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accelerated phase cml 2005:2010[pubdate] *count=100
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Items 1 to 100 of about 261
1.
Ding JH, Ma Y, Chen BA, Zhao G, Wang J, Sun YY, Cheng J, Su AL, Dong WM, Zhang Y:
[Nonmyeloablative peripheral blood stem cell transplantation for chronic myeloid leukemia in chronic and accelerated phases].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2008 Apr;16(2):373-6
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[Title]
[Nonmyeloablative peripheral blood stem cell transplantation for
chronic myeloid leukemia in chronic
and
accelerated
phases].
The aim of this study was to investigate the effect of nonmyeloablative peripheral blood stem cell transplantation in treatment of
chronic myeloid leukemia in chronic
phase
(
CML
-CP) and
accelerated phase
(
CML
-AP).
24 patients with
CML
including 16 in
CML
-CP and 8 in
CML
-AP were treated with nonmyeloablative conditioning regimen for peripheral blood stem cell transplantation (PBHSCT).
2 cases died of severe acute GVHD and 1 case died of
chronic
GVHD, 2 cases died of interstitial pneumonia and 1 case died of relapsed.
In conclusions, nonmyeloablative peripheral blood stem cell transplantation is an effective therapeutic method for
CML
patients
in chronic
phase
and
accelerated phase
.
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(PMID = 18426668.001).
[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
[Publication-country]
China
2.
Lee TS, Ma W, Zhang X, Giles F, Cortes J, Kantarjian H, Albitar M:
BCR-ABL alternative splicing as a common mechanism for imatinib resistance: evidence from molecular dynamics simulations.
Mol Cancer Ther
; 2008 Dec;7(12):3834-41
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[Title]
BCR
-ABL alternative splicing as a common mechanism for imatinib resistance: evidence from molecular dynamics simulations.
Rare cases of
chronic myelogenous leukemia
(
CML
) express high levels of alternatively spliced
BCR
-ABL mRNA with a 35-bp insertion (35INS) between ABL kinase domain exons 8 and 9.
This insertion results
in a
frameshift leading to the addition of 10 residues and truncation of 653 residues due to early termination.
Sensitive PCR-based testing showed that 32 of 52 (62%) imatinib-resistant
CML
patients
in chronic
phase
and 8 of 38 (21%) in
accelerated
or blast crisis expressed varying levels of the alternatively spliced
BCR
-ABL mRNA.
Simulation results showed that the new residues cause a significant global conformational change, altering imatinib binding
in a
way similar to that of the T315I mutation and, therefore, providing resistance to imatinib that depends on the level of expression.
[MeSH-major]
Alternative Splicing. Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Fusion Proteins,
bcr
-abl / physiology. Piperazines / pharmacology. Pyrimidines / pharmacology
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[CommentIn]
Mol Cancer Ther. 2010 Mar;9(3):772; author reply 772
[
20197392.001
]
[CommentIn]
Mol Cancer Ther. 2010 Jul;9(7):2152
[
20571070.001
]
(PMID = 19056677.001).
[ISSN]
1535-7163
[Journal-full-title]
Molecular cancer therapeutics
[ISO-abbreviation]
Mol. Cancer Ther.
[Language]
eng
[Grant]
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 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
3.
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
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4.
Galimberti S, Cervetti G, Guerrini F, Testi R, Pacini S, Fazzi R, Simi P, Petrini M:
Quantitative molecular monitoring of BCR-ABL and MDR1 transcripts in patients with chronic myeloid leukemia during Imatinib treatment.
Cancer Genet Cytogenet
; 2005 Oct 1;162(1):57-62
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[Title]
Quantitative molecular monitoring of
BCR
-ABL and MDR1 transcripts in patients with
chronic myeloid leukemia
during Imatinib treatment.
In search for a possible correlation,
BCR
-ABL and MDR1 expression were measured in 115 serial bone marrow samples from 33
CML
patients during Imatinib treatment.
All patients achieved complete hematologic responses, and 22 patients also achieved complete cytogenetic responses, with median
BCR
-ABL mRNA values significantly lower than those observed in the group of cases that were persistently Philadelphia
positive
.
All three cases treated during the
accelerated phase
showed
disease
progression after an initial period of remission; all presented either increased levels of
BCR
-ABL or MDR1 3 months before clinical progression.
In the subgroup of cases treated during the
chronic
phase
,
BCR
-ABL and MDR1 levels were significantly correlated after 3 and 6 months (88 and 80%, respectively) but not after 12 months of treatment (32%).
Reported data maintain that MDR1 expression would play an important role in Imatinib resistance when the
disease
is not fully controlled (e.g., progressive
disease
or during the first months of treatment).
[MeSH-major]
Fusion Proteins,
bcr
-abl / metabolism. Genes, MDR.
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 = 16157201.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
5.
Soverini S, Martinelli G, Rosti G, Bassi S, Amabile M, Poerio A, Giannini B, Trabacchi E, Castagnetti F, Testoni N, Luatti S, de Vivo A, Cilloni D, Izzo B, Fava M, Abruzzese E, Alberti D, Pane F, Saglio G, Baccarani M:
ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on Chronic Myeloid Leukemia.
J Clin Oncol
; 2005 Jun 20;23(18):4100-9
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[Title]
ABL mutations in late
chronic
phase
chronic myeloid leukemia
patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on
Chronic Myeloid Leukemia
.
PURPOSE: Point mutations within the ABL kinase domain of the
BCR
-ABL gene have been associated with clinical resistance to imatinib mesylate
in chronic myeloid leukemia
(
CML
) patients.
To shed further light on the frequency, distribution, and prognostic significance of ABL mutations, we retrospectively analyzed a homogeneous cohort of late
chronic
phase CML
patients who showed primary cytogenetic resistance to imatinib.
PATIENTS AND METHODS: Using denaturing high-performance liquid chromatography (D-HPLC) and sequencing, we screened for ABL mutations
in a
total of 178 bone marrow and/or peripheral blood samples from 40 late
chronic
phase CML
patients homogeneously treated with imatinib 400 mg/d, who did not reach a major cytogenetic response at 12 months.
The presence of a missense mutation was significantly associated with a greater likelihood of subsequent progression to
accelerated phase
/blast crisis (P = .0002) and shorter survival (P = .001).
[MeSH-major]
Antineoplastic Agents / therapeutic use. Cytogenetic Analysis / methods. Drug Resistance, Neoplasm / genetics. Genes, abl / genetics.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ genetics. Piperazines / therapeutic use. Point Mutation. Pyrimidines / therapeutic use
[MeSH-minor]
Adult. Aged. Benzamides. Blast Crisis. Chi-Square Distribution. Chromatography, High Pressure Liquid. DNA Mutational Analysis.
Disease
Progression. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Survival Analysis
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(PMID = 15867198.001).
[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
[Publication-type]
Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
6.
Imataki O, Shintani T, Waki F, Ohnishi H, Ishida T:
[Tolerability of imatinib for patients with chronic myelogeneous leukemia (CML)].
Gan To Kagaku Ryoho
; 2008 Nov;35(11):1863-7
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[Title]
[Tolerability of imatinib for patients with
chronic
myelogeneous
leukemia
(
CML
)].
We reviewed a patients' cohort treated with imatinib in our hospital in 2007 for
chronic
myelogeneous
leukemia
(
CML
).
The
disease
status at onset was
chronic
phase
in 13 patients and
accelerated phase
in 1.
In 4 of these 6 intolerant cases,
CR
was maintained 2 years after the start of imatinib therapy.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Drug Tolerance.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Benzamides.
Disease
Progression. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Stem Cell Transplantation. Survival Rate. Young Adult
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(PMID = 19011333.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
7.
Mauro MJ:
Tailoring tyrosine kinase inhibitor therapy in chronic myeloid leukemia.
Cancer Control
; 2009 Apr;16(2):108-21
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[Title]
Tailoring tyrosine kinase inhibitor therapy
in chronic myeloid leukemia
.
BACKGROUND: Research into
chronic myeloid leukemia
(
CML
) is increasingly focused on the problem of imatinib failure.
Dasatinib and nilotinib are both active
in chronic
- and
accelerated
-
phase CML
, including patients with imatinib-resistant or intolerant
disease
.
METHODS: This paper reviews advances in tailoring tyrosine kinase inhibition therapy according to patient risk profiles as well as hematologic, cytogenetic, and molecular responses,
BCR
-ABL mutation status, and emerging predictive factors.
CONCLUSIONS: Treatment for
CML
should be individualized and, when resistance to imatinib can be predicted, therapy should be modified so that patients do not progress beyond
chronic
phase
and respond as promptly and deeply as required to maximally reduce risk.
[MeSH-major]
Drug Resistance, Neoplasm / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / genetics
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(PMID = 19337197.001).
[ISSN]
1526-2359
[Journal-full-title]
Cancer control : journal of the Moffitt Cancer Center
[ISO-abbreviation]
Cancer Control
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[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; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; RBZ1571X5H / Dasatinib
[Number-of-references]
118
8.
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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(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
9.
Bhattacharyya J, Mihara K, Yasunaga S, Tanaka H, Hoshi M, Takihara Y, Kimura A:
BMI-1 expression is enhanced through transcriptional and posttranscriptional regulation during the progression of chronic myeloid leukemia.
Ann Hematol
; 2009 Apr;88(4):333-40
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[Title]
BMI-1 expression is enhanced through transcriptional and posttranscriptional regulation during the progression of
chronic myeloid leukemia
.
Patients with
chronic myeloid leukemia
(
CML
) are at a risk of developing blastic crisis (BC) even after the emergence of imatinib mesylate.
In this study, to determine the relevance of BMI-1 to BC, we investigated the expression of BMI-1 in CD34(+) cells at each of the
chronic
phase
(CP), the
accelerated phase
(AP), and BC by flow cytometry.
Interestingly, the level of BMI-1 expression was significantly higher in CP than in controls and was further increased during the course of the
disease
progression (control--5.66%; CP--36.93%; AP and BC--76.41%).
Curiously, mRNA levels for BMI-1 were almost consistent during the
disease
progression from CP to BC (control--2.21; CP--9.77; AP and BC--9.70 (BMI-1/glyceraldehyde-3-phosphate dehydrogenase ratio)).
Since we further found that overexpression of
BCR
-ABL in human embryonic kidney-293 cells enhanced BMI-1 expression and that BMI-1 expression was increased in K562 cells, derived from patients with BC, in the presence of proteasomal inhibitors, BMI-1 was presumed to be positively regulated by
BCR
-ABL and further by posttranscriptional modification in the course of the
disease
progression.
We suggest the usefulness of BMI-1 expression in CD34(+) cells as a molecular marker for monitoring patients with
CML
.
[MeSH-major]
Blast Crisis / pathology. Gene Expression Regulation, Leukemic.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ pathology. Nuclear Proteins / analysis. Proto-Oncogene Proteins / analysis. Repressor Proteins / analysis. Transcription, Genetic
[MeSH-minor]
Antigens, CD34. Cell Line, Tumor.
Disease
Progression. Fusion Proteins,
bcr
-abl / physiology. Humans. Neoplastic Stem Cells / pathology. Polycomb Repressive Complex 1. RNA Processing, Post-Transcriptional
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(PMID = 18781299.001).
[ISSN]
1432-0584
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, CD34; 0 / BMI1 protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 6.3.2.19 / Polycomb Repressive Complex 1
10.
Xing W, Gu BW, Zhu YM, Jiang CL, Zhao RH, Wang AH, Sun HP, Li JM, Shen ZX, Chen Z, Chen SJ:
[Detection and quantification of BCR-ABL transcripts in patients with chronic myeloid leukemia by real-time quantitative reverse transcriptase polymerase chain reaction].
Zhonghua Yi Xue Za Zhi
; 2005 Feb 23;85(7):453-7
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[Title]
[Detection and quantification of
BCR
-ABL transcripts in patients with
chronic myeloid leukemia
by real-time quantitative reverse transcriptase polymerase chain reaction].
OBJECTIVE: To investigate the effect of real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR) approach
in chronic myeloid leukemia
(
CML
) for detecting the minimal residual
disease
(MRD) or monitoring the treatment response and predicting the prognosis.
METHODS: Fifty-six
CML
patients, 39 males and 17 females, aged 39 (16 approximately 66), with
disease
history and frozen RNA specimens were studied, 31 of which were in the incipient
chronic
phase
, 7 in the
accelerated phase
, and 17 in the rapidly progressing
phase
.
Breakpoint cluster region-Abelson murine
leukemia
viral oncogene (
BCR
-ABL) of the patients in different
CML
stages was analyzed by RT-PCR approach.
RESULTS: The
BCR
-ABL transcript of those patients remaining
in chronic
period after treatment decreased to 1/3 that of the baseline level six months after the initiation of treatment and then remained at that level.
The
BCR
-ABL transcript of those in which progressing change occurred increased when such change occurred.
After allogeneic transplantation of peripheral blood stem cells the
BCR
-ABL level decreased significantly.
The median DoseN in the 17 progressing patients was 10 492, significantly higher than those of the 31 patients
in chronic
phase
(5920) and in the 7 patients in
accelerated phase
(4444, both P < 0.05).
The minimal residual
disease
and the treatment response were closely associated with the level and its variation of
BCR
-ABL transcripts, the transcripts level in blastic crisis was significantly higher than that
in chronic
phase
or
accelerated phase
.
CONCLUSION: Real-time quantitative RT-PCR is reliable and can be used to detect the minimal residual
disease
, monitor the treatment outcome, and predicting blastic crisis.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Fusion Proteins,
bcr
-abl / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use
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(PMID = 15854550.001).
[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 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
11.
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
12.
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
13.
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
14.
Lindauer M, Hochhaus A:
Dasatinib.
Recent Results Cancer Res
; 2010;184:83-102
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It potently inhibits
BCR
-ABL and SRC-family kinases (SRC, LCK, YES, FYN), but also c-KIT, PDGFR-alpha and beta, and ephrin receptor kinase.Dasatinib is about 300 times more potent than imatinib in cells expressing unmutated
BCR
-ABL in vitro.
The drug has demonstrated activity against clinically relevant mutations, including those associated with poor prognosis during ongoing imatinib therapy.Dasatinib is approved for the treatment of patients with
BCR
-ABL-
positive chronic myeloid leukemia
(
CML
), resistant or intolerant to imatinib
in chronic
,
accelerated
, and blast
phase
.
It also is approved for the treatment of Philadelphia Chromosome
positive
(Ph+) acute lymphoblastic
leukemia
(ALL) resistant or intolerant to imatinib.A single daily dose of 100 mg
in chronic
phase CML
results in high hematologic and molecular remission rates and prolongation of survival.
In
accelerated
and blastic
phase
as well as in ALL, 70 mg twice daily is recommended.
Complete hematologic and cytogenetic remissions (
CR
) frequently occur even in this patient group with poor prognosis.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
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(PMID = 20072833.001).
[ISSN]
0080-0015
[Journal-full-title]
Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
[ISO-abbreviation]
Recent Results Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Oncogene Proteins v-abl; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.2 / src-Family Kinases; RBZ1571X5H / Dasatinib
[Number-of-references]
68
15.
Zou WY, Xu DR, Su C, Chen M, Li J, Luo SK:
[Dynamic observations of beta-catenin in chronic myeloid leukemia and its relationship with cytogenetic response].
Nan Fang Yi Ke Da Xue Xue Bao
; 2010 Aug;30(8):1868-70, 1873
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[Title]
[Dynamic observations of beta-catenin
in chronic myeloid leukemia
and its relationship with cytogenetic response].
OBJECTIVE: To investigate the changes in the expression of beta-catenin in patients with
chronic myeloid leukemia
(
CML
) in different phases, and explore the relationship between beta-catenin and the cytogenetic response to imatinib mesylate.
METHODS: Beta-catenin mRNA and protein expressions were detected by RT-PCR and Western blotting in the bone marrow mononuclear cells (BMMNCs) from 99
CML
patients.
The expressions of
BCR
-ABL fusion gene at both the mRNA and protein levels were detected by fluorescence in situ hybridization (FISH) in 94 patients before and during the one-year treatment with imatinib mesylate at the interval of 3 months, and the relationship between beta-catenin and cytogenetic response to imatinib mesylate was analyzed.
RESULTS: The expression of beta-catenin increased significantly in patients with blast crisis and
accelerated phase
(P<0.001), but showed no significant difference between normal subjects and
CML
patients in the
chronic
phase
(P>0.05).
The main cytogenetic remission rate was significantly higher in patients who were consistently negative for beta-catenin than in those consistently
positive
for beta-catenin or those with
a positive
transformation (P<0.001).
CONCLUSION: Beta-catenin overexpression in the progression of
CML
, consistent high level of beta-catenin or
a positive
transformation may indicate a poor response to imatinib, and early measures should be taken to increase the remission rate.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ metabolism. beta Catenin / metabolism
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(PMID = 20813688.001).
[ISSN]
1673-4254
[Journal-full-title]
Nan fang yi ke da xue xue bao = Journal of Southern Medical University
[ISO-abbreviation]
Nan Fang Yi Ke Da Xue Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
China
[Chemical-registry-number]
0 / Benzamides; 0 / CTNNB1 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / beta Catenin; 8A1O1M485B / Imatinib Mesylate
16.
Kantarjian H, Talpaz M, O'Brien S, Giles F, Faderl S, Verstovsek S, Garcia-Manero G, Shan J, Rios MB, Champlin R, de Lima M, Cortes J:
Survival benefit with imatinib mesylate therapy in patients with accelerated-phase chronic myelogenous leukemia--comparison with historic experience.
Cancer
; 2005 May 15;103(10):2099-108
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[Title]
Survival benefit with imatinib mesylate therapy in patients with
accelerated
-
phase
chronic myelogenous leukemia
--comparison with historic experience.
BACKGROUND: The effect of imatinib mesylate on survival in the
accelerated phase
of
chronic myelogenous leukemia
(
CML
) is unknown.
The objectives of this study were to update the long-term experience with imatinib in patients who had
accelerated
-
phase CML
and to compare outcomes with historic experience.
METHODS: The outcomes of 176 patients who received treatment with imatinib were reviewed and compared with the outcomes of 213 historic control patients with
accelerated
-
phase CML
who received treatment with interferon-alpha or with other modalities.
This may have implications in relation to subsequent therapy, because, according to the outcomes of patients who underwent allogeneic transplantation in
accelerated phase
at the authors' institution and from literature reports, the estimates of 5-year survival were 25-30%.
CONCLUSIONS: The current results suggest that imatinib improved survival compared with other therapies in patients with
accelerated
-
phase CML
.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myeloid
,
Accelerated Phase
/ drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
[MeSH-minor]
Adult. Anemia / chemically induced. Benzamides. Bone Marrow Transplantation. Cohort Studies. Cytogenetic Analysis. Female. Follow-Up Studies. Fusion Proteins,
bcr
-abl / analysis. Hemoglobins / analysis. Humans. Imatinib Mesylate. Interferon-alpha / therapeutic use. Longitudinal Studies. Male. Middle Aged. Remission Induction. Survival Rate. Treatment Outcome
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(PMID = 15830345.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Hemoglobins; 0 / Interferon-alpha; 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
17.
Zhou L, Wang AH, Wang L, You JH, Li JM, Shen ZX:
[Efficacy and safety of imatinib in treatment of 151 chronic myeloid leukemia patients].
Zhonghua Xue Ye Xue Za Zhi
; 2008 Jan;29(1):13-7
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[Title]
[Efficacy and safety of imatinib in treatment of 151
chronic myeloid leukemia
patients].
OBJECTIVE: To evaluate the safety and efficacy of imatinib in treatment of
chronic myeloid leukemia
(
CML
) patients.
RESULTS: One hundred and forty-two patients were evaluable with a median follow-up duration of 21.5 (6 -78) months. (1) The rate of cumulative complete hematologic response (CHR), major cytogenetic response (MCyR), complete cytogenetic response (CCyR) and complete molecular response (CMoR)
in chronic
phase
(CP)
CML
patients were 96.9%, 82.6%, 76.1% and 29.4%, respectively.
These rates were significantly higher in patients with CP than in those with
accelerated phase
(AP) and blast crisis (BC) (P < 0.0001). (2) The overall survival (OS) rates at 1, 2 and 3 year were 100%, (97.3 +/- 1.9)% and (95.8 +/- 2.4)% for CP patients, they were (84.7 +/- 8.2)%, (77.0 +/- 10.4)% and (69.3 +/- 11.9)% for AP patients, and (62.9 +/- 8.9)%, (41.9 +/- 9.2)% and (28.5 +/- 9.1)% for BC patients, respectively (P < 0.0001).
Sokal score was also significantly associated with
disease
progression (P = 0.0467). (4) The adverse events of imatinib were moderate and tolerable.
CONCLUSIONS: Treatment of
CML
patients in CP with imatinib can induce high hematologic, cytogenetic and molecular response and overall survival, but can not do satisfactorily for patients in AP and BC.
[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 = 18512309.001).
[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
18.
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
19.
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
20.
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
21.
Crawley C, Szydlo R, Lalancette M, Bacigalupo A, Lange A, Brune M, Juliusson G, Nagler A, Gratwohl A, Passweg J, Komarnicki M, Vitek A, Mayer J, Zander A, Sierra J, Rambaldi A, Ringden O, Niederwieser D, Apperley JF, Chronic Leukemia Working Party of the EBMT:
Outcomes of reduced-intensity transplantation for chronic myeloid leukemia: an analysis of prognostic factors from the Chronic Leukemia Working Party of the EBMT.
Blood
; 2005 Nov 1;106(9):2969-76
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[Title]
Outcomes of reduced-intensity transplantation for
chronic myeloid leukemia
: an analysis of prognostic factors from the
Chronic Leukemia
Working Party of the EBMT.
This study reports outcomes of allogeneic hematopoietic stem cell transplantation with reduced-intensity conditioning (RIC) in 186 patients with
chronic myeloid leukemia
(
CML
) from the European Group for Blood and Marrow Transplantation (EBMT).
The median age was 50 years, and 64% were in first
chronic
phase
(CP1), CP2 13%,
accelerated phase
17%, and blast crises 6%.
Acute graft-versus-host
disease
(GvHD) grade II to IV occurred in 32% and
chronic
GvHD in 43% (extensive in 24%).
ATG was associated with a lower incidence of
chronic
GvHD (cGvHD).
Adverse OS was associated with advanced
disease
(relative risk [RR], 3.4).
PFS was inferior in advanced
disease
(RR, 2.7) and a trend to improved outcomes with Fd/Bu/ATG (RR, 0.58).
RIC allografts are feasible in
CML
in first or second CP.
[MeSH-major]
Bone Marrow Transplantation.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/
diagnosis
.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ surgery
[MeSH-minor]
Adolescent. Adult. Aged. Benzamides.
Disease
Progression. Europe. Female. Graft vs Host
Disease
. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / therapeutic use. Prognosis. Pyrimidines / therapeutic use. Risk Factors. Societies, Scientific. Survival Rate. Transplantation Conditioning. Treatment Outcome
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(PMID = 15998838.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
22.
Tedeschi FA, Zalazar FE:
HOXA9 gene expression in the chronic myeloid leukemia progression.
Leuk Res
; 2006 Nov;30(11):1453-6
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[Title]
HOXA9 gene expression in the
chronic myeloid leukemia
progression.
In the present work we study the HOXA9 expression in sequential samples of patients with
CML
using RT-PCR.
The relative HOXA9 expression was higher in patients in the
accelerated phase
of the
disease
(p<0.005).
These first results could be considered as an evidence of an actual biological phenomenon that could provide additional information about the HOXA9 role in the
CML
progression.
[MeSH-major]
Gene Expression Profiling. Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics
[MeSH-minor]
Adult.
Disease
Progression. Fusion Proteins,
bcr
-abl / genetics. Humans. Middle Aged. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
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(PMID = 16630659.001).
[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 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / homeobox protein HOXA9; EC 2.7.10.2 / Fusion Proteins, bcr-abl
23.
Stromskaya TP, Rybalkina EY, Kruglov SS, Zabotina TN, Mechetner EB, Turkina AG, Stavrovskaya AA:
Role of P-glycoprotein in evolution of populations of chronic myeloid leukemia cells treated with imatinib.
Biochemistry (Mosc)
; 2008 Jan;73(1):29-37
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[Title]
Role of P-glycoprotein in evolution of populations of
chronic myeloid leukemia
cells treated with imatinib.
Imatinib mesylate (imatinib) is a new generation preparation that is now successfully used for treatment of cancer, particularly for chemotherapy of
chronic myeloid leukemia
(
CML
).
Imatinib inhibits the activity of chimeric kinase
BCR
-ABL, which is responsible for the development of
CML
.
The goal of this study was to investigate the role of a multidrug resistance protein, P-glycoprotein (Pgp), in the evolution of
CML
treated with imatinib.
We demonstrate here that although imatinib is a substrate for Pgp, cultured
CML
cells (strain K562/i-S9), overexpressing active Pgp, do not exhibit imatinib resistance.
Studies of
CML
patients in the
accelerated phase
have shown variations in the number of Pgp-
positive
cells (Pgp+) among individual patients treated with imatinib.
During treatment of patients with imatinib for 6-12 months, the number of Pgp-
positive
cells significantly increased in most patients.
We also compared the mode of Rh123 efflux by cells from
CML
patients who underwent imatinib treatment for 6-24 months and the responsiveness of patients to this therapy.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. P-Glycoprotein / metabolism. Piperazines / therapeutic use. Pyrimidines / therapeutic use
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(PMID = 18294126.001).
[ISSN]
0006-2979
[Journal-full-title]
Biochemistry. Biokhimii︠a︡
[ISO-abbreviation]
Biochemistry Mosc.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Fluorescent Dyes; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Piperazines; 0 / Pyrimidines; 1N3CZ14C5O / Rhodamine 123; 8A1O1M485B / Imatinib Mesylate
24.
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
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11853795.001
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N Engl J Med. 2002 Feb 28;346(9):645-52
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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
25.
Agis H, Krauth MT, Böhm A, Mosberger I, Müllauer L, Simonitsch-Klupp I, Walls AF, Horny HP, Valent P:
Identification of basogranulin (BB1) as a novel immunohistochemical marker of basophils in normal bone marrow and patients with myeloproliferative disorders.
Am J Clin Pathol
; 2006 Feb;125(2):273-81
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In chronic myeloid leukemia
(
CML
), basophilia is a diagnostic and prognostic variable.
We applied the antibasogranulin antibody BB1 on paraffin-embedded BM sections in 21 control samples (normal BM), 45 patients with
CML
, 9 with
chronic
idiopathic myelofibrosis, 11 with polycythemia vera, 19 with essential thrombocythemia, and 7 with indolent systemic mastocytosis.
BB1+ BM cells were found to be highly elevated in patients with
CML
compared with normal BM or other MPDs, with maximum counts found in
accelerated phase CML
(median, 160 cells/mm(2)).
In summary, BB1 (basogranulin) is a new immunohistochemical basophil marker that should allow quantification of basophils in
CML
at
diagnosis
and during therapy.
[MeSH-major]
Basophils / chemistry. Bone Marrow / chemistry. DNA-Binding Proteins / analysis.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ blood. Phosphoproteins / analysis. Transcription Factors / analysis
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(PMID = 16393678.001).
[ISSN]
0002-9173
[Journal-full-title]
American journal of clinical pathology
[ISO-abbreviation]
Am. J. Clin. Pathol.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0500729
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers; 0 / DNA-Binding Proteins; 0 / Phosphoproteins; 0 / Transcription Factors; 148814-46-4 / BNC1 protein, human
26.
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
27.
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
28.
Hu Z, Pan XF, Wu FQ, Ma LY, Liu DP, Liu Y, Feng TT, Meng FY, Liu XL, Jiang QL, Chen XQ, Liu JL, Liu P, Chen Z, Chen SJ, Zhou GB:
Synergy between proteasome inhibitors and imatinib mesylate in chronic myeloid leukemia.
PLoS One
; 2009;4(7):e6257
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[Title]
Synergy between proteasome inhibitors and imatinib mesylate
in chronic myeloid leukemia
.
BACKGROUND: Resistance developed by leukemic cells, unsatisfactory efficacy on patients with
chronic myeloid leukemia
(
CML
) at
accelerated
and blastic phases, and potential cardiotoxity, have been limitations for imatinib mesylate (IM) in treating
CML
.
METHODS AND FINDINGS: We tested the therapeutic efficacies as well as adverse effects of low dose IM in combination with proteasome inhibitor, Bortezomib (BOR) or proteasome inhibitor I (PSI), in two
CML
murine models, and investigated possible mechanisms of action on
CML
cells.
Consistently, BOR and PSI enhanced IM-induced inhibition of long-term clonogenic activity and short-term cell growth of
CML
stem/progenitor cells, and potentiated IM-caused inhibition of proliferation and induction of apoptosis of
BCR
-ABL+ cells.
While exerting suppressive effects on
BCR
-ABL, E2F1, and beta-catenin, IM/BOR and IM/PSI inhibited proteasomal degradation of protein phosphatase 2A (PP2A), leading to a re-activation of this important negative regulator of
BCR
-ABL.
CONCLUSION: These data suggest that combined use of tyrosine kinase inhibitor and proteasome inhibitor might be helpful for optimizing
CML
treatment.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Protease Inhibitors / therapeutic use. Proteasome Inhibitors. Pyrimidines / therapeutic use
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.
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(PMID = 19606213.001).
[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
[Other-IDs]
NLM/ PMC2705802
29.
Kim SH, Kim D, Kim DW, Goh HG, Jang SE, Lee J, Kim WS, Kweon IY, Park SH:
Analysis of Bcr-Abl kinase domain mutations in Korean chronic myeloid leukaemia patients: poor clinical outcome of P-loop and T315I mutation is disease phase dependent.
Hematol Oncol
; 2009 Dec;27(4):190-7
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[Title]
Analysis of
Bcr
-Abl kinase domain mutations in Korean
chronic myeloid leukaemia
patients: poor clinical outcome of P-loop and T315I mutation is
disease
phase
dependent.
Despite durable responses to imatinib
in chronic myeloid leukaemia
(
CML
), mutations
in Bcr
-Abl kinase domain (KD) are known to induce imatinib resistance and cause poor clinical outcome.
We characterized
Bcr
-Abl KD mutations in 137 Korean
CML
patients with imatinib resistance (n = 111) or intolerance (n = 26) using allele specific oligonucleotide polymerase chain reaction (PCR) and direct sequencing.
Seventy (51%) patients harboured 81 mutations of 20 different types with increasing prevalence in advanced
phase
.
T315I was the most common mutation and P-loop was the hottest spot
in Bcr
-Abl KD.
Survival analysis according to
disease
phase
of mutation being detected and type of mutations provided correlation between P-loop or T315I mutation and poor overall survival in blast crisis, but not in
accelerated phase
(AP) or
chronic
phase
(CP), indicating poor clinical outcome of particular mutations depends on
disease
phase
.
CML
patients with imatinib resistance showed high rate (63%) of mutations
in Bcr
-Abl KD and therefore
CML
patients who do not respond to imatinib should be the candidates for mutation screening as molecular monitoring.
[MeSH-major]
Fusion Proteins,
bcr
-abl / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ enzymology. Piperazines / pharmacology. Pyrimidines / pharmacology
[MeSH-minor]
Adolescent. Adult. Aged. Antineoplastic Agents / pharmacology. Benzamides. DNA Mutational Analysis.
Disease
Progression. Drug Resistance, Neoplasm. Female. Humans. Imatinib Mesylate. Korea / epidemiology. Male. Middle Aged. Prognosis. Protein Kinase Inhibitors / pharmacology. Protein Structure, Tertiary. Survival Rate. Treatment Outcome. Young Adult
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[Copyright]
Copyright (c) 2009 John Wiley & Sons, Ltd.
(PMID = 19274615.001).
[ISSN]
1099-1069
[Journal-full-title]
Hematological oncology
[ISO-abbreviation]
Hematol Oncol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
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
30.
Liu Q, Zhu Y, Qiu HX, Qiu HR, Wang R, Xu W, Li JY:
[Analysis of chromosome-8 aberrations in myeloid malignancies with complex chromosome abnormalities].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2008 Oct;16(5):993-6
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[Title]
[Analysis of chromosome-8 aberrations
in myeloid
malignancies with complex chromosome abnormalities].
To investigate the chromosome-8 aberrations
in myeloid
malignancies with complex chromosome abnormalities (CCAs), 81 cases of
myeloid
malignancies with CCAs were analysed by conventional chromosome analysis and multiplex fluorescence in situ hybridization.
The 81 cases included 25 cases of acute
myeloid leukemia
(AML), 35 cases of
chronic myeloid leukemia
(
CML
) and 21 cases of myelodysplastic syndrome (MDS).
The results showed that all chromosomes were involved in CCAs, and the incidence of chromosome-8 abnormality was 35.8% (29 out of 81 cases)
in myeloid
malignancies with CCAs, which in AML,
CML
and MDS patients were 56% (14/25), 28.6% (10/35) and 23.81% (5/21), respectively.
In
CML
, the incidences of
accelerated phase
and blast
phase
were 20% (1/5) and 33.3% (9/27), respectively.
In conclusion, aberrations of chromosome 8 were common
in myeloid
malignancies with CCAs, and may be related to progression of the
disease
.
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(PMID = 18928581.001).
[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
[Publication-country]
China
31.
Hughes T, Saglio G, Branford S, Soverini S, Kim DW, Müller MC, Martinelli G, Cortes J, Beppu L, Gottardi E, Kim D, Erben P, Shou Y, Haque A, Gallagher N, Radich J, Hochhaus A:
Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase.
J Clin Oncol
; 2009 Sep 01;27(25):4204-10
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[Title]
Impact of baseline
BCR
-ABL mutations on response to nilotinib in patients with
chronic myeloid leukemia in chronic
phase
.
PURPOSE: Nilotinib is a second-generation tyrosine kinase inhibitor indicated for the treatment of patients with
chronic myeloid leukemia
(
CML
)
in chronic
phase
(CP;
CML
-CP) and
accelerated phase
(AP;
CML
-AP) who are resistant to or intolerant of prior imatinib therapy.
In this subanalysis of a
phase
II study of nilotinib in patients with imatinib-resistant or imatinib-intolerant
CML
-CP, the occurrence and impact of baseline and newly detectable
BCR
-ABL mutations were assessed.
PATIENTS AND METHODS: Baseline mutation data were assessed in 281 (88%) of 321 patients with
CML
-CP in the
phase
II nilotinib registration trial.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Fusion Proteins,
bcr
-abl / antagonists & inhibitors. Fusion Proteins,
bcr
-abl / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Mutation. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
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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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[Cites]
Blood. 2006 Jul 1;108(1):28-37
[
16522812.001
]
[Cites]
Clin Cancer Res. 2006 Dec 15;12(24):7374-9
[
17189410.001
]
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]
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]
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]
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[
15215876.001
]
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]
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Leukemia. 2002 Nov;16(11):2190-6
[
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]
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[
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]
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[
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]
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]
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[
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]
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Cancer. 2005 Apr 15;103(8):1659-69
[
15747376.001
]
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Blood. 2002 May 1;99(9):3472-5
[
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]
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[
17715389.001
]
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[
12576318.001
]
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J Clin Oncol. 2005 Jun 20;23(18):4100-9
[
15867198.001
]
[Cites]
Blood. 2003 Jul 1;102(1):276-83
[
12623848.001
]
[Cites]
Cancer Cell. 2002 Aug;2(2):117-25
[
12204532.001
]
[Cites]
Leukemia. 2006 Nov;20(11):1925-30
[
16990771.001
]
[Cites]
Haematologica. 2007 Mar;92(3):401-4
[
17339191.001
]
[Cites]
Cancer Res. 2008 Dec 1;68(23):9809-16
[
19047160.001
]
[Cites]
N Engl J Med. 2006 Dec 7;355(23):2408-17
[
17151364.001
]
[Cites]
Cancer. 2007 Oct 1;110(7):1509-19
[
17702093.001
]
[Cites]
Clin Cancer Res. 2005 Jul 1;11(13):4941-7
[
16000593.001
]
(PMID = 19652056.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[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 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
[Other-IDs]
NLM/ PMC4979230
32.
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
33.
Cavalcanti GB Jr, Scheiner MA, Simões Magluta EP, Vasconcelos FC, Klumb CE, Maia RC:
p53 flow cytometry evaluation in leukemias: correlation to factors affecting clinical outcome.
Cytometry B Clin Cytom
; 2010 Jul;78(4):253-9
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p53 is a cell cycle checkpoint control protein that assesses DNA damage and acts as a transcription factor regulating genes, which control cell growth, DNA repair, and apoptosis. p53 mutations have been found
in a
wide variety of different cancers including flow cytometric assessment of p53 protein expression using anti-p53 monoclonal antibodies.
We studied p53 protein expression by flow cytometry (FC) assay in 223 blood and/or bone marrow samples from 72 patients with
chronic myeloid leukemia
(
CML
): 54
in chronic
phase
(
CML
-CP), 7 in
accelerated phase
(
CML
-AP), and 11 in blastic
phase
(
CML
-BP); 64 patients with
chronic
lymphoid
leukemia
(CLL): (34 at
diagnosis
, 21 in previously treated, and 9 with Richter's syndrome); 44 patients with acute lymphoid
leukemia
(ALL): 36 at
diagnosis
and 8 in relapse; and 43 acute
myeloid leukemia
(AML): 27
de
novo, 7 in relapse, and 9 secondary. p53 protein expression was observed in 64 of 223 patient's samples: 14/64 (21.9%) CLL, 13/44 (29.5%) ALL, 19/43 (44.2%) AML, and 17/72 (23.6%)
CML
.
Highest levels were detected in the advanced phases of CLL, ALL, and
CML
.
In addition, in patients with AML, high levels of p53 expression were detected in secondary and relapse
disease
and also
in de
novo AML cases.
Our results demonstrated that p53 expression levels are strongly associated with advanced
disease
.
[MeSH-major]
Flow Cytometry / methods.
Leukemia
/ metabolism.
Leukemia
/ therapy. Tumor Suppressor Protein p53 / metabolism
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[Copyright]
(c) 2010 Clinical Cytometry Society.
(PMID = 20198607.001).
[ISSN]
1552-4957
[Journal-full-title]
Cytometry. Part B, Clinical cytometry
[ISO-abbreviation]
Cytometry B Clin Cytom
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Tumor Suppressor Protein p53
34.
Olsson-Strömberg U, Hermansson M, Lundán T, Ohm AC, Engdahl I, Höglund M, Simonsson B, Porkka K, Barbany G:
Molecular monitoring and mutation analysis of patients with advanced phase CML and Ph+ ALL receiving dasatinib.
Eur J Haematol
; 2010 Nov;85(5):399-404
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[Title]
Molecular monitoring and mutation analysis of patients with advanced
phase CML
and Ph+ ALL receiving dasatinib.
As a result of the excellent responses achieved
in chronic
phase
chronic myeloid leukemia
since the introduction of imatinib, sensitive techniques such as reverse transcriptase real-time PCR are warranted to monitor patients receiving tyrosine kinase inhibitors (TKI).
Our objective was to determine the value of molecular monitoring Ph-
positive
leukemias under dasatinib treatment.
We used real-time PCR and
ABL1
kinase domain sequencing on sequential samples from 11 patients with Philadelphia-
positive
leukemias who received dasatinib.
We were able to detect pre-existing mutations in the kinase domain of
BCR
-
ABL1 in
four patients, particularly in patients with high
BCR
-
ABL1
transcript levels.
We conclude that sensitive molecular monitoring with real-time PCR for
BCR
-
ABL1
transcripts and mutation screening of the
ABL1
kinase domain of patients with Philadelphia-
positive
leukemias are valuable for patient management, however, mutation findings should be interpreted with caution, as mutant clones not always behave in vivo as predicted by in vitro assays.
[MeSH-major]
DNA Mutational Analysis.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics.
Leukemia
,
Myeloid
,
Accelerated Phase
/ genetics. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
[MeSH-minor]
Adolescent. Adult. Aged. Clone Cells / pathology. Dasatinib. Female. Fusion Proteins,
bcr
-abl / genetics. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. RNA, Neoplasm / genetics. Young Adult
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[Copyright]
© 2010 John Wiley & Sons A/S.
(PMID = 20659155.001).
[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]
England
[Chemical-registry-number]
0 / Pyrimidines; 0 / RNA, Neoplasm; 0 / Thiazoles; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
35.
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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(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
36.
Quintás-Cardama A, Kantarjian H, O'brien S, Borthakur G, Bruzzi J, Munden R, Cortes J:
Pleural effusion in patients with chronic myelogenous leukemia treated with dasatinib after imatinib failure.
J Clin Oncol
; 2007 Sep 1;25(25):3908-14
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[Title]
Pleural effusion in patients with
chronic myelogenous leukemia
treated with dasatinib after imatinib failure.
PURPOSE: We investigated the risk factors and management of pleural effusion associated with dasatinib therapy for
chronic myelogenous leukemia
(
CML
) after failure of imatinib.
PATIENTS AND METHODS: We analyzed 138 patients with
CML
treated with dasatinib from November 2003 to January 2006 in one
phase
I (n = 50) and four
phase
II (n = 88) studies for the development of pleural effusion.
RESULTS: Pleural effusion occurred in 48 patients (35%; grade 3/4 in 23 [17%]), including 29% of those treated
in chronic
phase
(CP), 50% in
accelerated phase
(AP), and 33% in blast
phase
(BP).
By multivariate analysis, history of cardiac
disease
, hypertension, and use of a twice-daily schedule (v once daily) were identified as factors associated with development of pleural effusions.
A twice-daily schedule may result
in a
higher incidence of pleural effusion.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Pleural Effusion / chemically induced. Pyrimidines / adverse effects. Pyrimidines / therapeutic use. Thiazoles / adverse effects. Thiazoles / therapeutic use
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(PMID = 17761974.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Clinical Trial, Phase I; Clinical Trial, Phase II; Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
37.
Yin OQ, Gallagher N, Li A, Zhou W, Harrell R, Schran H:
Effect of grapefruit juice on the pharmacokinetics of nilotinib in healthy participants.
J Clin Pharmacol
; 2010 Feb;50(2):188-94
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Nilotinib (Tasigna; Novartis Pharmaceuticals) is a second-generation
BCR
-ABL tyrosine kinase inhibitor newly approved for the treatment of imatinib-resistant or imatinib-intolerant Philadelphia chromosome
positive
(Ph+)
chronic myeloid leukemia in chronic
phase
or
accelerated phase
.
All participants underwent 2 study periods during which they received a single oral dose of 400 mg nilotinib with 240 mL double-strength grapefruit juice or 240 mL water
in a
crossover fashion.
[MeSH-minor]
Adolescent. Adult. Aged. Antineoplastic Agents / adverse effects. Antineoplastic Agents / pharmacokinetics. Beverages. Cross-Over Studies. Fusion Proteins,
bcr
-abl / metabolism. Headache / chemically induced. Humans. Male. Middle Aged. Protein-Tyrosine Kinases / metabolism. Vomiting / chemically induced. Young Adult
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(PMID = 19948946.001).
[ISSN]
1552-4604
[Journal-full-title]
Journal of clinical pharmacology
[ISO-abbreviation]
J Clin Pharmacol
[Language]
eng
[Publication-type]
Journal Article; 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 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
38.
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
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(PMID = 18712183.001).
[ISSN]
0258-851X
[Journal-full-title]
In vivo (Athens, Greece)
[ISO-abbreviation]
In Vivo
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Proteins; 4Y8F71G49Q / Malondialdehyde
39.
Quintás-Cardama A, Kim TD, Cataldo V, le Coutre P:
Nilotinib.
Recent Results Cancer Res
; 2010;184:103-17
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Therapy with imatinib mesylate is a standard of care for most patients with Philadelphia chromosome-
positive chronic myeloid leukemia
(
CML
).
However, resistance or intolerance to imatinib develops
in a
considerable number of patients leading to relapse or discontinuation of treatment.
Nilotinib is a rationally designed second-generation tyrosine kinase inhibitor (TKI) with improved affinity and specificity against the
BCR
-ABL kinase, when compared with imatinib.
Considerable efficacy after imatinib failure has been demonstrated in clinical trials leading to nilotinib's current approval as second-line therapy for
CML
in chronic
and
accelerated phase
(AP).
The role of nilotinib as first-line treatment for
CML
, in combinatorial strategies and in the context of specific
BCR
-ABL mutations, requires future studies.
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(PMID = 20072834.001).
[ISSN]
0080-0015
[Journal-full-title]
Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
[ISO-abbreviation]
Recent Results Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[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 / Pyrimidines
[Number-of-references]
62
40.
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
41.
Lange T, Park B, Willis SG, Deininger MW:
BCR-ABL kinase domain mutations in chronic myeloid leukemia: not quite enough to cause resistance to imatinib therapy?
Cell Cycle
; 2005 Dec;4(12):1761-6
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[Title]
BCR
-ABL kinase domain mutations
in chronic myeloid leukemia
: not quite enough to cause resistance to imatinib therapy?
Patients with
chronic myeloid leukemia
(
CML
) treated with imatinib in early
chronic
phase
tend to have durable remissions, but there is a high rate of relapse in patients with advanced
disease
.
Mutations in the kinase domain of
BCR
-ABL that impair drug binding have been identified as the major mechanism of resistance.
In the present study we have used a highly sensitive PCR assay to screen for kinase domain mutations in pretherapeutic samples from
CML
patients, irrespective of their subsequent response to imatinib.
We find that kinase domain mutations are demonstrable in approximately 1/3 of patients with
accelerated phase
or blast crisis and that the presence of two copies of the Philadelphia chromosome is strongly correlated with mutation detection.
Unexpectedly, kinase domain mutant clones were not invariably selected in the presence of drug, suggesting that additional mechanisms must contribute to a fully drug resistant
leukemia
.
[MeSH-major]
Drug Resistance, Neoplasm / genetics. Fusion Proteins,
bcr
-abl / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Mutation / genetics. Phosphotransferases / genetics. Piperazines / pharmacology. Pyrimidines / pharmacology
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(PMID = 16319529.001).
[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 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.- / Phosphotransferases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
42.
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
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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
43.
Oehler VG, Yeung KY, Choi YE, Bumgarner RE, Raftery AE, Radich JP:
The derivation of diagnostic markers of chronic myeloid leukemia progression from microarray data.
Blood
; 2009 Oct 8;114(15):3292-8
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[Title]
The derivation of diagnostic markers of
chronic myeloid leukemia
progression from microarray data.
Currently, limited molecular markers exist that can determine where in the spectrum of
chronic myeloid leukemia
(
CML
) progression an individual patient falls at
diagnosis
.
Gene expression profiles can predict
disease
and prognosis, but most widely used microarray analytical methods yield lengthy gene candidate lists that are difficult to apply clinically.
Consequently, we applied a probabilistic method called Bayesian model averaging (BMA) to a large
CML
microarray dataset.
BMA identified 6 genes (NOB1, DDX47, IGSF2, LTB4R, SCARB1, and SLC25A3) that discriminated
chronic
phase
(CP) from blast crisis (BC)
CML
.
In
CML
,
phase
labels divide
disease
progression into discrete states.
In validation studies of 88 patients, the 6-gene signature discriminated early CP from late CP,
accelerated phase
, and BC.
This distinction between early and late CP is not possible with current classifications, which are based on known duration of
disease
.
Because therapeutic outcomes are so closely tied to
disease
phase
, these probabilities can be used to determine a risk-based treatment strategy at
diagnosis
.
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[
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Haematologica. 2006 Feb;91(2):152
[
16461297.001
]
(PMID = 19654405.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NICHD NIH HHS / HD / R01 HD054511; United States / NCI NIH HHS / CA / K25 CA106988-05; United States / NIAID NIH HHS / AI / U54 AI057141; United States / NCI NIH HHS / CA / CA18029; United States / NHLBI NIH HHS / HL / P50HL073996; United States / NCI NIH HHS / CA / R01 CA140371; United States / NCRR NIH HHS / RR / R24 RR021863; United States / NCI NIH HHS / CA / K25CA106988; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCRR NIH HHS / RR / R24RR021863-01A1; United States / NIGMS NIH HHS / GM / R01 GM084163-01A1; United States / PHS HHS / / R01HDO54511-01A1; United States / NIGMS NIH HHS / GM / GM084163-01A1; United States / NIGMS NIH HHS / GM / R01 GM084163; United States / NIDCR NIH HHS / DE / R01DE012212-06; United States / NHLBI NIH HHS / HL / P50 HL073996; United States / NIAID NIH HHS / AI / U54AI057141; United States / NIGMS NIH HHS / GM / R01 GM084163-02; None / None / / K25 CA106988-05; United States / NCRR NIH HHS / RR / UL1 RR025014; None / None / / R01 GM084163-02; United States / NIDCR NIH HHS / DE / R01 DE012212; United States / NCRR NIH HHS / RR / UL1RR025014-01; United States / NIGMS NIH HHS / GM / R01GM084163-01A1; United States / NICHD NIH HHS / HD / R24 HD042828; United States / NCI NIH HHS / CA / K25 CA106988
[Publication-type]
Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
[Other-IDs]
NLM/ PMC2759651
44.
Kantarjian H, Giles F, Wunderle L, Bhalla K, O'Brien S, Wassmann B, Tanaka C, Manley P, Rae P, Mietlowski W, Bochinski K, Hochhaus A, Griffin JD, Hoelzer D, Albitar M, Dugan M, Cortes J, Alland L, Ottmann OG:
Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL.
N Engl J Med
; 2006 Jun 15;354(24):2542-51
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[Title]
Nilotinib in imatinib-resistant
CML
and Philadelphia chromosome-
positive
ALL.
BACKGROUND: Resistance to imatinib mesylate can occur
in chronic myelogenous leukemia
(
CML
).
Preclinical in vitro studies have shown that nilotinib (AMN107), a new
BCR
-ABL tyrosine kinase inhibitor, is more potent than imatinib against
CML
cells by a factor of 20 to 50.
METHODS:
In a
phase
1 dose-escalation study, we assigned 119 patients with imatinib-resistant
CML
or acute lymphoblastic
leukemia
(ALL) to receive nilotinib orally at doses of 50 mg, 100 mg, 200 mg, 400 mg, 600 mg, 800 mg, and 1200 mg once daily and at 400 mg and 600 mg twice daily.
Of 33 patients with the blastic
phase
of
disease
, 13 had a hematologic response and 9 had a cytogenetic response; of 46 patients with the
accelerated phase
, 33 had a hematologic response and 22 had a cytogenetic response; 11 of 12 patients with the
chronic
phase
had a complete hematologic remission.
CONCLUSIONS: Nilotinib has a relatively favorable safety profile and is active in imatinib-resistant
CML
. (ClinicalTrials.gov number, NCT00109707 [ClinicalTrials.gov].).
[MeSH-major]
Antineoplastic Agents / administration & dosage. Fusion Proteins,
bcr
-abl / antagonists & inhibitors.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage
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[Copyright]
Copyright 2006 Massachusetts Medical Society.
[CommentIn]
N Engl J Med. 2006 Jun 15;354(24):2594-6
[
16775240.001
]
(PMID = 16775235.001).
[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/ NCT00109707
[Publication-type]
Clinical Trial, Phase I; 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 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
45.
Wei Y, Hardling M, Olsson B, Hezaveh R, Ricksten A, Stockelberg D, Wadenvik H:
Not all imatinib resistance in CML are BCR-ABL kinase domain mutations.
Ann Hematol
; 2006 Dec;85(12):841-7
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[Title]
Not all imatinib resistance in
CML
are
BCR
-ABL kinase domain mutations.
Point mutations within the ABL kinase domain of the
BCR
-ABL gene are associated with clinical resistance to imatinib mesylate
in chronic myeloid leukemia
(
CML
).
To obtain more information about the association between
BCR
-ABL mutations and type of imatinib resistance, we studied 30 early
chronic
phase
(CP)
CML
patients, commencing imatinib therapy, using a conventional sequencing technique.
Seven patients treated in late CP and three patients treated in the
accelerated phase
were included for comparison.
Likewise, none of 12 early CP patients with detectable
BCR
-ABL transcripts but in complete hematologic and cytogenetic remission at 12 months displayed any mutation.
We conclude that screening early CP patients for
BCR
-ABL mutations before start of imatinib therapy is not cost-effective.
BCR
-ABL kinase domain mutations do not appear to explain cytogenetic or molecular (detectable
BCR
-ABL transcripts by polymerase chain reaction)
disease
persistence in patients otherwise in stable
disease
.
However, in patients with signs of expanding
disease
burden, a search for
BCR
-ABL mutations is warranted.
[MeSH-major]
Drug Resistance, Neoplasm / genetics. 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
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
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.
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.
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.
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(PMID = 17006667.001).
[ISSN]
0939-5555
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.- / Protein Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
46.
Chen Y, Peng C, Li D, Li S:
Molecular and cellular bases of chronic myeloid leukemia.
Protein Cell
; 2010 Feb;1(2):124-32
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[Title]
Molecular and cellular bases of
chronic myeloid leukemia
.
Chronic myeloid leukemia
(
CML
) is a myeloproliferative
disease
characterized by the overproduction of granulocytes, which leads to high white blood cell counts and splenomegaly in patients.
Based on clinical symptoms and laboratory findings,
CML
is classified into three clinical phases, often starting with
a chronic
phase
, progressing to an
accelerated phase
and ultimately ending
in a
terminal
phase
called blast crisis.
Blast crisis
phase
of
CML
is clinically similar to an acute
leukemia
; in particular, B-cell acute lymphoblastic
leukemia
(B-ALL) is a severe form of acute
leukemia in
blast crisis, and there is no effective therapy for it yet.
CML
is induced by the
BCR
-ABL oncogene, whose gene product is
a BCR
-ABL tyrosine kinase.
Currently, inhibition of
BCR
-ABL kinase activity by its kinase inhibitor such as imatinib mesylate (Gleevec) is a major therapeutic strategy for
CML
.
However, the inability of
BCR
-ABL kinase inhibitors to completely kill
leukemia
stem cells (LSCs) indicates that these kinase inhibitors are unlikely to cure
CML
.
In addition, drug resistance due to the development of BCRABL mutations occurs before and during treatment of
CML
with kinase inhibitors.
In this review, we will focus on LSCs in
CML
by summarizing and discussing available experimental results, including the original studies from our own laboratory.
[MeSH-major]
Fusion Proteins,
bcr
-abl / metabolism.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ enzymology.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ pathology. Neoplastic Stem Cells / enzymology. Neoplastic Stem Cells / pathology. Protein-Tyrosine Kinases / metabolism
[MeSH-minor]
5-Lipoxygenase-Activating Proteins / metabolism. Animals. Benzamides.
Disease
Models, Animal. Humans. Imatinib Mesylate. Male. Mice. PTEN Phosphohydrolase / metabolism. Philadelphia Chromosome. Piperazines / therapeutic use. Point Mutation. Protein Structure, Tertiary. Pyrimidines / therapeutic use
Genetic Alliance.
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.
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.
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consumer health - Chronic Myeloid Leukemia
.
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.
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NCI CPTAC Assay Portal
.
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(PMID = 21203982.001).
[ISSN]
1674-8018
[Journal-full-title]
Protein & cell
[ISO-abbreviation]
Protein Cell
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / 5-Lipoxygenase-Activating Proteins; 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; EC 3.1.3.67 / PTEN Phosphohydrolase
[Other-IDs]
NLM/ PMC4875160
47.
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
Genetic Alliance.
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.
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consumer health - Leukemia, Myeloid
.
Genetic Alliance.
consumer health - Transplantation
.
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consumer health - Cancer Chemotherapy
.
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
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.
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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
48.
Singh RK, Tripathi AK, Tripathi P, Singh S, Singh R, Ahmad R:
Studies on biomarkers for oxidative stress in patients with chronic myeloid leukemia.
Hematol Oncol Stem Cell Ther
; 2009;2(1):285-8
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[Title]
Studies on biomarkers for oxidative stress in patients with
chronic myeloid leukemia
.
BACKGROUND:
Chronic myeloid leukemia
(
CML
) is a myeloproliferative
disorder
with a unique genetic rearrangement, the Philadelphia chromosome.
The aim of this study was to evaluate the products of protein oxidation and lipid peroxidation in plasma as biomarkers of oxidative stress in
CML
patients.
PATIENTS AND METHODS: The study included 40
CML
patients and 20 age- and sex-matched healthy volunteers.
Of 40
CML
patients, 28 were
in chronic
phase
(
CML
-CP) and 12 in
accelerated phase
(
CML
-AP).
RESULTS: There were significant differences (P < .05) in plasma levels of PC, TBARS and LOOH in
CML
,
CML
-CP and
CML
-AP patients as compared to controls.
CONCLUSION: PC, TBARS and LOOH might reflect oxidative stress in
CML
patients and might be used as biomarkers in such patients.
[MeSH-major]
Biomarkers, Tumor / analysis.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ blood.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ pathology. Oxidative Stress / physiology
Genetic Alliance.
consumer health - Chronic Myeloid Leukemia
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Chronic Myeloid Leukemia
.
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.
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.
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(PMID = 20063559.001).
[ISSN]
1658-3876
[Journal-full-title]
Hematology/oncology and stem cell therapy
[ISO-abbreviation]
Hematol Oncol Stem Cell Ther
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Lipid Peroxides; 0 / Thiobarbituric Acid Reactive Substances
49.
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.
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(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
50.
Hazarika M, Jiang X, Liu Q, Lee SL, Ramchandani R, Garnett C, Orr MS, Sridhara R, Booth B, Leighton JK, Timmer W, Harapanhalli R, Dagher R, Justice R, Pazdur R:
Tasigna for chronic and accelerated phase Philadelphia chromosome--positive chronic myelogenous leukemia resistant to or intolerant of imatinib.
Clin Cancer Res
; 2008 Sep 1;14(17):5325-31
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[Title]
Tasigna for
chronic
and
accelerated phase
Philadelphia chromosome--
positive chronic myelogenous leukemia
resistant to or intolerant of imatinib.
PURPOSE: This Food and Drug Administration (FDA) approval report describes the data and analyses leading to the approval by the FDA of nilotinib (Tasigna, AMN-107; Novartis Pharmaceuticals Corporation), an inhibitor of
Bcr
-Abl tyrosine kinase, for the treatment of
chronic
-
phase
(CP) and
accelerated
-
phase
(AP)
chronic myelogenous leukemia
(
CML
) resistant to or intolerant of imatinib.
EXPERIMENTAL DESIGN: The FDA approval of the efficacy and safety of nilotinib was based on the results of an ongoing single-arm, open-label,
phase
2 clinical trial.
The primary end point for
CML
-CP was unconfirmed major cytogenetic response.
The efficacy end point for
CML
-AP was confirmed hematologic response.
The median duration of response has not been reached for both
CML
-CP and
CML
-AP responding patients.
In
CML
-CP patients, the common serious drug-related adverse reactions were thrombocytopenia and neutropenia.
In
CML
-AP patients, the common serious drug-related adverse reactions were thrombocytopenia, neutropenia, pneumonia, febrile neutropenia, leukopenia, intracranial hemorrhage, elevated lipase, and pyrexia.
Nilotinib prolongs the QT interval and sudden deaths have been reported; these risks and appropriate risk minimization strategies are described
in a
boxed warning on the labeling.
FDA granted
accelerated
approval to nilotinib (Tasigna) for use in the treatment of CP and AP Philadelphia chromosome
positive
CML
in adult patients resistant to or intolerant of prior therapy that included imatinib.
[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]
Adult. Benzamides. Clinical Trials,
Phase
II as Topic. Drug Approval. Drug Resistance, Neoplasm. Fusion Proteins,
bcr
-abl. Humans. Imatinib Mesylate. Protein Kinase Inhibitors / therapeutic use. United States. United States Food and Drug Administration
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(PMID = 18765523.001).
[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 / 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 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
51.
Wu LL, Zeng QS, Yang MZ, Miao HW, Xia RX, Wang L, Ni J:
[Detection of ABL kinase domain point mutations in chronic myeloid leukemia patients receiving imatinib treatment].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2010 Feb;18(1):49-53
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[Title]
[Detection of ABL kinase domain point mutations
in chronic myeloid leukemia
patients receiving imatinib treatment].
This study was purposed to evaluate ABL tyrosine kinase point mutations in imatinib-treated
chronic myeloid leukemia
(
CML
) patients and their clinical significance.
51 bone marrow samples from 28 imatinib-resistant patients and 10 newly diagnosed
CML
patients were collected.
ABL kinase domain of
bcr
-abl allele was amplified by nested reverse transcription-polymerase chain reaction, followed by purifying, directly sequencing and sequence homology analysis of amplified products in order to determine the existence and type of point mutation.
The results showed that the point mutations were found in 12 of 38 patients, and all the 12 ones progressed to advanced
disease
or death.
The incidence of the point mutation was 17.6%, 45.5% and 44.4%
in chronic
,
accelerated
and blast
phase
respectively.
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(PMID = 20137117.001).
[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 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
52.
Vasconcelos FC, Gattass CR, Rumjanek VM, Maia RC:
Pomolic acid-induced apoptosis in cells from patients with chronic myeloid leukemia exhibiting different drug resistance profile.
Invest New Drugs
; 2007 Dec;25(6):525-33
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[Title]
Pomolic acid-induced apoptosis in cells from patients with
chronic myeloid leukemia
exhibiting different drug resistance profile.
Pomolic acid (PA) is a pentacyclic triterpene which has been previously described as active in inhibiting the growth of K562 cell line-originated from
chronic myeloid leukemia
(
CML
) in blast crisis-and its vincristine-resistant derivative K562-Lucena1.
In this work, cells from
CML
patients were treated with PA and the apoptotic index was compared with the multidrug resistance (MDR) profile and clinical status of the patients.
Our findings show that PA 12.5 microg/ml at 24 h (p = 0.000), at 48 h (p = 0.012) and at 72 h (p = 0.005) has a potent apoptotic index in
CML
cells as compared to mononuclear cells from healthy donors.
PA was capable to induce apoptosis in cells from
CML
patients exhibiting functional MDR phenotype but not in P-glycoprotein expression.
In addition, PA was effective
in chronic
as well as in blast
phase
of
CML
.
These results suggest that PA may be an effective agent for the treatment of
CML
.
[MeSH-major]
Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Drug Resistance, Neoplasm.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Oleanolic Acid / analogs & derivatives
[MeSH-minor]
Blast Crisis / drug therapy. Blast Crisis / pathology. Drug Resistance, Multiple. Humans.
Leukemia
,
Myeloid
,
Accelerated Phase
/ drug therapy.
Leukemia
,
Myeloid
,
Accelerated Phase
/ pathology.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ drug therapy.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ pathology
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[Cites]
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Pharmacol Ther. 2000 Mar;85(3):217-29
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10739876.001
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Leukemia. 2004 Aug;18(8):1406-12
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(PMID = 17520174.001).
[ISSN]
0167-6997
[Journal-full-title]
Investigational new drugs
[ISO-abbreviation]
Invest New Drugs
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / pomolic acid; 6SMK8R7TGJ / Oleanolic Acid
53.
Jabbour E, Cortés JE, Kantarjian H:
Optimizing treatment with Bcr-Abl tyrosine kinase inhibitors in Philadelphia chromosome-positive chronic myeloid leukemia: focus on dosing schedules.
Clin Lymphoma Myeloma
; 2008 Mar;8 Suppl 3:S75-81
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[Title]
Optimizing treatment with
Bcr
-Abl tyrosine kinase inhibitors in Philadelphia chromosome-
positive chronic myeloid leukemia
: focus on dosing schedules.
Chronic myeloid leukemia
(
CML
) is characterized by the presence of the Philadelphia chromosome (Ph), a genetic aberration that codes for bcrabl, which plays a key role
in disease
pathophysiology.
Dose-escalated imatinib (800 mg daily) has shown some limited activity in patients with imatinib-resistant
CML
, but the development of second-generation tyrosine kinase inhibitors has broadened the treatment options.
Dasatinib has demonstrated activity in all phases of
CML
and Ph+ acute lymphocytic
leukemia
and is approved for the treatment of adults in this setting.
Recent
phase
III data have demonstrated that, in patients with
chronic
-
phase CML
, dasatinib 100 mg once daily is equally effective, with improved tolerability, compared with the previously approved 70-mg twice-daily dose.
Nilotinib, which has been recently approved, has increased potency for Brc-Abl compared with imatinib and has demonstrated activity in patients with imatinib-resistant and -intolerant
chronic
- and
accelerated
-
phase CML
.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Philadelphia Chromosome. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
[MeSH-minor]
Clinical Trials as Topic. Dasatinib. Fusion Proteins,
bcr
-abl. Humans
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(PMID = 19254884.001).
[ISSN]
1557-9190
[Journal-full-title]
Clinical lymphoma & myeloma
[ISO-abbreviation]
Clin Lymphoma Myeloma
[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; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
[Number-of-references]
51
54.
Martin MG, Dipersio JF, Uy GL:
Management of the advanced phases of chronic myelogenous leukemia in the era of tyrosine kinase inhibitors.
Leuk Lymphoma
; 2009 Jan;50(1):14-23
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[Title]
Management of the advanced phases of
chronic myelogenous leukemia in
the era of tyrosine kinase inhibitors.
Imatinib has revolutionised the management of
chronic
phase
chronic myelogenous leukemia
(
CML
).
Unfortunately it has had less of an impact on the management of the advanced phases of
CML
.
These historically difficult-to-treat phases of
disease
remain largely resistant to therapy.
Even when responses are obtained with the tyrosine kinase inhibitors, they are brief, particularly in blast
phase
(BP)
disease
.
But transplant outcomes are dependent on cytogenetic and gross
disease
burden at the time of transplant.
This review will compare and contrast the various tyrosine kinase- and non-tyrosine kinase inhibitor-based treatments for
accelerated
and BP
CML
before allogeneic transplantation.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ pathology. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors
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(PMID = 19117213.001).
[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 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
[Number-of-references]
80
55.
Basak G, Torosian T, Snarski E, Niesiobedzka J, Majewski M, Gronkowska A, Urbanowska E, Jedrzejczak W:
Hematopoietic stem cell transplantation for T315I-mutated chronic myelogenous leukemia.
Ann Transplant
; 2010 Apr-Jun;15(2):68-70
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[Title]
Hematopoietic stem cell transplantation for T315I-mutated
chronic myelogenous leukemia
.
BACKGROUND: The T315I mutation of
BCR
/ABL gene is known to produce complete resistance of
chronic myelogenous leukemia
(
CML
) to all currently available
BCR
/ABL inhibitors.
However, evidence on efficiency of this treatment modality in
CML
with T315I mutation is lacking.
CASE REPORT: A 25-year-old patient was diagnosed with Philadelphia chromosome
positive
CML
in
accelerated phase
.
Moreover, despite escalation of imatinib dosage, the
disease
relapsed after further 3 months of treatment.
Molecular studies revealed T315I mutation of
BCR
/ABL gene.
The course of transplantation was complicated by staphylococcal sepsis, grade I skin acute GvHD and limited
chronic
skin GVHD.
CONCLUSIONS: The clinical course of this case supports the idea that allogeneic hematopoietic transplantation is a viable treatment option for patients with
CML
bearing T315I mutation.
[MeSH-major]
Genes, abl. Hematopoietic Stem Cell Transplantation.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy. Mutation, Missense
[MeSH-minor]
Adult. Amino Acid Substitution. Drug Resistance, Neoplasm / genetics. Fusion Proteins,
bcr
-abl / antagonists & inhibitors. Fusion Proteins,
bcr
-abl / genetics. Humans.
Leukemia
,
Myeloid
,
Accelerated Phase
/ drug therapy.
Leukemia
,
Myeloid
,
Accelerated Phase
/ genetics.
Leukemia
,
Myeloid
,
Accelerated Phase
/ therapy. Male. Protein Kinase Inhibitors / pharmacology. Remission Induction. Transplantation, Homologous
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(PMID = 20657522.001).
[ISSN]
2329-0358
[Journal-full-title]
Annals of transplantation
[ISO-abbreviation]
Ann. Transplant.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Poland
[Chemical-registry-number]
0 / Protein Kinase Inhibitors; EC 2.7.10.2 / Fusion Proteins, bcr-abl
56.
Tian J, Cheng H, Xu KL, Pan XY:
[Detection of phosphotyrosine in chronic myeloid leukemia cells with PY20 antibody and its clinical applications].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2009 Aug;17(4):1056-60
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[Title]
[Detection of phosphotyrosine
in chronic myeloid leukemia
cells with PY20 antibody and its clinical applications].
The objective of this study was to investigate the specificity of detecting the phosphotyrosine level with anti-phosphotyrosine monoclonal antibody PY20 for
diagnosis
and prognosis of patients with
chronic myeloid leukemia
(
CML
) and the possibility of its clinical application.
The
positive
rate of PY20 in 28 newly diagnosed
CML
patients was detected by flow cytometry using anti-PY20 antibody, the
bcr
-abl fusion gene was detected by nested RT-PCR, the Ph chromosome was measured by R-banding cytogenetic analysis, and the coincidence of PY20
positive
rate with results of
bcr
-abl fusion gene and Ph chromosome detection was compared.
In addition, the
positive
rate of PY20, the changes of
bcr
-abl fusion gene and Ph chromosome were determined in follow up 7
CML
patients after allo-hematopoietic stem cell transplantation.
The results indicated that the
positive
rates of PY20 in 28 newly diagnosed
CML
patients in groups of
chronic
phase
(CP),
accelerated phase
(AP), and blast
phase
(BP) were (40.31% +/- 1.22)%, (77.28 +/- 1.14)% and (78.12 +/- 1.32)% respectively.
The
positive
rate of PY20 in CP was lower than that in AP and BP (p < 0.05).
There was no difference
in positive
rate of PY20 between AP and BP (p > 0.05).
The
positive
rates of PY20 in patients with
CR
, PR and NR were (15.56% +/- 1.51)%, (38.73% +/- 2.31)% and (60.43% +/- 2.04)% respectively.
The
positive
and negative coincidence between PY20 and RT-PCR was 92.31% and 95.45% respectively.
The
positive
and negative coincidence between PY20 and Ph Chromosome in newly diagnosed patients was 88.46% and 95.46% respectively.
Ph chromosome and PY20 were all negative in 7
CML
patients after allo-HSCT.
Bcr
-abl fusion gene was negative persistently in 5 patients, but in the other 2 patients, the fusion gene was persistently
positive
.
In conclusion, the detection of the level of phosphotyrosine in
CML
cells has high sensitivity and specificity.
The results of PY20 cell
positive
rate combined with detection of
bcr
/abl fusion gene and Ph chromosome might be useful
in diagnosis
as a good index of monitoring.
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(PMID = 19698259.001).
[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
[Publication-country]
China
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 21820-51-9 / Phosphotyrosine; EC 2.7.10.2 / Fusion Proteins, bcr-abl
57.
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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[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
58.
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
59.
Kantarjian H, Shah NP, Hochhaus A, Cortes J, Shah S, Ayala M, Moiraghi B, Shen Z, Mayer J, Pasquini R, Nakamae H, Huguet F, Boqué C, Chuah C, Bleickardt E, Bradley-Garelik MB, Zhu C, Szatrowski T, Shapiro D, Baccarani M:
Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia.
N Engl J Med
; 2010 Jun 17;362(24):2260-70
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[Title]
Dasatinib versus imatinib in newly diagnosed
chronic
-
phase
chronic myeloid leukemia
.
BACKGROUND: Treatment with dasatinib, a highly potent
BCR
-ABL kinase inhibitor, has resulted in high rates of complete cytogenetic response and progression-free survival among patients with
chronic myeloid leukemia
(
CML
) in the
chronic
phase
, after failure of imatinib treatment.
We assessed the efficacy and safety of dasatinib, as compared with imatinib, for the first-line treatment of
chronic
-
phase CML
.
METHODS:
In a
multinational study, 519 patients with newly diagnosed
chronic
-
phase CML
were randomly assigned to receive dasatinib at a dose of 100 mg once daily (259 patients) or imatinib at a dose of 400 mg once daily (260 patients).
The rate of major molecular response was higher with dasatinib than with imatinib (46% vs. 28%, P<0.0001), and responses were achieved
in a
shorter time with dasatinib (P<0.0001).
Progression to the
accelerated
or blastic
phase
of
CML
occurred in 5 patients who were receiving dasatinib (1.9%) and in 9 patients who were receiving imatinib (3.5%).
Since achieving complete cytogenetic response within 12 months has been associated with better long-term, progression-free survival, dasatinib may improve the long-term outcomes among patients with newly diagnosed
chronic
-
phase CML
. (ClinicalTrials.gov number, NCT00481247. )
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Blast Crisis / prevention & control. Dasatinib.
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]
Expert Opin Pharmacother. 2011 Jan;12(1):157-63
[
21108601.001
]
[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]
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 = 20525995.001).
[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/ NCT00481247
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[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 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
60.
Notari M, Neviani P, Santhanam R, Blaser BW, Chang JS, Galietta A, Willis AE, Roy DC, Caligiuri MA, Marcucci G, Perrotti D:
A MAPK/HNRPK pathway controls BCR/ABL oncogenic potential by regulating MYC mRNA translation.
Blood
; 2006 Mar 15;107(6):2507-16
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[Title]
A MAPK/HNRPK pathway controls
BCR
/ABL oncogenic potential by regulating MYC mRNA translation.
Altered mRNA translation is one of the effects exerted by the
BCR
/ABL oncoprotein in the blast crisis
phase
of
chronic myelogenous leukemia
(
CML
).
Here, we report that
in BCR
/ABL+ cell lines and in patient-derived
CML
blast crisis mononuclear and CD34+ cells, p210(
BCR
/ABL) increases expression and activity of the transcriptional-inducer and translational-regulator heterogeneous nuclear ribonucleoprotein K (hnRNP K or HNRPK)
in a
dose- and kinase-dependent manner through the activation of the MAPK(ERK1/2) pathway.
Furthermore, HNRPK down-regulation and interference with HNRPK translation-but not transcription-regulatory activity impairs cytokine-independent proliferation, clonogenic potential, and in vivo leukemogenic activity of
BCR
/ABL-expressing
myeloid
32Dcl3 and/or primary CD34+
CML
-BC patient cells.
Mechanistically, we demonstrate that decreased internal ribosome entry site (IRES)-dependent Myc mRNA translation accounts for the phenotypic changes induced by inhibition of the
BCR
/ABL-ERK-dependent HNRPK translation-regulatory function.
Accordingly, MYC protein but not mRNA levels are increased in the CD34+ fraction of patients with
CML
in
accelerated
and blastic
phase
but not
in chronic
phase CML
patients and in the CD34+ fraction of marrow cells from healthy donors.
Thus,
BCR
/ABL-dependent enhancement of HNRPK translation-regulation is important for
BCR
/ABL leukemogenesis and, perhaps, it might contribute to blast crisis transformation.
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[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / CA16058
[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.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD34; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / Ribonucleoproteins; 146410-60-8 / HNRNPK protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
[Other-IDs]
NLM/ PMC1895740
61.
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
62.
Etienne G, Milpied B, Réa D, Rigal-Huguet F, Tulliez M, Nicolini FE, French Intergroup of CML (Fi-LMC group):
[Guidelines for the management of nilotinib (Tasigna)-induced side effects in chronic myelogenous leukemia: recommendations of French Intergroup of CML (Fi-LMC group)].
Bull Cancer
; 2010 Aug;97(8):997-1009
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[Title]
[Guidelines for the management of nilotinib (Tasigna)-induced side effects
in chronic myelogenous leukemia
: recommendations of French Intergroup of
CML
(Fi-
LMC
group)].
[Transliterated title]
Recommandations du groupe Fi-
LMC
pour la gestion des effets indésirables du traitement par nilotinib (Tasigna) au cours
de
la leucémie myéloïde
chronique
.
Nilotinib (Tasigna) is a second-generation
BCR
-ABL kinase inhibitor, recently introduced and used for the treatment of
chronic
or
accelerated phase CML
patients, intolerant or resistant to imatinib.
This treatment represents and important step forward for the
disease
control of such patients but can lead to side effects, sometimes serious, which can limit its optimal use.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Protein Kinase Inhibitors / adverse effects. Pyrimidines / adverse effects
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(PMID = 20529767.001).
[ISSN]
1769-6917
[Journal-full-title]
Bulletin du cancer
[ISO-abbreviation]
Bull Cancer
[Language]
fre
[Publication-type]
English Abstract; Journal Article; Practice Guideline
[Publication-country]
France
[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; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
63.
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
64.
Hochhaus A, O'Brien SG, Guilhot F, Druker BJ, Branford S, Foroni L, Goldman JM, Müller MC, Radich JP, Rudoltz M, Mone M, Gathmann I, Hughes TP, Larson RA, IRIS Investigators:
Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia.
Leukemia
; 2009 Jun;23(6):1054-61
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[Title]
Six-year follow-up of patients receiving imatinib for the first-line treatment of
chronic myeloid leukemia
.
Imatinib mesylate is considered standard of care for first-line treatment of
chronic
phase
chronic myeloid leukemia
(
CML
-CP).
In the
phase
III, randomized, open-label International Randomized Study of Interferon vs STI571 (IRIS) trial, previously untreated
CML
-CP patients were randomized to imatinib (n=553) or interferon-alpha (IFN) plus cytarabine (n=553).
This 6-year update focuses on patients randomized to receive imatinib as first-line therapy for newly diagnosed
CML
-CP.
During the sixth year of study treatment, there were no reports of
disease
progression to
accelerated phase
(AP) or blast crisis (BC).
The estimated overall survival was 88% -- or 95% when only
CML
-related deaths were considered.
This 6-year update of IRIS underscores the efficacy and safety of imatinib as first-line therapy for patients with
CML
.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
[MeSH-minor]
Benzamides.
Disease
Progression. Follow-Up Studies. Heart Failure / chemically induced. Humans. Imatinib Mesylate. Neoplasms, Second Primary / chemically induced. Remission Induction. Survival Analysis. Treatment Outcome
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[ErratumIn]
Leukemia. 2010 May;24(5):1102
(PMID = 19282833.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
[Investigator]
Hughes T; Taylor K; Durant S; Schwarer A; Joske D; Seymour J; Grigg A; Ma D; Arthur C; Bradstock K; Joshua D; Agis H; Verhoef G; Louwagie A; Martiat P; Bosly A; Shepherd J; Shistok C; Lipton J; Forrest D; Walker I; Roy DC; Rubinger M; Bence-Bruckler I; Stewart D; Kovacs M; Turner AR; Nielsen J; Birgens H; Bjerrum O; Rousselot P; Reiffers J; Facon T; Harousseau JL; Tulliez M; Guerci A; Blaise D; Maloisel F; Michallet M; Fischer T; Hochhaus A; Andreesen R; Nerl C; Freund M; Gattermann N; Ehninger G; Niederwieser D; Ottmann OG; Peschel C; Ho AD; Neubauer A; le Coutre P; Aulitzky W; Saglio G; Baccarani M; Fanin R; Rosti G; Mandelli F; Lazzarino M; Morra E; Carella A; Petrini M; Nobile F; Liso V; Ferrara F; Rizzoli V; Fiortoni G; Martinelli G; Cornelissen J; Ossenkoppele G; Browett P; Gedde-Dahl T; Tangen JM; Dahl I; Cervantes F; Odrizoala J; Hernandez Boulda JC; Steegmann JL; Canizo C; Diaz J; Grenena A; Fernandez M; Simonsson B; Stenke L; Paul C; Bjoreman M; Malm C; Wadenvik H; Nilsson PG; Turesson I; Gratwohl A; Hess U; Solenthaler M; Goldman JM; Clark RE; Green A; Holyoake T; Lucas G; Smith G; Milligan D; Rule S; Burnett A; Kantarjian H; Silver R; Stone R; Powell B; Gabrilove J; Moroose R; Wetzler M; Bearden J; Cataland S; Rabinowitz I; Meisenberg B; Thompson K; Graziano S; Emanuel P; Gross H; Cobb P; Bhatia R; Dakhil S; Irwin AD; Issell B; Pavletic S; Kuebler P; Layhe E; Butra P; Glass J; Moore J; Grant B; Neill H; Herzig R; Burris H; Petersen B; Kalaycio M; Stirewalt D; Samlowski W; Berman E; Limentani S; Seay T; Shea T; Akard L; Smith G; Becker P; Devine S; Hart R; Veith R; Wade J; Brunvad M; Kalman L; Strickland D; Shurafa M; Bashey A; Shadduck R; Safah H; Rubenstein M; Collins R; Keller A; Tallman M; Pecora A; Agha M; Homes H; Guidice R; Druker BJ; Guilhot F; Larson RA; O'Brien S; Rowe J; Schiffer CA; Buyse M; Baccarani M; Cervantes F; Cornelissen J; Fischer T; Hochhaus A; Hughes T; Lechner K; Nielsen JL; Reiffers J; Rousselot P; Saglio G; Shepherd J; Simonsson B; Gratwohl A; Goldman JM; Talpaz M; Taylor K; Verhoef G; Santini V
65.
Kosugi N, Ebihara Y, Nakahata T, Saisho H, Asano S, Tojo A:
CD34+CD7+ leukemic progenitor cells may be involved in maintenance and clonal evolution of chronic myeloid leukemia.
Clin Cancer Res
; 2005 Jan 15;11(2 Pt 1):505-11
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[Title]
CD34+CD7+ leukemic progenitor cells may be involved in maintenance and clonal evolution of
chronic myeloid leukemia
.
PURPOSE: We analyzed CD34+ cells coexpressing CD7
in chronic myeloid leukemia
(
CML
)
in chronic
phase
(CP) or
accelerated phase
(AP) to clarify their role in progression or regression of the
disease
during treatment.
EXPERIMENTAL DESIGN: Enumeration of CD34+CD7+ cells was done on bone marrow nucleated cells from normal donors and
CML
patients.
Fluorescence in situ hybridization analysis was done on sorted CD34+CD7+and CD34+CD7- cells to examine the occupancy rate of each fraction by
BCR
-ABL+ cells with or without additional cytogenetic abnormalities.
RESULTS: The proportion of CD34+CD7+cells was significantly affected by the treatment outcome and/or the
disease
status as follows: 20.5 +/- 10.4% in normal donors (n = 22), 18.1 +/- 10.2% in CP with major cytogenetic response (n = 14), 53.0 +/- 12.9% in CP at
diagnosis
(n = 18), 55.0 +/- 15.8% in CP with minor or no cytogenetic response (n = 28), and 70.2 +/- 18.1% in AP (n = 6).
In six untreated CP patients, the ratio of
BCR
-ABL+ cells was comparable between each fraction.
In three patients with major cytogenetic response, the ratio of
BCR
-ABL+ cells was remarkably lower in CD34+CD7- cells than in CD34+CD7+cells.
CONCLUSIONS: Our results suggest that CD34+CD7+ cells may be involved in maintenance and clonal evolution of
BCR
-ABL+ cells in
CML
.
[MeSH-major]
Antigens, CD34 / metabolism. Antigens, CD7 / metabolism. Hematopoietic Stem Cells / metabolism.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ metabolism.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ pathology. Stem Cells / metabolism
[MeSH-minor]
Adolescent. Adult. Bone Marrow. Chromosome Aberrations. Clone Cells. Cytogenetic Analysis.
Disease
Progression. Female. Fusion Proteins,
bcr
-abl / metabolism. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Tissue Donors
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(PMID = 15701834.001).
[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; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Antigens, CD7; EC 2.7.10.2 / Fusion Proteins, bcr-abl
66.
Huang Q:
Chronic myelogenous leukemia in accelerated phase.
Arch Pathol Lab Med
; 2005 May;129(5):710
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[Title]
Chronic myelogenous leukemia in
accelerated phase
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fusion Proteins,
bcr
-abl / genetics.
Leukemia
,
Myeloid
,
Accelerated Phase
. Philadelphia Chromosome. Translocation, Genetic
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(PMID = 15859653.001).
[ISSN]
1543-2165
[Journal-full-title]
Archives of pathology & laboratory medicine
[ISO-abbreviation]
Arch. Pathol. Lab. Med.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Arsenicals; 0 / Benzamides; 0 / Oxides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; S7V92P67HO / arsenic trioxide; X6Q56QN5QC / Hydroxyurea
67.
Yamamoto M, Kakihana K, Ohashi K, Yamaguchi T, Tadokoro K, Akiyama H, Sakamaki H:
Serial monitoring of T315I BCR-ABL mutation by Invader assay combined with RT-PCR.
Int J Hematol
; 2009 May;89(4):482-8
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[Title]
Serial monitoring of T315I
BCR
-ABL mutation by Invader assay combined with RT-PCR.
We recently developed an Invader assay combined with reverse transcriptase polymerase-chain-reaction in order to quantify T315I
bcr
-abl transcripts.
Using this assay, we serially monitored T315I
bcr
-abl transcripts
in chronic myeloid leukemia
(
CML
) patients whose
bcr
-abl transcripts were still detectable at 6 months after starting imatinib therapy.
Although, we continued to monitor
bcr
-abl transcripts in 14
CML
patients (13
chronic
phases and 1
accelerated phase
) for up to 12 months, there were no patients who were apparently resistant to imatinib due to the T315I mutation.
In contrast,
in a
case of Philadelphia chromosome-
positive
acute lymphoid
leukemia
being treated with chemotherapy including imatinib, we monitored both wild-type and T315I
bcr
-abl transcripts, and found increased levels of T315I transcripts during relapse (0% at the time of
diagnosis
and 54.8% at relapse).
[MeSH-major]
Fusion Proteins,
bcr
-abl / analysis. Fusion Proteins,
bcr
-abl / genetics. Genetic Techniques
[MeSH-minor]
Adult. Aged. Female. Humans.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Male. Middle Aged. Mutation / genetics
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[Cites]
Blood. 2006 Jul 1;108(1):28-37
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(PMID = 19343480.001).
[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
EC 2.7.10.2 / Fusion Proteins, bcr-abl
68.
Latagliata R, Breccia M, Carmosino I, Sarlo C, Montefusco E, Mancini M, Natalino F, Chistolini A, De Cuia R, Russo E, Morano GS, Biondo F, Spadea A, Mandelli F, Alimena G:
Elderly patients with Ph+ chronic myelogenous leukemia (CML): results of imatinib mesylate treatment.
Leuk Res
; 2005 Mar;29(3):287-91
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[Title]
Elderly patients with Ph+
chronic myelogenous leukemia
(
CML
): results of imatinib mesylate treatment.
Thirty-five patients with Ph+
CML
aged more than 60 years were treated with imatinib.
Twenty-four patients (group A) were in late
chronic
phase
(CP) and eleven patients (group B) were in
accelerated
/blastic
phase
(AP/BP).
In group A, complete haematological response (CHR) was achieved by all patients; seventeen patients (70.8%) attained a complete cytogenetic response (CCR), one (4.1%) attained a partial
CR
, one (4.1%) a minor
CR
(Ph+ 70%) and five (21%) were resistant (Ph+ 100%), toxicity was mild: seven patients had a transient cytopenia, three a skin reaction, one a moderate oedema and one muscular pain.
In group B, one patient died after 3 months in aplastic
phase
from sepsis, three patients were resistant and seven patients (63.7%) achieved CHR; of these, four obtained CCR.
After a median follow-up of 17 months, 4 patients have died from progressive
disease
, 6 are alive; 1 in AP and 5 in CHR (4 of them being in CCR).
[MeSH-major]
Aged.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
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[ErratumIn]
Leuk Res. 2005 Sep;29(9):1099. Roberto, Latagliata [corrected to Latagliata, Roberto]; Massimo, Breccia [corrected to Breccia, Massimo]; Ida, Carmosino [corrected to Carmosino, Ida]; Chiara, Sarlo [corrected to Sarlo, Chiara]; Enrico, Montefusco [corrected to Montefusco, Enrico]; Marco, Mancini [corrected to Mancini, Marco]; Fiammetta, Natalino [corrected to Natalino, Fiammetta]; Antonio, Chistolini [corrected to Chistolini, Antonio]; Rosa, De Cuia [corrected to De Cuia, Rosa]; Eleonora, Russo [corrected to Russo, Eleonora]; Giacomo, Morano Salvatore [corrected to Morano, Giacomo Salvatore]; Francesca, Biondo [corrected to Biondo, Francesca]; Antonio, Spadea [corrected to Spadea, Antonio]; Franco, Mandelli [corrected to Mandelli, Franco]; Giuliana, Alimena [corrected to Alimena, Giuliana]
(PMID = 15661264.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
69.
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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[Cites]
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[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
70.
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
71.
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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.
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.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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]
(PMID = 16477019.001).
[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
72.
De Souza CA, Vigorito AC, Ruiz MA, Nucci M, Dulley FL, Funcke V, Tabak D, Azevedo AM, Byington R, Macedo MC, Saboya R, Penteado Aranha FJ, Oliveira GB, Zulli R, Martins Miranda EC, Azevedo WM, Lodi FM, Voltarelli JC, Simões BP, Colturato V, De Souza MP, Silla L, Bittencourt H, Piron-Ruiz L, Maiolino A, Gratwohl A, Pasquini R:
Validation of the EBMT risk score in chronic myeloid leukemia in Brazil and allogeneic transplant outcome.
Haematologica
; 2005 Feb;90(2):232-7
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[Title]
Validation of the EBMT risk score
in chronic myeloid leukemia
in Brazil and allogeneic transplant outcome.
BACKGROUND AND OBJECTIVES: The management of
chronic myeloid leukemia
(
CML
) has changed radically since the introduction of imatinib therapy.
The aim of this retrospective analysis of 1,084
CML
patients who received an allogeneic HSCT in 10 Brazilian Centers between February 1983 and March 2003 was to validate the EBMT risk score.
DESIGN AND METHODS: The study population comprised 647 (60%) males and 437 (40%) females, with a median age of 32 years old (range 1 - 59); 898 (83%) were
in chronic
phase
, 146 (13%) were in
accelerated phase
and 40 (4%) were in blast crisis; 151 (14%) were younger than 20 years old, 620 (57%) were between 20 and 40 and 313 (29%) were older than 40; 1,025 (94%) received an HLA fully matched sibling transplant and only 59 (6%) received an unrelated transplant.
The interval from
diagnosis
to transplantation was less than 12 months in 223 (21%) cases and greater in 861 (79%).
The overall survival,
disease
-free survival, transplant-related mortality and relapse incidence were 49%, 50%, 45% and 25%, respectively.
Disease
-free survival (DFS) and transplant related mortality (TRM)
in a
patients with a score of 3 or more were 46% and 49%, respectively and the relapse rate beyond score 5-6 was 77%.
Disease
status had a negative impact on all outcomes (OS, DFS, TRM, and relapse).
DFS and TRM were significant for
disease
phase
and female donor-male recipient (p<0.001 and p<0.003, respectively).
In our experience, age and interval between
diagnosis
and transplant did influence OS, DFS, TRM, and relapse rate.
[MeSH-major]
Hematopoietic Stem Cell Transplantation / methods.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/
diagnosis
.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy
[MeSH-minor]
Adolescent. Adult. Brazil. Child. Child, Preschool.
Disease
-Free Survival. Female. Humans. Infant. Male. Middle Aged. Retrospective Studies. Risk. Sex Factors. Transplantation, Homologous. Treatment Outcome
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[CommentIn]
Haematologica. 2005 Feb;90(2):151
[
15713580.001
]
(PMID = 15710577.001).
[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
73.
Mai YJ, Qiu LG, Li ZJ, Yu Z, Li CH, Wang YF, Wang GR, Li Q:
[The expression of beta-catenin and its significance in leukemia cells].
Zhonghua Xue Ye Xue Za Zhi
; 2007 Aug;28(8):541-4
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[Title]
[The expression of beta-catenin and its significance
in leukemia
cells].
OBJECTIVE: To investigate the expression of beta-catenin in patients with
leukemia
and explore its significance in leukemias.
METHODS: RT-PCR was used to detect the expression of beta-catenin in bone marrow mononuclear cells (BMMNCs) from patients with
leukemia
.
RESULTS: Expression of beta-catenin was statistically higher in acute
myeloid leukemia
(AML) and acute lymphocytic
leukemia
(ALL) samples than in normal donors (P = 0.001 and 0.016 respectively) and
chronic
phase
chronic myeloid leukemia
(
CML
) patients (P = 0.001 and P = 0.008 respectively), while there was no statistic difference between AML and ALL patients (P = 0.58).
In addition, beta-catenin expression
in chronic
phase CML
patients was like that in normal donors (P = 0.49), but increased significantly in blast crisis and
accelerated phase
.
Immunocytochemical analysis revealed that BMMNCs from normal donors expressed beta-catenin on the plasma membrane and cytoplasma, while those from acute
leukemia
expressed beta-catenin to varying degrees in the nucleus as well.
No clinical features, such as, age, initial WBC count, therapy response rate, blast cell numbers or cytogenetic risk was found to be correlated with the expression of beta-catenin excepting for CD34+
positive
rate (P = 0.004) in AML.
CONCLUSION: As a key mediator of Wnt signal transduction way, overexpression of beta-catenin
in leukemia
cells indicates that it might be aberrantly activated in acute
leukemia
,
accelerated
or blastic
phase
of
CML
.
[MeSH-major]
Leukemia
/ metabolism. beta Catenin / metabolism
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(PMID = 18078131.001).
[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 / RNA, Messenger; 0 / beta Catenin
74.
Bornhäuser M, Kröger N, Schwerdtfeger R, Schafer-Eckart K, Sayer HG, Scheid C, Stelljes M, Kienast J, Mundhenk P, Fruehauf S, Kiehl MG, Wandt H, Theuser C, Ehninger G, Zander AR, Cooperative German Transplant Study Group:
Allogeneic haematopoietic cell transplantation for chronic myelogenous leukaemia in the era of imatinib: a retrospective multicentre study.
Eur J Haematol
; 2006 Jan;76(1):9-17
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[Title]
Allogeneic haematopoietic cell transplantation for
chronic myelogenous leukaemia in
the era of imatinib: a retrospective multicentre study.
OBJECTIVE: To analyse the results of allogeneic haematopoietic cell transplantation (HCT) in patients with advanced stages of Philadelphia chromosome-
positive chronic myelogenous leukaemia
(
CML
) who had previously been treated with imatinib mesylate (IM).
METHODS: We analysed the outcome of 61 patients with
CML
who had received allogeneic HCT from sibling (n = 18) or unrelated (n = 43) donors after having been treated with IM.
Forty-one patients had received IM because of
accelerated
or blast
phase CML
.
RESULTS: The incidence of grades II-IV and III-IV graft-versus-host
disease
was 66% and 38% respectively.
The probability of overall survival (OS),
disease
-free survival (DFS) and relapse at 18 months for the whole patient cohort were 37%, 33% and 24% respectively.
Univariate analysis showed that fludarabine-based conditioning therapy, age > or = 40 yr and >12 months interval between
diagnosis
and transplantation were associated with a significantly lower OS and DFS and a higher NRM.
CONCLUSION: These data suggest that although pretreatment with IM is not an independent negative prognostic factor, it cannot improve the dismal prognosis of
CML
patients at high risk for transplant-related mortality.
[MeSH-major]
Antineoplastic Agents / administration & dosage. Hematopoietic Stem Cell Transplantation.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Transplantation Conditioning
[MeSH-minor]
Adolescent. Adult. Benzamides. Busulfan / administration & dosage. Cohort Studies. Combined Modality Therapy. Cyclophosphamide / administration & dosage.
Disease
-Free Survival. Female. Graft vs Host
Disease
/ etiology. Graft vs Host
Disease
/ mortality. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloablative Agonists / administration & dosage. Recurrence. Retrospective Studies. Risk Factors. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Whole-Body Irradiation
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.
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.
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.
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BUSULFAN
.
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VIDARABINE
.
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(PMID = 16343266.001).
[ISSN]
0902-4441
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Myeloablative Agonists; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
75.
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
76.
Burchert A:
Roots of imatinib resistance: a question of self-renewal?
Drug Resist Updat
; 2007 Aug-Oct;10(4-5):152-61
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The
BCR
-ABL-fusion gene is critical for the development of
chronic myeloid leukemia
(
CML
) and
BCR
-ABL
positive
acute lymphatic
leukemia
(Ph+ ALL).
Blocking
BCR
-ABL by the ABL tyrosine kinase inhibitor imatinib mesylate (IM, Gleevec) is clinically highly efficient.
Treatment response is unfortunately compromised by the emergence of IM resistance, which is regularly seen in
accelerated
and blastic
phase
of
CML
(
CML
-AP/BP) and in Ph+ ALL.
BCR
-ABL kinase domain mutations are then considered the causative mechanism of IM resistance, because 50-60% of the IM resistant patients harbour such mutations.
In contrast, IM resistance arises very rarely in patients that are treated with IM in early
chronic
phase
of
CML
.
This implies that
BCR
-ABL independent factors such as the cellular context of
BCR
-ABL expression and stage of
disease
decisively control the evolution of IM resistance.
In line with this, novel Abl-kinase inhibitors such as dasatinib (DA) or nilotinib (NI) - although capable of inhibiting most of the
BCR
/-BL kinase mutants - still often fail to overcome resistance and do mostly not induce durable cytogenetic responses in IM resistant
CML
-AP/BC and Ph+ ALL patients.
On the basis of available evidence it is proposed here that alternative genetic aberrations, which synergize with
BCR
-ABL to enable leukemic self-renewal are of causal importance for the evolution of clinical kinase inhibitor resistance.
[MeSH-major]
Piperazines / therapeutic use. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
[MeSH-minor]
Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Benzamides. Drug Resistance, Neoplasm / genetics. Fusion Proteins,
bcr
-abl. Humans. Imatinib Mesylate. Models, Biological. Mutation
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(PMID = 17683977.001).
[ISSN]
1368-7646
[Journal-full-title]
Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
[ISO-abbreviation]
Drug Resist. Updat.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Scotland
[Chemical-registry-number]
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
[Number-of-references]
104
77.
Wang JX, Huang XJ, Wu DP, Hu JD, Liu T, Hu Y, Meng FY, Chen XQ, Hou M, Li Y, Wang SJ, Wang JM, Ren HY, Yu L, Chen FY, Qiu LG, Jiang B, Sun AN, Liu TB, Zhu HL, Guo T, Xu D, Ji CY, Lü XY, Jiao L, Song XM, Huang HH:
[Overview of chronic myelogenous leukemia and its current diagnosis and treatment patterns in 15 hospitals in China.].
Zhonghua Xue Ye Xue Za Zhi
; 2009 Nov;30(11):721-5
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[Title]
[Overview of
chronic myelogenous leukemia
and its current
diagnosis
and treatment patterns in 15 hospitals in China.].
OBJECTIVE: To explore demographic characteristics, current
diagnosis
and treatment patterns of
chronic myelogenous leukemia
(
CML
) patients in China.
METHODS: Data of hospitalized
CML
patients in 2005 whole year and outpatient information (July 1 through September 30, 2006) from 15 hospitals throughout China were analyzed.
RESULTS: A total of 1824
CML
cases were analyzed, including 722 inpatients and 1102 outpatients.
The median age at
diagnosis
was 40.02 (2.45 - 83.29) years old, 90.41% of the patients were diagnosed at
chronic
phase
.
Proportion of
accelerated phase
or blast crisis patients increased to 21.66% during study period.
93.20% of the patients received blood routine and bone marrow morphologic examination at
diagnosis
and in monitoring; 70.29% were performed cytogenetic analysis and 51.54% performed molecular measurement in addition.
The most common therapy for
CML
treatment was hydroxycarbamide.
The proportions of
accelerated phase
and blast crisis patients treated with imatinib were 48.28% and 48.42%, respectively, being significantly higher than that of
chronic
phase
patients (35.9%) (P < 0.05).
CONCLUSIONS:
CML
in China tends to afflict younger population than in Western countries.
Most patients were diagnosed in the
chronic
phase
.
Due to restriction of financial support, only one third of
CML
patients were treated with imatinib, and the majority of the treated were not monitored in time.
Clinicians should pay attention to resistance and intolerance to imatinib treatment in
accelerated phase
or blast crisis patients.
[MeSH-minor]
Benzamides / therapeutic use. China. Humans. Imatinib Mesylate.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy
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(PMID = 20137304.001).
[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; Review
[Publication-country]
China
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
78.
Lahaye T, Riehm B, Berger U, Paschka P, Müller MC, Kreil S, Merx K, Schwindel U, Schoch C, Hehlmann R, Hochhaus A:
Response and resistance in 300 patients with BCR-ABL-positive leukemias treated with imatinib in a single center: a 4.5-year follow-up.
Cancer
; 2005 Apr 15;103(8):1659-69
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[Title]
Response and resistance in 300 patients with
BCR
-ABL-
positive
leukemias treated with imatinib
in a
single center: a 4.5-year follow-up.
BACKGROUND: The advent of imatinib has considerably changed the treatment of
chronic myeloid leukemia
(
CML
).
Early studies demonstrated high rates of hematologic and cytogenetic responses in all phases of the
disease
after limited observation periods.
METHODS: The authors evaluated long-term outcome, rates of response, and resistance in 300 patients with
BCR
-ABL-
positive
leukemias (
CML
in chronic
phase
after failure to respond to interferon-alpha [CP], n = 139;
accelerated phase
[AP], n = 80;
myeloid
blast crisis [BC], n = 76; lymphoid BC and Philadelphia chromosome-
positive
acute lymphoblastic
leukemia
, n = 5) who entered clinical trials with imatinib
in a
single center after an observation time of 4.5 years.
The chance to achieve MCR was higher in patients commencing imatinib earlier in the course of
CML
.
In myeloid
BC, the median survival period after the start of imatinib and after
diagnosis
of BC was 6 and 9 months, respectively.
Hematologic resistance occurred in 25%, 41%, and 92% of patients in CP, AP, and
myeloid
BC, respectively, and was associated with
BCR
-ABL mutations in 45% of patients and with clonal evolution in 58% of patients.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Fusion Proteins,
bcr
-abl / metabolism.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Neoplasm Recurrence, Local / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
[MeSH-minor]
Adolescent. Adult. Aged. Benzamides. Blast Crisis. Cytogenetic Analysis. Female. Humans. Imatinib Mesylate. Interferon-alpha / adverse effects. Male. Middle Aged. Mutation. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / pathology. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction. Salvage Therapy. Survival Rate. Treatment Outcome
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[Copyright]
(c) 2005 American Cancer Society.
(PMID = 15747376.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
79.
Giles FJ, DeAngelo DJ, Baccarani M, Deininger M, Guilhot F, Hughes T, Mauro M, Radich J, Ottmann O, Cortes J:
Optimizing outcomes for patients with advanced disease in chronic myelogenous leukemia.
Semin Oncol
; 2008 Feb;35(1 Suppl 1):S1-17; quiz S18-20
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[Title]
Optimizing outcomes for patients with advanced
disease in chronic myelogenous leukemia
.
The treatment of
chronic myelogenous leukemia
(
CML
) has been revolutionized by the development of the small-molecule tyrosine kinase inhibitor imatinib.
The primary target for this drug is the oncogenic
BCR
-ABL kinase.
Five-year survival rates for patients
in chronic
phase CML
is now greater than 80%.
Patients who have advanced beyond the
chronic
phase
to the
accelerated phase
or blast crisis, however, have not faired as well.
Progression occurs for a variety of reasons, including late
diagnosis
, slow response to imatinib, and the development of imatinib-resistant clones.
Imatinib resistance has, in part, been addressed with the introduction of the new
BCR
-ABL inhibitors, namely dasatinib and nilotinib.
These drugs have shown efficacy in
CML
patients with wild-type
BCR
-ABL and some
BCR
-ABL mutants that are imatinib-resistant.
Unfortunately, some
BCR
-ABL mutations remain resistant to these therapies and will require the development of alternative treatments, and other mechanisms of imatinib resistance besides
BCR
-ABL mutation exist.
More
aggressive
therapies are being considered for high-risk patients, including increased dosage of the current tyrosine kinase inhibitors, along with combination therapies.
Aggressive
therapy holds promise, as the data suggest that responses are improved.
This is especially important for young
CML
patients, who hopefully will remain in remission for decades.
Polymerase chain reaction analysis has become of primary importance as a means of assessing
disease
burden, and given the idiosyncrasies of this technique, standards must be established to allow results to be compared across different institutions.
Additionally, the nature of advanced
disease
is being explored.
Increased activity of these pathways correlates with poor response and eventual
disease
progression.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Protein Kinase Inhibitors / therapeutic use
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(PMID = 18346528.001).
[ISSN]
0093-7754
[Journal-full-title]
Seminars in oncology
[ISO-abbreviation]
Semin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins c-jun; 0 / Wnt Proteins; 0 / beta Catenin
[Number-of-references]
131
80.
Nicolini FE, Corm S, Lê QH, Sorel N, Hayette S, Bories D, Leguay T, Roy L, Giraudier S, Tulliez M, Facon T, Mahon FX, Cayuela JM, Rousselot P, Michallet M, Preudhomme C, Guilhot F, Roche-Lestienne C:
Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients: a retrospective analysis from the French intergroup of CML (Fi(phi)-LMC GROUP).
Leukemia
; 2006 Jun;20(6):1061-6
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[Title]
Mutation status and clinical outcome of 89 imatinib mesylate-resistant
chronic myelogenous leukemia
patients: a retrospective analysis from the French intergroup of
CML
(Fi(phi)-
LMC
GROUP).
The emergence of ABL point mutations is the most frequent cause for imatinib resistance
in chronic myelogenous leukemia
(
CML
) patients and can occur during any
phase
of the
disease
; however, their clinical impact remains controversial.
In this study, we retrospectively analyzed the predictive impact of 94
BCR
-ABL kinase domain mutations (18 T315I, 26 P-loop, 50 in other sites) found in 89 imatinib-resistant
CML
patients.
At imatinib onset, 64% of patients (57/89) were
in chronic
phase
(CP), 24% (21/89) in
accelerated phase
(AP) and 12% (11/89) in blastic
phase
(BP).
T315I and P-loop mutations were preferentially discovered in
accelerated phase
of BP
CML
, and other types of mutations in CP (P=0.003).
Therefore, P-loop and T315I mutations selectively impair the outcome of imatinib-resistant
CML
patients, in contrast to other mutations, which may benefit from dose escalation of imatinib, able to improve or stabilize
disease
response.
[MeSH-major]
Drug Resistance, Neoplasm / genetics. Fusion Proteins,
bcr
-abl / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Piperazines / therapeutic use. Point Mutation. Pyrimidines / therapeutic use
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(PMID = 16642048.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
81.
Raza S, Ullah K, Ahmed P, Khan B, Kamal MK:
Post-transplant outcome in chronic myeloid leukaemia.
J Coll Physicians Surg Pak
; 2008 Oct;18(10):615-9
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[Title]
Post-transplant outcome
in chronic myeloid leukaemia
.
OBJECTIVE: To determine post-transplant survival
in chronic myeloid leukaemia
patients undergoing allogeneic stem cell transplant.
METHODOLOGY: All patients of
chronic myeloid leukaemia in chronic
phase
having HLA identical donor and age under 55 years, normal hepatic, renal and cardiac functions with good performance status were selected.
Patients in
accelerated phase
or blast crisis, poor performance status, impaired hepatic, renal, cardiac functions or pregnancy were excluded.
RESULTS: Thirty seven patients with
chronic myeloid leukaemia
underwent allogeneic stem cell transplant from HLA identical sibling donors.
All patients and donors were CMV
positive
.
Post-transplant complications encountered were acute GvHD (Grade II-IV) (n=13, 35.1%),
chronic
GvHD in 18.9% (n=7), Veno Occlusive
Disease
(VOD) in 5.4% (n=2), acute renal failure in 2.7% (n=1), haemorrhagic cystitis in 2.7% (n=1), bacterial infections in 40.5% (n=15), fungal infections in 16.2% (n=6), CMV infection in 5.4% (n=2), tuberculosis in 5.4% (n=2), Herpes Zoster infection 2.7% (n=1) and relapse in 2.7% (n=1).
Overall
Disease
Free Survival (DFS) was 73% with a median duration of follow-up of 47.4 +/-12 months.
CONCLUSION: Results of allogeneic stem cell transplant in standard risk group
CML
patients were good and comparable with other international centres, however, results in high-risk
CML
patients need further improvement, although, number of patients in this group is small.
[MeSH-major]
Hematopoietic Stem Cell Transplantation.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy
[MeSH-minor]
Adolescent. Adult. Child.
Disease
-Free Survival. Female. Humans. Longitudinal Studies. Male. Middle Aged. Survival Rate. Treatment Outcome. Young Adult
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(PMID = 18940118.001).
[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
82.
Qazilbash MH, Qu Z, Hosing C, Couriel D, Donato M, Giralt S, Champlin R:
Rituximab-induced acute liver failure after an allogeneic transplantation for chronic myeloid leukemia.
Am J Hematol
; 2005 Sep;80(1):43-5
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[Title]
Rituximab-induced acute liver failure after an allogeneic transplantation for
chronic myeloid leukemia
.
We report our experience with a 21-year-old female with
accelerated
-
phase
chronic myeloid leukemia
who underwent allogeneic hematopoietic stem cell transplantation from a matched, unrelated donor.
[MeSH-major]
Antibodies, Monoclonal / adverse effects. Antineoplastic Agents / adverse effects.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy. Liver Failure, Acute / chemically induced
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[Copyright]
Copyright 2005 Wiley-Liss, Inc.
[CommentIn]
Am J Hematol. 2005 Sep;80(1):92-3
[
16138348.001
]
(PMID = 16138357.001).
[ISSN]
0361-8609
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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.
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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.
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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
85.
Takagi Y, Aota Y, Gotoh A, Sakurai M:
[Effect of low-dose dasatinib in an elderly patient with chronic myelogenous leukemia (CML)].
Gan To Kagaku Ryoho
; 2010 Nov;37(11):2213-5
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[Title]
[Effect of low-dose dasatinib in an elderly patient with
chronic myelogenous leukemia
(
CML
)].
We experienced a case of
chronic myelogenous leukemia
(
CML
) treated successfully with low-dose dasatinib (20 mg/day).
An 87-year-old man was diagnosed with
CML
in January 2003 and was given imatinib (200 mg/day).
However, since the blood count was poorly controlled with HU, treatment with dasatinib, one of the second-generation tyrosine kinase inhibitors, was started at the
accelerated phase
(AP) in June 2009.
Dasatinib was given
in a
daily dose of 20 mg, intending dose escalation after confirmation of its safety.
Low-dose dasatinib might be a useful treatment in the control of selected patients with
CML
.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage
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(PMID = 21084830.001).
[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 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
86.
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
87.
Forrest DL, Trainor S, Brinkman RR, Barnett MJ, Hogge DE, Nevill TJ, Shepherd JD, Nantel SH, Toze CL, Sutherland HJ, Song KW, Lavoie JC, Power MM, Abou-Mourad Y, Smith CA:
Cytogenetic and molecular responses to standard-dose imatinib in chronic myeloid leukemia are correlated with Sokal risk scores and duration of therapy but not trough imatinib plasma levels.
Leuk Res
; 2009 Feb;33(2):271-5
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[Title]
Cytogenetic and molecular responses to standard-dose imatinib
in chronic myeloid leukemia
are correlated with Sokal risk scores and duration of therapy but not trough imatinib plasma levels.
Cytogenetic and molecular responses to standard-dose imatinib (IM) were correlated with trough IM plasma levels for 78 patients with
chronic myeloid leukemia
(
CML
) after a minimum of 12 months of IM therapy.
[MeSH-major]
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / blood. Pyrimidines / blood
[MeSH-minor]
Adult. 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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[CommentIn]
Leuk Res. 2009 Aug;33(8):1147-8; author reply 1149-50
[
19395027.001
]
(PMID = 18762338.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
88.
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
]
[Cites]
Science. 2001 Aug 3;293(5531):876-80
[
11423618.001
]
[Cites]
N Engl J Med. 2002 Feb 28;346(9):645-52
[
11870241.001
]
[Cites]
Blood. 2002 Sep 1;100(5):1628-33
[
12176881.001
]
[Cites]
Expert Opin Investig Drugs. 2005 Jan;14(1):89-91
[
15709925.001
]
[Cites]
Nature. 1973 Jun 1;243(5405):290-3
[
4126434.001
]
[Cites]
Science. 1990 Feb 16;247(4944):824-30
[
2406902.001
]
[Cites]
Am J Med. 1996 May;100(5):555-70
[
8644769.001
]
[Cites]
Cancer Cell. 2005 Feb;7(2):129-41
[
15710326.001
]
[Cites]
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
89.
Ghaith F, Abdou S, El-Bendary A, Shahin D, Eid M, Megeed WA, El-Sheikh I, Farrag W, Yousuf S:
Prognostic relevance of 9q34 deletion and the suppressor of cytokine signalling-1 in CML patients.
Int J Lab Hematol
; 2010 Feb;32(1 Pt 2):103-12
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[Title]
Prognostic relevance of 9q34 deletion and the suppressor of cytokine signalling-1 in
CML
patients.
Chronic myeloid leukemia
(
CML
) is characterized by formation of the
BCR
/ABL fusion gene.
This study aims to determine the incidence and prognostic value of the 9q34 deletion using fluorescence in situ hybridization and SOCS-1 mRNA aberrant expression by PCR in 43
CML
patients at different phases of the
disease
and in 10 normal controls and correlate the data to interferon response.
All patients were Philadelphia-
positive
, deletions of 9q34 were observed in 20.9% of all patients (13.3%
chronic
phase
, 10%
accelerated phase
and 33.3% in blast crisis).
SOCS expressions were
positive in
53.4% of all patients (40%
chronic
phase
, 50% AP and 66.67% in blast crisis).
Deletion of 9q34 and aberrant expression of SOCS-1 are associated with poor prognosis in
CML
patients with different phases of the
disease
under interferon therapy.
[MeSH-major]
Chromosome Deletion.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/
diagnosis
.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Suppressor of Cytokine Signaling Proteins / genetics
[MeSH-minor]
Disease
-Free Survival. Humans. In Situ Hybridization, Fluorescence. Polymerase Chain Reaction. Prognosis. RNA, Messenger / metabolism
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(PMID = 19222642.001).
[ISSN]
1751-553X
[Journal-full-title]
International journal of laboratory hematology
[ISO-abbreviation]
Int J Lab Hematol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / RNA, Messenger; 0 / Suppressor of Cytokine Signaling Proteins
90.
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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.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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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
91.
Quintas-Cardama A, Kantarjian H, Talpaz M, O'Brien S, Garcia-Manero G, Verstovsek S, Rios MB, Hayes K, Glassman A, Bekele BN, Zhou X, Cortes J:
Imatinib mesylate therapy may overcome the poor prognostic significance of deletions of derivative chromosome 9 in patients with chronic myelogenous leukemia.
Blood
; 2005 Mar 15;105(6):2281-6
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[Title]
Imatinib mesylate therapy may overcome the poor prognostic significance of deletions of derivative chromosome 9 in patients with
chronic myelogenous leukemia
.
Deletions of derivative chromosome 9 [der(9)] can be identified by fluorescence in situ hybridization (FISH) in 10% to 15% of patients with
chronic myeloid leukemia
(
CML
).
We investigated the frequency and prognostic significance of der(9) deletions among 352 patients with
CML
treated with imatinib mesylate at our institution, in whom a deletion status of der(9) was determined.
Thirty-three patients (9%; 95% CI 0.07, 0.13) (30
in chronic
phase
, 3 in
accelerated phase
) had der(9) deletions.
In a
multivariate analysis, der(9) deletions had no significant impact on response, survival, or response duration.
We conclude that treatment with imatinib mesylate overcomes the adverse prognostic significance of der(9) deletions in patients with
CML
.
[MeSH-major]
Antineoplastic Agents / administration & dosage. Chromosome Deletion. Chromosomes, Human, Pair 9.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
[MeSH-minor]
Adolescent. Adult. Aged. Benzamides.
Disease
-Free Survival. Female. Follow-Up Studies. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Interferons / administration & dosage. Interferons / adverse effects. Male. Middle Aged. Remission Induction. Treatment Outcome
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(PMID = 15572595.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; 9008-11-1 / Interferons
92.
Conte E, Stagno F, Guglielmo P, Scuto A, Consoli C, Messina A:
Survivin expression in chronic myeloid leukemia.
Cancer Lett
; 2005 Jul 8;225(1):105-10
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[Title]
Survivin expression
in chronic myeloid leukemia
.
In this study, we investigated the expression of survivin (SVV) in 44 patients with typical Ph-
positive chronic myeloid leukemia
(
CML
) in different phases of the
disease
as well as in 20 matched healthy donors.
We found a very high SVV expression
in a
predominant percentage of
CML
patients.
We also observed a significantly increased SVV expression in patients in
accelerated
/blastic
phase
of the
disease
compared to patients
in chronic
phase
.
Moreover, SVV expression levels correlated in all
CML
patients with % of Ph-chromosome
positive
cells, with
Bcr
-Abl expression levels and with WBC-count.
Based on this
finding
we suggest that SVV detection and monitoring in
CML
could represent both a useful biomarker and attractive candidate for devising new targeted and combined therapies in
CML
.
[MeSH-major]
Biomarkers, Tumor / blood. Gene Expression Profiling.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Microtubule-Associated Proteins / biosynthesis. Microtubule-Associated Proteins / blood
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(PMID = 15922862.001).
[ISSN]
0304-3835
[Journal-full-title]
Cancer letters
[ISO-abbreviation]
Cancer Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
93.
Talpaz M, Shah NP, Kantarjian H, Donato N, Nicoll J, Paquette R, Cortes J, O'Brien S, Nicaise C, Bleickardt E, Blackwood-Chirchir MA, Iyer V, Chen TT, Huang F, Decillis AP, Sawyers CL:
Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias.
N Engl J Med
; 2006 Jun 15;354(24):2531-41
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[Title]
Dasatinib in imatinib-resistant Philadelphia chromosome-
positive
leukemias.
BACKGROUND: The
BCR
-ABL tyrosine kinase inhibitor imatinib is effective in Philadelphia chromosome-
positive
(Ph-
positive
) leukemias, but relapse occurs, mainly as a result of the outgrowth of leukemic subclones with imatinib-resistant
BCR
-ABL mutations.
We evaluated dasatinib,
a BCR
-ABL inhibitor that targets most imatinib-resistant
BCR
-ABL mutations, in patients with
chronic myelogenous leukemia
(
CML
) or Ph-
positive
acute lymphoblastic
leukemia
(ALL).
METHODS: Patients with various phases of
CML
or with Ph-
positive
ALL who could not tolerate or were resistant to imatinib were enrolled
in a
phase
1 dose-escalation study.
RESULTS: A complete hematologic response was achieved in 37 of 40 patients with
chronic
-
phase CML
, and major hematologic responses were seen in 31 of 44 patients with
accelerated
-
phase CML
,
CML
with blast crisis, or Ph-
positive
ALL.
Responses were maintained in 95 percent of patients with
chronic
-
phase
disease
and in 82 percent of patients with
accelerated
-
phase
disease
, with a median follow-up more than 12 months and 5 months, respectively.
Nearly all patients with lymphoid blast crisis and Ph-
positive
ALL had a relapse within six months.
Responses occurred among all
BCR
-ABL genotypes, with the exception of the T315I mutation, which confers resistance to both dasatinib and imatinib in vitro.
CONCLUSIONS: Dasatinib induces hematologic and cytogenetic responses in patients with
CML
or Ph-
positive
ALL who cannot tolerate or are resistant to imatinib. (ClinicalTrials.gov number, NCT00064233 [ClinicalTrials.gov].).
[MeSH-major]
Antineoplastic Agents / administration & dosage. Fusion Proteins,
bcr
-abl / antagonists & inhibitors.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage
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[Copyright]
Copyright 2006 Massachusetts Medical Society.
[CommentIn]
N Engl J Med. 2006 Sep 7;355(10):1062; author reply 1063-4
[
16957155.001
]
[CommentIn]
N Engl J Med. 2006 Jun 15;354(24):2594-6
[
16775240.001
]
[CommentIn]
N Engl J Med. 2006 Sep 7;355(10):1062-3; author reply 1063-4
[
16960978.001
]
(PMID = 16775234.001).
[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/ NCT00064233
[Grant]
United States / NCRR NIH HHS / RR / M01-RR-00865
[Publication-type]
Clinical Trial, Phase I; 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 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
94.
Kim YR, Cho HI, Yoon SS, Park S, Kim BK, Lee YK, Chun H, Kim HC, Lee DS:
Interpretation of submicroscopic deletions of the BCR or ABL gene should not depend on extra signal-FISH: problems in interpretation of submicroscopic deletion of the BCR or ABL gene with extra signal-FISH.
Genes Chromosomes Cancer
; 2005 May;43(1):37-44
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[Title]
Interpretation of submicroscopic deletions of the
BCR
or ABL gene should not depend on extra signal-FISH: problems in interpretation of submicroscopic deletion of the
BCR
or ABL gene with extra signal-FISH.
Several groups have demonstrated that a submicroscopic gene deletion in Ph+
chronic myelogenous leukemia
(
CML
) is associated with a poor prognosis and reduced response to treatment.
To assess the variation between detection methods in the interpretation of a submicroscopic gene deletion, we performed an extra signal (ES)-FISH
BCR
/ABL and double-FISH (D-FISH)
BCR
/ABL on frozen bone marrow cells from 79 patients with
CML
(63 in the
chronic
phase
, 6 in the
accelerated phase
, and 10 in blast crisis) and 30 patients with
a BCR
/ABL-negative myeloproliferative
disorder
as determined by RT-PCR.
The cutoff values for false-
positive
signals from a juxtaposition of the
BCR
and ABL gene were 11% in ES-FISH and 13% in D-FISH.
Of the 14 patients who showed an ABL gene deletion by ES-FISH, 5 had an ABL deletion only, 5 had both
a BCR
and an ABL deletion, but 4 proved to have a classic
BCR
/ABL rearrangement without a submicroscopic deletion, as determined by D-FISH.
Discrepant results between ES- and D-FISH were observed in 12 of the 79 patients (15.8%), and the main causes of a discrepancy were a false-
positive
ABL deletion (4 of 12, 33%), a variant Philadelphia chromosome (3 of 12, 25%), an inversion of derivative chromosome 9 at the very breakpoint of the ABL gene (9q32) (1 of 12, 8.3%), a cryptic variant Ph chromosome (1 of 12, 8.3%), and a marker chromosome (1 of 12, 8.3%).
Although there was no significant difference in the sensitivity for the detection of the fusion signal between ES- and D-FISH, ES-FISH showed a high percentage of cells with false-
positive
fusion signals (1 orange, 1 green, 1 yellow), which makes it difficult to interpret the submicroscopic ABL deletion.
In conclusion, an interpretation of the submicroscopic deletions of the
BCR
or ABL gene should not depend on ES-FISH.
[MeSH-major]
Fusion Proteins,
bcr
-abl / genetics. Gene Deletion. Genes, abl.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics
[MeSH-minor]
Bone Marrow / pathology. Humans. In Situ Hybridization, Fluorescence. Prognosis. Proto-Oncogene Proteins c-
bcr
. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity
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[Copyright]
Copyright 2005 Wiley-Liss, Inc.
(PMID = 15723338.001).
[ISSN]
1045-2257
[Journal-full-title]
Genes, chromosomes & cancer
[ISO-abbreviation]
Genes Chromosomes Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
95.
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
96.
Velev N, Cortes J, Champlin R, Jones D, Rondon G, Giralt S, Borthakur G, Kantarjian HM, De Lima M:
Stem cell transplantation for patients with chronic myeloid leukemia resistant to tyrosine kinase inhibitors with BCR-ABL kinase domain mutation T315I.
Cancer
; 2010 Aug 1;116(15):3631-7
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[Title]
Stem cell transplantation for patients with
chronic myeloid leukemia
resistant to tyrosine kinase inhibitors with
BCR
-ABL kinase domain mutation T315I.
Although many imatinib-resistant mutations respond well to second-generation TKIs, the threonine-to-isoleucine mutation at codon 315 of the breakpoint cluster region/v-abl Abelson murine
leukemia
viral oncogene protein fusion
Bcr
-Abl (T315I) is insensitive to all currently available TKIs.
METHODS: Eight patients with TKI-resistant
CML
who had T315I mutations underwent 9 transplantations.
At the time of SCT, 2 patients were
in chronic
phase
, 3 patients were in
accelerated phase
; and 3 patients were in second
chronic
phase
.
The best outcome was for patients who underwent transplantation
in chronic
phase
, and both of those patients remained alive and in complete molecular remission 14 months and 42 months after SCT.
CONCLUSIONS: The current results indicated that SCT is an effective strategy for patients with
CML
who have the T315I mutation, particularly in earlier stages.
[MeSH-major]
Fusion Proteins,
bcr
-abl / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ therapy. Mutation. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Stem Cell Transplantation
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[Copyright]
Copyright (c) 2010 American Cancer Society.
(PMID = 20564073.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Evaluation Studies; 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
97.
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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[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
98.
Zhou L, Meng F, Yin O, Wang J, Wang Y, Wei Y, Hu P, Shen Z:
Nilotinib for imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase, accelerated phase, or blast crisis: a single- and multiple-dose, open-label pharmacokinetic study in Chinese patients.
Clin Ther
; 2009 Jul;31(7):1568-75
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[Title]
Nilotinib for imatinib-resistant or -intolerant
chronic myeloid leukemia in chronic
phase
,
accelerated phase
, or blast crisis: a single- and multiple-dose, open-label pharmacokinetic study in Chinese patients.
BACKGROUND: Nilotinib, an oral second-generation
Bcr
-Abi tyrosine kinase inhibitor, is approved in the United States and European Union for the treatment of Philadelphia chromosome-
positive
(Ph+),
chronic
-
phase
(CP) or
accelerated
-
phase
(AP)
chronic myeloid leukemia
(
CML
) resistant to or intolerant of prior therapy, including imatinib.
Information on the pharmacokinetics of nilotinib in Chinese patients with
CML
is lacking, and regulatory requirements for registration of this drug are needed in China.
OBJECTIVES: This study assessed the pharmacokinet-ics of single and multiple oral doses of nilotinib in Chinese patients with
CML
and compared the pharmacokinetic profiles of nilotinib between the Chinese patients and a subgroup of white patients with
CML
.
METHODS: Chinese patients aged > or =18 years with Ph+
CML
-CP,
CML
-AP, or
CML
-BC (blast crisis) resistant to or intolerant of imatinib were eligible.
RESULTS: Twenty-three patients were enrolled (18 men, 5 women; mean age, 40.0 years; mean weight, 68.3 kg;
CML
-CP, 22 patients;
CML
-AP, 1).
Steady-state C(max), C(min), AUC(0-tau), and CL/F were not significantly different from those previously reported
in a
subgroup of white patients with
CML
who received the same 400-mg BID dose.
CONCLUSIONS: In this pharmacokinetic study in Chinese patients with
CML
resistant to or intolerant of imatinib, nilotinib 400 mg BID was rapidly absorbed after a single dose and multiple doses.
The steady-state pharmacokinetic properties in this population were consistent with those reported previously in white patients with
CML
.
[MeSH-minor]
Administration, Oral. Adult. Aged. Area Under Curve. Asian Continental Ancestry Group. Benzamides. Blast Crisis / drug therapy. China. Chromatography, Liquid. Drug Administration Schedule. Drug Resistance, Neoplasm. European Continental Ancestry Group. Female. Humans. Imatinib Mesylate.
Leukemia
,
Myeloid
,
Accelerated Phase
/ drug therapy.
Leukemia
,
Myeloid
,
Chronic
-
Phase
/ drug therapy. Male. Middle Aged. Piperazines / administration & dosage. Tandem Mass Spectrometry. Young Adult
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(PMID = 19695406.001).
[ISSN]
1879-114X
[Journal-full-title]
Clinical therapeutics
[ISO-abbreviation]
Clin Ther
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00302016
[Publication-type]
Controlled Clinical Trial; 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 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
99.
Aleem A, Siddiqui N:
Chronic myeloid leukemia presenting with extramedullary disease as massive ascites responding to imatinib mesylate.
Leuk Lymphoma
; 2005 Jul;46(7):1097-9
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[Title]
Chronic myeloid leukemia
presenting with extramedullary
disease
as massive ascites responding to imatinib mesylate.
Patients with
chronic myeloid leukemia
(
CML
) can develop extramedullary involvement during the course of the illness.
This usually occurs during the
accelerated phase
or blast crisis.
We describe a patient who presented with massive ascites probably due to mesenteric/peritoneal infiltration during
chronic
phase CML
.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Ascites / drug therapy. Ascites / etiology. Blast Crisis / genetics.
Leukemia
,
Myelogenous
,
Chronic
,
BCR
-ABL
Positive
/ drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
[MeSH-minor]
Benzamides. Cytogenetic Analysis. Fusion Proteins,
bcr
-abl / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Remission Induction
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(PMID = 16019565.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Journal Article; 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
100.
Sessions J:
Chronic myeloid leukemia in 2007.
Am J Health Syst Pharm
; 2007 Dec 15;64(24 Suppl 15):S4-9
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[Title]
Chronic myeloid leukemia in
2007.
PURPOSE:
Chronic myeloid leukemia
(
CML
), a hematopoietic stem cell cancer representing 15-20% of adult leukemias, is discussed.
SUMMARY:
CML
is a myeloproliferative
disorder
that affects all lineages of hematopoiesis.
Final confirmation of
CML
comes with detection of the Philadelphia Chromosome (Ph) or
BCR
-ABL transcripts.
The
disease
presents in one of three phases:
chronic
phase
,
accelerated phase
, or blast crisis.
Progression from