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1
aml adult recurrent 2005:2010[pubdate] *count=100
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Items 1 to 98 of about 98
1.
Gregory TK, Wald D, Chen Y, Vermaat JM, Xiong Y, Tse W:
Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics.
J Hematol Oncol
; 2009;2:23
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[Title]
Molecular prognostic markers for
adult
acute myeloid leukemia
with normal cytogenetics.
Acute myeloid leukemia
(
AML
) is a heterogenous disorder that results from a block in the differentiation of hematopoietic progenitor cells along with uncontrolled proliferation.
In approximately 60% of cases, specific
recurrent
chromosomal aberrations can be identified by modern cytogenetic techniques.
Currently, favorable risk
AML
patients are usually treated with contemporary chemotherapy while poor risk
AML
patients receive allogeneic stem cell transplantation if suitable stem cell donors exist.
The largest subgroup of
AML
patients (aproximately 40%) have no identifiable cytogenetic abnormalities and are classified as intermediate risk.
Recently, it is becoming increasingly evident that it is possible to identify a subgroup of poorer risk patients among those with normal cytogenic
AML
(NC-
AML
).
Molecular risk stratification for NC-
AML
patients may be possible due to mutations of NPM1, FLT3, MLL, and CEBPalpha as well as alterations in expression levels of BAALC, MN1, ERG, and AF1q.
Further prospective studies are needed to confirm if poorer risk NC-
AML
patients have improved clinical outcomes after more aggressive therapy.
[MeSH-major]
Genetic Markers.
Leukemia
,
Myeloid
,
Acute
/ diagnosis.
Leukemia
,
Myeloid
,
Acute
/ genetics
[MeSH-minor]
Adult
. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Cytogenetics. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Humans. Neoplasm, Residual. Nuclear Proteins / genetics. Nuclear Proteins / physiology. Prognosis. fms-Like Tyrosine Kinase 3 / genetics. fms-Like Tyrosine Kinase 3 / physiology
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]
(PMID = 19490647.001).
[ISSN]
1756-8722
[Journal-full-title]
Journal of hematology & oncology
[ISO-abbreviation]
J Hematol Oncol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
[Number-of-references]
65
[Other-IDs]
NLM/ PMC2700131
2.
Gupta M, Raghavan M, Gale RE, Chelala C, Allen C, Molloy G, Chaplin T, Linch DC, Cazier JB, Young BD:
Novel regions of acquired uniparental disomy discovered in acute myeloid leukemia.
Genes Chromosomes Cancer
; 2008 Sep;47(9):729-39
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[Title]
Novel regions of acquired uniparental disomy discovered in
acute myeloid leukemia
.
The acquisition of uniparental disomy (aUPD) in
acute myeloid leukemia
(
AML
) results in homozygosity for known gene mutations.
We therefore aimed to develop a map of the regions of aUPD in
AML
.
Here, we have analyzed a large set of diagnostic
AML
samples (n = 454) from young adults (age: 15-55 years) using genotype arrays.
Novel
recurrent
regions of aUPD were uncovered at 2p, 17p, 2q, 17q, 1p, and Xq.
This study demonstrates aUPD is a frequent and significant finding in
AML
and pinpoints regions that may contain novel mutational targets.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics. Uniparental Disomy / genetics
[MeSH-minor]
Adult
. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 13 / genetics. DNA Mutational Analysis. Humans. Middle Aged. Models, Genetic. Mutation
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[Copyright]
2008 Wiley-Liss, Inc.
(PMID = 18506749.001).
[ISSN]
1098-2264
[Journal-full-title]
Genes, chromosomes & cancer
[ISO-abbreviation]
Genes Chromosomes Cancer
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789; United Kingdom / Cancer Research UK / /
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
3.
Peniket A, Wainscoat J, Side L, Daly S, Kusec R, Buck G, Wheatley K, Walker H, Chatters S, Harrison C, Boultwood J, Goldstone A, Burnett A:
Del (9q) AML: clinical and cytological characteristics and prognostic implications.
Br J Haematol
; 2005 Apr;129(2):210-20
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[Title]
Del (9q)
AML
: clinical and cytological characteristics and prognostic implications.
Del (9q) is a
recurrent
cytogenetic abnormality in
acute myeloid
leukaemia (
AML
).
We report an analysis of 81 patients with del(9q) as a diagnostic karyotypic abnormality entered into the Medical Research Council
AML
trials 10, 11 and 12.
It is likely that the deletion of single or multiple tumour suppressor genes located in this region may underlie the pathogenesis of del (9q)
AML
.
[MeSH-major]
Gene Deletion. Genes, Tumor Suppressor.
Leukemia
,
Myeloid
/ genetics
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Aged. Bone Marrow Cells / pathology. Child. Child, Preschool. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Cytogenetic Analysis. Disease-Free Survival. Female. Genetic Markers. Humans. Male. Middle Aged. Survival Rate. Translocation, Genetic
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[CommentIn]
Br J Haematol. 2005 Sep;130(6):969; author reply 969
[
16156871.001
]
(PMID = 15813849.001).
[ISSN]
0007-1048
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Genetic Markers
Advertisement
4.
Imataki O, Ohnishi H, Kitanaka A, Kubota Y, Tanaka T, Ishida T:
Isolated extramedullary relapse presenting as autologous lymphocyte response.
Am J Hematol
; 2008 Jun;83(6):512-4
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Isolated EMR in the CNS is a relatively rare form of
recurrent
leukemia
.
We report here a case of a 38-year-old man with inv(16)
acute myeloid leukemia
(
AML
, M2) who suffered a central nervous system (CNS) relapse after allogeneic bone marrow transplantation (BMT) from a human leukocyte antigen (HLA)-matched sibling donor.
His
leukemia relapsed
in the CNS 2.5 years after the allogeneic BMT.
Lumbar puncture revealed 780/muL white blood cells with 67.3%
leukemia
cells and 32.7% mature lymphocytes.
Fluorescent in situ hybridization (FISH) using a probe for the Y chromosome demonstrated that both
leukemia
cells and lymphocytes in the cerebrospinal fluid (CSF) were derived from the recipient, although the bone marrow cells were from the donor.
No
leukemia
cells with inv(16) were detected by FISH in the bone marrow.
This is the first report to clarify the chimerism of lymphocytes in the CSF of patients with isolated EMR in the CNS after allogeneic SCT, in which analysis revealed that autologous immunologic cells rather than donor lymphocytes responded to the
recurrent
isolated leukemic cells in CNS.
This observation suggests that the CNS is a "sanctuary" site not only from chemotherapy but also from the graft-versus-
leukemia
effect.
The present case contributes to our understanding of the possibility of immunological escape phenomenon of
recurrent
leukemia
cells in extramedullary sites.
[MeSH-major]
Central Nervous System Neoplasms / pathology.
Leukemia
,
Myeloid
,
Acute
/ pathology.
Leukemia
,
Myeloid
,
Acute
/ therapy
[MeSH-minor]
Adult
. Bone Marrow Transplantation / methods. Humans. Male. Recurrence. Sarcoma,
Myeloid
. Transplantation Chimera
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[Copyright]
Copyright 2008 Wiley-Liss, Inc.
(PMID = 18306363.001).
[ISSN]
1096-8652
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
5.
Rau R, Brown P:
Nucleophosmin (NPM1) mutations in adult and childhood acute myeloid leukaemia: towards definition of a new leukaemia entity.
Hematol Oncol
; 2009 Dec;27(4):171-81
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[Title]
Nucleophosmin (NPM1) mutations in
adult
and childhood
acute myeloid
leukaemia: towards definition of a new leukaemia entity.
Somatic mutations in exon 12 of the NPM gene (NPM1) are the most frequent genetic abnormality in
adult
acute myeloid
leukaemia (
AML
), found in approximately 35% of all cases and up to 60% of patients with normal karyotype (NK)
AML
.
In children, NPM1 mutations are far less frequent, occurring in 8-10% of all
AML
cases, and in approximately 25% of those with a NK.
NPM1 mutations lead to aberrant localization of the NPM protein into the cytoplasm, thus the designation, NPMc+
AML
.
NPMc+
AML
is seen predominantly in patients with a NK and is essentially mutually exclusive of
recurrent
chromosomal translocations.
NPMc+
AML
is also characterized by a unique gene expression signature and microRNA signature.
NPMc+
AML
has important prognostic significance, as NPMc+
AML
, in the absence of a coexisting FLT3-ITD mutation, is associated with a favourable outcome.
Given its distinctive biologic and clinical features and its clear clinical relevance, NPMc+
AML
is included as a provisional entity in the 2008 WHO classifications.
Further, it represents a potential therapeutic target warranting research aimed at identifying novel small molecules with activity in NPMc+
AML
.
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[Copyright]
Copyright (c) 2009 John Wiley & Sons, Ltd.
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(PMID = 19569254.001).
[ISSN]
1099-1069
[Journal-full-title]
Hematological oncology
[ISO-abbreviation]
Hematol Oncol
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA111728-05; United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / T32 CA060441; United States / NCI NIH HHS / CA / K23 CA111728-05
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
[Number-of-references]
102
[Other-IDs]
NLM/ NIHMS234930; NLM/ PMC3069851
6.
Kuwahara E, Otsuji Y, Iguro Y, Ueno T, Zhu F, Mizukami N, Kubota K, Nakashiki K, Yuasa T, Yu B, Uemura T, Takasaki K, Miyata M, Hamasaki S, Kisanuki A, Levine RA, Sakata R, Tei C:
Mechanism of recurrent/persistent ischemic/functional mitral regurgitation in the chronic phase after surgical annuloplasty: importance of augmented posterior leaflet tethering.
Circulation
; 2006 Jul 4;114(1 Suppl):I529-34
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[Title]
Mechanism of
recurrent
/persistent ischemic/functional mitral regurgitation in the chronic phase after surgical annuloplasty: importance of augmented posterior leaflet tethering.
BACKGROUND: Surgical annuloplasty can potentially hoist the posterior annulus anteriorly, exaggerate posterior leaflet (PML) tethering, and lead to
recurrent
ischemic/functional mitral regurgitation (MR).
METHODS AND RESULTS: In 30 patients with surgical annuloplasty for ischemic MR and 20 controls, the anterior leaflet (
AML
) and PML tethering angles relative to the line connecting annuli, posterior and apical displacement of the coaptation and the MR grade were measured by echocardiography before, early after, and late after surgery.
Early after surgery, grade of MR and
AML
tethering generally decreased (P<0.01), whereas PML tethering significantly worsened (P<0.01).
Nine of the 30 patients showed
recurrent
/persistent MR late after surgery.
CONCLUSIONS: Whereas both leaflets tethering is related to preoperative ischemic MR, both leaflets tethering but with predominant contribution from augmented and progressive PML tethering is related to
recurrent
/persistent ischemic/functional MR late after surgical annuloplasty.
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Chronic Disease. Coronary Artery Bypass. Female. Humans. Incidence. Male. Middle Aged. Motion. Papillary Muscles / pathology. Recurrence. Treatment Failure
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(PMID = 16820632.001).
[ISSN]
1524-4539
[Journal-full-title]
Circulation
[ISO-abbreviation]
Circulation
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
7.
Grandics P:
Complete remission achieved in a case of both primary and recurrent adult acute myelogeneous leukemia by a novel nutritional therapy.
J Altern Complement Med
; 2006 Apr;12(3):311-5
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[Title]
Complete remission achieved in a case of both primary and
recurrent adult
acute
myelogeneous
leukemia
by a novel nutritional therapy.
OBJECTIVES: The aim of this study was to determine the possible clinical benefit of molasses-based dietary compositions (designated as MSQ 13, MSQ 15, and MSQ 18) in a case of both primary and
recurrent adult AML
.
OUTCOME MEASURES: Clinical improvement and regression of
AML
were the outcome measures.
CONCLUSIONS: Treatment with the MSQ dietary compositions resulted in disease regression and the reversal of clinical manifestations over two episodes of
AML
.
Therefore, further studies are warranted to evaluate the utility of this approach for the clinical management of
AML
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ diet therapy. Molasses. Nutrition Therapy / methods
[MeSH-minor]
Adult
. Female. Humans. Remission Induction. Treatment Outcome
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(PMID = 16646731.001).
[ISSN]
1075-5535
[Journal-full-title]
Journal of alternative and complementary medicine (New York, N.Y.)
[ISO-abbreviation]
J Altern Complement Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
8.
Andersson BS, de Lima M, Thall PF, Madden T, Russell JA, Champlin RE:
Reduced-toxicity conditioning therapy with allogeneic stem cell transplantation for acute leukemia.
Curr Opin Oncol
; 2009 Jun;21 Suppl 1:S11-5
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[Title]
Reduced-toxicity conditioning therapy with allogeneic stem cell transplantation for
acute leukemia
.
We hypothesized that standardized systemic drug delivery would improve treatment safety and provide better
leukemia
control.
We used a Bayesian method to compare the outcomes of 67
acute myeloid leukemia
(
AML
)/myelodysplastic syndrome (MDS) patients who received intravenous busulfan-cyclophosphamide (BuCy2) with 148 subsequent
AML
/MDS patients who received busulfan-fludarabine (Bu-Flu).
Overall, the data support replacing BuCy2 with or without antithymocyte globulin (ATG) with Bu-Flu with or without rabbit-ATG for
AML
or MDS.
We further suggest that the high level of safety and fast recovery from conditioning therapy-related side effects after the Bu-Flu regimen makes it a suitable platform technology for testing additional adjuncts for improved posttransplant immune recovery and long-term disease control in patients who are at high risk of rapidly
recurrent
disease after alloSCT.
The extremely low one-year treatment-related mortality as well as high overall and event-free survival of patients in the Bu-Flu group indicate that it is time to revisit the value of alloSCT compared with conventional maintenance chemotherapy for patients in first complete remission of
AML
/MDS.
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]
(PMID = 19561406.001).
[ISSN]
1531-703X
[Journal-full-title]
Current opinion in oncology
[ISO-abbreviation]
Curr Opin Oncol
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / 2P30CA16672-26
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
[Other-IDs]
NLM/ NIHMS588342; NLM/ PMC4037323
9.
Kornblau SM, McCue D, Singh N, Chen W, Estrov Z, Coombes KR:
Recurrent expression signatures of cytokines and chemokines are present and are independently prognostic in acute myelogenous leukemia and myelodysplasia.
Blood
; 2010 Nov 18;116(20):4251-61
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[Title]
Recurrent
expression signatures of cytokines and chemokines are present and are independently prognostic in
acute myelogenous leukemia
and myelodysplasia.
We hypothesized that comprehensive profiling of C&Ckine expression in
leukemia
would provide greater insight compared with individual analyses.
We used multiplex array technology to simultaneously measure the level of 27 C&Ckines in serum from 176
acute myelogenous leukemia
(
AML
) and 114 myelodysplastic syndrome (MDS) patients and 19 normal controls.
C&Ckine levels in
AML
and MDS differed significantly from normal controls (5 higher, 13 lower) but were similar to each other for 24 of 27 analytes, with interleukin-8 and interleukin-13 higher in
AML
and vascular endothelial growth factor A higher in MDS.
Levels did not correlate with age, gender, infection, or blood counts; however, 3 correlated with specific cytognetic abnormalities in
AML
.
In newly diagnosed
AML
, 8 C&Ckine signatures, distinct from the normal control signature, were observed.
These patterns suggest specific therapeutic interventions to investigate in subsets of
AML
patients.
In conclusion, C&Ckine expression in
AML
and MDS differs from normal, is similar with one another, and forms
recurrent
patterns of expression with prognostic relevance.
[MeSH-major]
Chemokines / blood.
Leukemia
,
Myeloid
,
Acute
/ blood.
Leukemia
,
Myeloid
,
Acute
/ diagnosis. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / diagnosis
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Cluster Analysis. Cytogenetic Analysis. Female. Humans. Male. Middle Aged. Multivariate Analysis. Principal Component Analysis. Prognosis. Survival Analysis. Treatment Outcome. Young
Adult
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[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Chemokines
[Other-IDs]
NLM/ PMC4081283
10.
Fujieda A, Masuya M, Kitano S, Miyazaki K, Yazaki A, Sugimoto Y, Usui E, Miyata E, Shibasaki T, Yamamura K, Ohishi K, Nishii K, Nakase K, Takeuchi T, Katayama N:
Deletion of chromosome arm 15q in a case of minimally differentiated hypoplastic AML-M0.
Cancer Genet Cytogenet
; 2008 Jul;184(1):57-61
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[Title]
Deletion of chromosome arm 15q in a case of minimally differentiated hypoplastic
AML
-M0.
Deletion of the long arm of chromosome 15 is known as a rare but
recurrent
chromosomal abnormality in
myeloid
malignancies.
We report a novel case of minimally differentiated hypoplastic
acute myeloid leukemia
(
AML
M0) in a patient who initially had a normal karyotype, but clonal interstitial deletion of chromosome 15, del(15)(q11.2q22), coincided with increment of leukemic cells a year later.
We also summarize 18 published cases with
myeloid
malignancies and this chromosomal abnormality.
[MeSH-major]
Chromosome Deletion. Chromosomes, Human, Pair 15.
Leukemia
,
Myeloid
,
Acute
/ genetics
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Cell Differentiation. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Recurrence
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(PMID = 18558291.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
11.
Tanvetyanon T, Stiff PJ:
Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations.
Leuk Lymphoma
; 2005 Jan;46(1):151-4
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[Title]
Recurrent
steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations.
However, to date,
recurrent
acute
pancreatitis has never been described in association with MDS.
The vasculitic syndrome responded rapidly to corticosteroids, but soon after tapering of corticosteroids,
acute
pancreatitis developed.
Finally, his MDS transformed into
acute myeloid leukemia
(
AML
); severe
acute
pancreatitis closely accompanied.
A subsequent pancreatitis attack with pseudocyst formation occurred, but again was controlled with corticosteroids, although this was followed closely by another relapse of
AML
.
All etiologies for
recurrent
acute
pancreatitis were ruled out.
The dramatic response of his pancreatitis attacks to immunosuppression suggested its autoimmune origin, while the close relationship in both the timing and severity of
acute
pancreatitis and MDS/
AML
suggested that the autoimmune pancreatitis was a paraneoplastic phenomenon related to MDS.
[MeSH-minor]
Abdomen / pathology.
Adult
. Cell Transformation, Neoplastic. Humans. Male. Recurrence. Time Factors
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(PMID = 15621795.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Steroids
12.
Sazawal S, Kumar B, Hasan SK, Dutta P, Kumar R, Chaubey R, Mir R, Saxena R:
Haematological & molecular profile of acute myelogenous leukaemia in India.
Indian J Med Res
; 2009 Mar;129(3):256-61
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[Title]
Haematological & molecular profile of
acute myelogenous
leukaemia in India.
BACKGROUND & OBJECTIVE:
Recurrent
balanced translocations are generally recognized to be a major parameter for prognostication in
acute myeloid
leukaemia (
AML
).
Therefore, we screened the
AmL
patients for known specific genetic abnormalities that could lead to more definitive prognoses.
METHODS: A total of 113
AML
patients were evaluated at diagnosis based on routine morphology and cytochemistry and classified according to the WHO criteria.
The distribution of
AML
subtypes was M1(1), M2(32), M3(57), M4(14), M5(1), M6(1) and seven cases where morphological subtype could not be classified.
FLT3 internal tandem duplication (ITD) mutations were more frequent in patients with APL than in other
AML
subtypes (17.5 vs. 8.9%), the frequency greater in patients with bcr3 isoform (70%) than in those with in bcr1 isoform (30%).
FLT3 internal tandem duplication (ITD) mutation was predominant in
acute
promyelocytic leukaemia patients with bcr3 isoform.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ epidemiology.
Leukemia
,
Myeloid
,
Acute
/ genetics. Translocation, Genetic
[MeSH-minor]
Adolescent.
Adult
. Child. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Genetic Predisposition to Disease / epidemiology. Humans. India / epidemiology. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Prevalence. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Young
Adult
. fms-Like Tyrosine Kinase 3 / genetics
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(PMID = 19491417.001).
[ISSN]
0971-5916
[Journal-full-title]
The Indian journal of medical research
[ISO-abbreviation]
Indian J. Med. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
India
[Chemical-registry-number]
0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
13.
Chang ST, Hsieh YC, Lee LP, Tzeng CC, Chuang SS:
Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up.
Chang Gung Med J
; 2006 Sep-Oct;29(5):532-7
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[Title]
Acute
myelomonocytic
leukemia
with abnormal eosinophils: a case report with multi-modality diagnostic work-up.
Acute myeloid leukemia
(
AML
) with
recurrent
genetic abnormalities often carries a favorable prognosis.
AML
with inv(16)(p13q22) occurs predominantly in younger patients and usually shows granulocytic and monocytic differentiation with abnormal eosinophils.
It is referred to as
acute
myelomonocytic
leukemia
with abnormal eosinophils (AMML Eo).
[MeSH-major]
Eosinophils / pathology.
Leukemia
, Myelomonocytic,
Acute
/ diagnosis
[MeSH-minor]
Adult
. Bone Marrow Examination. Flow Cytometry. Humans. Immunohistochemistry. Male
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(PMID = 17214400.001).
[ISSN]
2072-0939
[Journal-full-title]
Chang Gung medical journal
[ISO-abbreviation]
Chang Gung Med J
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
China (Republic : 1949- )
14.
Mansour S, Connell F, Steward C, Ostergaard P, Brice G, Smithson S, Lunt P, Jeffery S, Dokal I, Vulliamy T, Gibson B, Hodgson S, Cottrell S, Kiely L, Tinworth L, Kalidas K, Mufti G, Cornish J, Keenan R, Mortimer P, Murday V, Lymphoedema Research Consortium:
Emberger syndrome-primary lymphedema with myelodysplasia: report of seven new cases.
Am J Med Genet A
; 2010 Sep;152A(9):2287-96
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Four reports have been published on an association between
acute myeloid
leukaemia (
AML
) and primary lymphedema, with or without congenital deafness.
The
AML
is often preceded by pancytopenia or myelodysplasia with a high incidence of monosomy 7 in the bone marrow (five propositi and two relatives).
Associated anomalies included hypotelorism, epicanthic folds, long tapering fingers and/or neck webbing (four patients),
recurrent
cellulitis in the affected limb (four patients), generalized warts (two patients), and congenital, high frequency sensorineural deafness (one patient).
[MeSH-minor]
Abnormalities, Multiple. Adolescent.
Adult
. Child. Child, Preschool. Chromosomes, Human, Pair 7. Female. Genitalia / abnormalities. Humans. Infant. Infant, Newborn.
Leukemia
,
Myeloid
,
Acute
/ complications.
Leukemia
,
Myeloid
,
Acute
/ genetics. Lower Extremity Deformities, Congenital. Male. Monosomy. Young
Adult
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.
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[Copyright]
Copyright 2010 Wiley-Liss, Inc.
(PMID = 20803646.001).
[ISSN]
1552-4833
[Journal-full-title]
American journal of medical genetics. Part A
[ISO-abbreviation]
Am. J. Med. Genet. A
[Language]
eng
[Grant]
United Kingdom / British Heart Foundation / / PG/10/58/28477; United Kingdom / British Heart Foundation / /
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
15.
Huh JY, Chung S, Oh D, Kang MS, Eom HS, Cho EH, Han MH, Kong SY:
Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.
Korean J Lab Med
; 2010 Apr;30(2):117-21
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[Title]
Clathrin assembly lymphoid
myeloid leukemia
-AF10-positive
acute
leukemias: a report of 2 cases with a review of the literature.
The translocation t(10;11)(p13;q14q21) has been found to be
recurrent
in
acute
lymphoblastic and
myeloid
leukemias, and results in the fusion of the clathrin assembly lymphoid
myeloid leukemia
(CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.
Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for
acute leukemia
.
The first patient (case 1) was diagnosed with T-cell ALL, and the second patient (case 2) was diagnosed with
AML
.
Both patient samples showed expression of the homeobox A gene cluster and the histone methyltransferase hDOT1L, which suggests that they mediate leukemic transformation in CALM-AF10-positive and mixed-lineage
leukemia
-AF10-positive leukemias.
The first patient (case 1)
relapsed
after double-unit cord blood transplantation; there was no evidence of relapse in the second patient (case 2) after allogenic peripheral blood stem cell transplantation.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics. Monomeric Clathrin Assembly Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Transcription Factors / genetics
[MeSH-minor]
Adolescent.
Adult
. Bone Marrow / pathology. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Cord Blood Stem Cell Transplantation. Female. Histone-Lysine N-Methyltransferase / genetics. Histone-Lysine N-Methyltransferase / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Recurrence. Translocation, Genetic
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(PMID = 20445327.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
[Number-of-references]
14
16.
Bedekovics J, Rejto L, Telek B, Udvardy M, Ujfalusi A, Oláh E, Hevessy Z, Kappelmayer J, Kajtár B, Méhes G:
[Immunohistochemical demonstration of mutant nucleophosmin in acute myeloid leukemia: biological and clinical features related to NPMc expression].
Orv Hetil
; 2009 May 31;150(22):1031-5
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[Title]
[Immunohistochemical demonstration of mutant nucleophosmin in
acute myeloid leukemia
: biological and clinical features related to NPMc expression].
[Transliterated title]
Mutáns nucleophosmin fehérje kimutatása akut
myeloid
leukaemiában: az NPMc+
AML
biológiai és klinikai jellemzôi.
The mutation of the nucleophosmin gene (NPM1) is the most frequently occurring genetic aberration in
acute myeloid leukemia
(
AML
).
Due to the high frequency and the obvious impact on disease outcome, the current WHO classification also defines the new (tentative) entity of "
AML
with NPM mutation".
The present study focused on further biological and clinical characterization of NPMc+
AML
determined by histological and cytological preparations of the bone marrow.
41
adult AML
cases were investigated in our center between 2005 and 2008, 6/41 cases were presented with cytoplasmic NPM immunostaining (14.6%).
All but one were female patients, and were diagnosed as de novo
AML
with no
recurrent
cytogenetic aberrations (6/23, 26.1%).
In conclusion, immunohistochemistry is well applicable for the identification of NPM mutated
AML
in the daily hematopathology practice.
[MeSH-major]
Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Bone Marrow / chemistry.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Mutation. Nuclear Proteins / analysis. Nuclear Proteins / genetics
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(PMID = 19465351.001).
[ISSN]
0030-6002
[Journal-full-title]
Orvosi hetilap
[ISO-abbreviation]
Orv Hetil
[Language]
hun
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Hungary
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
17.
Gil L, Styczynski J, Dytfeld D, Debski R, Kazmierczak M, Kolodziej B, Rafinska B, Kubicka M, Nowicki A, Komarnicki M, Wysocki M:
Activity of bortezomib in adult de novo and relapsed acute myeloid leukemia.
Anticancer Res
; 2007 Nov-Dec;27(6B):4021-5
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[Title]
Activity of bortezomib in
adult
de novo and
relapsed acute myeloid leukemia
.
AIM: The aim of the study was the analysis of in vitro drug resistance to bortezomib and other anticancer drugs in de novo and
relapsed
adult
acute myeloid leukemia
(
AML
).
PATIENTS AND METHODS: The leukemic cells of 46
adult
patients with
AML
were tested for the in vitro drug resistance profile.
The group included 20 de novo and 26
relapsed
AML
patients, among whom, 12
relapsed
after allogeneic hematopoietic stem cell transplantation (HSCT) and 4 after autologous HSCT.
RESULTS: No significant differences in drug resistance were found for all tested drugs between de novo and
relapsed
AML
samples, while expression of PGP, MRP1 and LRP was higher in
relapsed
patients.
Patients with refractory or
relapsed
disease, had higher resistance of myeloblasts to cyclophosphamide (RR = 2.4, p = 0.050), and better sensitivity to busulfan (RR = 0.4, p = 0.054) and topotecan (RR = 0.4, p = 0.031).
Those who have died due to refractory/
relapsed
disease (n = 16) had better sensitivity to bortezomib (RR = 0.6, p = 0.046) and treosulfan (RR = 0.1, p = 0.018).
CONCLUSION: In vitro drug resistance in
relapsed
adult AML
is comparable to that in de novo disease.
Activity in vitro of bortezomib might be a rationale for its use in refractory/
relapsed
AML adult
patients.
[MeSH-major]
Antineoplastic Agents / pharmacology. Boronic Acids / pharmacology.
Leukemia
,
Myeloid
/ drug therapy. Pyrazines / pharmacology
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Aged. Bortezomib. Drug Resistance, Neoplasm. Female. Flow Cytometry. HL-60 Cells. Humans. Male. Middle Aged. Multidrug Resistance-Associated Proteins / biosynthesis. Multidrug Resistance-Associated Proteins / metabolism. P-Glycoprotein / biosynthesis. P-Glycoprotein / metabolism. Vault Ribonucleoprotein Particles / biosynthesis. Vault Ribonucleoprotein Particles / metabolism
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(PMID = 18225565.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Pyrazines; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / multidrug resistance-associated protein 1; 69G8BD63PP / Bortezomib
18.
Olesen LH, Aggerholm A, Andersen BL, Nyvold CG, Guldberg P, Nørgaard JM, Hokland P:
Molecular typing of adult acute myeloid leukaemia: significance of translocations, tandem duplications, methylation, and selective gene expression profiling.
Br J Haematol
; 2005 Nov;131(4):457-67
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[Title]
Molecular typing of
adult
acute myeloid
leukaemia: significance of translocations, tandem duplications, methylation, and selective gene expression profiling.
Although a number of molecular aberrations have been described in
acute myeloid
leukaemia (
AML
), no study has yet determined their relative prognostic importance.
We have analysed blast cells from 250
adult
patients treated at the same institution during a 15-year period.
Compared with normal bone marrow, the chemotherapy resistance protein MRP1 and apoptosis related genes BAX and CASPASE3 were found to be overexpressed in
AML
blasts.
From these data, which are the first to compare these molecular aberrations directly, we conclude that, when a battery of molecular changes is evaluated for upfront significance in
AML
,
recurrent
translocations are of prime importance for treatment outcome.
[MeSH-major]
DNA Methylation.
Leukemia
,
Myeloid
/ genetics. Tandem Repeat Sequences / genetics. Translocation, Genetic
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. DNA, Neoplasm / genetics. Gene Expression Profiling. Genes, MDR. Humans. Middle Aged. Neoplasm Proteins / genetics. Promoter Regions, Genetic / genetics. Proportional Hazards Models. Retrospective Studies. Survival Analysis. fms-Like Tyrosine Kinase 3 / genetics
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(PMID = 16281935.001).
[ISSN]
0007-1048
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
19.
Metzgeroth G, Walz C, Score J, Siebert R, Schnittger S, Haferlach C, Popp H, Haferlach T, Erben P, Mix J, Müller MC, Beneke H, Müller L, Del Valle F, Aulitzky WE, Wittkowsky G, Schmitz N, Schulte C, Müller-Hermelink K, Hodges E, Whittaker SJ, Diecker F, Döhner H, Schuld P, Hehlmann R, Hochhaus A, Cross NC, Reiter A:
Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma.
Leukemia
; 2007 Jun;21(6):1183-8
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[Title]
Recurrent
finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated
acute myeloid leukemia
and lymphoblastic T-cell lymphoma.
Here, we report on seven FIP1L1-PDGFRA-positive patients who presented with
acute myeloid leukemia
(
AML
, n=5) or lymphoblastic T-cell
non
-Hodgkin-lymphoma (n=2) in conjunction with
AML
or Eos-MPD.
AML
patients were negative for common mutations of FLT3, NRAS, NPM1, KIT, MLL and JAK2; one patient revealed a splice mutation of RUNX1 exon 7.
We conclude that all eosinophilia-associated hematological malignancies should be screened for the presence of the FIP1L1-PDGFRA fusion gene as they are excellent candidates for treatment with tyrosine kinase inhibitors even if they present with an aggressive phenotype such as
AML
.
[MeSH-major]
Eosinophilia / drug therapy.
Leukemia
,
Myeloid
/ drug therapy. Oncogene Proteins, Fusion / analysis. Piperazines / administration & dosage. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha. mRNA Cleavage and Polyadenylation Factors
[MeSH-minor]
Acute
Disease.
Adult
. Aged. Benzamides. Disease-Free Survival. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloproliferative Disorders / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction / methods
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.
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.
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.
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.
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(PMID = 17377585.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Benzamides; 0 / FIP1L1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
20.
Yasar D, Karadogan I, Alanoglu G, Akkaya B, Luleci G, Salim O, Timuragaoglu A, Toruner GA, Berker-Karauzum S:
Array comparative genomic hybridization analysis of adult acute leukemia patients.
Cancer Genet Cytogenet
; 2010 Mar;197(2):122-9
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[Title]
Array comparative genomic hybridization analysis of
adult
acute leukemia
patients.
We have performed a retrospective array-based comparative hybridization (array-CGH) study on 41
acute leukemia
samples [n=17
acute
lymphoblastic
leukemia
(ALL) patients only at diagnosis, n=3 ALL patients both at diagnosis and relapse; n=20
acute myeloid leukemia
(
AML
) patients only at diagnosis and n=1
AML
patient both at diagnosis and relapse] using an Agilent 44K array.
In addition to previously detected cytogenetic aberrations, we observed cryptic aberrations in 95% of ALL and 90.5% of
AML
cases.
ALL-specific
recurrent
abnormalities were RB1 (n=3), PAX5 (n=4), and CDKN2B (n=3) deletions;
AML
-specific
recurrent
abnormalities were HOXA9 and HOXA10 (n=2) deletions and NOTCH1 duplication (n=2).
Recurrent
duplication of the ELK1 oncogene was observed in both ALL (n=2) and
AML
(n=3) cases.
[MeSH-major]
Comparative Genomic Hybridization / methods. Oligonucleotide Array Sequence Analysis / methods. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Chromosome Aberrations. Female. Humans. In Situ Hybridization, Fluorescence.
Leukemia
,
Myeloid
,
Acute
/ genetics. Male. Middle Aged. Mutation. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction
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(PMID = 20193845.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
21.
Garçon L, Libura M, Delabesse E, Valensi F, Asnafi V, Berger C, Schmitt C, Leblanc T, Buzyn A, Macintyre E:
DEK-CAN molecular monitoring of myeloid malignancies could aid therapeutic stratification.
Leukemia
; 2005 Aug;19(8):1338-44
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[Title]
DEK-CAN molecular monitoring of
myeloid
malignancies could aid therapeutic stratification.
The t(6;9)(p23;q34) is a
recurrent
chromosomal abnormality observed in 1% of
acute myelogenous leukemia
(
AML
), which generates a fusion transcript between DEK and CAN/NUP214 genes.
We conclude that DEK-CAN molecular monitoring by RQ-PCR in t(6;9) malignancies is a useful tool for individual patient management and that molecular negativity is indispensable for survival, but should not be a prerequisite for allografting in this rare, poor prognosis, subset of
AML
.
[MeSH-major]
Leukemia
,
Myeloid
/ diagnosis. Molecular Diagnostic Techniques. Oncogene Proteins / analysis. Recombinant Fusion Proteins / analysis
[MeSH-minor]
Adolescent.
Adult
. Child. Child, Preschool. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Oncogene Proteins, Fusion / analysis. Oncogene Proteins, Fusion / genetics. Polymerase Chain Reaction. Prognosis. Survival Rate
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[Copyright]
Leukemia (2005) 1344.19, 1338- doi
(PMID = 15973457.001).
[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 / DEK-CAN fusion protein, recombinant; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins
22.
Wakui M, Kuriyama K, Miyazaki Y, Hata T, Taniwaki M, Ohtake S, Sakamaki H, Miyawaki S, Naoe T, Ohno R, Tomonaga M:
Diagnosis of acute myeloid leukemia according to the WHO classification in the Japan Adult Leukemia Study Group AML-97 protocol.
Int J Hematol
; 2008 Mar;87(2):144-51
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[Title]
Diagnosis of
acute myeloid leukemia
according to the WHO classification in the Japan
Adult
Leukemia
Study Group
AML
-97 protocol.
We reviewed and categorized 638 of 809 patients who were registered in the Japan
Adult
Leukemia
Study Group
acute myeloid leukemia
(
AML
)-97 protocol using morphological means.
According to the WHO classification, 171 patients (26.8%) had
AML
with
recurrent
genetic abnormalities, 133 (20.8%) had
AML
with multilineage dysplasia (MLD), 331 (51.9%) had
AML
not otherwise categorized, and 3 (0.5%) had
acute leukemia
of ambiguous lineage.
The platelet count was higher and the rate of myeloperoxidase (MPO)-positive blasts was lower in
AML
with MLD than in the other WHO categories.
Our results confirmed that the cytogenetic profile, MLD phenotype, and MPO-positivity of blasts are associated with survival in patients with
AML
, and showed that each category had the characteristics of the WHO classification such as incidence, clinical features, and OS.
[MeSH-major]
Karyotyping.
Leukemia
,
Myeloid
,
Acute
/ classification.
Leukemia
,
Myeloid
,
Acute
/ genetics. Registries
[MeSH-minor]
Adolescent.
Adult
. Aged. Female. Humans. Japan. Kaplan-Meier Estimate. Male. Middle Aged
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(PMID = 18256787.001).
[ISSN]
0925-5710
[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]
United States
[Other-IDs]
NLM/ PMC2276241
23.
Sino US Leukemia Cooperative Group of Shanghai:
[Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification].
Zhonghua Xue Ye Xue Za Zhi
; 2007 Jul;28(7):444-8
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[Title]
[Clinical study of 572
adult
acute leukemia
patients in Shanghai according to WHO classification].
OBJECTIVE: To evaluate WHO classification of
acute leukemia
(AL) in Shanghai and compare the difference between WHO and FAB classification.
METHODS: Successive and unselected
leukemia
patients were referred to Sino-US
Leukemia
Cooperative Group of Shanghai from 2003 to 2006.
A total of 572
adult
AL cases were diagnosed and classified according to WHO and FAB classification.
RESULTS: Of the 572 AL patients, 436 (76.2%) were diagnosed as
acute myeloid leukemia
(
AML
), 119 (20.8%)
acute
lymphoblastic
leukemia
(ALL).
The
AML
and ALL percentage ratio was 3.66: 1.
AML
with
recurrent
cytogenetic abnormalities accounted for 35.3%, and with multilineage dysplasia for 13.1%, therapy-related
AML
accounted for 0.9%, and
AML
not otherwise categorized for 50.7%.
The percentage of therapy-related
AML
in Shanghai was lower than that in the Western.
According to FAB classification,
AML
-M4 was the most (38.5%) common subtype.
The percentage of
AML
-M3 and M4 in Shanghai were higher than that in the Western, but that of
AML
-M, was lower.
The incidence of karyotypic abnormalities in
AML
was 60.8%.
The incidence of
AML
with t (15;17) was higher than that in the Western.
Favorable cytogenetic risk group accounted for 30.6%, intermediate group for 51.5%, unfavorable group for 17.9% of
AML
.
CONCLUSIONS: The percentages of
AML
with t (15;17) and
AML
-M4 in Shanghai and the incidence of cytogenetic favorable group were higher than that in the Western.
It was different in WHO classification and karyotypic abnormalities of
AML
between Shanghai and the Western.
Comparing to the AL data of Shanghai
Leukemia
Group between 1984 and 1994, the percentage of
AML
-M4 was increased, but that of
AML
-M1 and M5 were decreased.
[MeSH-major]
Leukemia
/ classification
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Aged. Aged, 80 and over. China. Female. Humans. Karyotyping. Male. Middle Aged
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(PMID = 18072625.001).
[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
[Publication-country]
China
24.
Wang Y, Xue Y, Chen S, Wu Y, Pan J, Zhang J, Shen J:
[A clinical and laboratory study on acute myeloid leukemia with t(6;9)(p23;q34)].
Zhonghua Yi Xue Yi Chuan Xue Za Zhi
; 2010 Feb;27(1):34-7
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[Title]
[A clinical and laboratory study on
acute myeloid leukemia
with t(6;9)(p23;q34)].
OBJECTIVE: To explore the clinical and laboratory features of 6 cases of
acute myeloid leukemia
(
AML
) with t(6;9)(p23;q34).
CONCLUSION: The t(6;9)(p23;q34) is a rare
recurrent
abnormity.
AML
with t(6;9)(p23;q34) has unique clinical and laboratory features and its prognosis is poor in most cases.
[MeSH-major]
Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 9 / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Translocation, Genetic
[MeSH-minor]
Adult
. Antigens, CD / genetics. Antigens, CD13 / genetics. Antigens, CD34 / genetics. Antigens, Differentiation, Myelomonocytic / genetics. Female. Humans. Male. Middle Aged. Proto-Oncogene Proteins c-kit / genetics. Sialic Acid Binding Ig-like Lectin 3
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(PMID = 20140864.001).
[ISSN]
1003-9406
[Journal-full-title]
Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
[ISO-abbreviation]
Zhonghua Yi Xue Yi Chuan Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.11.2 / Antigens, CD13
25.
Cunningham I:
Extramedullary sites of leukemia relapse after transplant.
Leuk Lymphoma
; 2006 Sep;47(9):1754-67
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[Title]
Extramedullary sites of
leukemia
relapse after transplant.
Recurrent
or residual
leukemia
found in extramedullary sites after intensive treatments adversely affects prognosis.
The most commonly reported sites are soft tissue in
acute
leukemias and bone in CML.
Extramedullary relapse occurred typically within 2 years in ALL, but later in one-third of
myeloid
leukemias.
Most testicular relapses reported in
AML
followed
non
-TBI conditioning.
Intensive therapy has produced lengthy remissions in cases of
acute
leukemias involving various sites, whereas CML cases, particularly involving bone, were most resistant to treatment.
[MeSH-major]
Bone Neoplasms / pathology.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / pathology.
Leukemia
,
Myeloid
,
Acute
/ pathology. Neoplasm Recurrence, Local / pathology. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / pathology. Soft Tissue Neoplasms / pathology. Stem Cell Transplantation
[MeSH-minor]
Adolescent.
Adult
. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Male. Middle Aged
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(PMID = 17064985.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
26.
Reisch N, Roehnisch T, Sadeghi M, Greiner L, Regenbogen C, Rieger J, Emmerich B, Oduncu F:
AML M1 presenting with recurrent acute large arterial vessel thromboembolism.
Leuk Res
; 2007 Jun;31(6):869-71
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[Title]
AML
M1 presenting with
recurrent
acute
large arterial vessel thromboembolism.
Acute leukemia
may be associated with coagulopathy, predominantly severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.
Disordered hemostasis is characteristic for
acute
promyelocytic
leukemia
(APL, FAB M3).
We report a case of severe
recurrent
acute
arterial thromboembolism at presentation in
AML
FAB M1.
Most likely, the ischemic events in our patient resulted from
leukemia
as the thrombus material included many leukemic blasts.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ complications. Thromboembolism / etiology
[MeSH-minor]
Adult
. Amputation. Disseminated Intravascular Coagulation / etiology. Female. Hemorrhagic Disorders / etiology. Humans. Iliac Artery / pathology. Iliac Artery / radiography. Ischemia / etiology. Ischemia / pathology. Ischemia / radiography. Ischemia / surgery. Leg / blood supply. Leg / pathology. Leg / radiography. Leg / surgery.
Leukemia
, Promyelocytic,
Acute
/ complications
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(PMID = 17011031.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
27.
Pan J, Xue Y, Qiu H, Chen S, Zhang J, Wu Y, Shen J, Wang Y:
A pericentric inv(9)(p22q34) of the der(9)t(9;22)(q34;q11.2) is a recurrent secondary anomaly in Ph-positive leukemia.
Cancer Genet Cytogenet
; 2010 Dec;203(2):333-40
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[Title]
A pericentric inv(9)(p22q34) of the der(9)t(9;22)(q34;q11.2) is a
recurrent
secondary anomaly in Ph-positive
leukemia
.
A pericentric inv(9)(p22q34) of the derivative chromosome 9 that resulted from a standard t(9;22)(q34;q11.2) was identified by R-banding karyotypic analysis and fluorescence in situ hybridization (FISH) assays in 4 (0.18%) of 2,200 Philadelphia chromosome (Ph)-positive
leukemia
patients, including 3 with chronic
myeloid leukemia
(CML) in chronic phase and 1 with
acute myeloid leukemia
(
AML
) in our hospital since 2004.
FISH also found a deletion of partial sequence of BCR on der(9)t(9;22)(q34;q11.2)inv(9)(p22q34) in 67.5% of bone marrow cells in the
AML
patient, but did not detect the deletion of the sequence of ASS/9q34 in these four patients.
Reverse transcriptase-polymerase chain reaction revealed a b3a2 type of BCR/ABL1 fusion transcript in all of them, proving their disease to be Ph-positive
leukemia
.
On reviewing the literature, only two solitary Ph-positive
leukemia
patients have been noticed to have the inv(9)(p22q34) anomaly.
These two patients, together with our four documented patients, indicate that inv(9)(p22q34) is a novel, rare, but
recurrent
secondary chromosomal abnormality for Ph-positive
leukemia
.
Despite receiving hydroxyurea therapy (n = 3 patients), combined chemotherapy (n = 2), even imatinib treatment (n = 1), three patients, including one with
AML
and two with CML (one of whom progressed into the lymphoblastic blast phase), died with survival times of 28 days, 13 months, and 34 months, respectively.
[MeSH-major]
Chromosome Inversion. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / genetics
[MeSH-minor]
Adult
. Bone Marrow Cells / cytology. Chromosome Aberrations. Disease Progression. Female. Gene Deletion. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction
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[Copyright]
Copyright © 2010 Elsevier Inc. All rights reserved.
(PMID = 21156255.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
28.
Lu G, Yin CC, Medeiros LJ, Abruzzo LV:
Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.
Cancer Genet Cytogenet
; 2009 Jan 15;188(2):118-23
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[Title]
Deletion 15q as the sole abnormality in
acute myeloid leukemia
: report of three cases and review of the literature.
Deletions within the long arm of chromosome 15, a
recurrent
abnormality in
myeloid
malignancies, have been reported previously as a sole abnormality in only eight cases of
acute myeloid leukemia
(
AML
).
We describe three new cases of
AML
with this abnormality, all
adult
women (age, 41-66 years).
Two cases were
acute
myelomonocytic
leukemia
(FAB
AML
-M4), and one was
acute
myeloblastic
leukemia
with maturation (FAB
AML
-M2).
Taken together with the eight previously reported cases, we conclude that deletions in chromosome 15 are associated with
AML
, both in cases that arise de novo or in the setting of a myeloproliferative disorder or myelodysplastic syndrome.
The prognosis is poor, with survival similar to other
AML
cases with unfavorable cytogenetic changes.
[MeSH-major]
Chromosomes, Human, Pair 15.
Leukemia
,
Myeloid
,
Acute
/ genetics. Sequence Deletion
[MeSH-minor]
Adult
. Aged. Chromosome Banding. Fatal Outcome. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping
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(PMID = 19100517.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Number-of-references]
20
29.
Shimoyama M, Yamamoto K, Nishikawa S, Minagawa K, Katayama Y, Matsui T:
Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia.
Cancer Genet Cytogenet
; 2009 Oct;194(1):38-43
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[Title]
Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in
acute myeloid leukemia
with multilineage dysplasia.
Isodicentric chromosome 21, idic(21)(p11.2), is a rare but
recurrent
cytogenetic aberration in
acute
lymphoblastic
leukemia
.
We describe here a novel case of
acute myeloid leukemia
(
AML
) with double idic(21)(p11.2).
A 35-year-old man was diagnosed as having de novo
AML
with multilineage dysplasia because of 30% myeloperoxidase-positive blasts and trilineage dysplasia in the bone marrow.
These results suggest that the idic(21)(p11.2) could be implicated also in the pathogenesis of
AML
through amplification of genes including RUNX1 located on 21q.
[MeSH-major]
Aneuploidy. Chromosomes, Human, Pair 21 / genetics. Gene Duplication.
Leukemia
,
Myeloid
/ genetics
[MeSH-minor]
Acute
Disease.
Adult
. Antigens, CD / blood. Antigens, CD13 / blood. Antigens, CD34 / blood. Antigens, CD7 / blood. Antigens, Differentiation, Myelomonocytic / blood. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. HLA-DR Antigens / blood. Humans. In Situ Hybridization, Fluorescence. Male. Sialic Acid Binding Ig-like Lectin 3. Spectral Karyotyping
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(PMID = 19737652.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / HLA-DR Antigens; 0 / RUNX1 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
30.
Sakamaki H:
[The role of gemtuzumab ozogamicin in the treatment of acute myeloid leukemia patients].
Gan To Kagaku Ryoho
; 2008 Sep;35(9):1629-34
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[Title]
[The role of gemtuzumab ozogamicin in the treatment of
acute myeloid leukemia
patients].
Gemtuzumab Ozogamicin (GO) targets
leukemia
cells expressing CD33 by means of a monoclonal antibody conjugated to a cytotoxic agent, calicheamicin.
GO has been approved in Japan as monotherapy for the treatment of patients with
relapsed
/refractory
acute myeloid leukemia
(
AML
)since 2005.
GO administered as a single agent has resulted in overall response rates of about 30% in previously
relapsed
adult AML
.
Although caution is advised when administering GO within 115 days of a stem cell transplantation (SCT) procedure because of veno-occlusive disease, recent clinical studies overseas suggest that GO can be integrated into reduced-intensity conditioning therapy before allogeneic SCT in patients with
relapsed
AML
.
[MeSH-major]
Aminoglycosides / immunology. Aminoglycosides / therapeutic use. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / immunology. Antineoplastic Agents / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ immunology
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(PMID = 18799927.001).
[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 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab
31.
Bao L, Wang X, Ryder J, Ji M, Chen Y, Chen H, Sun H, Yang Y, Du X, Kerzic P, Gross SA, Yao L, Lv L, Fu H, Lin G, Irons RD:
Prospective study of 174 de novo acute myelogenous leukemias according to the WHO classification: subtypes, cytogenetic features and FLT3 mutations.
Eur J Haematol
; 2006 Jul;77(1):35-45
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[Title]
Prospective study of 174 de novo
acute myelogenous
leukemias according to the WHO classification: subtypes, cytogenetic features and FLT3 mutations.
We report a prospective study of 174 unselected
adult
de novo
acute myeloid leukemia
(
AML
) cases diagnosed using the WHO classification.
Of those, 57 (33%) were
AML
with
recurrent
cytogenetic abnormalities, 41 were (24%)
AML
with multilineage dysplasia, 74 (42%) were
AML
not otherwise categorized, and two were
acute
leukemias of ambiguous lineage.
Clonal cytogenetic abnormalities were detected in 64% of the WHO
AML
cases with t(15;17) (15%), t(8;21) (12%), +8 (11%), -7/del7q (8%) and del9q (5%) being the most common ones.
The FLT3/ITD mutations (FMS-like tyrosine kinase 3/internal tandem duplication) were observed in 12% of the WHO
AML
cases, which is much lower than ones in the literature, while the 6% incidence of the FLT3-activating loop mutations (either FLT3/D835 or FLT3/I836) was comparable with others.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ classification.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation. fms-Like Tyrosine Kinase 3 / genetics
[MeSH-minor]
Adolescent.
Adult
. Aged. Aged, 80 and over. Classification. Cytogenetic Analysis. Female. Humans. Leukocytosis / genetics. Male. Middle Aged. Prospective Studies. World Health Organization
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(PMID = 16573742.001).
[ISSN]
0902-4441
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Denmark
[Chemical-registry-number]
EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
32.
Biggio V, Renneville A, Nibourel O, Philippe N, Terriou L, Roumier C, Amouyel P, Cottel D, Castaigne S, Dombret H, Thomas X, Fenaux P, Preudhomme C, French alfa group:
Recurrent in-frame insertion in C/EBPalpha TAD2 region is a polymorphism without prognostic value in AML.
Leukemia
; 2008 Mar;22(3):655-7
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[Title]
Recurrent
in-frame insertion in C/EBPalpha TAD2 region is a polymorphism without prognostic value in
AML
.
[MeSH-major]
CCAAT-Enhancer-Binding Protein-alpha / genetics.
Leukemia
,
Myeloid
/ genetics. Neoplasm Proteins / genetics. Polymorphism, Genetic
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic / statistics & numerical data. Disease-Free Survival. Female. Humans. Male. Middle Aged. Mutagenesis, Insertional. Prognosis. Protein Structure, Tertiary. Risk. Survival Analysis
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(PMID = 17851556.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Letter
[Publication-country]
England
[Chemical-registry-number]
0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Neoplasm Proteins
33.
Carnicer MJ, Lasa A, Buschbeck M, Serrano E, Carricondo M, Brunet S, Aventin A, Sierra J, Di Croce L, Nomdedeu JF:
K313dup is a recurrent CEBPA mutation in de novo acute myeloid leukemia (AML).
Ann Hematol
; 2008 Oct;87(10):819-27
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[Title]
K313dup is a
recurrent
CEBPA mutation in de novo
acute myeloid leukemia
(
AML
).
The CEBPA gene codes for a transcription factor that has a pivotal role in controlling proliferation and differentiation of
myeloid
progenitors.
Acquired CEBPA mutations have been found in
acute myeloid
leukemias (
AML
) with a good prognosis, and most of these patients have a normal karyotype.
All four had an
AML
-M1 with CD7 positivity and T-cell receptor gamma chain (TCR-gamma) rearrangement.
K313dup seems to be selected in leukemic cells, and its frequency in other
AML
series could be determined using the screening method reported in this paper.
[MeSH-major]
CCAAT-Enhancer-Binding Proteins / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation
[MeSH-minor]
Adolescent.
Adult
. Aged. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Receptors, Antigen, T-Cell, gamma-delta / genetics. Receptors, Antigen, T-Cell, gamma-delta / metabolism
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(PMID = 18587575.001).
[ISSN]
0939-5555
[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 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Receptors, Antigen, T-Cell, gamma-delta
34.
Lee MY, Tan TD, Feng AC:
Clinicopathologic analysis of acute myeloid leukemia in a single institution: biphenotypic acute myeloid leukemia may not be an aggressive subtype.
J Chin Med Assoc
; 2007 Jul;70(7):269-73
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[Title]
Clinicopathologic analysis of
acute myeloid leukemia
in a single institution: biphenotypic
acute myeloid leukemia
may not be an aggressive subtype.
BACKGROUND: Most
acute
leukemias are classified as lymphoid or
myeloid
lineages by standard microscopic morphology, cytochemistry and a panel of immunologic markers.
The World Health Organization classification of
acute leukemia
incorporates morphologic, cytogenetic, immunologic and clinical features to define the entities that are biologically homogeneous and that have clinical relevance.
The purpose of this study was to determine the clinicopathologic characteristics of
acute myeloid leukemia
(
AML
) in Taiwan.
The median age at onset of disease was 49 years (range, 2-78 years), which was younger in biphenotypic
AML
(23.5 years) and older in multilineage dysplasia-related
AML
(61 years).
There were 9 cases (13%) with
recurrent
cytogenetic abnormality, 7 (10%) multilineage dysplasia-related, 7 (10%) therapy-related, 39 (56%) not other categorized and 8 (11%) of ambiguous lineage.
The 2- and 5-year overall survival rates of
AML
were 26.5% and 20.6%, respectively.
The median survivals of therapyrelated, multilineage dysplasia-related and biphenotypic
AML
were 2 months, 9 months and 30.5 months, respectively.
CONCLUSION: This was a clinicopathologic study of
AML
in Taiwan.
Multilineage dysplasia- and therapy-related
AML
have worse prognosis.
Biphenotypic
AML
may not be an aggressive subtype.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ pathology
[MeSH-minor]
Adolescent.
Adult
. Aged. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Myelodysplastic Syndromes / pathology. Phenotype
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(PMID = 17631462.001).
[ISSN]
1726-4901
[Journal-full-title]
Journal of the Chinese Medical Association : JCMA
[ISO-abbreviation]
J Chin Med Assoc
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
China (Republic : 1949- )
35.
Bullinger L, Krönke J, Schön C, Radtke I, Urlbauer K, Botzenhardt U, Gaidzik V, Carió A, Senger C, Schlenk RF, Downing JR, Holzmann K, Döhner K, Döhner H:
Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis.
Leukemia
; 2010 Feb;24(2):438-49
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[Title]
Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal
acute myeloid leukemia
using high-resolution single-nucleotide polymorphism analysis.
As
acute myeloid leukemia
(
AML
) represents a genetically heterogeneous disease, this technology might prove helpful, especially for cytogenetically normal
AML
(CN-
AML
) cases.
Thus, we performed high-resolution SNP analyses in 157
adult
cases of CN-
AML
.
Furthermore, we identified two cases with a cryptic t(6;11) as well as several
non
-
recurrent
aberrations pointing to
leukemia
-relevant regions.
These data show the potential of high-resolution SNP analysis for identifying genomic regions of potential pathogenic and clinical relevance in
AML
.
[MeSH-major]
Gene Dosage.
Leukemia
,
Myeloid
,
Acute
/ genetics. Polymorphism, Single Nucleotide / genetics. Uniparental Disomy / genetics
[MeSH-minor]
Adolescent.
Adult
. CCAAT-Enhancer-Binding Proteins / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 6 / genetics. Female. Gene Expression Regulation, Leukemic. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Nuclear Proteins / genetics. Young
Adult
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(PMID = 20016533.001).
[ISSN]
1476-5551
[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 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
36.
Verhaak RG, Valk PJ:
Genes predictive of outcome and novel molecular classification schemes in adult acute myeloid leukemia.
Cancer Treat Res
; 2010;145:67-83
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[Title]
Genes predictive of outcome and novel molecular classification schemes in
adult
acute myeloid leukemia
.
The pretreatment karyotype of leukemic blasts is currently the key determinant in therapy decision making in
acute myeloid leukemia
(
AML
).
The World Health Organization (WHO) has recognized this important information by including, besides clinical, cytological, cytochemical, and immunophenotypical features,
recurrent
cytogenetic abnormalities in its classification (Table 1).
In addition, novel molecular approaches in genomics, like monitoring the expression levels of thousands of genes in parallel using DNA microarray technology, open possibilities for further refinement of prognostication of
AML
.
Gene expression profiling in
AML
is already well established and has proven to be valuable to recognize various cytogenetic subtypes, discover novel
AML
subclasses, and predict clinical outcome.
The current advances made in molecular understanding of
AML
will ultimately lead to a further refinement of prognostics of
AML
.
[MeSH-major]
Genes, Neoplasm.
Leukemia
,
Myeloid
,
Acute
/ genetics
[MeSH-minor]
Adult
. Chromosome Aberrations. Gene Expression Profiling. Humans. Neoplasm Proteins / genetics. Neoplasm Proteins / physiology. Oligonucleotide Array Sequence Analysis. Prognosis. Treatment Outcome
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(PMID = 20306246.001).
[ISSN]
0927-3042
[Journal-full-title]
Cancer treatment and research
[ISO-abbreviation]
Cancer Treat. Res.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Neoplasm Proteins
[Number-of-references]
81
37.
Tullu MS, Date NB, Ghildiyal RG, Modi CJ:
Acute myelogenous leukemia in a child with HIV infection.
Eur J Pediatr
; 2010 May;169(5):629-31
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[Title]
Acute myelogenous leukemia
in a child with HIV infection.
The occurrence of
acute myelogenous leukemia
(
AML
) in HIV-infected patients is extremely rare with only
adult
patients reported so far.
The child also had
recurrent
parotid swellings, melena, and purulent otitis media.
The patient's bone marrow aspiration and biopsy suggested
AML
, and the
leukemia
panel 1 study showed CD13, CD33, CD34, and HLA DR-positive
AML
with CD7 expression.
AML
can occur in pediatric patients with HIV infection.
This is the first HIV-infected pediatric patient (<12 years) with
AML
reported in the medical literature.
[MeSH-major]
HIV Infections / complications.
Leukemia
,
Myeloid
,
Acute
/ complications
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[Cites]
Br J Haematol. 2001 Mar;112(4):900-8
[
11298584.001
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Int J STD AIDS. 1997 Apr;8(4):272-4
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[
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]
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J Infect. 1995 Jul;31(1):69-70
[
8522839.001
]
(PMID = 19802631.001).
[ISSN]
1432-1076
[Journal-full-title]
European journal of pediatrics
[ISO-abbreviation]
Eur. J. Pediatr.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
38.
Chelghoum Y, Vey N, Raffoux E, Huguet F, Pigneux A, Witz B, Pautas C, de Botton S, Guyotat D, Lioure B, Fegueux N, Garban F, Saad H, Thomas X:
Acute leukemia during pregnancy: a report on 37 patients and a review of the literature.
Cancer
; 2005 Jul 1;104(1):110-7
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[Title]
Acute leukemia
during pregnancy: a report on 37 patients and a review of the literature.
BACKGROUND:
Acute leukemia
(AL) requiring cytotoxic treatment occurring during pregnancy poses a very difficult therapeutic dilemma.
RESULTS: Thirty-one patients had
acute myeloid leukemia
(
AML
), and 6 patients had
acute
lymphoblastic
leukemia
(ALL).
Ten patients developed
recurrent
disease.
Overall, 12 of 37 pregnant women died from
leukemia
.
[MeSH-major]
Leukemia
/ drug therapy. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Pregnancy Complications, Neoplastic
[MeSH-minor]
Acute
Disease.
Adult
. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans.
Leukemia
,
Myeloid
/ drug therapy. Pregnancy. Pregnancy Outcome. Pregnancy Trimesters. Remission Induction
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(PMID = 15912518.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
13
39.
Kothary N, Soulen MC, Clark TW, Wein AJ, Shlansky-Goldberg RD, Crino PB, Stavropoulos SW:
Renal angiomyolipoma: long-term results after arterial embolization.
J Vasc Interv Radiol
; 2005 Jan;16(1):45-50
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This study was conducted to evaluate the long-term efficacy of
AML
embolization.
Of these, 10 patients had tuberous sclerosis (TS) with multiple AMLs and nine patients had a solitary sporadic
AML
.
Recurrence was defined as an increase in tumor size of greater than 2 cm on follow-up imaging and/or
recurrent
symptoms that required repeat embolization.
AML
recurrence was noted in 31.6% of patients (n = 19) and for 30% of lesions overall (n = 9).
Six of 10 patients in the TS group had
AML
recurrences.
No recurrences occurred in the patients with sporadic
AML
.
Six lesions in four patients had to be reembolized because of
recurrent
symptoms, including one hemorrhage, and three lesions in two patients required repeat embolization because of a greater than 2 cm increase in size.
However, long-term follow-up revealed a high
AML
recurrence rate in patients with TS.
Lifelong surveillance for recurrence after
AML
embolization is essential in patients with TS.
[MeSH-minor]
Adult
. Aged. Female. Follow-Up Studies. Hemorrhage / prevention & control. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Treatment Outcome. Tuberous Sclerosis / complications
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[CommentIn]
J Vasc Interv Radiol. 2005 Aug;16(8):1153-4; author reply 1154
[
16105930.001
]
(PMID = 15640409.001).
[ISSN]
1051-0443
[Journal-full-title]
Journal of vascular and interventional radiology : JVIR
[ISO-abbreviation]
J Vasc Interv Radiol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
40.
Sinclair P, Harrison CJ, Jarosová M, Foroni L:
Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36).
Haematologica
; 2005 May;90(5):602-11
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[Title]
Analysis of balanced rearrangements of chromosome 6 in
acute leukemia
: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new
recurrent
translocation, t(6;7)(q23;q32 through 36).
BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of
recurrent
chromosomal rearrangements in
acute leukemia
.
In this study we investigated the significance of novel translocations and inversions of 6q in
acute
lymphoblastic
leukemia
(ALL) and
acute myeloid leukemia
(
AML
).
RESULTS: Six of seven breakpoints in ALL and two in a single case of
AML
were localized to within a 10.5 Mb hotspot at 6q22-q23 with five analyzed to the level of a single probe.
INTERPRETATION AND CONCLUSIONS: We identified a new primary
recurrent
translocation t(6;7) (q22;q23 through q26) in pediatric T-ALL.
Other translocations interrupting the 6q22-q23 breakpoint cluster region did not appear to be
recurrent
and may contribute to leukemogenesis through a novel mechanism.
[MeSH-major]
Chromosome Breakage. Chromosome Inversion / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Genes, myb.
Leukemia
,
Myeloid
/ genetics.
Leukemia
-Lymphoma,
Adult
T-Cell / genetics. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Translocation, Genetic / genetics
[MeSH-minor]
Acute
Disease. Adaptor Proteins, Signal Transducing / genetics. Adolescent. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Banding. Clone Cells / pathology. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor B-Cell Lymphoblastic
Leukemia
-Lymphoma / pathology
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(PMID = 15921375.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / AHI1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Oncogene Proteins, Fusion
41.
Zhang L, Alsabeh R, Mecucci C, La Starza R, Gorello P, Lee S, Lill M, Schreck R:
Rare t(1;11)(q23;p15) in therapy-related myelodysplastic syndrome evolving into acute myelomonocytic leukemia: a case report and review of the literature.
Cancer Genet Cytogenet
; 2007 Oct 1;178(1):42-8
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[Title]
Rare t(1;11)(q23;p15) in therapy-related myelodysplastic syndrome evolving into
acute
myelomonocytic
leukemia
: a case report and review of the literature.
Balanced chromosome rearrangements are the hallmark of therapy-related
leukemia
that develops in patients treated with topoisomerase II inhibitors.
Many of these rearrangements involve
recurrent
chromosomal sites and associated genes (11q23/MLL, 21q22.3/AML1, and 11p15/NUP98), which can interact with a variety of partner genes.
With time, the patient's disorder progressed to
acute
myelomonocytic
leukemia
with cytogenetic evidence of clonal evolution.
To our knowledge, this is the first report of a patient presenting with a myelodysplastic syndrome with isolated t(1;11) (q23;p15), which evolved into therapy-related
acute myeloid leukemia
(t-
AML
).
This patient is the third reported with this cytogenetic rearrangement and t-
AML
, and is compared with the other two reports of t(1;11)(q23;p15).
[MeSH-major]
Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11.
Leukemia
, Myelomonocytic,
Acute
/ genetics. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Myelodysplastic Syndromes / therapy. Translocation, Genetic
[MeSH-minor]
Adult
. Aged. Disease Progression. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Neutrophils / metabolism
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(PMID = 17889707.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
42.
Schnittger S, Kohl TM, Haferlach T, Kern W, Hiddemann W, Spiekermann K, Schoch C:
KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival.
Blood
; 2006 Mar 1;107(5):1791-9
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[Title]
KIT-D816 mutations in AML1-ETO-positive
AML
are associated with impaired event-free and overall survival.
Mutations in codon D816 of the KIT gene represent a
recurrent
genetic alteration in
acute myeloid leukemia
(
AML
).
To clarify the biologic implication of activation loop mutations of the KIT gene, 1940 randomly selected
AML
patients were analyzed.
In contrast, other activating mutations like FLT3 and NRAS mutations were very rarely detected in AML1-rearranged
leukemia
.
Our findings clearly indicate that activating mutations of receptor tyrosine kinases are associated with distinct genetic subtypes in
AML
.
The KIT-D816 mutations confer a poor prognosis to AML1-ETO-positive
AML
and should therefore be included in the diagnostic workup.
Patients with KIT-D816-positive/AML1-ETO-positive
AML
might benefit from early intensification of treatment or combination of conventional chemotherapy with KIT PTK inhibitors.
[MeSH-major]
Amino Acid Substitution. Core Binding Factor Alpha 2 Subunit / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Oncogene Proteins, Fusion / genetics. Point Mutation. Proto-Oncogene Proteins c-kit / genetics
[MeSH-minor]
Adult
. Aged. Cell Line. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Codon / genetics. Disease-Free Survival. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Female. Gene Expression / genetics. Humans. Male. Middle Aged. Prognosis. Protein Kinase Inhibitors / pharmacology. Retrospective Studies. Translocation, Genetic / genetics
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(PMID = 16254134.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / AML1-ETO fusion protein, human; 0 / Codon; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
43.
Chamberlain MC, Raizer J:
Extended exposure to alkylator chemotherapy: delayed appearance of myelodysplasia.
J Neurooncol
; 2009 Jun;93(2):229-32
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OBJECTIVE: A case series of gliomas treated with alkylator-based chemotherapy who subsequently developed myelodysplastic syndrome (tMDS) or
acute
myelocytic
leukemia
(
AML
).
Three patients were diagnosed with
AML
as well (in two determined by bone marrow and one at autopsy).
Interval from last chemotherapy exposure to diagnosis of tMDS/
AML
ranged from 3 to 31 months (median 24 months).
Five patients have died, 2 as a consequence of
recurrent
brain tumor, 1 as a complication of transplantation, and 2 due to
AML
.
CONCLUSIONS: Although rare, induction of tMDS/
AML
following extended use of alkylator-based chemotherapy may become more relevant with the evolving practice to treat gliomas for protracted periods.
[MeSH-minor]
Adult
. Aged. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Female. Follow-Up Studies. Humans. Male. Middle Aged. Nitrosourea Compounds / therapeutic use. Reoperation / statistics & numerical data. Survival Analysis. Survivors. Time Factors
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N Engl J Med. 2005 Mar 10;352(10 ):987-96
[
15758009.001
]
(PMID = 19099199.001).
[ISSN]
1573-7373
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Alkylating; 0 / Nitrosourea Compounds; 7GR28W0FJI / Dacarbazine; YF1K15M17Y / temozolomide
44.
Fagnoni P, Limat S, Hintzy-Fein E, Martin F, Deconinck E, Cahn JY, Arveux P, Dussaucy A, Woronoff-Lemsi MC:
[Cost of hospital-based management of acute myeloid leukemia: from analytical to procedure-based tarification].
Bull Cancer
; 2006 Aug;93(8):813-9
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[Title]
[Cost of hospital-based management of
acute myeloid leukemia
: from analytical to procedure-based tarification].
The confrontation of the macro- and micro-economic approaches of hospital costs is a
recurrent
question, in particular for pathologies where length of stay is highly variable, like
acute myeloid
leukemias (
AML
).
This monocentric and retrospective study compares direct hospital medical costs of induction and relapse treatment sequences for
AML
, valued according to four different approaches: the analytic accounting system of our hospital, the French Diagnosis Related Group (DRG) cost databases of hospital discharges (readjusted, or not, to actual hospital stay duration), and official tariffs from the new French DRG prospective payment system.
The average cost of hospital
AML
care valued by the analytic accounting system of our hospital is 61,248 euros for the induction phase and 91,702 euros for the relapse phase.
[MeSH-major]
Hospital Costs.
Leukemia
,
Myeloid
/ economics. Prospective Payment System / economics
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Diagnosis-Related Groups / economics. Female. France. Humans. Length of Stay / economics. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies
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(PMID = 16935786.001).
[ISSN]
1769-6917
[Journal-full-title]
Bulletin du cancer
[ISO-abbreviation]
Bull Cancer
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
45.
Ley TJ, Ding L, Walter MJ, McLellan MD, Lamprecht T, Larson DE, Kandoth C, Payton JE, Baty J, Welch J, Harris CC, Lichti CF, Townsend RR, Fulton RS, Dooling DJ, Koboldt DC, Schmidt H, Zhang Q, Osborne JR, Lin L, O'Laughlin M, McMichael JF, Delehaunty KD, McGrath SD, Fulton LA, Magrini VJ, Vickery TL, Hundal J, Cook LL, Conyers JJ, Swift GW, Reed JP, Alldredge PA, Wylie T, Walker J, Kalicki J, Watson MA, Heath S, Shannon WD, Varghese N, Nagarajan R, Westervelt P, Tomasson MH, Link DC, Graubert TA, DiPersio JF, Mardis ER, Wilson RK:
DNMT3A mutations in acute myeloid leukemia.
N Engl J Med
; 2010 Dec 16;363(25):2424-33
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[Title]
DNMT3A mutations in
acute myeloid leukemia
.
BACKGROUND: The genetic alterations responsible for an adverse outcome in most patients with
acute myeloid leukemia
(
AML
) are unknown.
METHODS: Using massively parallel DNA sequencing, we identified a somatic mutation in DNMT3A, encoding a DNA methyltransferase, in the genome of cells from a patient with
AML
with a normal karyotype.
We sequenced the exons of DNMT3A in 280 additional patients with de novo
AML
to define recurring mutations.
CONCLUSIONS: DNMT3A mutations are highly
recurrent
in patients with de novo
AML
with an intermediate-risk cytogenetic profile and are independently associated with a poor outcome. (Funded by the National Institutes of Health and others.).
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[CommentIn]
N Engl J Med. 2010 Dec 16;363(25):2460-1
[
21067376.001
]
(PMID = 21067377.001).
[ISSN]
1533-4406
[Journal-full-title]
The New England journal of medicine
[ISO-abbreviation]
N. Engl. J. Med.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01CA101937; United States / NCRR NIH HHS / RR / UL1 RR024992; United States / NCI NIH HHS / CA / P01 CA101937; United States / NHGRI NIH HHS / HG / U54 HG003079; United States / NCRR NIH HHS / RR / P41 RR000954; United States / NCRR NIH HHS / RR / P41RR000954
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3A
[Other-IDs]
NLM/ NIHMS320791; NLM/ PMC3201818
46.
Niparuck P, Chuncharunee S, Ungkanont A, Udomtrupayakul U, Aungchaisuksiri P, Rerkamnuatchoke B, Jootar S, Atichartakarn V:
Long-term outcomes of de novo acute myeloid leukemia in Thai patients.
J Med Assoc Thai
; 2009 Sep;92(9):1143-9
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[Title]
Long-term outcomes of de novo
acute myeloid leukemia
in Thai patients.
BACKGROUND:
Acute myeloid leukemia
(
AML
) is the heterogeneous disease.
As per previous reports, there are some differences in clinical features and cytogenetic biomarkers of
AML
among different ethnic backgrounds.
Therefore, we conducted a retrospective study to analyze clinical outcomes and predictive factors of Thai
AML
patients receiving chemotherapy treatment.
MATERIAL AND METHOD: The authors performed a retrospective analysis of 106 adults with newly diagnosed de novo
AML
at Ramathibodi Hospital between 2003 and 2007.
Of 101 patients with
non
- M3 subtype, the patients received induction and consolidation chemotherapy with anthracyclin plus cytarabine based regimens (3 + 7).
AML
with
recurrent
cytogenetic translocations, complex chromosome, trisomy 8, polyploidy, del 5q and del 7q were found in 16.8, 6.3, 5.3, 5.3, 2.1 and 3.2%, respectively.
CONCLUSION: The overall complete remission rate of Thai
AML
patients is in 60%.
Only a small proportion of the presented patients have long-term DFS and OS, the significant factor for predicting survival of Thai
AML
patients is the complete remission status.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ epidemiology.
Leukemia
,
Myeloid
,
Acute
/ therapy
[MeSH-minor]
Adolescent.
Adult
. Aged. Antineoplastic Agents / therapeutic use. Cohort Studies. Disease-Free Survival. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Rate. Thailand. Treatment Outcome. Young
Adult
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(PMID = 19772172.001).
[ISSN]
0125-2208
[Journal-full-title]
Journal of the Medical Association of Thailand = Chotmaihet thangphaet
[ISO-abbreviation]
J Med Assoc Thai
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Thailand
[Chemical-registry-number]
0 / Antineoplastic Agents
47.
Ando T, Mitani N, Matsui K, Yamashita K, Nomiyama J, Tsuru M, Yujiri T, Tanizawa Y:
Recurrent extramedullary relapse of acute myelogenous leukemia after allogeneic hematopoietic stem cell transplantation in a patient with the chromosomal abnormality t(8;21) and CD56-positivity.
Int J Hematol
; 2009 Oct;90(3):374-7
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[Title]
Recurrent
extramedullary relapse of
acute myelogenous leukemia
after allogeneic hematopoietic stem cell transplantation in a patient with the chromosomal abnormality t(8;21) and CD56-positivity.
Isolated extramedullary (EM) relapse of
acute myelogenous leukemia
(
AML
) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is rare.
We describe an
AML
patient showing the chromosomal abnormality t(8;21) and CD56 expression who experienced a unique EM relapse after allo-HSCT.
These findings suggest that the graft-versus-
leukemia
effect may preferentially maintain marrow remission rather than prevent EM relapse.
In addition, our findings show that extended survival is possible after EM relapse following allo-HSCT in patients with marrow hematopoiesis of donor origin, and that augmentation of the graft-versus-
leukemia
effect may be useful.
[MeSH-major]
Graft vs
Leukemia
Effect. Hematopoietic Stem Cell Transplantation.
Leukemia
,
Myeloid
,
Acute
. Stomach Neoplasms. Translocation, Genetic
[MeSH-minor]
Antigens, CD56 / metabolism. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Gastric Mucosa / pathology. Humans. Male. Recurrence. Transplantation, Homologous. Young
Adult
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.
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1865-3774
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International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
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Case Reports; Journal Article
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Japan
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0 / Antigens, CD56
48.
Tibes R, Keating MJ, Ferrajoli A, Wierda W, Ravandi F, Garcia-Manero G, O'Brien S, Cortes J, Verstovsek S, Browning ML, Faderl S:
Activity of alemtuzumab in patients with CD52-positive acute leukemia.
Cancer
; 2006 Jun 15;106(12):2645-51
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[Title]
Activity of alemtuzumab in patients with CD52-positive
acute leukemia
.
BACKGROUND: Alemtuzumab is a humanized monoclonal antibody directed against the cell surface antigen CD52 and has demonstrated activity in chronic
lymphocytic leukemia
and other CD52-positive lymphoproliferative disorders.
Because CD52 also is expressed on
acute
leukemic blasts, the authors investigated the safety and efficacy of alemtuzumab in patients with
acute myeloid leukemia
(
AML
) and
acute
lymphoblastic
leukemia
(ALL).
METHODS: Fifteen patients with CD52-positive (> or = 20%),
recurrent
or refractory
acute leukemia
(9 patients with
AML
and 6 patients with ALL) received alemtuzumab at a dose of 30 mg intravenously given 3 times a week (dose escalation during Week 1) for a total of 4 to 12 weeks.
CONCLUSIONS: Single-agent alemtuzumab was found to have limited activity in
recurrent
or refractory
acute leukemia
.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antigens, CD / immunology. Antigens, Neoplasm / immunology. Glycoproteins / immunology.
Leukemia
,
Myeloid
/ drug therapy. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Aged. Antibodies, Monoclonal, Humanized. Bacteremia / diagnosis. Bacteremia / etiology. Bone Marrow / drug effects. Bone Marrow / pathology. Disease Progression. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. Fungemia / diagnosis. Fungemia / etiology. Humans. Male. Middle Aged. Pneumonia / diagnosis. Pneumonia / etiology. Treatment Outcome
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[Copyright]
Copyright 2006 American Cancer Society.
(PMID = 16688777.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
49.
Parkin B, Ouillette P, Wang Y, Liu Y, Wright W, Roulston D, Purkayastha A, Dressel A, Karp J, Bockenstedt P, Al-Zoubi A, Talpaz M, Kujawski L, Liu Y, Shedden K, Shakhan S, Li C, Erba H, Malek SN:
NF1 inactivation in adult acute myelogenous leukemia.
Clin Cancer Res
; 2010 Aug 15;16(16):4135-47
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[Title]
NF1 inactivation in
adult
acute myelogenous leukemia
.
PURPOSE: This study was conducted to identify novel genes with importance to the biology of
adult
acute myelogenous leukemia
(
AML
).
EXPERIMENTAL DESIGN: We analyzed DNA from highly purified
AML
blasts and paired buccal cells from 95 patients for
recurrent
genomic microdeletions using ultra-high density Affymetrix single nucleotide polymorphism 6.0 array-based genomic profiling.
Sequence analysis of all NF1 coding exons in the 11
AML
cases with NF1 copy number changes identified acquired truncating frameshift mutations in two patients.
Subsequent expression analysis of NF1 mRNA in the entire
AML
cohort using fluorescence-activated cell sorting sorted blasts as a source of RNA identified six patients (one with a NF1 mutation) with absent NF1 expression.
The NF1 null states were associated with increased Ras-bound GTP, and short hairpin RNA-mediated NF1 suppression in primary
AML
blasts with wild-type NF1 facilitated colony formation in methylcellulose.
Primary
AML
blasts without functional NF1, unlike blasts with functional NF1, displayed sensitivity to rapamycin-induced apoptosis, thus identifying a dependence on mammalian target of rapamycin (mTOR) signaling for survival.
Finally, colony formation in methylcellulose ex vivo of NF1 null CD34+/CD38- cells sorted from
AML
bone marrow samples was inhibited by low-dose rapamycin.
CONCLUSIONS: NF1 null states are present in 7 of 95 (7%) of
adult AML
and delineate a disease subset that could be preferentially targeted by Ras or mammalian target of rapamycin-directed therapeutics.
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Clin Cancer Res. 2010 Aug 15;16(16):4074-6
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20587590.001
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(PMID = 20505189.001).
[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 States / NCI NIH HHS / CA / R01 CA136537; United States / NCI NIH HHS / CA / 1R01 CA136537-01; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / R01 CA136537-02; United States / NCI NIH HHS / CA / CA136537-02
[Publication-type]
Comment; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
EC 3.6.5.2 / ras Proteins
[Other-IDs]
NLM/ NIHMS210184; NLM/ PMC2921448
50.
Owen C, Fitzgibbon J, Paschka P:
The clinical relevance of Wilms Tumour 1 (WT1) gene mutations in acute leukaemia.
Hematol Oncol
; 2010 Mar;28(1):13-9
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[Title]
The clinical relevance of Wilms Tumour 1 (WT1) gene mutations in
acute
leukaemia.
Recurrent
genetic aberrations are important predictors of outcome in
acute myeloid
leukaemia (
AML
).
WT1 mutations occur in approximately 10% of
adult AML
patients at diagnosis and are most frequent in the cytogenetically normal (CN)
AML
subgroup.
Herein, we discuss the importance of WT1 mutations in
AML
.
[MeSH-major]
Genes, Wilms Tumor.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation / genetics
[MeSH-minor]
Adult
. Humans. Prognosis. WT1 Proteins / genetics. WT1 Proteins / metabolism
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(PMID = 20013787.001).
[ISSN]
1099-1069
[Journal-full-title]
Hematological oncology
[ISO-abbreviation]
Hematol Oncol
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0700052; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / WT1 Proteins
[Number-of-references]
75
51.
De Stefano V, Sorà F, Rossi E, Chiusolo P, Laurenti L, Fianchi L, Zini G, Pagano L, Sica S, Leone G:
The risk of thrombosis in patients with acute leukemia: occurrence of thrombosis at diagnosis and during treatment.
J Thromb Haemost
; 2005 Sep;3(9):1985-92
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[Title]
The risk of thrombosis in patients with
acute leukemia
: occurrence of thrombosis at diagnosis and during treatment.
BACKGROUND: Thromboembolism can occur during
acute leukemia
, especially
acute
lymphoid
leukemia
(ALL) treated with L-asparaginase.
Yet, most reports are anecdotical and scarce data are available on the risk of thrombosis in
acute myeloid leukemia
(
AML
).
OBJECTIVES: To evaluate the risk of thrombosis in patients with
acute leukemia
.
PATIENTS AND METHODS: Three-hundred and seventy-nine consecutive
adult
patients with newly diagnosed
acute leukemia
were recruited in an observational cohort study conducted from January 1994 to December 2003.
Diagnosis was ALL in 69 patients,
acute
promyelocytic
leukemia
(APL; FAB subtype M3) in 31, and
non
-M3
AML
in 279.
All first or
recurrent
symptomatic thromboembolic events objectively diagnosed were recorded.
At diagnosis, thrombosis was a presenting manifestation in 13 cases (3.4% of the whole cohort): 1.4% in ALL, 9.6% in APL, and 3.2% in
non
-M3
AML
patients.
At 6 months from diagnosis, the cumulative incidence of thrombosis was 10.6% in ALL, 8.4% in APL, and 1.7% in
non
-M3
AML
patients.
CONCLUSIONS: In patients with
acute leukemia
, the risk of thrombosis is not negligible.
Thombosis can be a presenting symptom at diagnosis in a significant portion of cases with APL (9.6%) and
non
-M3
AML
(3.2%); a similar rate of thrombosis can occur during the subsequent course of the disease.
[MeSH-major]
Leukemia
/ complications. Thrombosis / etiology
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Aged. Asparaginase / adverse effects. Female. Follow-Up Studies. Genetic Predisposition to Disease. Humans. Incidence. Male. Middle Aged. Risk
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.
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(PMID = 16102104.001).
[ISSN]
1538-7933
[Journal-full-title]
Journal of thrombosis and haemostasis : JTH
[ISO-abbreviation]
J. Thromb. Haemost.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
EC 3.5.1.1 / Asparaginase
52.
Erkeland SJ, Verhaak RG, Valk PJ, Delwel R, Löwenberg B, Touw IP:
Significance of murine retroviral mutagenesis for identification of disease genes in human acute myeloid leukemia.
Cancer Res
; 2006 Jan 15;66(2):622-6
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[Title]
Significance of murine retroviral mutagenesis for identification of disease genes in human
acute myeloid leukemia
.
Acute myeloid leukemia
(
AML
) is a heterogeneous disease with a variable response to treatment.
Recurrent
cytogenetic defects and acquired mutations in regulatory genes are associated with
AML
subtypes and prognosis.
Recently, gene expression profiling (GEP) has been applied to further risk stratify
AML
.
Here, we show that mouse
leukemia
genes identified by retroviral insertion mutagenesis are more frequently differentially expressed in distinct subclasses of
adult
and pediatric
AML
than randomly selected genes or genes located more distantly from a virus integration site.
The candidate proto-oncogenes showing discriminative expression in primary
AML
could be placed in regulatory networks mainly involved in signal transduction and transcriptional control.
Our data support the validity of retroviral insertion mutagenesis in mice for human disease and indicate that combining these murine screens for potential proto-oncogenes with GEP in human
AML
may help to identify critical disease genes and novel pathogenetic networks in
leukemia
.
[MeSH-major]
Gene Expression Profiling.
Leukemia
,
Myeloid
/ genetics. Mutagenesis, Insertional. Proto-Oncogenes
[MeSH-minor]
Acute
Disease.
Adult
. Animals. Child. Humans. Mice. Retroviridae / genetics. Signal Transduction. Transcription, Genetic
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(PMID = 16423987.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
53.
Falini B, Mecucci C, Saglio G, Lo Coco F, Diverio D, Brown P, Pane F, Mancini M, Martelli MP, Pileri S, Haferlach T, Haferlach C, Schnittger S:
NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities: a comparative analysis of 2562 patients with acute myeloid leukemia.
Haematologica
; 2008 Mar;93(3):439-42
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[Title]
NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of
recurrent
genetic abnormalities: a comparative analysis of 2562 patients with
acute myeloid leukemia
.
Acute myeloid leukemia
carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc(+)
acute myeloid leukemia
) represents one-third of
adult AML
(50-60% of all
acute myeloid leukemia
with normal karyotype) and shows distinct biological, pathological and clinical features.
We confirm in 2562 patients with
acute myeloid leukemia
our previous observation that NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of
recurrent
genetic abnormalities.
Taken together, these findings make NPMc+
acute myeloid leukemia
a good candidate for inclusion in the upcoming World Health Organization classification.
[MeSH-major]
Cytoplasm / chemistry.
Leukemia
,
Myeloid
/ genetics. Nuclear Proteins / genetics
[MeSH-minor]
Acute
Disease. Bone Marrow / pathology. Cell Nucleus / chemistry. Chromosome Aberrations. Chromosome Inversion. Cohort Studies. DNA Mutational Analysis. Germany / epidemiology. Humans. In Situ Hybridization, Fluorescence. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic
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(PMID = 18268276.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin
54.
Ahmad F, Dalvi R, Mandava S, Das BR:
Acute Myelogeneous Leukemia (M0/M1) with novel chromosomal abnormality of t(14;17) (q32; q11.2).
Am J Hematol
; 2007 Jul;82(7):676-8
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[Title]
Acute
Myelogeneous
Leukemia
(M0/M1) with novel chromosomal abnormality of t(14;17) (q32; q11.2).
Acute
Myelogeneous
Leukemia
(
AML
) is a heterogeneous disease with respect to morphology, immunophenotype, and genetic rearrangements.
Multiple
recurrent
chromosomal aberrations have been identified by conventional cytogenetic analysis.
In this study, we report a case whose clinical features were suggestive of
AML
-M1 subtype with t(14;17) (q32; q11.2) karyotype involving rearrangement of chromosomal segments 17q11.2 and 14q32.
This is the first report of novel chromosomal translocation in this subset of
AML
and has not yet been reported elsewhere.
[MeSH-major]
Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 17 / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Translocation, Genetic / genetics
[MeSH-minor]
Adult
. Female. Humans. Karyotyping
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(PMID = 17177193.001).
[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
55.
Sindt A, Deau B, Brahim W, Staal A, Visanica S, Villarese P, Rault JP, Macintyre E, Delabesse E:
Acute monocytic leukemia with coexpression of minor BCR-ABL1 and PICALM-MLLT10 fusion genes along with overexpression of HOXA9.
Genes Chromosomes Cancer
; 2006 Jun;45(6):575-82
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[Title]
Acute
monocytic
leukemia
with coexpression of minor BCR-ABL1 and PICALM-MLLT10 fusion genes along with overexpression of HOXA9.
The t(9;22)(q34;q11) translocation occurs in chronic
myeloid leukemia
(CML) and
adult
B-cell
acute
lymphoblastic
leukemia
(ALL), leading to fusion of BCR to ABL1 and constitutive activation of ABL1 tyrosine kinase activity.
The latter is found in almost all cases of CML and in one third of the cases of t(9;22)-positive
adult
B-ALL.
P190 BCR-ABL1 is found in the remaining two thirds of t(9;22)-positive
adult
B-ALL cases but only exceptionally in CML.
We describe here the first case of t(9;22)(q34;q11) associated with t(10;11)(p13;q14) in
acute
monocytic
leukemia
.
The
recurrent
t(10;11)(p13;q14) translocation, usually found in
acute myeloid leukemia
(
AML
) and T-ALL, merges PICALM to MLLT10.
RT-PCR enabled identification of PICALM-MLLT10 and BCR-ABL1 e1-a2 fusion transcripts; in the context of chronic and
acute myeloid leukemia
, the latter usually has a monocytic presentation.
We also identified overexpression of HOXA9, a gene essential to
myeloid
differentiation that is expressed in PICALM-MLLT10 and MLL-rearranged
acute
leukemias.
This case fits with and extends a recently proposed multistage
AML
model in which constitutive activation of tyrosine kinases by mutations (BCR-ABL1) are associated with deregulation of transcription factors central to
myeloid
differentiation (HOXA9 secondary to PICALM-MLLT10).
[MeSH-major]
Fusion Proteins, bcr-abl / metabolism. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / metabolism.
Leukemia
, Monocytic,
Acute
/ genetics. Oncogene Proteins, Fusion / metabolism
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[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 16518848.001).
[ISSN]
1045-2257
[Journal-full-title]
Genes, chromosomes & cancer
[ISO-abbreviation]
Genes Chromosomes Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / PICALM-MLLT10 fusion protein, human; 0 / Transcription Factors; 0 / homeobox protein HOXA9; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Fusion Proteins, bcr-abl
56.
Landrette SF, Kuo YH, Hensen K, Barjesteh van Waalwijk van Doorn-Khosrovani S, Perrat PN, Van de Ven WJ, Delwel R, Castilla LH:
Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11.
Blood
; 2005 Apr 1;105(7):2900-7
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[Title]
Plag1 and Plagl2 are oncogenes that induce
acute myeloid leukemia
in cooperation with Cbfb-MYH11.
Recurrent
chromosomal rearrangements are associated with the development of
acute myeloid leukemia
(
AML
).
This fusion protein inhibits the core-binding factor (CBF), resulting in a block of hematopoietic differentiation, and induces
leukemia
upon the acquisition of additional mutations.
In this study, we demonstrate that Plag1 and Plagl2 independently cooperate with CBF beta-SMMHC in vivo to efficiently trigger
leukemia
with short latency in the mouse.
Finally, PLAG1 and PLAGL2 expression was increased in 20% of human
AML
samples.
Interestingly, PLAGL2 was preferentially increased in samples with chromosome 16 inversion, suggesting that PLAG1 and PLAGL2 may also contribute to human
AML
.
Overall, this study shows that Plag1 and Plagl2 are novel
leukemia
oncogenes that act by expanding hematopoietic progenitors expressing CbF beta-SMMHC.
[MeSH-major]
DNA-Binding Proteins / genetics.
Leukemia
,
Myeloid
/ genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Proteins / genetics. Transcription Factors / genetics
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Animals. Female. G1 Phase / immunology. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / cytology. Humans. Male. Mice. Mice, Mutant Strains. Middle Aged. Mutagenesis, Insertional. Retroviridae / genetics. S Phase / immunology
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.
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gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
SciCrunch.
HGNC: Data: Gene Annotation
.
SciCrunch.
Marmoset Gene list: Data: Gene Annotation
.
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(PMID = 15585652.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA096983-01
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / CBFbeta-MYH11 fusion protein; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / PLAG1 protein, human; 0 / PLAGL2 protein, human; 0 / RNA-Binding Proteins; 0 / Transcription Factors
57.
Shali W, Hélias C, Fohrer C, Struski S, Gervais C, Falkenrodt A, Leymarie V, Lioure B, Raby P, Herbrecht R, Lessard M:
Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/acute myeloid leukemias: conventional cytogenetics, FISH, and multiplex FISH.
Cancer Genet Cytogenet
; 2006 Jul 15;168(2):133-45
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[Title]
Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/
acute myeloid
leukemias: conventional cytogenetics, FISH, and multiplex FISH.
We report a series of 43 consecutive therapy-related myelodysplastic syndromes (t-MDS) or
acute myeloid
leukemias (t-
AML
) observed for 6 years.
Conventional cytogenetic and fluorescent in situ hybridization (FISH)/ multiplex FISH (M-FISH) methods were used to analyze cytogenetic characteristics of secondary MDS/
AML
.
A considerable proportion of
recurrent
balanced translocations characterized t-
AML
secondary to therapy.
Compared to other series,
recurrent
translocations appeared to be more numerous (25%), probably reflecting an evolution of therapeutic modalities.
[MeSH-major]
In Situ Hybridization, Fluorescence / methods.
Leukemia
,
Myeloid
,
Acute
/ genetics. Myelodysplastic Syndromes / genetics
[MeSH-minor]
Adolescent.
Adult
. Aged. Aged, 80 and over. Child. Female. Gene Amplification. Gene Deletion. Humans. Karyotyping. Male. Middle Aged. Translocation, Genetic
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(PMID = 16843103.001).
[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
58.
Katsanos K, Sabharwal T, Ahmad F, Dourado R, Adam A:
Onyx embolization of sporadic angiomyolipoma.
Cardiovasc Intervent Radiol
; 2009 Nov;32(6):1291-5
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We present what is to our knowledge the first case of successful embolization of a solitary sporadic
AML
with the use of a new nonadhesive liquid embolic agent (ethylene vinyl alcohol copolymer; Onyx).
Short-term follow-up magnetic resonance imaging showed complete tumor necrosis without any
recurrent
pathologic vessels.
The specific features, potential advantages in
AML
treatment, and technical limitations of this new liquid embolic agent are discussed.
[MeSH-minor]
Adult
. Angiography. Contrast Media. Female. Humans. Magnetic Resonance Imaging
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DIMETHYL SULFOXIDE
.
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(PMID = 19083054.001).
[ISSN]
1432-086X
[Journal-full-title]
Cardiovascular and interventional radiology
[ISO-abbreviation]
Cardiovasc Intervent Radiol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Contrast Media; 0 / Onyx copolymer; 0 / Polyvinyls; YOW8V9698H / Dimethyl Sulfoxide
59.
Boissel N, Nibourel O, Renneville A, Gardin C, Reman O, Contentin N, Bordessoule D, Pautas C, de Revel T, Quesnel B, Huchette P, Philippe N, Geffroy S, Terre C, Thomas X, Castaigne S, Dombret H, Preudhomme C:
Prognostic impact of isocitrate dehydrogenase enzyme isoforms 1 and 2 mutations in acute myeloid leukemia: a study by the Acute Leukemia French Association group.
J Clin Oncol
; 2010 Aug 10;28(23):3717-23
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[Title]
Prognostic impact of isocitrate dehydrogenase enzyme isoforms 1 and 2 mutations in
acute myeloid leukemia
: a study by the
Acute Leukemia
French Association group.
PURPOSE: Recently, whole-genome sequencing in
acute myeloid leukemia
(
AML
) identified
recurrent
isocitrate dehydrogenase enzyme isoform (IDH1) mutations (IDH1m), previously reported to be involved in gliomas as well as IDH2 mutations (IDH2m).
The prognosis of both IDH1m and IDH2m in
AML
remains unclear.
PATIENTS AND METHODS: The prevalence and the prognostic impact of R132 IDH1 and R172 IDH2 mutations were evaluated in a cohort of 520 adults with
AML
homogeneously treated in the French
Acute Leukemia
French Association (ALFA) -9801 and -9802 trials.
In patients with CN-
AML
, IDH1m were associated with NPM1m (P = .008), but exclusive of CEBPAm (P = .03).
In CN-
AML
patients, IDH1m were found in 19% of favorable genotype ([NPM1m or CEBPAm] without fms-related tyrosine kinase 3 [FLT3] internal tandem duplication [ITD]) and were associated with a higher risk of relapse (RR) and a shorter overall survival (OS).
Favorable genotype in CN-
AML
could thus be defined by the association of NPM1m or CEBPAm with neither FLT3-ITD nor IDH1m.
In IDH2m CN-
AML
patients, we observed a higher risk of induction failure, a higher RR and a shorter OS.
CONCLUSION: Contrarily to what is reported in gliomas, IDH1m and IDH2m in
AML
are associated with a poor prognosis.
Screening of IDH1m could help to identify high-risk patients within the subset of CN-
AML
with a favorable genotype.
[MeSH-major]
Isocitrate Dehydrogenase / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics
[MeSH-minor]
Adolescent.
Adult
. Aged. Humans. Middle Aged. Mutation. Prevalence. Prognosis. Protein Isoforms / genetics. Randomized Controlled Trials as Topic. Retrospective Studies. Young
Adult
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(PMID = 20625116.001).
[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
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00880243/ NCT00931138
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Protein Isoforms; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human
60.
Mulrooney DA, Dover DC, Li S, Yasui Y, Ness KK, Mertens AC, Neglia JP, Sklar CA, Robison LL, Davies SM, Childhood Cancer Survivor Study:
Twenty years of follow-up among survivors of childhood and young adult acute myeloid leukemia: a report from the Childhood Cancer Survivor Study.
Cancer
; 2008 May 1;112(9):2071-9
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[Title]
Twenty years of follow-up among survivors of childhood and young
adult
acute myeloid leukemia
: a report from the Childhood Cancer Survivor Study.
BACKGROUND: Limited data exist on the comprehensive assessment of late medical and social effects experienced by survivors of childhood and young
adult
acute myeloid leukemia
(
AML
).
METHODS: This analysis included 272 5-year
AML
survivors who participated in the Childhood Cancer Survivor Study (CCSS).
The cumulative incidence of
recurrent AML
was 6.6% at 10 years (95% CI, 3.7%-9.6%) and 8.6% at 20 years (95% CI, 5.1%-12.1%).
CONCLUSIONS: Long-term survival from childhood
AML
> or =5-years after diagnosis was favorable.
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(PMID = 18327823.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
ENG
[Grant]
United States / NCRR NIH HHS / RR / K12 RR023247; United States / NCI NIH HHS / CA / U24 CA055727; United States / NCRR NIH HHS / RR / 1 K12 RR 023247; United States / NCI NIH HHS / CA / U24 CA 55727
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Investigator]
Robison LL; Hudson M; Armstrong G; Perkins J; O'Leary M; Friedman D; Pendergrass T; Greffe B; Odom L; Ruccione K; Mulvihill J; Ginsberg J; Meadows A; Tersak J; Ritchey A; Blatt J; Reaman G; Packer R; Davies S; Bhatia S; Qualman S; Hammond S; Termuhlen A; Ruymann F; Diller L; Grier H; Li F; Meacham L; Mertens A; Leisenring W; Potter J; Greenberg M; Nathan PC; Boice J; Rodriguez V; Smithson WA; Gilchrist G; Sklar C; Oeffinger K; Finklestein J; Anderson B; Inskip P; Vik TA; Weetman R; Green DM; Hayashi R; Vietti T; Marina N; Donaldson SS; Link MP; Dreyer Z; Whelan K; Sande J; Berkow R; Yasui Y; Casallis J; Zeltzer L; Goldsby R; Ablin A; Hutchinson R; Neglia J; Deapen D; Breslow N; Bowers D; Tomlinson G; Buchanan GR; Strong L; Stovall M
61.
Montoto S, Canals C, Rohatiner AZ, Taghipour G, Sureda A, Schmitz N, Gisselbrecht C, Fouillard L, Milpied N, Haioun C, Slavin S, Conde E, Fruchart C, Ferrant A, Leblond V, Tilly H, Lister TA, Goldstone AH, EBMT Lymphoma Working Party:
Long-term follow-up of high-dose treatment with autologous haematopoietic progenitor cell support in 693 patients with follicular lymphoma: an EBMT registry study.
Leukemia
; 2007 Nov;21(11):2324-31
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A total of 375 patients (54%) developed
recurrent
lymphoma, 10-year progression-free survival (PFS) being 31%.
Thirty-nine patients developed secondary myelodysplastic syndrome/
acute myeloid
leukaemia (MDS/
AML
), in 34 cases having received TBI as the conditioning regimen.
The 5-year
non
-relapse mortality (NRM) was 9%.
[MeSH-minor]
Adolescent.
Adult
. Bone Marrow Cells / cytology. Bone Marrow Transplantation. Disease-Free Survival. Female. Humans. Male. Middle Aged. Registries. Remission Induction. Stem Cells / cytology. Transplantation, Autologous. Treatment Outcome
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(PMID = 17637813.001).
[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
62.
Bacher U, Kern W, Schnittger S, Hiddemann W, Haferlach T, Schoch C:
Population-based age-specific incidences of cytogenetic subgroups of acute myeloid leukemia.
Haematologica
; 2005 Nov;90(11):1502-10
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[Title]
Population-based age-specific incidences of cytogenetic subgroups of
acute myeloid leukemia
.
BACKGROUND AND OBJECTIVES: It is well known that the different cytogenetic subgroups of
acute myeloid leukemia
(
AML
) show different age-specific frequencies.
For example, balanced translocations tend to be found in younger patients while complex aberrant karyotypes are usually found in elderly patients with
AML
.
DESIGN AND METHODS: We evaluated the population-based age-specific incidences of different cytogenetic subgroups in 2555 patients with
AML
between 21 and 70 years of age.
There were also different age-specific incidences of some
recurrent
molecular mutations.
INTERPRETATION AND CONCLUSIONS: These results are suggestive of different mechanisms in the pathogenesis of
AML
.
[MeSH-major]
Cytogenetics.
Leukemia
,
Myeloid
,
Acute
/ epidemiology.
Leukemia
,
Myeloid
,
Acute
/ genetics
[MeSH-minor]
Adult
. Age Factors. Aged. Female. Genetic Markers / genetics. Genetics, Population. Humans. Incidence. Male. Middle Aged. Translocation, Genetic / genetics
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(PMID = 16266897.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Genetic Markers
63.
Walter MJ, Payton JE, Ries RE, Shannon WD, Deshmukh H, Zhao Y, Baty J, Heath S, Westervelt P, Watson MA, Tomasson MH, Nagarajan R, O'Gara BP, Bloomfield CD, Mrózek K, Selzer RR, Richmond TA, Kitzman J, Geoghegan J, Eis PS, Maupin R, Fulton RS, McLellan M, Wilson RK, Mardis ER, Link DC, Graubert TA, DiPersio JF, Ley TJ:
Acquired copy number alterations in adult acute myeloid leukemia genomes.
Proc Natl Acad Sci U S A
; 2009 Aug 4;106(31):12950-5
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[Title]
Acquired copy number alterations in
adult
acute myeloid leukemia
genomes.
Cytogenetic analysis of
acute myeloid leukemia
(
AML
) cells has accelerated the identification of genes important for
AML
pathogenesis.
To complement cytogenetic studies and to identify genes altered in
AML
genomes, we performed genome-wide copy number analysis with paired normal and tumor DNA obtained from 86
adult
patients with de novo
AML
using 1.85 million feature SNP arrays.
A total of 201 somatic CNAs were found in the 86
AML
genomes (mean, 2.34 CNAs per genome), with French-American-British system M6 and M7 genomes containing the most changes (10-29 CNAs per genome).
Twenty-four percent of
AML
patients with normal cytogenetics had CNA, whereas 40% of patients with an abnormal karyotype had additional CNA detected by SNP array, and several CNA regions were
recurrent
.
The mRNA expression levels of 57 genes were significantly altered in 27 of 50
recurrent
CNA regions <5 megabases in size.
Collectively, 34 of 86
AML
genomes (40%) contained alterations not found with cytogenetics, and 98% of these regions contained genes.
In this study of 86
adult AML
genomes, the use of an unbiased high-resolution genomic screen identified many genes not previously implicated in
AML
that may be relevant for pathogenesis, along with many known oncogenes and tumor suppressor genes.
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[Cites]
Blood. 2001 Jun 1;97(11):3581-8
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[
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]
(PMID = 19651600.001).
[ISSN]
1091-6490
[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
[Grant]
United States / NHLBI NIH HHS / HL / K08 HL083012; United States / NCI NIH HHS / CA / P01 CA101937; United States / NHLBI NIH HHS / HL / T32 HL007088; United States / NCI NIH HHS / CA / U10 CA101140
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Intracellular Signaling Peptides and Proteins; 0 / NSD1 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Nuclear Proteins; 0 / Nup98 protein, human
[Other-IDs]
NLM/ PMC2716381
64.
Park HK, Zhang S, Wong MK, Kim HL:
Clinical presentation of epithelioid angiomyolipoma.
Int J Urol
; 2007 Jan;14(1):21-5
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OBJECTIVE: Epithelioid angiomyolipomas (
AML
) of the kidney are malignant tumors with aggressive clinical behavior.
METHODS: We reviewed cases of epithelioid
AML
recently diagnosed at our institution to highlight the spectrum of clinical presentations.
The diagnosis of epithelioid
AML
was established by positive staining for melanoma and smooth muscle cell markers, and presence of perivascular epithelioid cells.
Two patients developed
recurrent
, metastatic disease following nephrectomy.
One patient with tuberous sclerosis and multiple, bilateral
AML
developed an enhancing renal tumor that did not contain any fat densities.
A partial nephrectomy was performed and pathology revealed epithelioid
AML
adjacent to conventional
AML
.
Epithelioid
AML
may be locally aggressive and metastasize.
[MeSH-minor]
Adult
. Aged. Carcinoma, Renal Cell / diagnosis. Diagnosis, Differential. Female. Humans. Male. Middle Aged
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(PMID = 17199855.001).
[ISSN]
0919-8172
[Journal-full-title]
International journal of urology : official journal of the Japanese Urological Association
[ISO-abbreviation]
Int. J. Urol.
[Language]
eng
[Publication-type]
Duplicate Publication; Journal Article
[Publication-country]
Australia
65.
Cornely OA, Böhme A, Reichert D, Reuter S, Maschmeyer G, Maertens J, Buchheidt D, Paluszewska M, Arenz D, Bethe U, Effelsberg J, Lövenich H, Sieniawski M, Haas A, Einsele H, Eimermacher H, Martino R, Silling G, Hahn M, Wacker S, Ullmann AJ, Karthaus M, Multinational Case Registry of the Infectious Diseases Working Party of the German Society for Hematology and Oncology:
Risk factors for breakthrough invasive fungal infection during secondary prophylaxis.
J Antimicrob Chemother
; 2008 Apr;61(4):939-46
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Secondary prophylaxis of IFI is widely administered, but reliable data on outcome and risk factors for
recurrent
IFI during subsequent chemotherapy are not available.
This study determines risk factors for
recurrent
IFI in leukaemia patients.
METHODS: From 25 European cancer centres, 166 consecutive patients with
acute myelogenous
leukaemia (
AML
) and a recent history of proven or probable pulmonary IFI were included.
Recurrent
IFI occurred in 26 patients (15.7%).
Multiple logistic regressions yielded predisposing factors: duration of neutropenia [per additional day; odds ratio (OR) 1.043, confidence interval (CI) 1.008-1.078], high-dose cytarabine (OR 3.920, CI 1.120-12.706), number of antibiotics (per antibiotic; OR 1.504, CI 1.089-2.086), partial response as outcome of prior IFI (OR 4.037, CI 1.301-12.524) and newly diagnosed
AML
(OR 3.823, CI 0.953-15.340).
CONCLUSIONS: Duration of neutropenia, high-dose cytarabine, prior antibiotic therapy and a partial response to the first IFI therapy were risk factors for
recurrent
IFI and should be considered in
AML
patients with prior pulmonary IFI undergoing further chemotherapy.
[MeSH-minor]
Adolescent.
Adult
. Aged. Aged, 80 and over. Chemoprevention. Child. Child, Preschool. Female. Humans.
Leukemia
,
Myeloid
,
Acute
/ complications.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Logistic Models. Male. Middle Aged. Recurrence. Risk Factors. Treatment Outcome
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(PMID = 18272515.001).
[ISSN]
1460-2091
[Journal-full-title]
The Journal of antimicrobial chemotherapy
[ISO-abbreviation]
J. Antimicrob. Chemother.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antifungal Agents
66.
Davis CJ, Barton JH, Sesterhenn IA:
Cystic angiomyolipoma of the kidney: a clinicopathologic description of 11 cases.
Mod Pathol
; 2006 May;19(5):669-74
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This report deals with 11 examples of renal angiomyolipomas (
AML
) which appear to include an epithelial element as a part of the neoplasm in the form of gross or microscopic cysts-usually both.
Three of these were known to be symptomatic: intermittent flank pain and gross hematuria for 2 months;
recurrent
hematuria both before and after flank trauma and a third patient with
acute
abdomen due to a ruptured tumor blood vessel.
[MeSH-minor]
Actins / analysis.
Adult
. Aged. Antigens, Neoplasm. Desmin / analysis. Female. Humans. Immunohistochemistry. MART-1 Antigen. Male. Melanoma-Specific Antigens. Middle Aged. Muscle, Smooth / chemistry. Neoplasm Proteins / analysis. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis
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(PMID = 16528375.001).
[ISSN]
0893-3952
[Journal-full-title]
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
[ISO-abbreviation]
Mod. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Actins; 0 / Antigens, Neoplasm; 0 / Desmin; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
67.
Lai YY, Qiu JY, Jiang B, Lu XJ, Huang XJ, Zhang Y, Liu YR, Shi HL, Lu DP:
Characteristics and prognostic factors of acute myeloid leukemia with t (8; 21) (q22; q22).
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2005 Oct;13(5):733-40
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[Title]
Characteristics and prognostic factors of
acute myeloid leukemia
with t (8; 21) (q22; q22).
q22) frequently associated with additional chromosomal aberrations is one of the most
recurrent
chromosomal abnormalities in
AML
.
Clinically, this type of
AML
usually shows some specific characteristics and has a good response to chemotherapy with a high remission rate and a relatively long median survival.
On the other hand, some reports also showed poor prognosis in
AML
patients with t (8; 21), and the associated bad-prognosis factors have not been strongly established to date.
21)
AML
in China, 75 Chinese
AML
patients with t (8;.
Cytogenetically, 62.5% cases had additional chromosomal abnormalities, and the main associated
recurrent
additional abnormalities were loss of a sex chromosome (LOS), trisomy 4, del (9q) and trisomy 8.
With a follow-up of 1 to 96 months, 19 cases
relapsed
at a median time of 10.5 months (range 3 to 42 months).
In multivariate analyses of prognostic factors, karyotype, extramedullary
leukemia
, age and post-remission therapy were of prognostic value for OS.
Extramedullary
leukemia
was an adverse prognostic factor (P = 0.012).
It is concluded that Chinese
AML
patients with t (8;.
21) had some different characteristics as compared with patients from other countries, a relatively poor outcome was observed in our patients, especially in those with extramedullary
leukemia
or additional chromosomal abnormalities.
21)
AML
in China, especially to those with adverse prognostic factors.
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(PMID = 16277833.001).
[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]
ENG
[Publication-type]
Journal Article
[Publication-country]
China
68.
Anwar Iqbal M, Al-Omar HM, Owaidah T, Al-Humaidan H, Bhuiyan ZA, Sahovic E:
del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality.
Eur J Haematol
; 2006 Sep;77(3):245-50
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[Title]
del(6)(p23) in two cases of de novo
AML
--a new
recurrent
primary chromosome abnormality.
OBJECTIVE: Previously, deletion 6p23 was generally reported in therapy-related secondary
acute myeloid leukemia
(
AML
) as part of complex karyotypes.
In this report, we present two young
adult
patients with de novo
AML
-M2 and a terminal deletion 6p23 as a sole primary abnormality, confirmed by chromosome 6 specific subtelomeric probes.
RESULTS: A diagnosis of
AML
-M2 was confirmed in both patients by morphological and immunophenotyping studies.
The common morphological, immunophenotypic, and cytogenetic features in our two patients strongly support a separate new entity of de novo
AML
with deletion 6p23.
[MeSH-major]
Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics
[MeSH-minor]
Adult
. Chromosomal Proteins,
Non
-Histone / genetics. Cytogenetics. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Oncogene Proteins / genetics. Oncogenes. Recurrence
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(PMID = 16856925.001).
[ISSN]
0902-4441
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Chromosomal Proteins, Non-Histone; 0 / Dek protein, human; 0 / Oncogene Proteins
69.
Maserati E, Pressato B, Valli R, Minelli A, Sainati L, Patitucci F, Marletta C, Mastronuzzi A, Poli F, Lo Curto F, Locatelli F, Danesino C, Pasquali F:
The route to development of myelodysplastic syndrome/acute myeloid leukaemia in Shwachman-Diamond syndrome: the role of ageing, karyotype instability, and acquired chromosome anomalies.
Br J Haematol
; 2009 Apr;145(2):190-7
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[Title]
The route to development of myelodysplastic syndrome/
acute myeloid
leukaemia in Shwachman-Diamond syndrome: the role of ageing, karyotype instability, and acquired chromosome anomalies.
An investigation of 22 new patients with Shwachman-Diamond syndrome (SDS) and the follow-up of 14 previously reported cases showed that (i) clonal chromosome changes of chromosomes 7 and 20 were present in the bone marrow (BM) of 16 out of 36 cases, but if
non
-clonal changes were taken into account, the frequency of anomalies affecting these chromosomes was 20/36: a specific SDS karyotype instability was thus confirmed;.
(ii) the
recurrent
isochromosome i(7)(q10) did not include short arm material, whereas it retained two arrays of D7Z1 alphoid sequences;.
(iii) the deletion del(20)(q11) involved the minimal region of deletion typical of myelodysplastic syndromes (MDS) and
acute myeloid
leukaemia (
AML
);.
We conclude that karyotype instability is part of the natural history of SDS through a specific mutator effect, linked to lacking SBDS protein, with consequent clonal anomalies of chromosomes 7 and 20 in BM, which may eventually promote MDS/
AML
with the patients' ageing.
[MeSH-major]
Aging / genetics. Chromosome Aberrations.
Leukemia
,
Myeloid
,
Acute
/ genetics. Myelodysplastic Syndromes / genetics
[MeSH-minor]
Adolescent.
Adult
. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Breakage. Chromosomes, Human, Pair 20. Chromosomes, Human, Pair 7. DNA Mutational Analysis. Disease Progression. Female. Follow-Up Studies. Humans. In Situ Hybridization, Fluorescence. Isochromosomes. Karyotyping. Male. Proteins / genetics. Young
Adult
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(PMID = 19222471.001).
[ISSN]
1365-2141
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Proteins; 0 / SBDS protein, human
70.
McCormack E, Bruserud O, Gjertsen BT:
Review: genetic models of acute myeloid leukaemia.
Oncogene
; 2008 Jun 19;27(27):3765-79
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[Title]
Review: genetic models of
acute myeloid
leukaemia.
The use of genetically engineered mice (GEM) have been critical in understanding disease states such as cancer, and none more so than
acute myelogenous
leukaemia (
AML
), a disease characterized by over 100 distinct chromosomal translocations.
A substantial proportion of cases exhibiting
recurrent
reciprocal translocations at diagnosis, such as t(8;21) or t(15;17) have been exhaustively studied and are currently employed in clinical diagnosis.
Furthermore, little emphasis has been paid to the effect of chromosomal translocations other than
recurrent
genetic abnormalities, with no models reflecting the multiple abnormalities observed in high-risk cases of
AML
accounting for 8-10% of
adult AML
.
Here we review the differing technologies employed in generation of GEM of
AML
.
We discuss the relevance of GEM
AML
from embryonic stem cell-mediated (for example retinoic acid receptor-alpha fusions and AML1/ETO) models; through to the valuable retroviral-mediated gene transfer models.
The latter have been used to great effect in defining the transforming properties of chromosomal translocation products such as MLL (found in 5-6% of all
AML
cases) and NUP98 (denoting poor prognosis in therapy-related disease) and particularly when co-transduced with bad prognostic factors such as Flt3 mutations.
[MeSH-major]
Animals, Genetically Modified / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Models, Genetic
[MeSH-minor]
Animals. Chromosome Aberrations. Disease Models, Animal. Exons. Humans.
Leukemia
, Promyelocytic,
Acute
/ genetics. Mice. Mice, Transgenic. Prognosis
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(PMID = 18264136.001).
[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
111
71.
Trubia M, Albano F, Cavazzini F, Cambrin GR, Quarta G, Fabbiano F, Ciambelli F, Magro D, Hernandezo JM, Mancini M, Diverio D, Pelicci PG, Coco FL, Mecucci C, Specchia G, Rocchi M, Liso V, Castoldi G, Cuneo A:
Characterization of a recurrent translocation t(2;3)(p15-22;q26) occurring in acute myeloid leukaemia.
Leukemia
; 2006 Jan;20(1):48-54
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[Title]
Characterization of a
recurrent
translocation t(2;3)(p15-22;q26) occurring in
acute myeloid
leukaemia.
Six patients with de novo
acute myeloid leukemia
(
AML
) and a t(2;3)(p15-21;q26-27) were identified among approximately 1000 cases enrolled in the GIMEMA trial.
The patients showed dysplasia of at least two
myeloid
cell lineages in all cases; they had a low-to-normal platelet count and displayed an immature CD34+ CD117+ immunophenotype.
We arrived at the following conclusions: (a) the t(2;3) is a
recurrent
translocation having an approximate 0.5% incidence in
adult AML
;.
[MeSH-major]
Chromosomes, Human, Pair 2 / genetics. Chromosomes, Human, Pair 3 / genetics.
Leukemia
,
Myeloid
/ genetics. Translocation, Genetic / genetics
[MeSH-minor]
Acute
Disease.
Adult
. Cytogenetic Analysis / methods. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Polymerase Chain Reaction. Predictive Value of Tests. Prognosis. Trisomy
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(PMID = 16619048.001).
[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
72.
Park SH, Chi HS, Park SJ, Jang S, Park CJ:
[Clinical importance of morphological multilineage dysplasia in acute myeloid leukemia with myelodysplasia related changes].
Korean J Lab Med
; 2010 Jun;30(3):231-8
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[Title]
[Clinical importance of morphological multilineage dysplasia in
acute myeloid leukemia
with myelodysplasia related changes].
BACKGROUND:
AML
with myelodysplasia related changes (
AML
MRC) is known to show a poor prognosis compared with de novo
AML
, but controversies exist about the prognostic impact of multilineage dysplasia (MLD) among MRC.
We investigated the prognostic impact of MLD in
AML
MRC.
METHODS: A total of 357 patients newly diagnosed as
AML
at Asan Medical Center from January 2001 to December 2005 were analyzed.
They were diagnosed and classified as
AML
with
recurrent
genetic abnormalities,
AML
MRC, and
AML
not otherwise specified (
AML
NOS).
RESULTS:
AML
MRC patients showed a lower complete remission (CR) rate (44.7% vs. 64.9%, P=0.002) and shorter OS (297 vs. 561 days, P=0.004) and EFS (229 vs. 374 days, P=0.004) than
AML
NOS patients.
Patients with MLD among
AML
MRC also showed a lower CR rate (37.7%, P=0.001) and shorter OS (351 days, P=0.036) and EFS (242 days, P=0.076) than
AML
NOS patients.
However, among
AML
MRC patients, there were no differences in OS, EFS and CR between patients with and without MLD.
CONCLUSIONS:
AML
MRC patients showed a lower CR rate and shorter OS and EFS than
AML
NOS patients.
AML
MRC patients with MLD showed similar results and their prognosis was not different from those without MLD.
MLD findings among
AML
MRC could be an independent poor prognostic factor in de novo
AML
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ mortality. Myelodysplastic Syndromes / diagnosis
[MeSH-minor]
Adolescent.
Adult
. Aged. Aged, 80 and over. Cell Lineage. Child. Child, Preschool. Data Interpretation, Statistical. Disease-Free Survival. Female. Humans. Infant. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis
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(PMID = 20603581.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
kor
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Korea (South)
73.
Tang JM, Meng FY, Chen AW:
[Gene expression profile of refractory acute myeloid leukemia (M2a)].
Ai Zheng
; 2005 Jun;24(6):676-9
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[Title]
[Gene expression profile of refractory
acute myeloid leukemia
(M2a)].
BACKGROUND & OBJECTIVE: Recurrence is the major cause of treatment failure of
acute myeloid leukemia
(
AML
).
Drug resistance, the main cause of refractoriness of
AML
, is related to abnormal genes expression.
This study was to detect differential expression of genes in naive and
recurrent
/refractory
AML
, and explore potential mechanisms of
recurrent
/refractory
AML
.
METHODS: Differential gene expressions of bone marrow mononuclear cells between naive and
recurrent
/refractory diseases in 5 self-paired patients with
AML
-M(2a) were detected by DNA microarray.
RESULTS: In 925 tested genes, 14 were differentially expressed between naive and
recurrent
/refractory diseases in the 5 self-paired patients.
Of the 14 genes, 12 (involved in signal transduction, DNA replication, regulation of transcription, RNA processing, and regulation of cell cycle) were obviously up-regulated in
recurrent
diseases, and up-regulation of RRM1 (involved in DNA replication) was the most obvious.
CONCLUSIONS: Development of
recurrent
/refractory
AML
-M(2a) is concerned with various genes.
Up-regulation of these genes suggests that proliferation of
recurrent
/refractory
AML
-M(2a) blasts may be higher than that of naive
AML
-M(2a) blasts.
[MeSH-major]
Gene Expression Profiling. Immunophenotyping.
Leukemia
,
Myeloid
/ genetics
[MeSH-minor]
Acute
Disease.
Adult
. Antigens, CD / metabolism. Cell Proliferation. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Recurrence. Tumor Suppressor Proteins / metabolism. Up-Regulation
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(PMID = 15946477.001).
[Journal-full-title]
Ai zheng = Aizheng = Chinese journal of cancer
[ISO-abbreviation]
Ai Zheng
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD; 0 / RRM1 protein, human; 0 / Tumor Suppressor Proteins
74.
Kaya M, Nagoya S, Sasaki M, Kukita Y, Yamashita T:
Primary total hip arthroplasty with Asian-type AML total hip prosthesis: follow-up for more than 10 years.
J Orthop Sci
; 2008 Jul;13(4):324-7
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[Title]
Primary total hip arthroplasty with Asian-type
AML
total hip prosthesis: follow-up for more than 10 years.
BACKGROUND: We retrospectively reviewed 137 consecutive total hip arthroplasties performed with
AML
-A stems and Tri-Lock cups to see whether design modifications made to these components would achieve durable biological fixation in the Japanese population in whom developmental dysplasia of the hip (DDH) is relatively common.
METHODS: Between April 1988 and June 1994, we performed 137 total hip arthroplasties using the
AML
-A prosthesis for the patients with osteoarthritis of the hip joint.
Another seven hips underwent revision surgery for
recurrent
dislocation.
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Japan. Kaplan-Meier Estimate. Male. Middle Aged. Reoperation. Young
Adult
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(PMID = 18696190.001).
[ISSN]
0949-2658
[Journal-full-title]
Journal of orthopaedic science : official journal of the Japanese Orthopaedic Association
[ISO-abbreviation]
J Orthop Sci
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
75.
Horton TM, Thompson PA, Berg SL, Adamson PC, Ingle AM, Dolan ME, Delaney SM, Hedge M, Weiss HL, Wu MF, Blaney SM, Children's Oncology Group Study:
Phase I pharmacokinetic and pharmacodynamic study of temozolomide in pediatric patients with refractory or recurrent leukemia: a Children's Oncology Group Study.
J Clin Oncol
; 2007 Nov 1;25(31):4922-8
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[Title]
Phase I pharmacokinetic and pharmacodynamic study of temozolomide in pediatric patients with refractory or
recurrent
leukemia
: a Children's Oncology Group Study.
PURPOSE: To determine the tolerability, pharmacokinetics, and mechanisms of temozolomide resistance in children with
relapsed
or refractory
leukemia
.
Pretreatment
leukemia
cell O6-methylguanine-DNA methyltransferase (MGMT) activity, tumor and plasma MGMT promoter methylation, and microsatellite instability (MSI) were examined in 14 of 16 study patients and in tissue bank samples from children with
acute leukemia
not treated with temozolomide (MGMT, n = 67; MSI, n = 65).
RESULTS: Sixteen patients (nine female, seven male;
acute
lymphoblastic
leukemia
[ALL], n = 8;
acute myeloid leukemia
[
AML
], n = 8), median age 11 years (range, 1 to 19 years), received either 200 mg/m2/d (nine enrolled, three assessable for toxicity) or 260 mg/m2/d (seven enrolled, three assessable for toxicity) of temozolomide.
MGMT activity in
leukemia
cells was quite variable and was highest in patients with
relapsed
ALL.
CONCLUSION: Temozolomide was well tolerated at doses as high as 260 mg/m2/d for 5 days in children with
relapsed
or refractory
leukemia
.
Increased MGMT activity may account for the temozolomide resistance in children with
relapsed leukemia
.
Leukemia
cell MGMT activity was higher in pediatric ALL than
AML
(P < .0001).
[MeSH-major]
Antineoplastic Agents, Alkylating / pharmacokinetics. Dacarbazine / analogs & derivatives. Drug Resistance, Neoplasm / genetics.
Leukemia
/ drug therapy. Neoplasm Recurrence, Local / drug therapy
[MeSH-minor]
Adolescent.
Adult
. Child. Child, Preschool. DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Female. Humans. Infant. Male. Microsatellite Instability. Tumor Suppressor Proteins / metabolism
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(PMID = 17971589.001).
[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
[Grant]
United States / NCI NIH HHS / CA / K12CA90433; United States / NCI NIH HHS / CA / P30 CA14599; United States / NCI NIH HHS / CA / U01CA63187; United States / NCI NIH HHS / CA / UO1-CA97452
[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, Alkylating; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
76.
Yamamoto K, Yakushijin K, Kawamori Y, Minagawa K, Katayama Y, Matsui T:
Translocation (7;9)(q22;q34) in therapy-related myelodysplastic syndrome after allogeneic bone marrow transplantation for acute myeloblastic leukemia.
Cancer Genet Cytogenet
; 2007 Jul 1;176(1):61-6
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[Title]
Translocation (7;9)(q22;q34) in therapy-related myelodysplastic syndrome after allogeneic bone marrow transplantation for
acute
myeloblastic
leukemia
.
Reciprocal translocations involving the long arm of chromosome 7 are relatively rare cytogenetic aberrations in myelodysplastic syndrome (MDS) and
acute
myeloblastic
leukemia
(
AML
).
A 44-year-old woman was initially given a diagnosis of de novo
AML
M6A with a normal karyotype.
Considering two other such reported cases of
AML
, the t(7;9)(q22;q34) may be a novel
recurrent
translocation in
myeloid
malignancies.
[MeSH-major]
Bone Marrow Transplantation / adverse effects. Chromosomes, Human, Pair 7. Chromosomes, Human, Pair 9.
Leukemia
,
Myeloid
,
Acute
/ therapy. Myelodysplastic Syndromes / genetics. Translocation, Genetic
[MeSH-minor]
Adult
. Female. Humans. Spectral Karyotyping
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(PMID = 17574966.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
77.
Lu SH, Hou YY, Tan YS, Xu JF, Zeng HY, Sujie AK, Wang XD, Bai CX:
Clinical and histopathological alterations of lymphangioleiomyomatosis in 14 Chinese patients.
Chin Med J (Engl)
; 2009 Aug 20;122(16):1895-900
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The clinical course of LAM is characterized by progressive dyspnea on exertion,
recurrent
pneumothorax, and chylous fluid collections.
Extrapulmonary findings such as renal angiomyolipoma (
AML
), enlarged abdominal lymph nodes, liver
AML
and retroperitoneal lymphangioleiomyoma were seen in 21.4%, 14.3%, 7.14% and 7.14% in 14 cases respectively, which is remarkably lower than in the previously reported.
CONCLUSIONS: Women with unexplained
recurrent
pneumothorax, tuberous sclerosis, or a diagnosis of primary spontaneous pneumothorax or emphysema in the setting of limited or absent tobacco use should undergo high-resolution computed tomography (HRCT) scan screening for LAM.
[MeSH-minor]
Adolescent.
Adult
. Aged. Contraceptives, Oral, Synthetic. Female. Humans. Immunohistochemistry. Medroxyprogesterone / therapeutic use. Middle Aged. Ovariectomy. Progesterone / therapeutic use. Progestins / therapeutic use. Young
Adult
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(PMID = 19781367.001).
[ISSN]
0366-6999
[Journal-full-title]
Chinese medical journal
[ISO-abbreviation]
Chin. Med. J.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Contraceptives, Oral, Synthetic; 0 / Progestins; 4G7DS2Q64Y / Progesterone; HSU1C9YRES / Medroxyprogesterone
78.
de Lima M, Giralt S, Thall PF, de Padua Silva L, Jones RB, Komanduri K, Braun TM, Nguyen HQ, Champlin R, Garcia-Manero G:
Maintenance therapy with low-dose azacitidine after allogeneic hematopoietic stem cell transplantation for recurrent acute myelogenous leukemia or myelodysplastic syndrome: a dose and schedule finding study.
Cancer
; 2010 Dec 01;116(23):5420-31
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[Title]
Maintenance therapy with low-dose azacitidine after allogeneic hematopoietic stem cell transplantation for
recurrent
acute myelogenous leukemia
or myelodysplastic syndrome: a dose and schedule finding study.
BACKGROUND: Recurrence is a major cause of treatment failure after allogeneic transplantation for
acute myelogenous leukemia
(
AML
) and myelodysplastic syndrome (MDS), and treatment options are very limited.
Azacitidine is a DNA methyltransferase inhibitor with activity in
myeloid
disease.
CONCLUSIONS: Azacitidine at 32 mg/m2 given for 5 days is safe and can be administered after allogeneic transplant for at least 4 cycles to heavily pretreated
AML
/MDS patients.
[MeSH-major]
Azacitidine / administration & dosage. Hematopoietic Stem Cell Transplantation.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ surgery. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / surgery
[MeSH-minor]
Adult
. Aged. DNA Methylation. Disease-Free Survival. Drug Administration Schedule. Female. Graft vs Host Disease / epidemiology. Humans. Male. Middle Aged. Recurrence. Transplantation, Homologous
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[Copyright]
Copyright © 2010 American Cancer Society.
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Leukemia. 2007 Dec;21(12):2540-4
[
17611563.001
]
[Cites]
Curr Opin Hematol. 2009 Mar;16(2):112-23
[
19468273.001
]
[Cites]
Blood. 1984 Oct;64(4):922-9
[
6206904.001
]
(PMID = 20672358.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA083932
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
M801H13NRU / Azacitidine
79.
Graziano A, Santangelo M, Umana DS:
Clinical evaluation of epithelioid angiomyolipoma.
Ann Ital Chir
; 2008 Mar-Apr;79(2):135-8
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OBJECTIVE: Epithelioid angiomyolipomas (
AML
) of the kidney are malignant tumors with aggressive clinical behavior.
The diagnosis of epithelioid
AML
was established by positive staining for melanoma and smooth muscle cell markers, and presence of perivascular epithelioid cells.
Two patients developed
recurrent
, metastatic disease following nephrectomy.
Epithelioid
AML
, may be locally aggressive and metastasized.
[MeSH-minor]
Adult
. Aged. Carcinoma, Renal Cell / diagnosis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Kidney / pathology. Male. Middle Aged. Nephrectomy. Tomography, X-Ray Computed
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(PMID = 18727277.001).
[ISSN]
0003-469X
[Journal-full-title]
Annali italiani di chirurgia
[ISO-abbreviation]
Ann Ital Chir
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Italy
80.
Arnaud B, Douet-Guilbert N, Morel F, Le Bris MJ, Herry A, Banzakour S, Bourquard P, Morice P, Le Calvez G, Marion V, Abgrall JF, Berthou C, De Braekeleer M:
Screening by fluorescence in situ hybridization for MLL status at diagnosis in 239 unselected patients with acute myeloblastic leukemia.
Cancer Genet Cytogenet
; 2005 Sep;161(2):110-5
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[Title]
Screening by fluorescence in situ hybridization for MLL status at diagnosis in 239 unselected patients with
acute
myeloblastic
leukemia
.
A large number of abnormalities involving the MLL gene have been associated with hematological malignancies, including
acute
myeloblastic leukemias (
AML
).
Given the overall unfavorable prognosis of
AML
with an MLL abnormality, its reliable and accurate detection is needed for informed treatment decision.
We therefore investigated the occurrence of MLL abnormalities in 239 unselected consecutive
AML
patients, using conventional cytogenetic and fluorescent in situ hybridization (FISH) analyses.
MLL abnormalities were more frequently found in
AML
-M5 and M4, mainly as rearrangements, and in
AML
-M2, mainly as overrepresentation.
All M2, M4, and M5
AML
patients without known
recurrent
translocations, such as t(8;21) and inv(16), should be investigated by FISH with an MLL probe because it allows the detection of MLL rearrangement that would go undetected by conventional cytogenetics and because it has the ability of detecting multiple copies of the MLL gene in, for example, marker chromosomes and double minutes.
[MeSH-major]
Chromosome Aberrations. Chromosomes, Human, Pair 11. DNA-Binding Proteins / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
[MeSH-minor]
Adult
. Aged. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Infant, Newborn. Male. Middle Aged.
Myeloid
-Lymphoid
Leukemia
Protein
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(PMID = 16102580.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Comparative Study; Evaluation Studies; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
81.
Yang L, Zhang Y, Zhang MR, Xiao ZJ:
[Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations].
Zhonghua Yi Xue Za Zhi
; 2005 Aug 31;85(33):2312-6
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[Title]
[Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and
acute myeloid leukemia
and
recurrent
chromosome translocations].
OBJECTIVE: To investigate the impact of GSTM1, GSTT1 and NQO1 genotypes on susceptibility to
acute myeloid leukemia
(
AML
) and
recurrent
chromosome translocations of
AML
.
METHODS: GSTT1, GSTM1 and NQO1 genotypes were detected in 228
adult
patients with de novo
AML
and 241 controls by PCR or PCR-RFLP.
RESULTS: The frequency of GSTM1 null genotype in the
AML
patients was 62.3%, significantly higher than that in the normal controls (52.7%, P = 0.036), however, no significant difference was found in the incidence of GSTT1 null genotype.
The frequencies of NQO1(C609T) C/T and T/T genotypes were 53.1% and 25.0% respectively among the total
AML
patients (53.1% and 25.0% respectively), 64.3% and 25.0% respectively among the
AML
patients with t (8;.
21) (q22; q22)/
AML
-ETO fusion gene, and 57.1% and 26.0% respectively among the
AML
patient with t (15;.
21) (q22; q22)/
AML
-ETO (+)
AML
was 4.487 (95% CI: 1.282-15.705) for the subjects with NQO1(C609T) C/T genotype, and was 6.293 (95% CI: 1.536-25.782) for the subjects with NQO1(C609T) T/T genotype.
17) (q22; q11)/PML-RARalpha (+)
AML
was 2.531 (95% CI: 1.286-4.981) for the subjects with NQO1(C609T) C/T genotype, and was 4.149 (95% CI: 1.856-9.275) for the subjects with NQO1(C609T) T/T genotype.
CONCLUSION: Determination of the NQO1(C609T) genotypes may be used as a stratification marker to predict high-risk individuals for
AML
, especially for
AML
with t (8;.
21) (q22; q22)/
AML
-ETO fusion gene and t (15;.
[MeSH-major]
Chromosome Aberrations. Glutathione Transferase / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics
[MeSH-minor]
Adolescent.
Adult
. Aged. Aged, 80 and over. Case-Control Studies. Female. Gene Frequency. Genotype. Humans. Male. Middle Aged. NAD(P)H Dehydrogenase (Quinone) / genetics. Translocation, Genetic. Young
Adult
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(PMID = 16321221.001).
[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; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
82.
Balgobind BV, Van Vlierberghe P, van den Ouweland AM, Beverloo HB, Terlouw-Kromosoeto JN, van Wering ER, Reinhardt D, Horstmann M, Kaspers GJ, Pieters R, Zwaan CM, Van den Heuvel-Eibrink MM, Meijerink JP:
Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.
Blood
; 2008 Apr 15;111(8):4322-8
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[Title]
Leukemia
-associated NF1 inactivation in patients with pediatric T-ALL and
AML
lacking evidence for neurofibromatosis.
Patients with NF1 have a higher risk to develop juvenile myelomonocytic
leukemia
(JMML) with a possible progression toward
acute myeloid leukemia
(
AML
).
In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell
acute
lymphoblastic
leukemia
(T-ALL) and 71 patients with MLL-rearranged
AML
, a
recurrent
cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged
AML
.
Since the NF1 protein is a negative regulator of the RAS pathway (RAS-GTPase activating protein), homozygous NF1 inactivation represent a novel type I mutation in pediatric MLL-rearranged
AML
and T-ALL with a predicted frequency that is less than 10%.
NF1 inactivation may provide an additional proliferative signal toward the development of
leukemia
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
-Lymphoma,
Adult
T-Cell / genetics. Mutation / genetics. Neurofibromatoses / genetics. Neurofibromin 1 / genetics
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(PMID = 18172006.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Neurofibromin 1; 0 / RNA, Messenger
83.
Marcucci G, Maharry K, Wu YZ, Radmacher MD, Mrózek K, Margeson D, Holland KB, Whitman SP, Becker H, Schwind S, Metzeler KH, Powell BL, Carter TH, Kolitz JE, Wetzler M, Carroll AJ, Baer MR, Caligiuri MA, Larson RA, Bloomfield CD:
IDH1 and IDH2 gene mutations identify novel molecular subsets within de novo cytogenetically normal acute myeloid leukemia: a Cancer and Leukemia Group B study.
J Clin Oncol
; 2010 May 10;28(14):2348-55
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[Title]
IDH1 and IDH2 gene mutations identify novel molecular subsets within de novo cytogenetically normal
acute myeloid leukemia
: a Cancer and
Leukemia
Group B study.
PURPOSE To analyze the frequency and associations with prognostic markers and outcome of mutations in IDH genes encoding isocitrate dehydrogenases in
adult
de novo cytogenetically normal
acute myeloid leukemia
(CN-
AML
).
IDH2 mutations, previously unreported in
AML
, were detected in 69 patients (19%; 13 with R172 and 56 with R140).
The highest expressed gene and microRNAs in R172 IDH2-mutated patients compared with the IDH1/IDH2wt patients were APP (previously associated with complex karyotype
AML
) and miR-1 and miR-133 (involved in embryonal stem-cell differentiation), respectively.
CONCLUSION IDH1 and IDH2 mutations are
recurrent
in CN-
AML
and have an unfavorable impact on outcome.
The R172 IDH2 mutations, previously unreported in
AML
, characterize a novel subset of CN-
AML
patients lacking other prognostic mutations and associate with unique gene- and microRNA-expression profiles that may lead to the discovery of novel, therapeutically targetable leukemogenic mechanisms.
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[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
[Grant]
United States / NCI NIH HHS / CA / CA33601; United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / CA140158; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / U10 CA031946; United States / NCI NIH HHS / CA / R21 CA129657; United States / NCI NIH HHS / CA / U10 CA033601; United States / NCI NIH HHS / CA / U24 CA114725; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / CA129657; United States / NCI NIH HHS / CA / CA114725; United States / NCI NIH HHS / CA / CA31946
[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 / MicroRNAs; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human
[Other-IDs]
NLM/ PMC2881719
84.
Falini B, Mecucci C, Tiacci E, Alcalay M, Rosati R, Pasqualucci L, La Starza R, Diverio D, Colombo E, Santucci A, Bigerna B, Pacini R, Pucciarini A, Liso A, Vignetti M, Fazi P, Meani N, Pettirossi V, Saglio G, Mandelli F, Lo-Coco F, Pelicci PG, Martelli MF, GIMEMA Acute Leukemia Working Party:
Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype.
N Engl J Med
; 2005 Jan 20;352(3):254-66
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[Title]
Cytoplasmic nucleophosmin in
acute myelogenous leukemia
with a normal karyotype.
METHODS: We used immunohistochemical methods to study the subcellular localization of NPM in bone marrow-biopsy specimens from 591 patients with primary
acute myelogenous leukemia
(
AML
).
RESULTS: Cytoplasmic NPM was detected in 208 (35.2 percent) of the 591 specimens from patients with primary
AML
but not in 135 secondary
AML
specimens or in 980 hematopoietic or extrahematopoietic neoplasms other than
AML
.
It was associated with a wide spectrum of morphologic subtypes of the disease, a normal karyotype, and responsiveness to induction chemotherapy, but not with
recurrent
genetic abnormalities.
There was a high frequency of FLT3 internal tandem duplications and absence of CD34 and CD133 in
AML
specimens with a normal karyotype and cytoplasmic dislocation of NPM, but not in those in which the protein was restricted to the nucleus.
AML
specimens with cytoplasmic NPM carried mutations of the NPM gene that were predicted to alter the protein at its C-terminal; this mutant gene caused cytoplasmic localization of NPM in transfected cells.
CONCLUSIONS: Cytoplasmic NPM is a characteristic feature of a large subgroup of patients with
AML
who have a normal karyotype, NPM gene mutations, and responsiveness to induction chemotherapy.
[MeSH-major]
Bone Marrow / pathology. Cytoplasm / chemistry.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation. Nuclear Proteins / genetics
[MeSH-minor]
Adolescent.
Adult
. Antibodies, Monoclonal. Antineoplastic Agents / therapeutic use. Base Sequence. Cell Nucleolus. DNA Mutational Analysis. Humans. Karyotyping. Middle Aged. Remission Induction. Transfection. Translocation, Genetic
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[Copyright]
Copyright 2005 Massachusetts Medical Society.
[CommentIn]
N Engl J Med. 2005 Jan 20;352(3):291-2
[
15659732.001
]
[CommentIn]
N Engl J Med. 2005 Apr 28;352(17):1819-20; author reply 1819-20
[
15858195.001
]
[ErratumIn]
N Engl J Med. 2005 Feb 17;352(7):740
(PMID = 15659725.001).
[ISSN]
1533-4406
[Journal-full-title]
The New England journal of medicine
[ISO-abbreviation]
N. Engl. J. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
85.
Nimer SD:
Is it important to decipher the heterogeneity of "normal karyotype AML"?
Best Pract Res Clin Haematol
; 2008 Mar;21(1):43-52
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[Title]
Is it important to decipher the heterogeneity of "normal karyotype
AML
"?
Almost half of
adult
acute myelogenous leukemia
(
AML
) is normal cytogenetically, and this subgroup shows a remarkable heterogeneity of genetic mutations at the molecular level and an intermediate response to therapy.
The finding of
recurrent
cytogenetic abnormalities has influenced, in a primary way, the understanding and treatment of leukemias.
Yet "normal karyotype
AML
" lacks such obvious abnormalities, but has a variety of prognostically important genetic abnormalities.
Although resistance to treatment is associated with specific mutations, the degree to which the
leukemia
resembles a stem cell in its functional properties may provide greater protection from the effects of treatment.
Although usually all of the circulating
leukemia
cells are cleared following treatment, a small residual population of leukemic cells in the bone marrow persists, making this disease hard to eradicate.
Increased understanding of the biological consequences of at least some of these mutations in "normal karyotype
AML
" is leading to more targeted approaches to develop more effective treatments for this disease.
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(PMID = 18342811.001).
[ISSN]
1521-6926
[Journal-full-title]
Best practice & research. Clinical haematology
[ISO-abbreviation]
Best Pract Res Clin Haematol
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK052621; United States / NIDDK NIH HHS / DK / R01 DK052621-08; United States / NIDDK NIH HHS / DK / R56 DK052208-09A1; United States / NCI NIH HHS / CA / R01 CA102202-01; United States / NCI NIH HHS / CA / CA102202-01; United States / NIDDK NIH HHS / DK / R56 DK052208; United States / NCI NIH HHS / CA / R01 CA102202; United States / NIDDK NIH HHS / DK / DK052208-09A1; United States / NIDDK NIH HHS / DK / DK052621-08
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Number-of-references]
76
[Other-IDs]
NLM/ NIHMS44325; NLM/ PMC2654590
86.
Abbas S, Lugthart S, Kavelaars FG, Schelen A, Koenders JE, Zeilemaker A, van Putten WJ, Rijneveld AW, Löwenberg B, Valk PJ:
Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value.
Blood
; 2010 Sep 23;116(12):2122-6
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[Title]
Acquired mutations in the genes encoding IDH1 and IDH2 both are
recurrent
aberrations in
acute myeloid leukemia
: prevalence and prognostic value.
Somatic mutations in isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) were recently demonstrated in
acute myeloid leukemia
(
AML
), but their prevalence and prognostic impact remain to be explored in large extensively characterized
AML
series, and also in various other hematologic malignancies.
Here, we demonstrate in 893 newly diagnosed cases of
AML
mutations in the IDH1 (6%) and IDH2 (11%) genes.
Moreover, we identified IDH mutations in 2 JAK2 V617F myeloproliferative neoplasias (n = 96), a single case of
acute
lymphoblastic
leukemia
(n = 96), and none in chronic
myeloid
leukemias (n = 81).
In
AML
, IDH1 and IDH2 mutations are more common among
AML
with normal karyotype and NPM1(mutant) genotypes.
Thus, IDH1 and IDH2 mutations are common genetic aberrations in
AML
, and IDH1 mutations may carry prognostic value in distinct subtypes of
AML
.
[MeSH-major]
Isocitrate Dehydrogenase / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation
[MeSH-minor]
Adolescent.
Adult
. Aged. Female. Hematologic Diseases. Humans. Janus Kinase 2 / genetics. Male. Middle Aged. Prevalence. Prognosis. Young
Adult
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(PMID = 20538800.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / Janus Kinase 2
87.
Druhan LJ, Ai J, Massullo P, Kindwall-Keller T, Ranalli MA, Avalos BR:
Novel mechanism of G-CSF refractoriness in patients with severe congenital neutropenia.
Blood
; 2005 Jan 15;105(2):584-91
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Severe congenital neutropenia (SCN) is a rare disease diagnosed at or soon after birth, characterized by a
myeloid
maturation arrest in the bone marrow, ineffective neutrophil production, and
recurrent
infections.
In the subset of patients with SCN transforming to
acute myeloid leukemia
(
AML
), mutations that truncate the cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected.
Here, we report a novel mutation in the extracellular portion of the G-CSFR within the WSXWS motif in a patient with SCN without
AML
who was refractory to G-CSF treatment.
Expression of the mutant receptor in either
myeloid
or lymphoid cells was shown to alter subcellular trafficking of the wild-type (WT) G-CSFR by constitutively heterodimerizing with it.
[MeSH-minor]
Adult
. Cells, Cultured. Dimerization. Drug Resistance. Female. Gene Expression. Humans. Infant, Newborn. Ligands. Male. Parents. Point Mutation. Signal Transduction / drug effects. Signal Transduction / immunology
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(PMID = 15353486.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA75226; United States / NCI NIH HHS / CA / CA82859
[Publication-type]
Case Reports; Journal Article; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Ligands; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor
88.
Chou WC, Hou HA, Chen CY, Tang JL, Yao M, Tsay W, Ko BS, Wu SJ, Huang SY, Hsu SC, Chen YC, Huang YN, Chang YC, Lee FY, Liu MC, Liu CW, Tseng MH, Huang CF, Tien HF:
Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation.
Blood
; 2010 Apr 8;115(14):2749-54
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[Title]
Distinct clinical and biologic characteristics in
adult
acute myeloid leukemia
bearing the isocitrate dehydrogenase 1 mutation.
Recent genome-wide screening also revealed IDH1 mutation as a
recurrent
event in
acute myeloid leukemia
(
AML
), but its clinical implications in
AML
are largely unknown.
We analyzed 493
adult
Chinese
AML
patients in Taiwan and found 27 patients (5.5%) harboring this mutation.
[MeSH-major]
Chromosomes, Human, Pair 8 / genetics. Isocitrate Dehydrogenase / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Monosomy. Neoplasm Proteins / genetics
[MeSH-minor]
Adult
. Aged. Antigens, CD13 / biosynthesis. Antigens, CD13 / genetics. Antigens, CD14 / biosynthesis. Antigens, CD14 / genetics. Female. Gene Expression Regulation, Leukemic / genetics. Genome-Wide Association Study. HLA-DR Antigens / biosynthesis. HLA-DR Antigens / genetics. Humans. Male. Middle Aged. Recurrence. Remission Induction. Taiwan
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[CommentIn]
Blood. 2010 Jul 22;116(3):495-6
[
20651083.001
]
(PMID = 20097881.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD14; 0 / HLA-DR Antigens; 0 / Neoplasm Proteins; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 3.4.11.2 / Antigens, CD13
89.
Camera A, Rinaldi CR, Palmieri S, Cantore N, Mele G, Mettivier V, Miraglia E, Mastrullo L, Grimaldi F, Luciano L, Guerriero A, Rotoli B, Ferrara F:
Sequential continuous infusion of fludarabine and cytarabine associated with liposomal daunorubicin (DaunoXome) (FLAD) in primary refractory or relapsed adult acute myeloid leukemia patients.
Ann Hematol
; 2009 Feb;88(2):151-8
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[Title]
Sequential continuous infusion of fludarabine and cytarabine associated with liposomal daunorubicin (DaunoXome) (FLAD) in primary refractory or
relapsed
adult
acute myeloid leukemia
patients.
A large proportion of
adult
patients with
acute myeloid leukemia
(
AML
) relapse after treatment, and some of them are resistant to primary induction chemotherapy.
Sixty-one patients from seven hematological centers with poor-risk
AML
, primary refractory (n = 16), or
relapsed
(n = 45) were treated with a salvage regimen, including fludarabine (2 days) and cytarabine (3 days) in a sequential continuous infusion, associated with liposomal daunorubicin (3 days) (FLAD).
Complete response rate was 44% and 56% for refractory and
relapsed
patients, respectively, with an overall response rate of 52% (32 of 61).
Twenty patients (62.5%)
relapsed
after this treatment in a median of 7.3 months; ten patients
relapsed
after a SCT procedure.
A better response rate was obtained in the subgroup of
relapsed
patients, compared to patients treated for refractory disease.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / therapeutic use. Daunorubicin / administration & dosage. Daunorubicin / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Vidarabine / analogs & derivatives
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Infusions, Intravenous. Liposomes. Male. Middle Aged. Recurrence. Salvage Therapy. Stem Cell Transplantation. Survival Rate. Time Factors
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Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
DAUNORUBICIN
.
Hazardous Substances Data Bank.
FLUDARABINE
.
Hazardous Substances Data Bank.
VIDARABINE
.
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(PMID = 18709502.001).
[ISSN]
1432-0584
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Liposomes; 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZS7284E0ZP / Daunorubicin
90.
Shearer BM, Knudson RA, Flynn HC, Ketterling RP:
Development of a D-FISH method to detect DEK/CAN fusion resulting from t(6;9)(p23;q34) in patients with acute myelogenous leukemia.
Leukemia
; 2005 Jan;19(1):126-31
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[Title]
Development of a D-FISH method to detect DEK/CAN fusion resulting from t(6;9)(p23;q34) in patients with
acute myelogenous leukemia
.
The t(6;9)(p23;q34)-DEK/CAN fusion occurs with an incidence of 1-5% in
adult
patients with
acute myelogenous leukemia
(
AML
) and tends to have an unfavorable prognosis at diagnosis.
Unfortunately, no commercial or previously published fluorescence in situ hybridization (FISH) strategies exist for this
recurrent
anomaly.
The development of this sensitive D-FISH strategy for the detection of the t(6;9)(p23;q34) adds to the
AML
FISH testing repertoire, and is effective in the detection of low-level disease in post-treatment samples in these patients.
[MeSH-major]
Chromosomes, Human, Pair 6. Chromosomes, Human, Pair 9. In Situ Hybridization, Fluorescence / methods.
Leukemia
,
Myeloid
,
Acute
/ genetics. Oncogene Proteins / genetics. Recombinant Fusion Proteins / genetics. Translocation, Genetic
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(PMID = 15510206.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / DEK-CAN fusion protein, recombinant; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins
91.
Yanada M, Suzuki M, Kawashima K, Kiyoi H, Kinoshita T, Emi N, Saito H, Naoe T:
Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience.
Eur J Haematol
; 2005 May;74(5):418-23
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[Title]
Long-term outcomes for unselected patients with
acute myeloid leukemia
categorized according to the World Health Organization classification: a single-center experience.
The actual utility of a new classification system of
acute myeloid leukemia
(
AML
) recently introduced by the World Health Organization (WHO) has not been thoroughly investigated yet.
In this study, we evaluated long-term outcomes of unselected
AML
patients categorized according to the new WHO classification.
Between 1990 and 2002, 109
adult AML
cases were referred to our hospital.
AML
with
recurrent
genetic abnormalities accounted for 26%,
AML
with multilineage dysplasia for 29%, therapy-related
AML
for 13%, and
AML
not otherwise categorized for 32% of classifiable cases.
These results indicate that outcomes for
AML
patients appear to be distinguished on the basis of the WHO classification, but the prognostic significance of multilineage dysplasia and prior therapy is lost after adjusting for cytogenetic risk and age.
[MeSH-major]
Leukemia
,
Myeloid
/ classification.
Leukemia
,
Myeloid
/ therapy
[MeSH-minor]
Adolescent.
Adult
. Aged. Aged, 80 and over. Humans. Middle Aged. Palliative Care. Retrospective Studies. Survival Analysis. Survivors. Treatment Outcome. World Health Organization
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(PMID = 15813916.001).
[ISSN]
0902-4441
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Denmark
92.
Sperr WR, Mitterbauer M, Mitterbauer G, Kundi M, Jäger U, Lechner K, Valent P:
Quantitation of minimal residual disease in acute myeloid leukemia by tryptase monitoring identifies a group of patients with a high risk of relapse.
Clin Cancer Res
; 2005 Sep 15;11(18):6536-43
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[Title]
Quantitation of minimal residual disease in
acute myeloid leukemia
by tryptase monitoring identifies a group of patients with a high risk of relapse.
PURPOSE: Recent data suggest that tryptase is produced by blast cells in a group of patients with
acute myeloid leukemia
(
AML
).
PATIENTS: In this study, we examined the value of tryptase as a marker of minimal residual
AML
.
In 61 patients with de novo
AML
exhibiting elevated serum tryptase (>15 ng/mL) at diagnosis, tryptase levels were measured serially during and after chemotherapy by a fluoroenzyme immunoassay.
Thus,
AML
relapses occurred in 15 of 29 patients with CR + BR (52%) and in 12 of 13 patients with CR without BR (92%), resulting in a significantly reduced probability of continuous CR for patients with CR without BR (P < 0.05).
In all patients with continuous hematologic CR, tryptase levels remained constantly normal, whereas a
recurrent
elevation of tryptase in CR was invariably followed by a hematologic relapse.
CONCLUSION: A persistently elevated tryptase level in
AML
in CR is indicative of minimal residual
AML
and associated with a high risk of relapse.
[MeSH-major]
Leukemia
,
Myeloid
/ pathology. Neoplasm, Residual / pathology. Serine Endopeptidases / blood
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Recurrence, Local. Oncogene Proteins, Fusion / genetics. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Survival Analysis. Time Factors. Tryptases
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(PMID = 16166430.001).
[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]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / CBFbeta-MYH11 fusion protein; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.59 / Tryptases
93.
Inaba H, Stewart CF, Crews KR, Yang S, Pounds S, Pui CH, Rubnitz JE, Razzouk BI, Ribeiro RC:
Combination of cladribine plus topotecan for recurrent or refractory pediatric acute myeloid leukemia.
Cancer
; 2010 Jan 1;116(1):98-105
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[Title]
Combination of cladribine plus topotecan for
recurrent
or refractory pediatric
acute myeloid leukemia
.
BACKGROUND: The prognosis after recurrence of pediatric
acute myeloid leukemia
(
AML
) is poor, and effective salvage regimens are urgently needed.
METHODS: In phase 1 and pilot studies, the authors evaluated the maximum tolerated dose (MTD) and dose-limiting toxicities (DLTs) of a 5-day course of cladribine followed by topotecan in pediatric patients with
recurrent
/refractory
AML
.
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.
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.
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[Copyright]
Copyright 2010 American Cancer Society.
[Cites]
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]
(PMID = 19885837.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / P30 CA021765-31
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
47M74X9YT5 / Cladribine; 7M7YKX2N15 / Topotecan
[Other-IDs]
NLM/ NIHMS151111; NLM/ PMC2920745
94.
Pereira FG, Metze K, Costa FP, Lima CS, Lorand-Metze I:
Phenotypic quantitative features of patients with acute myeloid leukemia.
Neoplasma
; 2006;53(2):155-60
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[Title]
Phenotypic quantitative features of patients with
acute myeloid leukemia
.
The recent WHO classification for
acute myeloid
leukemias (
AML
) separates entities by
recurrent
cytogenetic abnormalities and immunophenotypic features presenting prognostic impact.
We have examined the expression of several lineage and maturation linked antigens used in routine immunophenotyping of patients with de novo
AML
, using a 3-color two-step panel.
[MeSH-major]
Biomarkers, Tumor / analysis. Immunophenotyping / methods.
Leukemia
,
Myeloid
/ diagnosis.
Leukemia
,
Myeloid
/ metabolism
[MeSH-minor]
Acute
Disease. Adolescent.
Adult
. Aged. Antibodies, Monoclonal. Antigens, CD / metabolism. Female. Flow Cytometry. Humans. Male. Middle Aged. Neoplasm, Residual. Phenotype. Prognosis. Survival Analysis
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(PMID = 16575472.001).
[ISSN]
0028-2685
[Journal-full-title]
Neoplasma
[ISO-abbreviation]
Neoplasma
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Slovakia
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Biomarkers, Tumor
95.
Hijiya N, Ness KK, Ribeiro RC, Hudson MM:
Acute leukemia as a secondary malignancy in children and adolescents: current findings and issues.
Cancer
; 2009 Jan 1;115(1):23-35
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[Title]
Acute leukemia
as a secondary malignancy in children and adolescents: current findings and issues.
Secondary
acute leukemia
is a devastating complication in children and adolescents who have been treated for cancer.
Secondary
acute
lymphoblastic
leukemia
(s-ALL) was rarely reported previously but can be distinguished today from
recurrent
primary ALL by comparison of immunoglobulin and T-cell receptor rearrangement.
Secondary
acute myeloid leukemia
(s-
AML
) is much more common, and some cases actually may be second primary cancers.
Treatment-related and host-related characteristics and their interactions have been identified as risk factors for s-
AML
.
A high cumulative dose of alkylating agents is well known to predispose to s-
AML
.
The prevalence of alkylator-associated s-
AML
has diminished among pediatric oncology patients with the reduction of cumulative alkylator dose and limited use of the more leukemogenic alkylators.
The best-documented topoisomerase II inhibitor-associated s-
AML
is s-
AML
associated with epipodophyllotoxins.
The risk of s-
AML
in these cases is influenced by the schedule of drug administration and by interaction with other antineoplastic agents but is not consistently found to be related to cumulative dose.
The unpredictable risk of s-
AML
after epipodophyllotoxin therapy may discourage the use of these agents, even in patients at a high risk of disease recurrence, although the benefit of recurrence prevention may outweigh the risk of s-
AML
.
Studies in survivors of
adult
cancers suggest that, contrary to previous beliefs, the outcome of s-
AML
is not necessarily worse than that of de novo
AML
when adjusted for cytogenetic features.
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[Copyright]
Copyright (c) 2008 American Cancer Society.
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[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / P30 CA021765-31
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
L36H50F353 / Podophyllotoxin
[Number-of-references]
99
[Other-IDs]
NLM/ NIHMS135594; NLM/ PMC2767267
96.
La Starza R, Matteucci C, Gorello P, Brandimarte L, Pierini V, Crescenzi B, Nofrini V, Rosati R, Gottardi E, Saglio G, Santucci A, Berchicci L, Arcioni F, Falini B, Martelli MF, Sambani C, Aventin A, Mecucci C:
NPM1 deletion is associated with gross chromosomal rearrangements in leukemia.
PLoS One
; 2010;5(9):e12855
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[Title]
NPM1 deletion is associated with gross chromosomal rearrangements in
leukemia
.
BACKGROUND: NPM1 gene at chromosome 5q35 is involved in
recurrent
translocations in
leukemia
and lymphoma.
It also undergoes mutations in 60% of
adult
acute myeloid leukemia
(
AML
) cases with normal karyotype.
The incidence and significance of NPM1 deletion in human
leukemia
have not been elucidated.
METHODOLOGY AND PRINCIPAL FINDINGS: Bone marrow samples from 145 patients with myelodysplastic syndromes (MDS) and
AML
were included in this study.
NPM1 deletion was an uncommon event in the "5q- syndrome" but occurred in over 40% of cases with high risk MDS/
AML
with complex karyotypes and 5q loss.
CONCLUSIONS AND SIGNIFICANCE: NPM1/5q35 deletion is a consistent event in MDS/
AML
with a 5q-/-5 in complex karyotypes.
NPM1 deletion and NPM1 exon 12 mutations appear to be mutually exclusive and are associated with two distinct cytogenetic subsets of MDS and
AML
.
[MeSH-major]
Gene Deletion.
Leukemia
,
Myeloid
/ genetics. Nuclear Proteins / genetics. Translocation, Genetic
[MeSH-minor]
Adolescent.
Adult
. Aged. Aged, 80 and over. Base Sequence. Child. Chromosome Deletion. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 5 / metabolism. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Young
Adult
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(PMID = 20877721.001).
[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 / Nuclear Proteins; 117896-08-9 / nucleophosmin
[Other-IDs]
NLM/ PMC2943467
97.
Gong H, Liu WL, Zhou JF, Xu HZ:
[Expression of mitosis checkpoint gene CHFR in acute leukemia].
Zhonghua Yi Xue Za Zhi
; 2005 Apr 27;85(16):1085-8
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[Title]
[Expression of mitosis checkpoint gene CHFR in
acute leukemia
].
OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in
adult
patients with
acute leukemia
(AL) and its clinical significance.
METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with
acute
myelocytic
leukemia
(
AML
) and 22 with
acute lymphocytic leukemia
(ALL), 45 de novo patients and 20
recurrent
patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
(1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the
recurrent
acute
lymphoblastic
leukemia
(ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in
adult
patients with
acute leukemia
.
Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of
acute leukemia
to chemotherapy.
[MeSH-major]
Cell Cycle Proteins / biosynthesis.
Leukemia
,
Myeloid
,
Acute
/ genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic
Leukemia
-Lymphoma / genetics
[MeSH-minor]
Adolescent.
Adult
. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics
MedlinePlus Health Information.
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(PMID = 16029562.001).
[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; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
98.
Ahmad F, Dalvi R, Das BR, Mandava S:
Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population.
Cancer Detect Prev
; 2008;32(2):168-77
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[Title]
Specific chromosomal aberrations in de novo
acute myeloid leukemia
: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population.
BACKGROUND:
Acute myeloid leukemia
(
AML
) is a heterogeneous disease with regard to morphology, immunophenotype, and genetic rearrangements.
Multiple
recurrent
chromosomal aberrations have been identified by conventional cytogenetic analysis, which is now widely recognized as one of the most important diagnostic and prognostic determinants in
AML
.
METHOD: Conventional cytogenetic analysis was done on 200 de novo
AML
subjects.
Similarly, the frequency of other
recurrent
FAB associated abnormalities viz.
Furthermore, ongoing cytogenetic studies are warranted in larger groups of
AML
cases to identify newly acquired chromosomal aberrations that may aid in cloning novel genes involved in the neoplastic process, ultimately helping in the development of targeted therapeutic drugs.
[MeSH-major]
Chromosome Aberrations.
Leukemia
,
Myeloid
,
Acute
/ genetics
[MeSH-minor]
Adolescent.
Adult
. Age Distribution. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Humans. India. Infant. Karyotyping. Male. Middle Aged
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
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(PMID = 18639991.001).
[ISSN]
1525-1500
[Journal-full-title]
Cancer detection and prevention
[ISO-abbreviation]
Cancer Detect. Prev.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
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