova Y, Pospisil Z, Racil Z, Dvorakova D, Lengerova M, Horky O, Koristek Z, Dolezal T, Vorlicek J:
Clinical outcomes and direct hospital costs of reduced-intensity allogeneic transplantation in chronic myeloid leukemia.
Bone Marrow Transplant
; 2006 Oct;38(7):483-91
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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
17.
Amin HM, Hoshino K, Yang H, Lin Q, Lai R, Garcia-Manero G:
Decreased expression level of SH2 domain-containing protein tyrosine phosphatase-1 (Shp1) is associated with progression of chronic myeloid leukaemia.
J Pathol
; 2007 Aug;212(4):402-10
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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
18.
Babicka L, Zemanova Z, Pavlistova L, Brezinova J, Ransdorfova S, Houskova L, Moravcova J, Klamova H, Michalova K:
Complex chromosomal rearrangements in patients with chronic myeloid leukemia.
Cancer Genet Cytogenet
; 2006 Jul 1;168(1):22-9
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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
19.
Akhlynina TV, Gerasimova LP, Sarkisian GP, Borovkova TV, Dukhovenskaia EA, Manakova TE, Naĭdenova NM, Timofeev AM, Grineva NI:
[Kinetics of proliferation, differentiation and transcription of genes regulating apoptosis in cultured human BCR/ABL+ Ph+-cells].
Tsitologiia
; 2007;49(10):889-900
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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
20.
Keam SJ:
Dasatinib: in chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia.
BioDrugs
; 2008;22(1):59-69
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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
21.
Tam CS, Kantarjian H, Garcia-Manero G, Borthakur G, O'Brien S, Ravandi F, Shan J, Cortes J:
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.
Blood
; 2008 Aug 1;112(3):516-8
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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
]
[Cites]
Haematologica. 2005 Mar;90(3):335-40
[
15749665.001
]
[Cites]
Blood. 2005 Dec 1;106(12):3948-54
[
16105974.001
]
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Blood. 2007 Jun 15;109(12):5143-50
[
17317857.001
]
[Cites]
Blood. 2006 Sep 15;108(6):1809-20
[
16709930.001
]
[Cites]
Cancer Res. 2006 Dec 1;66(23):11314-22
[
17114238.001
]
[Cites]
N Engl J Med. 2006 Dec 7;355(23):2408-17
[
17151364.001
]
[Cites]
Cancer. 2007 Jan 15;109(2):248-55
[
17154172.001
]
[Cites]
Blood. 2006 Sep 1;108(5):1478-84
[
16627756.001
]
(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
22.
Dutcher JP, Lee S, Gallagher RE, Makary AZ, Hines JD, Londer H, Farnen JP, Bennett JM, Paietta E, Rowe JM, Goloubeva O, Wiernik PH, Eastern Cooperative Oncology Group:
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).
Leuk Lymphoma
; 2005 Mar;46(3):377-85
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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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.
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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
23.
Yeh CH, Tseng R, Zhang Z, Cortes J, O'Brien S, Giles F, Hannah A, Estrov Z, Keating M, Kantarjian H, Albitar M:
Circulating heat shock protein 70 and progression in patients with chronic myeloid leukemia.
Leuk Res
; 2009 Feb;33(2):212-7
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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
24.
Wodarz D:
Stem cell regulation and the development of blast crisis in chronic myeloid leukemia: Implications for the outcome of Imatinib treatment and discontinuation.
Med Hypotheses
; 2008;70(1):128-36
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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
25.
Wang GR, Zhao YZ, Qian LS, Zou DH, Li R, Mi YC, Wang XX, Qiu LG:
[Analysis of long-term treatment outcome and related factors in 95 chronic myeloid leukemia patients treated with imatinib].
Zhonghua Xue Ye Xue Za Zhi
; 2008 Jan;29(1):18-22
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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
26.
Saglio G, Kim DW, Issaragrisil S, le Coutre P, Etienne G, Lobo C, Pasquini R, Clark RE, Hochhaus A, Hughes TP, Gallagher N, Hoenekopp A, Dong M, Haque A, Larson RA, Kantarjian HM, ENESTnd Investigators:
Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia.
N Engl J Med
; 2010 Jun 17;362(24):2251-9
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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
27.
Zhu ZH, Qian J, Lin J, Qian Z, Yao DM, Wang YL, Chen Q, Xiao GF:
[Quantification of prame gene transcript in chronic myeloid leukemia].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2010 Aug;18(4):855-8
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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
28.
Li X, Yang J, Chen X, Liu J, Li H, Zheng J, He Y, Chen Z, Huang S:
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.
Cancer Genet Cytogenet
; 2007 Jul 15;176(2):166-8
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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
29.
Jørgensen HG, Holyoake TL:
Characterization of cancer stem cells in chronic myeloid leukaemia.
Biochem Soc Trans
; 2007 Nov;35(Pt 5):1347-51
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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
30.
Anand M, Ghara N, Kumar R, Singh S, Sengar M, Panikar N, Raina V, Sharma A:
Myeloperoxidase cytochemical negativity: an unexpected but intrinsic property of blasts of all phases of chronic myeloid leukemia.
Ann Hematol
; 2005 Nov;84(12):767-70
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[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[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
31.
Nakazato T, Suzuki K, Mihara A, Sanada Y, Kakimoto T:
[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].
Gan To Kagaku Ryoho
; 2010 Mar;37(3):539-42
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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
32.
Wang XR, Kang HY, Cen J, Li YH, Wang LL, Yu L:
[Methylation status of id4 gene promoter in patients with chronic myeloid leukemia].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2010 Dec;18(6):1402-4
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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
33.
Mahon FX, Molimard M:
Correlation between trough imatinib plasma concentration and clinical response in chronic myeloid leukemia.
Leuk Res
; 2009 Aug;33(8):1147-8; author reply 1149-50
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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
34.
Gratwohl A, Heim D:
Current role of stem cell transplantation in chronic myeloid leukaemia.
Best Pract Res Clin Haematol
; 2009 Sep;22(3):431-43
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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
35.
Fausel CA:
Novel treatment strategies for chronic myeloid leukemia.
Am J Health Syst Pharm
; 2006 Dec 1;63(23 Suppl 8):S15-20; quiz S21-2
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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
36.
Popova EY, Claxton DF, Lukasova E, Bird PI, Grigoryev SA:
Epigenetic heterochromatin markers distinguish terminally differentiated leukocytes from incompletely differentiated leukemia cells in human blood.
Exp Hematol
; 2006 Apr;34(4):453-62
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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
37.
Fausel C:
Targeted chronic myeloid leukemia therapy: seeking a cure.
J Manag Care Pharm
; 2007 Oct;13(8 Suppl A):8-12
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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
38.
Terasawa T, Dahabreh I, Trikalinos TA:
BCR-ABL mutation testing to predict response to tyrosine kinase inhibitors in patients with chronic myeloid leukemia.
PLoS Curr
; 2010 Dec 07;2:RRN1204
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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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[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
39.
le Coutre P, Ottmann OG, Giles F, Kim DW, Cortes J, Gattermann N, Apperley JF, Larson RA, Abruzzese E, O'Brien SG, Kuliczkowski K, Hochhaus A, Mahon FX, Saglio G, Gobbi M, Kwong YL, Baccarani M, Hughes T, Martinelli G, Radich JP, Zheng M, Shou Y, Kantarjian H:
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.
Blood
; 2008 Feb 15;111(4):1834-9
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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
40.
Chen ZC, You Y, Zhu XM, Li QB, Li WM, Zou P:
[A clinical study of treating 120 cases of adult chronic myelocytic leukemia with imatinib mesylate].
Zhonghua Nei Ke Za Zhi
; 2007 Dec;46(12):1003-6
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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
46.
Rosti G, Castagnetti F, Gugliotta G, Palandri F, Martinelli G, Baccarani M:
Dasatinib and nilotinib in imatinib-resistant Philadelphia-positive chronic myelogenous leukemia: a 'head-to-head comparison'.
Leuk Lymphoma
; 2010 Apr;51(4):583-91
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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
47.
Rao S, Sen R, Singh S, Ghalaut PS, Arora BB:
Grading of marrow fibrosis in chronic myeloid leukemia--a comprehensive approach.
Indian J Pathol Microbiol
; 2005 Jul;48(3):341-4
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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
48.
Sailaja K, Surekha D, Rao DN, Rao DR, Vishnupriya S:
Association of the GSTP1 gene (Ile105Val) polymorphism with chronic myeloid leukemia.
Asian Pac J Cancer Prev
; 2010;11(2):461-4
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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
49.
Aguilera DG, Tsimberidou AM:
Dasatinib in chronic myeloid leukemia: a review.
Ther Clin Risk Manag
; 2009 Apr;5(2):281-9
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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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[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
50.
Hochhaus A, Druker B, Sawyers C, Guilhot F, Schiffer CA, Cortes J, Niederwieser DW, Gambacorti-Passerini C, Stone RM, Goldman J, Fischer T, O'Brien SG, Reiffers JJ, Mone M, Krahnke T, Talpaz M, Kantarjian HM:
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.
Blood
; 2008 Feb 1;111(3):1039-43
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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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.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
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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
51.
Baron F, Maris MB, Storer BE, Sandmaier BM, Stuart MJ, McSweeney PA, Radich JP, Pulsipher MA, Agura ED, Chauncey TR, Maloney DG, Shizuru JA, Storb R:
HLA-matched unrelated donor hematopoietic cell transplantation after nonmyeloablative conditioning for patients with chronic myeloid leukemia.
Biol Blood Marrow Transplant
; 2005 Apr;11(4):272-9
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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
52.
Keller G, Brassat U, Braig M, Heim D, Wege H, Brümmendorf TH:
Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy.
Hematol Oncol
; 2009 Sep;27(3):123-9
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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
53.
DeAngelo DJ, Attar EC:
Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice.
Leuk Lymphoma
; 2010 Mar;51(3):363-75
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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
54.
Xiao-Jun H, Lan-Ping X, Kai-Yan L, Dai-Hong L, Huan C, Wei H, Yu-Hong C, Jing-Zhi W, Yao C, Xiao-Hui Z, Hong-Xia S, Dao-Pei L:
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.
Ann Med
; 2008;40(6):444-55
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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
55.
Jørgensen HG, Copland M, Allan EK, Jiang X, Eaves A, Eaves C, Holyoake TL:
Intermittent exposure of primitive quiescent chronic myeloid leukemia cells to granulocyte-colony stimulating factor in vitro promotes their elimination by imatinib mesylate.
Clin Cancer Res
; 2006 Jan 15;12(2):626-33
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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
56.
Otero L, Ornellas MH, de Azevedo AM, Tavares Rde C, Pires V, Abdelhay E, Bouzas LF, Fernandez Tde S:
Karyotype abnormalities and their clinical significance in a group of chronic myeloid leukemia patients treated with hematopoietic stem cell transplantation.
Sao Paulo Med J
; 2007 Jul 5;125(4):246-9
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[Title]
Karyotype abnormalities and their clinical significance
in a
group of
chronic myeloid leukemia
patients treated with hematopoietic stem cell transplantation.
CONTEXT AND OBJECTIVE: Following hematopoietic stem cell transplantation (HSCT), karyotyping is a valuable tool for monitoring engraftment and
disease
status.
Few studies have examined the prognostic significance of karyotypes in patients who underwent HSCT for
chronic myeloid leukemia
(
CML
).
The objective of this study was to evaluate the significance of pretransplantation cytogenetic status in relation to outcomes following HSCT
in CML
patients.
DESIGN AND SETTING: Case series study at Instituto Nacional do Câncer (INCA), Rio
de
Janeiro, Brazil.
RESULTS: Thirty-one patients were in the
chronic phase
and eight were in the
accelerated phase
.
[MeSH-major]
Chromosome Aberrations. Hematopoietic Stem Cell Transplantation.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Philadelphia Chromosome
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(PMID = 17992398.001).
[ISSN]
1516-3180
[Journal-full-title]
São Paulo medical journal = Revista paulista de medicina
[ISO-abbreviation]
Sao Paulo Med J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Brazil
57.
Holzerová M, Faber E, Veselovská J, Urbánková H, Balcárková J, Rozmanová S, Voglová J, Muzík J, Chroust K, Indrák K, Jarosová M, CAMELIA-Chronic Myeloid Leukaemia Project:
Imatinib mesylate efficacy in 72 previously treated Philadelphia-positive chronic myeloid leukemia patients with and without additional chromosomal changes: single-center results.
Cancer Genet Cytogenet
; 2009 May;191(1):1-9
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[Title]
Imatinib mesylate efficacy in 72 previously treated Philadelphia-
positive
chronic myeloid leukemia
patients with and without additional chromosomal changes: single-center results.
Reported here are 72 previously treated Philadelphia chromosome-
positive
(Ph+)
CML
patients on imatinib (IM) therapy, with a focus on patients with additional chromosomal aberrations (CAs).
Patients in
accelerated phase
had significantly worse overall survival on IM, regardless of additional CAs.
The present results confirm that the majority of previously treated Ph+
CML
patients benefit from starting IM therapy, including patients with defined additional changes.
[MeSH-major]
Chromosome Aberrations.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
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(PMID = 19389502.001).
[ISSN]
1873-4456
[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 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
58.
Agis H, Krauth MT, Mosberger I, Müllauer L, Simonitsch-Klupp I, Schwartz LB, Printz D, Böhm A, Fritsch G, Horny HP, Valent P:
Enumeration and immunohistochemical characterisation of bone marrow basophils in myeloproliferative disorders using the basophil specific monoclonal antibody 2D7.
J Clin Pathol
; 2006 Apr;59(4):396-402
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In
chronic myeloid
leukaemia
(
CML
), basophilia is a diagnostic and prognostic determinant.
OBJECTIVE: To detect and enumerate basophils in bone marrow sections in patients with
CML
and other MPD.
METHODS: The anti-basophil antibody 2D7 was applied to paraffin embedded bone marrow sections from normal/reactive subjects (n = 31), patients with
CML
(
chronic phase
, n = 37;
accelerated phase
, n = 9), and other MPD (
chronic
idiopathic myelofibrosis (CIMF), n = 20; polycythaemia vera (PV), n = 20; essential thrombocythaemia (ET), n = 20; indolent systemic mastocytosis (ISM), n = 7).
2D7(+) bone marrow cells were found to increase
in CML
compared with normal/reactive bone marrow and other MPD (median numbers of 2D7(+) cells/mm(2):
CML
, 33; normal/reactive bone marrow, 6; CIMF, 10; PV, 6; ET, 5; ISM, 3; p<0.05).
The highest basophil counts were recorded in
accelerated phase
CML
(115/mm(2)).
This approach should help in the quantification of bone marrow basophils at
diagnosis
and during anti-leukaemic treatment.
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Clin Exp Allergy. 2001 Nov;31(11):1705-13
[
11696046.001
]
[Cites]
Blood. 2002 Oct 1;100(7):2292-302
[
12239137.001
]
(PMID = 16461568.001).
[ISSN]
0021-9746
[Journal-full-title]
Journal of clinical pathology
[ISO-abbreviation]
J. Clin. Pathol.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / R01 AI020487; United States / NIAID NIH HHS / AI / R21 AI020487; United States / NIAID NIH HHS / AI / R37 AI020487; United States / NIAID NIH HHS / AI / AI20487
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Biomarkers; 820484N8I3 / Histamine
[Other-IDs]
NLM/ PMC1860377
59.
Liu L, Liu Q, Hao MW, Chen RA, Zhang JL, Wang LH, He H, Jiang SS, Liang YM:
[Nonmyleoablative allogeneic stem cell transplantation combined with imatinib in treatment of chronic myeloid leukemia: a clinical study].
Zhonghua Yi Xue Za Zhi
; 2005 Apr 27;85(16):1102-5
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[Title]
[Nonmyleoablative allogeneic stem cell transplantation combined with imatinib in treatment of
chronic myeloid leukemia
: a clinical study].
OBJECTIVE: To study the effect of nonmyeloablative allogeneic peripheral blood stem cell (NST) transplantation combined with imatinib in the treatment of
chronic myeloid leukemia
(
CML
).
METHODS: Ten
CML
patients, 5 males and 5 females, aged 21-41, 3 in
chronic phase
(CP), 4 in
accelerated phase
(AP) and 3 in blast crisis
phase
(BP), were treated with imatinib (400-1500 mg/d) before (n = 10) and/or after (n = 6) NST transplantation.
Graft-versus-host
disease
(GVHD) prophylaxis consisted of cyclosporine (CSA) and mycophenolate mofetil (MMF), or with low-dose methotrexate (MTX) or zenapax.
6 cases had I-II degrees acute and
chronic
GVHD of skin.
2 case had III-IV degrees
chronic
GVHD.
The time needed for
bcr
/abl becoming negative was 33-130 days.
CONCLUSION: An effective and safer method for
CML
, especially advanced
CML
treatment of NST transplantation combined with imatinib before and after transplantation reduces the leukemic cell load before transplantation, inhibits the proliferation of residual leukemic cells, promotes full chimerism change and enhanced the effect of graft versus
leukemia
.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy. Peripheral Blood Stem Cell Transplantation. Piperazines / therapeutic use. Pyrimidines / therapeutic use
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(PMID = 16029566.001).
[ISSN]
0376-2491
[Journal-full-title]
Zhonghua yi xue za zhi
[ISO-abbreviation]
Zhonghua Yi Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
60.
Valent P, Agis H, Sperr W, Sillaber C, Horny HP:
Diagnostic and prognostic value of new biochemical and immunohistochemical parameters in chronic myeloid leukemia.
Leuk Lymphoma
; 2008 Apr;49(4):635-8
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[Title]
Diagnostic and prognostic value of new biochemical and immunohistochemical parameters in
chronic myeloid leukemia
.
Chronic myeloid leukemia
(
CML
) is a stem-cell
disease
characterized by multilineage expansion of clonal
BCR
/ABL+ cells.
Transformation from
chronic
into
accelerated
and blast
phase
of
CML
is usually associated with drug resistance and is accompanied by typical clinical and/or laboratory features, such as splenomegaly, increase in precursor cells, disturbed megakaryopoiesis, basophilia or marrow fibrosis.
Because of new treatment options, early recognition of
disease
-acceleration is of importance.
These tests are useful to quantitate basophil-lineage cells in the peripheral blood
in CML
, to determine and quantify basophilia in the bone marrow, and to detect focal accumulations of blast cells and megakaryocytes as well as increased angiogenesis and fibrosis in bone marrow sections.
Application of these markers may assist in determining the
phase
of
disease
and may help to better predict the prognosis in individual patients.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/
diagnosis
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(PMID = 18398724.001).
[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 / Biomarkers
[Number-of-references]
15
61.
Qian J, Wang YL, Lin J, Yao DM, Xu WR, Wu CY:
Aberrant methylation of the death-associated protein kinase 1 (DAPK1) CpG island in chronic myeloid leukemia.
Eur J Haematol
; 2009 Feb;82(2):119-23
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[Title]
Aberrant methylation of the death-associated protein kinase 1 (DAPK1) CpG island in
chronic myeloid leukemia
.
The epigenetic changes of TSGs are now recognized as a mechanism contributing to the development of
chronic myeloid leukemia
(
CML
).
To clarify the role of DAPK1
in CML
, we examined the methylation status of DAPK1 in 49 patients with
CML
using methylation-specific polymerase chain reaction.
The aberrant methylation of the DAPK1 gene was found in 25 of 49 (51.0%)
CML
cases, not in all controls.
No correlation was found between DAPK1 gene methylation and the age, hematologic parameters, chromosomal abnormalities, the types and levels of
bcr
/abl transcripts of
CML
patients.
However, correlation could be observed between the sex and the status of DAPK1 methylation
in CML
patients (R = 0.374, P = 0.008).
Furthermore, there was a significant correlation between DAPK1 methylation and the stages of
CML
(R = 0.354, P = 0.013).
The
CML
patients in
accelerated phase
(AP) and blast crisis (BC) had higher frequency of DAPK1 methylation than those in
chronic phase
(CP) (75.0% vs. 34.5%) (chi(2) = 7.776, P = 0.005).
In one patient, the status of DAPK1 methylation became
positive
on the transition from CP to AP and BC.
These results suggested that DAPK1 promoter methylation might play a significant role in the progression of
CML
.
[MeSH-major]
Apoptosis Regulatory Proteins / genetics. Calcium-Calmodulin-Dependent Protein Kinases / genetics. CpG Islands. DNA Methylation.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics
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(PMID = 19018866.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / DNA Primers; EC 2.7.11.1 / DAPK1 protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
62.
Guilhot F, Druker B, Larson RA, Gathmann I, So C, Waltzman R, O'Brien SG:
High rates of durable response are achieved with imatinib after treatment with interferon alpha plus cytarabine: results from the International Randomized Study of Interferon and STI571 (IRIS) trial.
Haematologica
; 2009 Dec;94(12):1669-75
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BACKGROUND: Imatinib is the standard of care for newly diagnosed
chronic
-
phase chronic myeloid leukemia
.
DESIGN AND METHODS: Patients were allowed to cross over to the opposite treatment for intolerance, lack of response,
disease
progression, and, following release of the initial efficacy data, reluctance to remain on therapy with interferon-alpha plus cytarabine.
Estimated rates of freedom from progression to
accelerated
or blast
phase
and overall survival were 91% and 89%, respectively, at 48 months after starting imatinib.
CONCLUSIONS: This is the largest analysis to date describing the efficacy of imatinib in patients who have received prior therapies for
chronic myeloid leukemia
and it demonstrates excellent responses to this treatment. (ClinicalTrials.gov identifier: NCT00006343).
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy
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[Cites]
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[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00006343
[Publication-type]
Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate
[Other-IDs]
NLM/ PMC2791923
63.
Radich JP, Dai H, Mao M, Oehler V, Schelter J, Druker B, Sawyers C, Shah N, Stock W, Willman CL, Friend S, Linsley PS:
Gene expression changes associated with progression and response in chronic myeloid leukemia.
Proc Natl Acad Sci U S A
; 2006 Feb 21;103(8):2794-9
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[Title]
Gene expression changes associated with progression and response in
chronic myeloid leukemia
.
Chronic myeloid leukemia
(
CML
) is a hematopoietic stem cell
disease
with distinct biological and clinical features.
The biologic basis of the stereotypical progression from
chronic phase
through
accelerated phase
to blast crisis is poorly understood.
We used DNA microarrays to compare gene expression in 91 cases of
CML in
chronic
(42 cases),
accelerated
(17 cases), and blast phases (32 cases).
Three thousand genes were found to be significantly (P < 10(-10)) associated with
phase
of
disease
.
A comparison of the gene signatures of
chronic
,
accelerated
, and blast phases suggest that the progression of
chronic phase
CML
to advanced
phase
(
accelerated
and blast crisis)
CML
is a two-step rather than a three-step process, with new gene expression changes occurring early in
accelerated phase
before the accumulation of increased numbers of
leukemia
blast cells.
Studies of
CML
patients who relapsed after initially successful treatment with imatinib demonstrated a gene expression pattern closely related to advanced
phase
disease
.
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[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Databank-accession-numbers]
GEO/ GSE4170
[Grant]
United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / CA-18029; United States / NCI NIH HHS / CA / CA-85053
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / DNA-Binding Proteins; 0 / Kruppel-Like Transcription Factors; 0 / MZF1 protein, human; 0 / Peptide Elongation Factor 1; 0 / Piperazines; 0 / Pyrimidines; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate
[Other-IDs]
NLM/ PMC1413797
64.
Landstrom AP, Knudson RA, Dewald GW, Ketterling RP, Tefferi A:
Philadelphia chromosome mosaicism at diagnosis in chronic myeloid leukemia: clinical correlates and effect on imatinib mesylate treatment outcome.
Leuk Lymphoma
; 2007 Nov;48(11):2137-40
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[Title]
Philadelphia chromosome mosaicism at
diagnosis in
chronic myeloid leukemia
: clinical correlates and effect on imatinib mesylate treatment outcome.
In chemotherapy-treated patients with
chronic myeloid leukemia
(
CML
), the karyotypic detection of Philadelphia chromosome (Ph)-negative metaphases at
diagnosis
(i.e.
In the current retrospective study, clinical correlates and prognostic relevance of Ph mosaicism were evaluated in 63 Ph-
positive
patients with
CML
, including 59 in
chronic phase
and 4 in
accelerated phase
, receiving imatinib mesylate as either first (n = 46) or second (n = 17) line therapy.
Thirteen patients (21%) displayed Ph-negative metaphases at
diagnosis
and, compared to the other 50 patients with 100% Ph-
positive
metaphases, presented with significantly lower leukocyte count (p = 0.0004), circulating blast percentage (p = 0.02), and incidence of palpable splenomegaly (p = 0.02).
Ph mosaicism did not correlate with other
CML
-pertinent prognostic factors including Sokal score (p = 0.4) or the presence of additional chromosome changes (p = 0.96) found in 10 patients (16%).
Due to the small sample size, the current preliminary observations require validation
in a
larger group of patients.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/
diagnosis
.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Mosaicism. Philadelphia Chromosome. Piperazines / therapeutic use. Pyrimidines / therapeutic use
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(PMID = 17926177.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Grant]
United States / NIGMS NIH HHS / GM / T32 GM072474
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
65.
Wright MP, Shepherd JD, Barnett MJ, Nantel SH, Sutherland HJ, Toze CL, Hogge DE, Nevill TJ, Song KW, Abou Mourad YR, Narayanan S, Power MM, Smith CA, Forrest DL:
Response to tyrosine kinase inhibitor therapy in patients with chronic myelogenous leukemia relapsing in chronic and advanced phase following allogeneic hematopoietic stem cell transplantation.
Biol Blood Marrow Transplant
; 2010 May;16(5):639-46
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[Title]
Response to tyrosine kinase inhibitor therapy in patients with
chronic
myelogenous
leukemia
relapsing in
chronic
and advanced
phase
following allogeneic hematopoietic stem cell transplantation.
Tyrosine kinase inhibitors (TKI) have been used to treat relapse of
chronic
myelogenous
leukemia
(
CML
) after allogeneic stem cell transplant (HSCT), with responses seen predominantly in
chronic phase
(CP) patients.
This study aimed to analyze the response to TKI therapy and overall survival for patients relapsing predominantly in advanced
phase
.
We retrospectively reviewed 22 patients treated with imatinib (n=20) and/or dasatinib (n=6) for relapsed
CML
after HSCT; 8 patients were in CP, and 14 patients had advanced
disease
.
In advanced
phase
patients, 11 (79%) achieved CHR, 10 (71%) CCR, and 8 (57%) achieved CMR.
TKI therapy is capable of inducing durable molecular responses for
CML
relapsing after HSCT, both in
chronic
and advanced phases.
The achievement of CMR appears to be crucial in providing long-term
disease
control for these patients.
[MeSH-major]
Hematopoietic Stem Cell Transplantation / methods.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy. Protein Kinase Inhibitors / therapeutic use
[MeSH-minor]
Adult. Female. Humans.
Leukemia
,
Myeloid
,
Accelerated Phase
/ mortality.
Leukemia
,
Myeloid
,
Accelerated Phase
/ therapy.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ mortality.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ therapy. Male. Middle Aged. Protein-Tyrosine Kinases / antagonists & inhibitors. Recurrence. Remission Induction. Retrospective Studies. Survival Rate. Transplantation, Homologous
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[Copyright]
Copyright 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
(PMID = 20005967.001).
[ISSN]
1523-6536
[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
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
66.
Verma D, Kantarjian H, Shan J, O'Brien S, Estrov Z, Garcia-Manero G, Koller C, Borthakur G, Cortes J:
Survival outcomes for clonal evolution in chronic myeloid leukemia patients on second generation tyrosine kinase inhibitor therapy.
Cancer
; 2010 Jun 1;116(11):2673-81
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[Title]
Survival outcomes for clonal evolution in
chronic myeloid leukemia
patients on second generation tyrosine kinase inhibitor therapy.
METHODS: The authors analyzed the outcome of 177
CML
patients after second tyrosine kinase inhibitor therapy.
RESULTS: Ninety-five patients were in
chronic phase
, 30 had clonal evolution, 28 were in
accelerated phase
(AP), and 24 were in AP plus clonal evolution.
The hematologic and cytogenetic response rates, OS, and EFS were no different between patients in
chronic phase
with clonal evolution and patients with
chronic phase
and no clonal evolution.
The factors predicting increasing major cytogenetic response to second generation tyrosine kinase inhibitors were prior achievement of major cytogenetic response with imatinib, higher hemoglobin levels, no splenomegaly, lower percentage of Philadelphia chromosome-
positive
metaphases, and no prior chemotherapy.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ mortality. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
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[Copyright]
(c) 2010 American Cancer Society.
[Cites]
N Engl J Med. 2002 Feb 28;346(9):645-52
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Blood. 2002 Mar 15;99(6):1928-37
[
11877262.001
]
(PMID = 20499401.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Journal Article; 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 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
[Other-IDs]
NLM/ NIHMS593644; NLM/ PMC4216809
67.
Kim DH, Popradi G, Sriharsha L, Kamel-Reid S, Chang H, Messner HA, Lipton JH:
No significance of derivative chromosome 9 deletion on the clearance kinetics of BCR/ABL fusion transcripts, cytogenetic or molecular response, loss of response, or treatment failure to imatinib mesylate therapy for chronic myeloid leukemia.
Cancer
; 2008 Aug 15;113(4):772-81
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[Title]
No significance of derivative chromosome 9 deletion on the clearance kinetics of
BCR
/ABL fusion transcripts, cytogenetic or molecular response, loss of response, or treatment failure to imatinib mesylate therapy for
chronic myeloid leukemia
.
BACKGROUND: Although deletion of the derivative chromosome 9 (der 9; del-der 9) carries a poor prognosis in patients with
chronic myeloid leukemia
(
CML
) who are treated with hydroxyurea or interferon, its significance in patients on imatinib mesylate (IM) therapy is debated.
METHODS: In the current study, the authors used a locus-specific indicator breakpoint cluster region/receptor tyrosine kinase (
BCR
/ABL) probe to evaluate the significance of del-der 9 in 163 patients with
CML
who had fluorescence in situ hybridization (FISH) results available.
Serial changes
in BCR
/ABL fusion transcript levels also were monitored by using messenger RNA (mRNA) quantitative polymerase chain reaction (PCR).
The results of serial
BCR
/ABL mRNA quantitative PCR revealed similar patterns of
BCR
/ABL fusion gene reduction between the 2 groups.
CONCLUSIONS: The presence of del-der 9 in patients with
CML
did not influence 1) the response to IM therapy in terms of hematologic response, CyR, or MoR;. 2) LOR;.
4) progression to
accelerated phase
/blast crisis; or 5) time to dose escalation of IM.
Therefore, the authors concluded that the detection of del-der 9 does not have an impact on the current management of patients with
CML
who are receiving IM therapy.
[MeSH-major]
Chromosome Deletion. Chromosomes, Human, Pair 9. Fusion Proteins,
bcr
-abl / metabolism.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use
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[Copyright]
2008 American Cancer Society
(PMID = 18543309.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
68.
Rodzaj M, Gałazka K, Majewski M, Zduńczyk A:
A diagnostically difficult case of chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA effectively treated with imatinib in accelerated phase: case report.
Pol Arch Med Wewn
; 2009 Dec;119(12):838-41
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[Title]
A diagnostically difficult case of
chronic myeloid
neoplasm with eosinophilia and abnormalities of PDGFRA effectively treated with imatinib in
accelerated phase
: case report.
Chronic myeloid
neoplasm with eosinophilia and abnormalities of platelet-derived growth factor receptor alpha (PDGFRA), referred to until 2008 as
chronic
eosinophilic
leukemia
, is distinguished from hypereosinophilic syndrome (HES), if accompanied by genetic abnormalities that enable to determine eosinophil clonality.
In
chronic myeloid
neoplasm with eosinophilia and abnormalities of PDGFRA the FIP1L1-PDGFRA fusion gene can be detected.
Differential
diagnosis
of HES is often difficult because hypereosinophilia may also be reactive and may occur in many nonhematological as well as hematological disorders.
Traditional treatment of
chronic myeloid
neoplasm with cytostatic drugs results
in a
short-term and transient remission or stabilization of the
disease
.
We present the case of a 52-year-old patient with
chronic myeloid
neoplasm with eosinophilia and abnormalities of PDGFRA, in whom acceleration occurred after a year of cytostatic therapy with hydroxyurea and was successfully treated with imatinib.
It was impossible to unequivocally determine the type of bone marrow
disease
based on histologic criteria, and a wide spectrum of molecular tests differentiating the type of
myeloid
proliferation were necessary to establish the
diagnosis
.
RT-PCR did not reveal
BCR
-ABL or JAK2 V617F mutation.
[MeSH-major]
Hypereosinophilic Syndrome /
diagnosis
. Hypereosinophilic Syndrome / drug therapy.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/
diagnosis
.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Oncogene Proteins, Fusion / metabolism. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha / metabolism. mRNA Cleavage and Polyadenylation Factors / metabolism
[MeSH-minor]
Antineoplastic Agents / administration & dosage. Benzamides.
Disease
Progression. Gene Rearrangement. Humans. Imatinib Mesylate. Middle Aged. Protein Kinase Inhibitors / administration & dosage
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(PMID = 20010473.001).
[ISSN]
1897-9483
[Journal-full-title]
Polskie Archiwum Medycyny Wewnetrznej
[ISO-abbreviation]
Pol. Arch. Med. Wewn.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Poland
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FIP1L1-PDGFRA fusion protein, human; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
69.
Luk'ianova AS, Pien'kovs'ka-Hrelia B, Masliak ZV:
[Complex cytogenetic aberrations in a patient with chronic myeloid leukemia: a case report].
Tsitol Genet
; 2009 May-Jun;43(3):48-54
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[Title]
[Complex cytogenetic aberrations
in a
patient with
chronic myeloid leukemia
: a case report].
In this article is presented a case of multiple chromosomal aberrations
in a
patient with
CML
accelerated phase
.
Our data suggested that detected changes can be correlated with previous treatment regimens and the influence of these changes on progression of
disease
is discussed.
[MeSH-major]
Chromosome Aberrations.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics
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(PMID = 19938637.001).
[ISSN]
0564-3783
[Journal-full-title]
T︠S︡itologii︠a︡ i genetika
[ISO-abbreviation]
Tsitol. Genet.
[Language]
ukr
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Ukraine
70.
Palandri F, Castagnetti F, Alimena G, Testoni N, Breccia M, Luatti S, Rege-Cambrin G, Stagno F, Specchia G, Martino B, Levato L, Merante S, Liberati AM, Pane F, Saglio G, Alberti D, Martinelli G, Baccarani M, Rosti G:
The long-term durability of cytogenetic responses in patients with accelerated phase chronic myeloid leukemia treated with imatinib 600 mg: the GIMEMA CML Working Party experience after a 7-year follow-up.
Haematologica
; 2009 Feb;94(2):205-12
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[Title]
The long-term durability of cytogenetic responses in patients with
accelerated phase chronic myeloid leukemia
treated with imatinib 600 mg: the GIMEMA
CML
Working Party experience after a 7-year follow-up.
BACKGROUND: Imatinib mesylate is the first line treatment for
chronic myeloid leukemia
.
The advent of imatinib increased survival significantly in patients in an advanced
phase
of the
disease
.
DESIGN AND METHODS: A
phase
2 multicenter trial of the use of imatinib 600 mg/daily in patients with
accelerated phase chronic myeloid leukemia
was sponsored and promoted by the Italian Cooperative Study Group on
Chronic Myeloid Leukemia
in 2001.
One hundred and seven patients (96%) returned to
chronic phase
and 79 patients (71%) achieved a complete hematologic response.
CONCLUSIONS: Imatinib may induce durable responses, associated with prolonged survival, in patients with
accelerated phase chronic myeloid leukemia
.
[MeSH-major]
Leukemia
,
Myeloid
,
Accelerated Phase
/ drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
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[CommentIn]
Haematologica. 2009 May;94(5):743-4
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(PMID = 19144656.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
[Other-IDs]
NLM/ PMC2635408
71.
Jabbour E, Kantarjian H, Jones D, Talpaz M, Bekele N, O'Brien S, Zhou X, Luthra R, Garcia-Manero G, Giles F, Rios MB, Verstovsek S, Cortes J:
Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate.
Leukemia
; 2006 Oct;20(10):1767-73
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[Title]
Frequency and clinical significance of
BCR
-ABL mutations in patients with
chronic myeloid leukemia
treated with imatinib mesylate.
Mutations of the
BCR
-ABL kinase domain are a common mechanism of resistance to imatinib in
chronic myeloid leukemia
.
By multivariate analysis, factors associated with development of mutations were older age (P=0.026) prior interferon therapy (P=0.026), and
accelerated phase
or blast
phase
at time of imatinib failure (P=0.001).
[MeSH-major]
Antineoplastic Agents / therapeutic use. Fusion Proteins,
bcr
-abl / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use
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(PMID = 16855631.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article
[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
72.
Druker BJ, Guilhot F, O'Brien SG, Gathmann I, Kantarjian H, Gattermann N, Deininger MW, Silver RT, Goldman JM, Stone RM, Cervantes F, Hochhaus A, Powell BL, Gabrilove JL, Rousselot P, Reiffers J, Cornelissen JJ, Hughes T, Agis H, Fischer T, Verhoef G, Shepherd J, Saglio G, Gratwohl A, Nielsen JL, Radich JP, Simonsson B, Taylor K, Baccarani M, So C, Letvak L, Larson RA, IRIS Investigators:
Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.
N Engl J Med
; 2006 Dec 7;355(23):2408-17
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[Title]
Five-year follow-up of patients receiving imatinib for
chronic myeloid leukemia
.
BACKGROUND: The cause of
chronic myeloid leukemia
(
CML
) is a constitutively active
BCR
-ABL tyrosine kinase.
Imatinib inhibits this kinase, and
in a
short-term study was superior to interferon alfa plus cytarabine for newly diagnosed
CML in
the
chronic phase
.
For 5 years, we followed patients with
CML
who received imatinib as initial therapy.
METHODS: We randomly assigned 553 patients to receive imatinib and 553 to receive interferon alfa plus cytarabine and then evaluated them for overall and event-free survival; progression to
accelerated
-
phase
CML
or blast crisis; hematologic, cytogenetic, and molecular responses; and adverse events.
An estimated 7% of patients progressed to
accelerated
-
phase
CML
or blast crisis, and the estimated overall survival of patients who received imatinib as initial therapy was 89% at 60 months.
Patients who had a complete cytogenetic response or in whom levels of
BCR
-ABL transcripts had fallen by at least 3 log had a significantly lower risk of
disease
progression than did patients without a complete cytogenetic response (P<0.001).
CONCLUSIONS: After 5 years of follow-up, continuous treatment of
chronic
-
phase
CML
with imatinib as initial therapy was found to induce durable responses
in a
high proportion of patients. (ClinicalTrials.gov number, NCT00006343 [ClinicalTrials.gov]. )
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
[MeSH-minor]
Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Cytarabine / administration & dosage.
Disease
-Free Survival. Female. Follow-Up Studies. Fusion Proteins,
bcr
-abl / blood. Humans. Imatinib Mesylate. Interferon-alpha / administration & dosage. Kaplan-Meier Estimate. Male. Survival Analysis. Survival Rate. Treatment Outcome
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[Copyright]
Copyright 2006 Massachusetts Medical Society.
[CommentIn]
N Engl J Med. 2007 Apr 26;356(17):1780; author reply 1780
[
17460235.001
]
(PMID = 17151364.001).
[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/ NCT00006343
[Publication-type]
Journal Article; Multicenter Study; Randomized Controlled Trial
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
73.
Bee PC, Gan GG, Teh A, Haris AR:
Imatinib mesylate in the treatment of chronic myeloid leukemia: a local experience.
Med J Malaysia
; 2006 Dec;61(5):547-52
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[Title]
Imatinib mesylate in the treatment of
chronic myeloid leukemia
: a local experience.
This study was done to assess the overall response rate of imatinib mesylate in local patients with
chronic myeloid
leukaemia
.
Of the 69 patients; 35% were in the
chronic phase
, 41% were in the
accelerated phase
, 17% were in blast crisis and the remaining 7% were after stem cell transplantation.
Complete haematological response rates of patients in
chronic phase
,
accelerated phase
and blast crisis were 95.8%, 96.4% and 41.7% respectively.
The cytogenetic response rates were 80%, 41.7% and 18.2% in
chronic
,
accelerated
and blast crisis
phase
respectively (p < 0.005).
This was affected by the different phases of
disease
(
chronic phase
was better than
accelerated
and blast crisis) (p < 0.001).
In conclusion, our local
CML
patients did well on treatment with imatinib.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Treatment Outcome
[MeSH-minor]
Benzamides. Cytogenetics.
Disease
Progression. Female. Humans. Imatinib Mesylate. Malaysia. Male. Prognosis. Prospective Studies
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(PMID = 17623954.001).
[ISSN]
0300-5283
[Journal-full-title]
The Medical journal of Malaysia
[ISO-abbreviation]
Med. J. Malaysia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Malaysia
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
74.
Zang C, Liu H, Waechter M, Eucker J, Bertz J, Possinger K, Koeffler HP, Elstner E:
Dual PPARalpha/gamma ligand TZD18 either alone or in combination with imatinib inhibits proliferation and induces apoptosis of human CML cell lines.
Cell Cycle
; 2006 Oct;5(19):2237-43
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[Title]
Dual PPARalpha/gamma ligand TZD18 either alone or in combination with imatinib inhibits proliferation and induces apoptosis of human
CML
cell lines.
Despite progress in the treatment of early-stage
chronic myeloid leukemia
(
CML
), the
accelerated
and blastic phases of
CML
still remain a therapeutic challenge.
Persistence of
BCR
-ABL-
positive
(
bcr
-abl(+)) cells or secondary resistance during imatinib therapy frequently occurs.
In this study, we investigated the activity of a novel dual ligand specific for peroxisome proliferator-activated receptor alpha and gamma (PPARalpha/gamma) against
CML
blast crisis cell lines.
Exposure of these cell lines (K562, KU812 and KCL22) to TZD18 resulted
in a
growth inhibition
in a
dose- and time-dependent manner.
Overall, our findings strongly suggest that either TZD18, either alone or in combination with imatinib may be beneficial for the treatment of
CML in
myeloid
blast crisis.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / pharmacology.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Phenyl Ethers / pharmacology. Piperazines / pharmacology. Pyrimidines / pharmacology. Thiazolidinediones / pharmacology
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(PMID = 17102607.001).
[ISSN]
1551-4005
[Journal-full-title]
Cell cycle (Georgetown, Tex.)
[ISO-abbreviation]
Cell Cycle
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / 5-(3-(3-(4-phenoxy-2-propylphenoxy)propoxy)phenyl)-2,4-thiazolidinedione; 0 / Benzamides; 0 / PPAR alpha; 0 / PPAR gamma; 0 / Phenyl Ethers; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazolidinediones; 8A1O1M485B / Imatinib Mesylate
75.
Perrotti D, Jamieson C, Goldman J, Skorski T:
Chronic myeloid leukemia: mechanisms of blastic transformation.
J Clin Invest
; 2010 Jul;120(7):2254-64
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[Title]
Chronic myeloid leukemia
: mechanisms of blastic transformation.
The
BCR
-
ABL1
oncoprotein transforms pluripotent HSCs and initiates
chronic myeloid leukemia
(
CML
).
Patients with early
phase
(also known as
chronic phase
[CP])
disease
usually respond to treatment with ABL tyrosine kinase inhibitors (TKIs), although some patients who respond initially later become resistant.
In most patients, TKIs reduce the
leukemia
cell load substantially, but the cells from which the
leukemia
cells are derived during CP (so-called
leukemia
stem cells [LSCs]) are intrinsically insensitive to TKIs and survive long term.
LSCs or their progeny can acquire additional genetic and/or epigenetic changes that cause the
leukemia
to transform from CP to a more advanced
phase
, which has been subclassified as either
accelerated phase
or blastic
phase
disease
.
Here, we discuss what is known about the molecular mechanisms leading to blastic transformation of
CML
and propose some novel therapeutic approaches.
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[Cites]
Mutat Res. 2002 Jun;511(2):145-78
[
12052432.001
]
[Cites]
Cancer. 2002 Jun 1;94(11):2996-9
[
12115389.001
]
[Cites]
Leuk Res. 2002 Nov;26(11):1011-6
[
12363470.001
]
[Cites]
Blood. 2003 Jan 15;101(2):655-63
[
12393654.001
]
[Cites]
Blood. 2003 Jan 15;101(2):690-8
[
12509383.001
]
(PMID = 20592475.001).
[ISSN]
1558-8238
[Journal-full-title]
The Journal of clinical investigation
[ISO-abbreviation]
J. Clin. Invest.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA123014; United States / NCI NIH HHS / CA / R21 CA133646; United States / NCI NIH HHS / CA / R01 CA123014; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA133646; United States / NCI NIH HHS / CA / CA095512
[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.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Protein Kinase Inhibitors
[Number-of-references]
144
[Other-IDs]
NLM/ PMC2898591
76.
Deininger M, Schleuning M, Greinix H, Sayer HG, Fischer T, Martinez J, Maziarz R, Olavarria E, Verdonck L, Schaefer K, Boqué C, Faber E, Nagler A, Pogliani E, Russell N, Volin L, Schanz U, Doelken G, Kiehl M, Fauser A, Druker B, Sureda A, Iacobelli S, Brand R, Krahl R, Lange T, Hochhaus A, Gratwohl A, Kolb H, Niederwieser D, European Blood and Marrow Transplantation Group:
The effect of prior exposure to imatinib on transplant-related mortality.
Haematologica
; 2006 Apr;91(4):452-9
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BACKGROUND AND OBJECTIVES: Imatinib is an effective treatment for
chronic myeloid leukemia
(
CML
) and Philadelphia chromosome-
positive
(Ph+) acute lymphoblastic
leukemia
(ALL).
However, relapse is common in patients with advanced or high risk
disease
.
DESIGN AND METHODS: We retrospectively analyzed 70 patients with
CML
and 21 with Ph+ ALL who had received imatinib prior to SCT.
Multivariate analysis was used to define factors associated with major outcomes (engraftment, graft-versus-host
disease
, relapse, non-relapse mortality) in addition to descriptive statistics.
For the
CML
patients major outcomes were compared with those of historical controls drawn from the EBMT registry.
RESULTS: At SCT, 44% of
CML
patients were in
accelerated phase
or blast crisis and 40% of ALL patients had active
disease
compared to 84% and 95% prior to imatinib.
Factors associated with shorter overall and progression-free survival were advanced
disease
at SCT and a female donor/male recipient pairing.
Compared to historical controls, prior imatinib treatment did not influence overall survival, progression-free survival or non-relapse mortality, while there was a trend towards higher relapse mortality and significantly less
chronic
graft-versus-host
disease
.
[MeSH-minor]
Adolescent. Adult. Benzamides. Child. Child, Preschool. Female. Humans. Imatinib Mesylate.
Leukemia
/ mortality.
Leukemia
/ therapy. Male. Middle Aged. Mortality. Retrospective Studies. Treatment Outcome
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(PMID = 16585011.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
77.
Litzow MR, Dietz AB, Bulur PA, Butler GW, Gastineau DA, Hoering A, Fink SR, Letendre L, Padley DJ, Paternoster SF, Tefferi A, Vuk-Pavlović S:
Testing the safety of clinical-grade mature autologous myeloid DC in a phase I clinical immunotherapy trial of CML.
Cytotherapy
; 2006;8(3):290-8
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[Title]
Testing the safety of clinical-grade mature autologous
myeloid
DC
in a
phase
I clinical immunotherapy trial of
CML
.
BACKGROUND: We conducted a
phase
I clinical immunotherapy trial of
CML
to evaluate the safety of a clinical-grade leukemic DC product standardized for purity and mature phenotype.
METHODS: We injected autologous DC into patients in late
chronic
or
accelerated
phases of
CML
.
The patients received mature CD83+ and
bcr
-abl+ DC prepared from CD14+ cells.
T cells drawn later in the course of therapy were more sensitive to stimulation by
CML
DC in vitro.
DISCUSSION: The increase in T-cell sensitivity to
CML
-specific stimulation that accompanied active immunization by
CML
DC justifies further clinical studies, possibly with modifications such as an increased frequency and number of DC injections.
[MeSH-major]
Dendritic Cells / transplantation. Immunotherapy, Active / methods.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy
[MeSH-minor]
Aged. Antigens, CD / analysis. Antigens, CD14 / analysis. Antigens, CD86 / analysis. Bone Marrow Cells / cytology. Cell Count. Cell Proliferation. Coculture Techniques. Female. Fusion Proteins,
bcr
-abl / analysis. Humans. Immunoglobulins / analysis. Interferon-gamma / metabolism. Leukocytes, Mononuclear / cytology. Lymphocyte Activation / immunology. Male. Membrane Glycoproteins / analysis. Middle Aged.
Myeloid
Cells / cytology.
Myeloid
Cells / immunology.
Myeloid
Cells / transplantation. T-Lymphocytes / immunology. T-Lymphocytes / metabolism. Transplantation, Autologous. Treatment Outcome
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(PMID = 16793737.001).
[ISSN]
1465-3249
[Journal-full-title]
Cytotherapy
[ISO-abbreviation]
Cytotherapy
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 15083; United States / NCI NIH HHS / CA / R01 CA 84368
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD14; 0 / Antigens, CD86; 0 / CD83 antigen; 0 / CD86 protein, human; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 82115-62-6 / Interferon-gamma; EC 2.7.10.2 / Fusion Proteins, bcr-abl
78.
Voglová J, Maisnar V, Beránek M, Chrobák L:
[Combination of imatinib and anagrelide in treatment of chronic myeloid leukemia in blastic phase].
Vnitr Lek
; 2006 Sep;52(9):819-22
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[Title]
[Combination of imatinib and anagrelide in treatment of
chronic myeloid leukemia
in blastic
phase
].
[Transliterated title]
Kombinace imatinibu s anagrelidem v lécbe blastického zvratu chronické myeloidní
leukemie
.
Chronic myeloid leukemia
in blast
phase
(BP) is resistant to chemotherapy and majority of patients die within 6 months.
Inhibitor
Bcr
-Abl tyrosine kinase imatinib mesylate dramatically improved outcome of patients in
chronic phase
(CP) and is also effective in BP of
CML
.
High platelet counts are often observed at
diagnosis
or in the subsequent course of the
CML in
about 25% of patients.
Anagrelide selectively reduces circulating platelets and is used in treatment of thrombocythemia in
chronic
myeloproliferative disorders.
Efficacy and safety of combination imatinib mesylate with anagrelide was demonstrated in
chronic
and
accelerated phase
of
CML
.
51-year-old white man with
CML
presented in blast
phase
was followed for 4 years.
[MeSH-major]
Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / administration & dosage. Platelet Aggregation Inhibitors / administration & dosage. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Quinazolines / administration & dosage. Thrombocytosis / drug therapy
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.
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.
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.
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.
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(PMID = 17091608.001).
[ISSN]
0042-773X
[Journal-full-title]
Vnitr̆ní lékar̆ství
[ISO-abbreviation]
Vnitr Lek
[Language]
cze
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Czech Republic
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Platelet Aggregation Inhibitors; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Quinazolines; 0 / anagrelide; 8A1O1M485B / Imatinib Mesylate
79.
Salerni BL, Bates DJ, Albershardt TC, Lowrey CH, Eastman A:
Vinblastine induces acute, cell cycle phase-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed.
Mol Cancer Ther
; 2010 Apr;9(4):791-802
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[Title]
Vinblastine induces acute, cell cycle
phase
-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed.
Inhibition of the extracellular signal-regulated kinase by PD98059 dramatically accelerates vinblastine-mediated apoptosis in ML-1
leukemia
with cells dying in 4 hours from all phases of the cell cycle.
Inhibition of protein synthesis by cycloheximide also markedly
accelerated
vinblastine-induced apoptosis, showing that the proteins required for this acute apoptosis are constitutively expressed.
We also investigated the response of 13 other
leukemia
and lymphoma cell lines and cells from seven
chronic
lymphocytic
leukemia
patients.
Four cell lines and all
chronic
lymphocytic
leukemia
cells were killed in 6 hours by vinblastine alone.
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.
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.
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(PMID = 20371726.001).
[ISSN]
1538-8514
[Journal-full-title]
Molecular cancer therapeutics
[ISO-abbreviation]
Mol. Cancer Ther.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / T32 CA009658-17; United States / NCI NIH HHS / CA / CA23108; United States / NCI NIH HHS / CA / CA009658-17; United States / NCI NIH HHS / CA / T32 CA009658; United States / NCI NIH HHS / CA / R01 CA050224; United States / NCI NIH HHS / CA / P30 CA023108-315657; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / CA023108-315657; United States / NCI NIH HHS / CA / CA050224-14; United States / NCI NIH HHS / CA / R01 CA050224-14; United States / NCI NIH HHS / CA / CA50224
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 5V9KLZ54CY / Vinblastine; 98600C0908 / Cycloheximide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
[Other-IDs]
NLM/ NIHMS184304; NLM/ PMC2852489
80.
Zhu Y, Li JY, Xu W, Qiu HR, Chen LJ, Pan JL, Shen YF, Xue YQ:
[Multiplex fluorescence in situ hybridization for detecting complex chromosomal aberrations in chronic myeloid leukemia in blast crisis].
Zhonghua Xue Ye Xue Za Zhi
; 2007 Jul;28(7):458-61
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[Title]
[Multiplex fluorescence in situ hybridization for detecting complex chromosomal aberrations in
chronic myeloid leukemia
in blast crisis].
OBJECTIVE: To investigate the value of multiplex fluorescence in situ hybridization (M-FISH) for the detection of complex chromosomal abnormalities (CCA) of
chronic myeloid leukemia
in blast crisis (
CML
-BC).
METHODS: M-FISH was used to study 26 cases of
CML
-BC with CCA assayed by conventional cytogenetics (CC).
All chromosomes were involved
in CML
-BC, and chromosomes 17, 2, 8, 16 involvements were the most frequent.
CONCLUSIONS: M-FISH can refine CCA
in CML
-BC, find out or correct the missed or misidentified abnormalities by CC.
The frequent secondary chromosomal abnormalities
in CML
-BC with CCA are different from that
in CML
.
[MeSH-major]
Blast Crisis / genetics. Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods.
Leukemia
,
Myeloid
,
Accelerated Phase
/ genetics
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(PMID = 18072628.001).
[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
81.
Brave M, Goodman V, Kaminskas E, Farrell A, Timmer W, Pope S, Harapanhalli R, Saber H, Morse D, Bullock J, Men A, Noory C, Ramchandani R, Kenna L, Booth B, Gobburu J, Jiang X, Sridhara R, Justice R, Pazdur R:
Sprycel for chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant to or intolerant of imatinib mesylate.
Clin Cancer Res
; 2008 Jan 15;14(2):352-9
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[Title]
Sprycel for
chronic myeloid leukemia
and Philadelphia chromosome-
positive
acute lymphoblastic
leukemia
resistant to or intolerant of imatinib mesylate.
Food and Drug Administration approved dasatinib (Sprycel; Bristol-Myers Squibb), a new small-molecule inhibitor of multiple tyrosine kinases, for the treatment of adults with
chronic phase
,
accelerated phase
, or
myeloid
or lymphoid blast
phase chronic myeloid leukemia
(
CML
) or Philadelphia chromosome-
positive
acute lymphoblastic
leukemia
(Ph(+) ALL) with resistance or intolerance to prior therapy including imatinib.
The primary efficacy end point in
chronic phase
CML
was major cytogenetic response.
The primary end point in
accelerated phase
,
myeloid phase
, and lymphoid blast
phase
CML
, and Ph(+) ALL was major hematologic response.
In patients with
chronic phase
CML
, the major cytogenetic response rate was 45% with a complete cytogenetic response rate of 33%.
Major hematologic response rates in patients with
accelerated phase
CML
,
myeloid
CML
, lymphoid blast
CML
, and Ph(+) ALL were 59%, 32%, 31%, and 42%, respectively.
Median response durations in
chronic phase
,
accelerated phase
, and
myeloid phase
CML
had not been reached.
The median durations of major hematologic response were 3.7 months in lymphoid blast
CML
and 4.8 months in Ph(+) ALL.
CONCLUSIONS: This report describes the Food and Drug Administration review supporting the approval of dasatinib for
CML
and Ph(+) ALL based on the rates and durability of cytogenetic and hematologic responses.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ drug therapy. Piperazines / therapeutic use. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
[MeSH-minor]
Benzamides. Clinical Trials,
Phase
I as Topic. Clinical Trials,
Phase
II as Topic. Dasatinib. Drug Approval. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Multicenter Studies as Topic. Protein Kinase Inhibitors / adverse effects. Protein Kinase Inhibitors / chemistry. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. United States. United States Food and Drug Administration
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(PMID = 18223208.001).
[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
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
82.
Jabbour E, Cortes J, Kantarjian HM, Giralt S, Jones D, Jones R, Giles F, Andersson BS, Champlin R, de Lima M:
Allogeneic stem cell transplantation for patients with chronic myeloid leukemia and acute lymphocytic leukemia after Bcr-Abl kinase mutation-related imatinib failure.
Blood
; 2006 Aug 15;108(4):1421-3
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[Title]
Allogeneic stem cell transplantation for patients with
chronic myeloid leukemia
and acute lymphocytic
leukemia
after
Bcr
-Abl kinase mutation-related imatinib failure.
Resistance to imatinib mesylate is an emerging problem in the treatment of
chronic myeloid leukemia
(
CML
), often associated with point mutations in the
Bcr
-Abl kinase domain.
Ten imatinib-resistant patients with
Bcr
-Abl kinase mutations received a transplant: 9 had
CML
(3 in
chronic phase
, 4 in
accelerated phase
, and 2 in blast
phase
) and 1 had Philadelphia-
positive
acute lymphocytic
leukemia
(ALL).
Disease
response was complete molecular (CMR; n = 7), major molecular (n = 2), and no response (n = 1).
Allo-SCT remains an important salvage option for patients who develop resistance to imatinib through
Bcr
-Abl mutations.
[MeSH-major]
Drug Resistance, Neoplasm / genetics. Fusion Proteins,
bcr
-abl / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy. Point Mutation. Stem Cell Transplantation
[MeSH-minor]
Adult. Benzamides. Blast Crisis / genetics. Blast Crisis / metabolism. Blast Crisis / mortality. Blast Crisis / therapy.
Disease
-Free Survival. Female. Graft Survival / drug effects. Graft Survival / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / administration & dosage. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / metabolism. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / mortality. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Recurrence. Salvage Therapy. Transplantation, Homologous. Treatment Outcome
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(PMID = 16601247.001).
[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 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
83.
Walther JU, Pohl I, Rausch A, Fuehrer M:
Proliferation studies on chromosome preparations of bone marrow in hematological disease.
Oncol Rep
; 2006 Oct;16(4):893-9
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[Title]
Proliferation studies on chromosome preparations of bone marrow in hematological
disease
.
The disorders studied were: Acute lymphoblastic
leukemia
(ALL) (N=107),
chronic myeloid leukemia
(
CML
) (N=166) and aplastic anemia in childhood (AA) (N=39).
ii)
CML
: Philadelphia-
positive CML
shows proliferation activities quite distinct from Philadelphia-negative
CML
; however there is only a small change in the proliferative activity from the
chronic phase
to the
accelerated phase
or blast crisis.
Higher levels at
diagnosis
are associated with a faster and better response to therapy.
In conclusion, assessment of the proliferative activity in cytogenetic preparations made from bone marrow samples of patients with haematological
disease
may add valuable information as to diagnostic sub-groups and clinical course and may contribute to therapeutic decisions.
[MeSH-major]
Bone Marrow Cells / cytology. Chromosomes / ultrastructure. Hematologic Neoplasms / drug therapy.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ metabolism. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / metabolism
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(PMID = 16969511.001).
[ISSN]
1021-335X
[Journal-full-title]
Oncology reports
[ISO-abbreviation]
Oncol. Rep.
[Language]
eng
[Publication-type]
Historical Article; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
84.
Labussière H, Hayette S, Tigaud I, Michallet M, Nicolini FE:
[Treatment of chronic myeloid leukemia in 2007].
Bull Cancer
; 2007 Oct;94(10):863-9
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[Title]
[Treatment of
chronic myeloid leukemia
in 2007].
[Transliterated title]
Le traitement
de
la leucémie myéloïde
chronique en
2007.
The treatment of
chronic myeloid leukemia
(
CML
) has considerably evolved since imatinib mesylate has been introduced as a new therapeutic weapon for this
disease
.
The 5-year updated results of the IRIS study confirmed that imatinib mesylate is the best first line therapy for
chronic phase
CML
with an overall survival of 90%.
However, despite these remarkable improvements, new problems arise as sub-optimal responses, imatinib-resistances with recently identified
BCR
-ABL protein point mutations, responsible for a variety of therapeutic consequences : imatinib dose increase, alternative treatments with second generation tyrosine kinase inhibitors (TKIs : dastinib, nilotinib) or allogeneic stem cell transplantation.
The treatment of
accelerated
and blastic phases relies on imatinib +/- conventional chemotherapy, ideally followed by allogeneic stem cell transplantation, as newly developed TKIs are currently evaluated within this frame.
Finally,
BCR
-ABL(T315I) mutations remain a new therapeutic critical challenge as none of the three TKIs (imatinib, nilotinib, dasatinib) can efficiently control such diseases.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
[MeSH-minor]
Benzamides. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ drug therapy
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(PMID = 17964980.001).
[ISSN]
1769-6917
[Journal-full-title]
Bulletin du cancer
[ISO-abbreviation]
Bull Cancer
[Language]
fre
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
France
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
[Number-of-references]
36
85.
Paydas S, Tanriverdi K, Yavuz S, Seydaoglu G:
PRAME mRNA levels in cases with chronic leukemia: Clinical importance and review of the literature.
Leuk Res
; 2007 Mar;31(3):365-9
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[Title]
PRAME mRNA levels in cases with
chronic leukemia
: Clinical importance and review of the literature.
The aim of this study is to determine the frequency and the clinical importance of PRAME expression in
chronic myeloid leukemia
(
CML
)/
chronic
myeloproliferative disorders (CMPD) and
chronic
lymphocytic
leukemia
(CLL).
PRAME mRNA was measured by real time RT-PCR in 88 cases with
chronic leukemia
(CL) and 42 controls.
Seventy cases had
CML
/CMPD (56 had
chronic phase
(CP)-14 had
accelerated
/blastic
phase
disease
(AP/BP) and 18 cases had CLL (11 had early stage (Rai 0-I-II) and 7 had late stage (Rai III-IV).
Twenty-four of 70 (34%) cases with
CML
/CMPD and 5 of 18 (28%) cases with CLL showed PRAME expression.
PRAME (+) and PRAME (-) cases were not different for age, Hb, Hct, WBC count, platelet count, stage of the
disease
and response to therapy.
PRAME was monitorised in eight cases during follow-up: in three cases PRAME was negative at CP and expression developed at the AP/BP
disease
.
PRAME was
positive
at the beginning in five cases (4
CML
-1CLL) and expression disappeared after chemotherapy.
PRAME mRNA may be a useful marker to detect the minimal residual
disease
(MRD) and to determine the response to therapy in CLs.
[MeSH-major]
Antigens, Neoplasm / genetics. Biomarkers, Tumor / genetics.
Leukemia
, Lymphocytic,
Chronic
, B-Cell / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Myeloproliferative Disorders / genetics. RNA, Messenger / genetics
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Chronic
Disease
.
Disease
Progression. Female. Follow-Up Studies. Gene Expression Profiling. Humans. Male. Middle Aged. Neoplasm Staging. Reverse Transcriptase Polymerase Chain Reaction / methods. Treatment Outcome
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(PMID = 16914202.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / PRAME protein, human; 0 / RNA, Messenger
86.
Oztop I, Yaren A, Demirpence M, Alacacioglu I, Tuna B, Piskin O, Yilmaz U:
The development of metachronous prostate cancer and chronic myeloid leukemia in a patient with metastatic rectal cancer.
J BUON
; 2008 Apr-Jun;13(2):267-70
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[Title]
The development of metachronous prostate cancer and
chronic myeloid leukemia
in a
patient with metastatic rectal cancer.
We report herein an unusual case of metachronous triple cancers (rectum, prostate and Philadelphia(+) [Ph(+)]
chronic myeloid leukemia
[
CML
]).
A metastatic rectal cancer was diagnosed
in a
76-year-old male patient, who was treated with transanal tumor resection and chemotherapy.
Thirty months from the initial rectal cancer
diagnosis
, prostate cancer was diagnosed and the patient was administered maximal androgen blockade and received palliative radiotherapy to the lumbar spine because of painful bone metastases.
Thirty months after the
diagnosis
of rectal cancer and 12 months after the
diagnosis
of prostate cancer the patient developed Ph(+)
CML
and imatinib treatment was started.
After one-year period in remission,
CML
evolved into
accelerated phase
and the patient died of intracranial hemorrhage.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ pathology. Neoplasms, Multiple Primary / pathology. Prostatic Neoplasms / pathology. Rectal Neoplasms / pathology. Stomach Neoplasms / pathology
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(PMID = 18555476.001).
[ISSN]
1107-0625
[Journal-full-title]
Journal of B.U.ON. : official journal of the Balkan Union of Oncology
[ISO-abbreviation]
J BUON
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
87.
Jabbour E, Cortes J, Kantarjian H, Giralt S, Andersson BS, Giles F, Shpall E, Kebriaei P, Champlin R, de Lima M:
Novel tyrosine kinase inhibitor therapy before allogeneic stem cell transplantation in patients with chronic myeloid leukemia: no evidence for increased transplant-related toxicity.
Cancer
; 2007 Jul 15;110(2):340-4
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[Title]
Novel tyrosine kinase inhibitor therapy before allogeneic stem cell transplantation in patients with
chronic myeloid leukemia
: no evidence for increased transplant-related toxicity.
BACKGROUND: Patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) for
chronic myeloid leukemia
(
CML
) are increasingly likely to have received a novel tyrosine kinase inhibitor (NTKI) after failing imatinib mesylate.
METHODS: The outcome of 12 patients with
CML
(1 in
chronic phase
, 6 in the
accelerated phase
, and 5 in the blastic
phase
) who received dasatinib (n = 2), nilotinib (n = 7), or both (n = 3) before HSCT were retrospectively analyzed.
Acute and
chronic
graft-versus-host
disease
(GVHD) was observed in 7 and 6 patients, respectively.
Three patients had
disease
progression by Day 30 after HSCT.
Two patients developed
disease
recurrence after a median of 12 months.
After a median follow-up of 10 months, 7 patients were alive in molecular response and 5 patients had died, 4 of
disease
progression and 1 of extensive
chronic
GVHD.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
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(PMID = 17559140.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
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 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Protein-Tyrosine Kinases; RBZ1571X5H / Dasatinib
88.
Jabbour E, Kantarjian H, Jones D, Breeden M, Garcia-Manero G, O'Brien S, Ravandi F, Borthakur G, Cortes J:
Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy.
Blood
; 2008 Jul 1;112(1):53-5
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[Title]
Characteristics and outcomes of patients with
chronic myeloid leukemia
and T315I mutation following failure of imatinib mesylate therapy.
Chronic myeloid leukemia
(
CML
) with T315I mutation has been reported to have poor prognosis.
At the time of T315I detection, 10 were in
chronic phase
(CP), 9 in
accelerated phase
, and 8 in blast
phase
.
Although the T315I mutation is resistant to currently available TKIs, survival of patients with T315I remains mostly dependent on the stage of the
disease
, with many CP patients having an indolent course.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Piperazines / therapeutic use. Point Mutation. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Amino Acid Substitution. Benzamides. Child. Drug Resistance, Neoplasm / genetics. Female. Fusion Proteins,
bcr
-abl. Humans. Imatinib Mesylate. Male. Middle Aged. Treatment Outcome
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[Cites]
Lancet. 2002 Feb 9;359(9305):487-91
[
11853795.001
]
[Cites]
Blood. 2007 Dec 1;110(12):4005-11
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16775235.001
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17189410.001
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16990603.001
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Haematologica. 2007 Sep;92(9):1238-41
[
17768119.001
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Leukemia. 2007 Oct;21(10):2204-6
[
17541396.001
]
[Cites]
N Engl J Med. 2002 Feb 28;346(9):645-52
[
11870241.001
]
(PMID = 18403620.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
[Other-IDs]
NLM/ PMC4081375
89.
Vidović A, Janković G, Tomin D, Perunicić-Jovanović M, Djunić I, Djurasinović V, Colović M:
[Prognostic significance of cellular vascular endothelial growth factor (VEGF) expression in the course of chronic myeloid leukaemia].
Srp Arh Celok Lek
; 2009 Jul-Aug;137(7-8):379-83
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[Title]
[Prognostic significance of cellular vascular endothelial growth factor (VEGF) expression in the course of
chronic myeloid
leukaemia
].
INTRODUCTION: Increased angiogenesis in bone marrow is one of the characteristics of
chronic myeloid
leukaemia
(
CML
), a clonal myeloproliferative
disorder
that expresses a chimeric
bcr
/abl protein.
The impact of elevated VEGF expression on the course of
chronic myeloid
leukaemia
is unknown.
OBJECTIVE: The aim of this study was the follow-up of VEGF expression during the course of
CML
.
METHODS: We studied VEGF expression of 85
CML
patients (median age 50 years, range 16-75 years).
At the commencement of the study, 29 patients were in
chronic phase
(CP), 25 in an
accelerated phase
(AP), and 31 in the blast crisis (BC).
The temporal expression (percentage positivity per 1000 analysed cells) VEGF proteins over the course of
CML
were studied using the immunohistochemical technique utilizing relevant monoclonal antibodies.
It was correlated with the laboratory (Hb, WBC and platelet counts, and the percentage of blasts) and clinical parameters (organomegaly, duration of CP, AP, and BC) of
disease
progression.
CONCLUSION: Immunohistochemically confirmed significance of the expression of VEGF in dependence of the
CML
stage could be of clinical importance in deciding on the timing therapy.
These data suggest that VEGF plays a role in the biology of
CML
and that VEGF inhibitors should be investigated
in CML
.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ metabolism. Vascular Endothelial Growth Factor A / metabolism
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(PMID = 19764591.001).
[ISSN]
0370-8179
[Journal-full-title]
Srpski arhiv za celokupno lekarstvo
[ISO-abbreviation]
Srp Arh Celok Lek
[Language]
srp
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Serbia
[Chemical-registry-number]
0 / Vascular Endothelial Growth Factor A
90.
Li ZJ, Qiu LG, Li X, Mai YJ, Wang GR, Yu Z, Wang YF, Li CH, Li Q:
[Expression of beta-Catenin Gene in CML and its relationship with bcr/abl].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2007 Oct;15(5):931-5
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[Title]
[Expression of beta-Catenin Gene
in CML
and its relationship with
bcr
/abl].
This study was aimed to quantitatively detect the expression level of beta-catenin and
bcr
/abl in different phases of
chronic myeloid leukemia
(
CML
) and to analyze their potential relationship and significance in the progression of
CML
.
First, the total RNA isolated from BMMNC of patients with
CML
and donors was reversely transcribed into cDNA.
The real-time quantitative PCR method was used to analyze the expression level of beta-catenin and
bcr
/abl.
The expression level of beta-catenin and
bcr
/abl in different phases of
CML
was compared and the correlation was analyzed between the two genes.
The results showed that the beta-catenin gene in BMMNC of blast crisis of
CML
patients was expressed significantly higher than that in
chronic phase
(p < 0.001) and
accelerated phase
(p = 0.016) of
CML
patients and in normal donors (p = 0.004).
The expression of
bcr
/abl in blast crisis of
CML
was statistically higher than that in
chronic phase
of
CML
(p = 0.001).
The expression levels of beta-catenin and
bcr
/abl were correlated with each other
in CML
patients (r = 0.620, p < 0.001).
It is concluded that the beta-catenin gene in blast crisis of
CML
patients express higher than that in
chronic phase
and
accelerated phase
of
CML
, and its expression level is correlated with the level of
bcr
/abl expression.
The increased expression of beta-catenin may be account partly for the blast crisis of
CML
.
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(PMID = 17956664.001).
[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 / beta Catenin; EC 2.7.10.2 / Fusion Proteins, bcr-abl
91.
Gouda HM, Abdel Mohsen MM:
Frequency of expression of RHAMM/CD168 in Egyptian patients with CML.
J Egypt Natl Canc Inst
; 2009 Jun;21(2):93-9
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[Title]
Frequency of expression of RHAMM/CD168 in Egyptian patients with
CML
.
It is one of the
leukemia
-associated antigens (LAA) identified in patients with
myeloid
leukemias.
WE AIMED: at studying the frequency of expression of RHAMM/CD168 in Egyptian patients with
CML
, both in
chronic phase
and
accelerated
/blastic
phase
, as a potential target structure for cellular immunotherapies, and to compare it with available western records.
PATIENTS AND METHODS: RHAMM expression was tested by RT-PCR in peripheral blood mononuclear cells of 60
CML
patients divided into 2 groups, group A: 44
chronic phase
CML
patients, group B: 16
accelerated
/ blastic
phase
patients as well as 15 healthy volunteers.
OUR RESULTS: Demonstrated that 14/44 (31.8%) of
chronic
CML
patients showed
positive
RHAMM expression in contrast to 15/16 ( 93.7%) in the
accelerated
/blastic
phase
patients.
Moreover within the
chronic phase
patients the RHAMM
positive
patients had a significantly higher level of
bcr
-abl/abl ratio.
This highlighted the contribution of RHAMM expression with
CML disease
progression.
CONCLUSION: Our work demonstrated a similar proportion of RHAMM expression in both Egyptian and western
CML
patients.
This may pave the way for subsequent studies suggesting the concomitant use of RHAMM R3 peptide vaccination with conventional
CML
therapy especially in
accelerated phase
, in order to achieve complete molecular remission for our patient.
[MeSH-major]
Antigens, CD44 / genetics. Biomarkers, Tumor / genetics. Cell Proliferation. Extracellular Matrix Proteins / genetics.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ genetics
[MeSH-minor]
Adult. Blast Crisis. Case-Control Studies. Female. Fusion Proteins,
bcr
-abl / genetics. Humans. Male. Middle Aged. Prognosis. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction
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(PMID = 21057560.001).
[ISSN]
1110-0362
[Journal-full-title]
Journal of the Egyptian National Cancer Institute
[ISO-abbreviation]
J Egypt Natl Canc Inst
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Randomized Controlled Trial
[Publication-country]
Egypt
[Chemical-registry-number]
0 / Antigens, CD44; 0 / Biomarkers, Tumor; 0 / Extracellular Matrix Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / hyaluronan-mediated motility receptor; EC 2.7.10.2 / Fusion Proteins, bcr-abl
92.
Gucluler G, Baran Y:
Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia positive human chronic myeloid leukemia cells.
Hematology
; 2009 Jun;14(3):139-44
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[Title]
Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia
positive
human
chronic myeloid leukemia
cells.
Chronic
myelogenous
leukemia
(
CML
) results from a translocation between chromosomes 9 and 22 which generates
BCR
/ABL fusion protein and characterized by uncontrolled proliferation of immature white blood cells.
Imatinib, a molecularly targeting anticancer agent, is used widely for the treatment of
CML
and showed significant activity in
chronic
and
accelerated
phases but much less in blast crisis
phase
.
The resistance to imatinib especially in blast crisis
phase
is recognized as a major problem in the treatment of
CML
patients.
Docetaxel is shown to arrest cells in G2/M
phase
of the cell cycle which makes cells more sensitive to chemo- and radiotherapy.
In this study, we aimed to increase chemosensitivity of human K562
CML
cells to imatinib in combination with docetaxel.
Taken together, our results showed that the combination of imatinib and docetaxel decreased cellular proliferation and increased apoptosis in human K562
chronic myeloid leukemia
cells as compared to any agent alone.
[MeSH-major]
Antineoplastic Agents / pharmacology. Apoptosis / drug effects.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / pharmacology. Pyrimidines / pharmacology. Radiation-Sensitizing Agents / pharmacology. Taxoids / pharmacology
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(PMID = 19490758.001).
[ISSN]
1607-8454
[Journal-full-title]
Hematology (Amsterdam, Netherlands)
[ISO-abbreviation]
Hematology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Radiation-Sensitizing Agents; 0 / Taxoids; 15H5577CQD / docetaxel; 8A1O1M485B / Imatinib Mesylate; EC 3.4.22.- / Caspase 3
93.
Quintás-Cardama A, Kantarjian H, Ravandi F, O'Brien S, Thomas D, Vidal-Senmache G, Wierda W, Kornblau S, Cortes J:
Bleeding diathesis in patients with chronic myelogenous leukemia receiving dasatinib therapy.
Cancer
; 2009 Jun 1;115(11):2482-90
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[Title]
Bleeding diathesis in patients with
chronic
myelogenous
leukemia
receiving dasatinib therapy.
BACKGROUND: The most frequent nonhematologic side effects associated with dasatinib therapy in patients with
chronic myeloid leukemia
(
CML
) are gastrointestinal, rash, and fluid retention syndromes.
In the current study, the authors investigated the risk factors and management of bleeding associated with dasatinib therapy for
CML
after imatinib failure.
METHODS: The bleeding episodes associated with dasatinib therapy in 138 patients with
CML
who were consecutively treated at the study institution in clinical trials were evaluated.
RESULTS: Bleeding occurred in 32 (23%) patients (grade >or=3 in 9 [7%] patients [according to National Cancer Institute Common Toxicity Criteria]), including in 12% of patients treated in
chronic phase
, 31% of patients treated in
accelerated phase
(AP), and 35% of patients treated in blast
phase
(BP) (P = .02).
Although 37% of episodes occurred with platelet counts >100 x 10(9)/L, multivariate analysis identified thrombocytopenia and advanced
phase
CML
as risk factors for bleeding.
CONCLUSIONS: Bleeding occurs during dasatinib therapy, particularly in patients with AP or BP
disease
and low platelet counts.
[MeSH-major]
Hemorrhagic Disorders / chemically induced.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ complications.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ drug therapy. Pyrimidines / adverse effects. Thiazoles / adverse effects
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[Copyright]
(c) 2009 American Cancer Society.
[Cites]
Science. 2000 Sep 15;289(5486):1938-42
[
10988075.001
]
[Cites]
J Natl Cancer Inst. 2008 Jul 2;100(13):926-39
[
18577747.001
]
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[
15615512.001
]
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[
16436588.001
]
[Cites]
N Engl J Med. 2006 Jun 15;354(24):2531-41
[
16775234.001
]
[Cites]
Blood. 2007 Apr 15;109(8):3207-13
[
17185463.001
]
[Cites]
Drug Metab Dispos. 2008 Jul;36(7):1357-64
[
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]
[Cites]
J Clin Oncol. 2008 Jul 1;26(19):3204-12
[
18541900.001
]
[Cites]
Blood. 2001 Apr 1;97(7):1990-8
[
11264163.001
]
(PMID = 19280591.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Clinical Trial, Phase I; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
[Other-IDs]
NLM/ NIHMS629436; NLM/ PMC4180711
94.
Imatinib: a second look. Longer follow-up in chronic myeloid leukaemia: clear advantages.
Prescrire Int
; 2008 Dec;17(98):226-8
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[Title]
Imatinib: a second look. Longer follow-up in
chronic myeloid
leukaemia
: clear advantages.
(1) In 2002/2003, the clinical evaluation of imatinib, a tyrosine kinase inhibitor, in the treatment of
chronic myeloid
leukaemia
left many questions unanswered.
(3) As second-line treatment for patients in the
chronic phase
, we now have non-comparative follow-up data on 532 patients in whom interferon had failed.
(4) As second-line treatment for patients in the
accelerated phase
, we now have non-comparative follow-up data on 235 patients.
(9) In practice, imatinib seems to increase survival time when used as a first-line or second-line treatment for patients in different phases of
chronic myeloid
leukaemia
.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
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(PMID = 19415889.001).
[ISSN]
1167-7422
[Journal-full-title]
Prescrire international
[ISO-abbreviation]
Prescrire Int
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines
95.
Shi P, Chandra J, Sun X, Gergely M, Cortes JE, Garcia-Manero G, Arlinghaus RB, Lai R, Amin HM:
Inhibition of IGF-IR tyrosine kinase induces apoptosis and cell cycle arrest in imatinib-resistant chronic myeloid leukaemia cells.
J Cell Mol Med
; 2010 Jun;14(6B):1777-92
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[Title]
Inhibition of IGF-IR tyrosine kinase induces apoptosis and cell cycle arrest in imatinib-resistant
chronic myeloid
leukaemia
cells.
Chronic myeloid
leukaemia
(
CML
) is the most common subtype of
chronic
myeloproliferative diseases.
Typically,
CML
evolves as a
chronic phase
(CP)
disease
that progresses into
accelerated
(AP) and blast
phase
(BP) stages.
In this study, we show that IGF-IR is universally expressed in four
CML
cell lines.
Increased expression levels of IGF-IR with
CML
progression was supported by quantitative real-time PCR that demonstrated significantly higher levels of IGF-IR mRNA in BP patients.
Inhibition of IGF-IR decreased the viability and proliferation of
CML
cell lines and abrogated their growth in soft agar.
Importantly, inhibition of IGF-IR decreased the viability of cells resistant to imatinib mesylate including BaF3 cells transfected with p210
BCR
-ABL mutants,
CML
cell lines and primary neoplastic cells from patients.
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(PMID = 19508387.001).
[ISSN]
1582-4934
[Journal-full-title]
Journal of cellular and molecular medicine
[ISO-abbreviation]
J. Cell. Mol. Med.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / K08 CA114395; 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 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.2 / Fusion Proteins, bcr-abl
[Other-IDs]
NLM/ NIHMS405889; NLM/ PMC3444523
96.
Vidović A, Janković G, Colović M, Tomin D, Perunicić M, Bila J, Marković O, Bosković D:
The proto-oncogene expression varies over the course of chronic myeloid leukemia.
Hematology
; 2008 Feb;13(1):34-40
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[Title]
The proto-oncogene expression varies over the course of
chronic myeloid leukemia
.
The
chronic phase
(CP) of
chronic myeloid leukemia
(
CML
) is characterized by the expression of chimeric
BCR
/ABL gene, extended survival, and profligate growth of maturing granulocyte stemline.
The
accelerated phase
(AP) and blast crisis (BC) of
CML
are usually manifested by additionally acquired oncogene aberrations, resistance to therapy, advancing anaplasia, progressive organomegaly, and increased blast count.
Abnormal expression of some proto-oncogenes may accompany or even precede AP or BC of
CML
.
Our objective was to follow-up oncogene expression over time covering different clinical phases of
CML
.
Temporal variation in expression (percentage positivity per 1000 analyzed cells) of c-kit, c-myc, H-Ras, cyclin A1, p53, bcl-2 and VEGF oncogenic proteins in CP, AP, and BC of
CML
was studied by immunohistochemical procedures.
This was then correlated with parameters of clinical
disease
(organomegaly, duration of CP, AP, and BC) and laboratory (Hb, WBC and platelet counts, and the percentage of blasts) data.
The level of c-kit expression differed significantly over the course of
disease
(x(2), p = 0 x 025).
Antiapoptotic bcl-2 protein increased significantly with the progression of
CML
(x(2), p = 0 x 005).
There was no significant difference in the level of expression of H-Ras, cyclin A1 and p53 over the course of
disease
.
CONCLUSION: The changes in oncogene expression, assessed by immunohistochemical approach over the course of
CML
may have clinical relevance in deciding on and timing of therapy.
Temporal distribution of changes in oncoprotein expression
in CML
requires further study at the molecular level.
[MeSH-major]
Blast Crisis / metabolism.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Proto-Oncogene Proteins c-myc / metabolism
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(PMID = 18534064.001).
[ISSN]
1607-8454
[Journal-full-title]
Hematology (Amsterdam, Netherlands)
[ISO-abbreviation]
Hematology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
97.
Schmidt S, Wolf D, Thaler J, Burgstaller S, Linkesch W, Petzer A, Fridrik M, Lang A, Agis H, Valent P, Krieger O, Walder A, Korger M, Schlögl E, Sliwa T, Wöll E, Mitterer M, Eisterer W, Pober M, Gastl G, ASHO CML registry:
First annual report of the Austrian CML registry.
Wien Klin Wochenschr
; 2010 Oct;122(19-20):558-66
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[Title]
First annual report of the Austrian
CML
registry.
The Austrian
chronic myeloid leukemia
(
CML
) registry monitors individual
disease
courses, treatments applied, clinical outcome, and side effects of
CML
patients on a nationwide basis to provide data on the "real-life" situation and to complement the information and interpretation gained from the selected patient population observed in clinical trials.
This report summarizes the Austrian
CML
registry data as of March 2009.
At
diagnosis
most patients (n = 163) were in
chronic phase
(early, late, and secondary), whereas only 4 were in advanced
phase
.
A total of 5 patients progressed from
chronic phase
to
accelerated
(n = 3) and blastic
phase
(n = 2) while receiving imatinib standard dose.
Estimated overall survival (OS) rate at 60 months was 90% and progression free survival (PFS) according to European
Leukemia
Net (ELN) failure definition was 58%.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ mortality.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy. Registries / statistics & numerical data
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J Clin Oncol. 2009 Dec 10;27(35):6041-51
[
19884523.001
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Leukemia. 2008 Oct;22(10):1963-6
[
18754023.001
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(PMID = 20936366.001).
[ISSN]
1613-7671
[Journal-full-title]
Wiener klinische Wochenschrift
[ISO-abbreviation]
Wien. Klin. Wochenschr.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Austria
98.
Luo Y, Pan J, Shi JM:
[Clinical observation of Gleevec combined with myeloablative allogeneic stem cells transplantation in treatment of chronic myeloid leukemia].
Zhejiang Da Xue Xue Bao Yi Xue Ban
; 2007 Jul;36(4):343-7
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[Title]
[Clinical observation of Gleevec combined with myeloablative allogeneic stem cells transplantation in treatment of
chronic myeloid leukemia
].
OBJECTIVE: To observe the efficacy of Gleevec combined with myeloablative allogeneic stem cells transplantation(Allo-SCT) for the treatment of
chronic myeloid leukemia
(
CML
).
METHODS: Nine patients with
CML
were treated with Gleevec before and after Allo-SCT, with 5 in the
chronic phase
(CP), 2 in the
accelerated phase
(AP) and 2 in the blast-crisis
phase
(BP).
Three cases suffered from acute GVHD and 4 from
chronic
GVHD.
The rate of
disease
free survival was 88.9% after a median follow-up of 31 m (range 7 approximately 34 m).
CONCLUSION: The treatment of
CML
consisting of myeloablative Allo-SCT combined with Gleevec before and after transplantation is an effective and safe method for
CML
.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy. Peripheral Blood Stem Cell Transplantation. Piperazines / therapeutic use. Pyrimidines / therapeutic use
Genetic Alliance.
consumer health - Chronic Myeloid Leukemia
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
Genetic Alliance.
consumer health - Transplantation
.
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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(PMID = 17717824.001).
[ISSN]
1008-9292
[Journal-full-title]
Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
[ISO-abbreviation]
Zhejiang Da Xue Xue Bao Yi Xue Ban
[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
99.
Piazza RG, Magistroni V, Franceschino A, Andreoni F, Tornaghi L, Colnaghi F, Corneo G, Pogliani EM, Gambacorti-Passerini C:
The achievement of durable complete cytogenetic remission in late chronic and accelerated phase patients with CML treated with Imatinib mesylate predicts for prolonged response at 6 years.
Blood Cells Mol Dis
; 2006 Sep-Oct;37(2):111-5
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[Title]
The achievement of durable complete cytogenetic remission in late
chronic
and
accelerated phase
patients with
CML
treated with Imatinib mesylate predicts for prolonged response at 6 years.
Despite the
positive
results achieved by Imatinib mesylate (Imatinib) in the treatment of
chronic myeloid leukemia
(
CML
), over the past several years, Imatinib does not eradicate the leukemic clone.
Long-term follow-up of
CML
patients treated with Imatinib will ultimately define the durability of such treatment and the frequency of reemergence of progressive
disease
.
We present the results of a 6-year follow-up of 40
CML
patients either in
chronic
or
accelerated phase
who obtained a durable (>6 months) complete cytogenetic remission (CCyR) after treatment with Imatinib
in a
single center.
No progressions to more advanced phases of
disease
have been detected during the follow-up period.
Cytogenetic relapse was predicted by either a decrease in the amount of
BCR
-ABL transcript of less than 2 logs after the achievement of CCyR (p=0.0041) or a time-to-CCyR of more than 12 months (p<0.0001).
This 6-year follow-up of the efficacy of Imatinib therapy
in CML
patients who obtained a durable CCyR indicates that the relapses rate is low over this period of observation and that the rate of relapse does not increase over time.
[MeSH-major]
Cytogenetic Analysis / methods.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
[Email]
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(PMID = 16908206.001).
[ISSN]
1079-9796
[Journal-full-title]
Blood cells, molecules & diseases
[ISO-abbreviation]
Blood Cells Mol. Dis.
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
100.
Ahmad R, Tripathi AK, Tripathi P, Singh S, Singh R, Singh RK:
Malondialdehyde and protein carbonyl as biomarkers for oxidative stress and disease progression in patients with chronic myeloid leukemia.
In Vivo
; 2008 Jul-Aug;22(4):525-8
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[Title]
Malondialdehyde and protein carbonyl as biomarkers for oxidative stress and
disease
progression in patients with
chronic myeloid leukemia
.
However, evidence for this association has often been lacking because of a lack of specific biomarkers and methods available to evaluate oxidative stress status in humans with
disease
conditions.
The aim of this study was to investigate the plasma levels of malondialdehyde (MDA) and protein carbonyl (PC) as biomarkers for oxidative stress and
disease
progression in patients with
chronic myeloid leukemia
(
CML
).
MATERIALS AND METHODS: The study included 20
CML
patients and 10 age-and sex-matched healthy control volunteers.
The mean age of
CML
patients was 37.11+/-11.36 years and that of controls was 31.07+/-7.60 years.
RESULTS: There was a significant increase (p<0.05) in plasma MDA and PC levels
in CML
patients as compared to healthy volunteers.
Our results also showed that plasma MDA and PC levels were significantly higher (p<0.001) in both
chronic phase
(
CML
-CP) and
accelerated phase
(
CML
-AP) as compared to healthy volunteers.
During the follow-up of 12 months, two patients of
CML
-CP progressed to the
accelerated phase
.
The mean plasma levels of MDA and PC in patients with
CML
-CP who progressed to
CML
-AP were found to be higher than in patients with
CML
-CP who did not progress to the
accelerated phase
.
CONCLUSION: Plasma MDA and PC appears to reflect the oxidative stress status and
disease
progression
in CML
and can be used as biomarkers for oxidative stress and
disease
progression.
[MeSH-major]
Biomarkers, Tumor / metabolism.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ metabolism.
Leukemia
,
Myeloid
,
Accelerated Phase
/ metabolism.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ metabolism. Malondialdehyde / metabolism. Oxidative Stress. Protein Carbonylation. Proteins / metabolism
[MeSH-minor]
Adult. Case-Control Studies.
Disease
Progression. Humans. Time Factors