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1
acute myelocytic leukaemia 2005:2010[pubdate] *count=100
10481 results
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acute myelocytic leukaemia
' expanded to all its synonyms;
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Items 1 to 100 of about 10481
1.
Wang HP, Yen YF, Chen WS, Chou YL, Tsai CY, Chang HN, Chou CT:
An unusual case of Candida tropicalis and Candida krusei arthritis in a patient with acute myelogenous leukemia before chemotherapy.
Clin Rheumatol
; 2007 Jul;26(7):1195-7
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[Title]
An unusual case of Candida tropicalis and Candida krusei arthritis in a patient with
acute
myelogenous leukemia
before chemotherapy.
A 79-year-old male with
acute
myelogenous leukemia
developed
acute
right knee arthritis during admission, after the use of broad-spectrum antibiotics before chemotherapy.
The initial synovial fluid sample appeared to be mildly inflammatory with a low white
cell
count.
The fungal septic arthritis was
not
diagnosed until Candida tropicalis, a rare species of Candida, was isolated in the synovial fluid.
Although fluconazole is effective in treating the microorganism, the untreated
leukemia
rendered the infection incurable and led to the growth of fluconazole-resistant Candida krusei.
[MeSH-major]
Arthritis, Infectious / pathology. Candida / isolation & purification. Candidiasis / pathology.
Leukemia
,
Myeloid
,
Acute
/ pathology
Genetic Alliance.
consumer health - Acute Myeloid Leukemia, Adult
.
Genetic Alliance.
consumer health - Arthritis
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Infectious Arthritis
.
MedlinePlus Health Information.
consumer health - Yeast Infections
.
Hazardous Substances Data Bank.
FLUCONAZOLE
.
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[Cites]
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[ISSN]
0770-3198
[Journal-full-title]
Clinical rheumatology
[ISO-abbreviation]
Clin. Rheumatol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antifungal Agents; 8VZV102JFY / Fluconazole
2.
Tsujimura A, Kiyoi H, Shiotsu Y, Ishikawa Y, Mori Y, Ishida H, Toki T, Ito E, Naoe T:
Selective KIT inhibitor KI-328 and HSP90 inhibitor show different potency against the type of KIT mutations recurrently identified in acute myeloid leukemia.
Int J Hematol
; 2010 Nov;92(4):624-33
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[Title]
Selective KIT inhibitor KI-328 and HSP90 inhibitor show different potency against the type of KIT mutations recurrently identified in
acute
myeloid leukemia
.
Activating mutations of KIT play an important role in the pathophysiology of several human malignancies, including
acute
myeloid leukemia
.
Here we examined the potency
of a
novel KIT inhibitor KI-328 against different types of mutant KIT kinases recurrently identified in
AML
.
Furthermore, HSP90 inhibitors suppress the growth of D816V-KIT-expressing cells at the concentration at which the growth of other mutant-KIT-expressing cells is
not
affected.
[MeSH-major]
Antineoplastic Agents / pharmacology. Carbamates / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-kit / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology
[MeSH-minor]
Cell
Line, Tumor. Humans. K562 Cells
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
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[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Carbamates; 0 / HSP90 Heat-Shock Proteins; 0 / KI 328; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
3.
Mneimneh WS, Bonte H, Bernheim A, Martin A:
Myeloid sarcoma of the prostate revealed by urinary retention: a case report.
BMJ Case Rep
; 2009;2009
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[Title]
Myeloid
sarcoma of the prostate revealed by urinary retention: a case report.
Myeloid
sarcoma (MS) of the prostate is very uncommon with only 17 reported cases in the literature.
Here, a singular case
of a
MS of the prostate discovered through investigations for urinary retention and revealing an
acute leukaemia
classified as an
acute
myeloid
leukaemia
(
AML
) with inversion 16 (inv16) according to the World Health Organization (WHO)
classification
(
AML
-M4 with inv16 in the French-American-British (FAB)
classification
) in a 65-year-old man is presented.
None of the previously reported and reviewed cases of prostatic MS were
of AML
-M4 type.
Such a translocation was recently described in some
acute
myeloid
processes.
Radiation therapy could be beneficial for the localised
disease of
the prostate.
Allogenic haematopoietic stem
cell
transplantation is also a promising therapy for MS.
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G Gerontol. 1967 May;15(5):605-14
[
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Cancer. 1983 Jun 15;51(12):2164-7
[
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[Cites]
Am J Hematol. 1996 Dec;53(4):267-71
[
8948669.001
]
(PMID = 21686890.001).
[ISSN]
1757-790X
[Journal-full-title]
BMJ case reports
[ISO-abbreviation]
BMJ Case Rep
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC3029613
Advertisement
4.
Yang XP, Li Y, Wang Y, Wang Y, Wang P:
beta-Tryptase up-regulates vascular endothelial growth factor expression via proteinase-activated receptor-2 and mitogen-activated protein kinase pathways in bone marrow stromal cells in acute myeloid leukemia.
Leuk Lymphoma
; 2010 Aug;51(8):1550-8
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[Title]
beta-Tryptase up-regulates vascular endothelial growth factor expression via proteinase-activated receptor-2 and mitogen-activated protein kinase pathways in bone marrow stromal cells in
acute
myeloid leukemia
.
Tryptases are predominantly mast
cell
-specific serine proteases with pleiotropic biological activities.
Recently, significant amounts of tryptases have been shown to be produced by myeloblasts in certain patients with
acute
myeloid leukemia
(
AML
), but the function of secreted tryptases in pathological circumstances remains unknown.
In this study, we investigated whether beta-tryptase affects the expression of vascular endothelial growth factor (VEGF) in bone marrow stromal cells (BMSCs) in
AML
.
We detected the expression of proteinase-activated receptor-2 (PAR-2) on
AML
BMSCs and found that beta-tryptase significantly up-regulated VEGF mRNA and protein expression in a dose-dependent manner by real-time PCR, Western blot, and ELISA.
These results suggest that beta-tryptase up-regulates VEGF production in
AML
BMSCs via the PAR-2, ERK1/2, and p38MAPK signaling pathways.
[MeSH-major]
Bone Marrow Cells / metabolism.
Leukemia
,
Myeloid
,
Acute
/ metabolism.
Leukemia
, Promyelocytic,
Acute
/ metabolism. Mitogen-Activated Protein Kinases / metabolism. Receptor, PAR-2 / metabolism. Stromal Cells / metabolism. Tryptases / metabolism. Vascular Endothelial Growth Factor A / metabolism
[MeSH-minor]
Blotting, Western.
Cell
Proliferation. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoenzyme Techniques. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Up-Regulation
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(PMID = 20578818.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / RNA, Messenger; 0 / Receptor, PAR-2; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.21.59 / Tryptases
5.
Kroeger H, Jelinek J, Estécio MR, He R, Kondo K, Chung W, Zhang L, Shen L, Kantarjian HM, Bueso-Ramos CE, Issa JP:
Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse.
Blood
; 2008 Aug 15;112(4):1366-73
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[Title]
Aberrant CpG island methylation in
acute
myeloid leukemia
is accentuated at relapse.
DNA methylation of CpG islands around gene transcription start sites results in gene silencing and plays a role in
leukemia
pathophysiology.
Its impact in
leukemia
progression is
not
fully understood.
We performed genomewide screening for methylated CpG islands and identified 8 genes frequently methylated in
leukemia cell
lines and in patients with
acute
myeloid leukemia
(
AML
): NOR1, CDH13, p15, NPM2, OLIG2, PGR, HIN1, and SLC26A4.
We assessed the methylation status of these genes and of the repetitive element LINE-1 in 30 patients with
AML
, both at
diagnosis
and relapse.
Abnormal methylation was found in 23% to 83% of patients at
diagnosis
and in 47% to 93% at relapse, with CDH13 being the most frequently methylated.
We observed concordance in methylation of several genes, confirming the presence
of a
hypermethylator pathway in
AML
.
DNA methylation levels increased at relapse in 25 of 30 (83%) patients with
AML
.
These changes represent much larger epigenetic dysregulation, since methylation microarray analysis of 9008 autosomal genes in 4 patients showed hypermethylation ranging from 5.9% to 13.6% (median 8.3%) genes at
diagnosis
and 8.0% to 15.2% (median 10.6%) genes in relapse (P < .001).
Our data suggest that DNA methylation is involved in
AML
progression and provide a rationale for the use of epigenetic agents in remission maintenance.
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Blood. 2001 May 1;97(9):2823-9
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Oncogene. 2002 Apr 18;21(17):2741-9
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11965547.001
]
(PMID = 18523155.001).
[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 / P50 CA100632; United States / NCI NIH HHS / CA / 5P01CA108631-03; United States / NCI NIH HHS / CA / 5P50CA100632-05
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2515110
6.
Papiez MA, Dybala M, Sowa-Kucma M, Krzysciak W, Taha H, Jozkowicz A, Nowak G:
Evaluation of oxidative status and depression-like responses in Brown Norway rats with acute myeloid leukemia.
Prog Neuropsychopharmacol Biol Psychiatry
; 2009 Jun 15;33(4):596-604
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[Title]
Evaluation of oxidative status and depression-like responses in Brown Norway rats with
acute
myeloid leukemia
.
It has been proved that oxidative stress increases when
leukemia
is accompanied by depression.
The aim of this study was to determine whether the
acute
myeloid leukemia
of Brown Norway rats, which is accompanied by oxidative stress, evoked behavioral and receptor changes resembling alterations characteristic of rat models of depression.
Leukemia
was induced through intraperitoneal injection of 10(7) promyelocytic
leukemia
cells to the Brown Norway rats.
Radioligand binding assay was used to assess of the effect
of leukemia
on cortical receptors.
Leukemia
influenced locomotory activity as well as forced swim test behavior in a 34-day series of experiments.
Signs of oxidative stress in leukemic rats were observed in each examined stage
of leukemia
development.
Upregulation of 5-HT(2A) receptors was observed in rat cortex after 30 days
of leukemia
development but
not
in 34-days series compared with the control.
It is concluded that disturbances in antioxidant system in brain cortex were accompanied by an activation of glycine sites of the NMDA receptor complex, regardless of stage
of leukemia
development, which are characteristic of model of depression.
Findings of our study demonstrate the link between glutamatergic activity, oxidative stress and
leukemia
.
[MeSH-major]
Depression / etiology.
Disease
Models, Animal.
Leukemia
,
Myeloid
,
Acute
/ complications. Oxidative Stress / physiology
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(PMID = 19268504.001).
[ISSN]
1878-4216
[Journal-full-title]
Progress in neuro-psychopharmacology & biological psychiatry
[ISO-abbreviation]
Prog. Neuropsychopharmacol. Biol. Psychiatry
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Receptors, Biogenic Amine; 9007-73-2 / Ferritins; EC 1.14.99.3 / Heme Oxygenase (Decyclizing); GAN16C9B8O / Glutathione; O9MIA842K9 / Biliverdine
7.
Bacher U, Haferlach T, Alpermann T, Zenger M, Kröger N, Beelen DW, Kern W, Schnittger S, Haferlach C:
Comparison of cytogenetic clonal evolution patterns following allogeneic hematopoietic transplantation versus conventional treatment in patients at relapse of AML.
Biol Blood Marrow Transplant
; 2010 Dec;16(12):1649-57
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[Title]
Comparison of cytogenetic clonal evolution patterns following allogeneic hematopoietic transplantation versus conventional treatment in patients at relapse
of AML
.
Relapse of
acute
myelogenous leukemia
has been associated with clonal cytogenetic evolution, but no study focused specifically on relapse after allogeneic hematopoietic stem
cell
transplantation (HSCT).
We compared karyotypes in 160 patients at both
diagnosis
and relapse either after allo-HSCT (n = 26) or standard chemotherapy (n = 134) using chromosome banding analysis combined with fluorescein in situ hybridization.
At
diagnosis
, aberrant karyotypes were more frequent in the HSCT than in the chemotherapy cohort (16 of 26; 61.5% versus 63 of 134; 47.0%).
Differences in the karyotypes between
diagnosis
and relapse were more frequent in the allo-cohort (14 of 26; 53.8% versus 49 of 134; 36.6%) than in the conventional cohort (n.s.
The mean number of cytogenetic alterations per patient was increasing from 2.0 at
diagnosis
to 4.0 at relapse in the allo-cohort, in the conventionally treated patients from 0.9 to 1.3 (both P < .001).
Thus, higher frequencies of clonal evolution and increasing cytogenetic complexity were observed in the stem
cell
recipients probably related to the more unfavorable cytogenetic profiles already depicted at
diagnosis
.
[MeSH-major]
Hematopoietic Stem
Cell
Transplantation / methods.
Leukemia
,
Myeloid
,
Acute
/ pathology.
Leukemia
,
Myeloid
,
Acute
/ therapy
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[Copyright]
Copyright © 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
(PMID = 20558312.001).
[ISSN]
1523-6536
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
8.
Suzuki K, Irie M, Kadowaki H, Shibata T, Kumagai M, Nishida A:
Genetic parameter estimates of meat quality traits in Duroc pigs selected for average daily gain, longissimus muscle area, backfat thickness, and intramuscular fat content.
J Anim Sci
; 2005 Sep;83(9):2058-65
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[Title]
Genetic parameter estimates of meat quality traits in Duroc pigs selected for average daily gain, longissimus muscle
area
, backfat thickness, and intramuscular fat content.
Using a multitrait animal model BLUP, selection was conducted over seven generations for growth rate (ADG), real-time ultrasound LM
area
(
LMA
), backfat thickness (BF), and intramuscular fat content (IMF) to develop a new line of purebred Duroc pigs with enhanced meat production and meat quality.
Genetic correlations of IMF with ADG and BF were low and positive, but low and negative with
LMA
.
Tenderness was correlated negatively with ADG (-0.44) and BF (-0.59), but positively correlated with
LMA
(0.32).
The genetic correlation between
LMA
and DL was positive and high (0.64).
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(PMID = 16100060.001).
[ISSN]
1525-3163
[Journal-full-title]
Journal of animal science
[ISO-abbreviation]
J. Anim. Sci.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
9007-34-5 / Collagen
9.
Møller T, Nielsen OJ, Welinder P, Dünweber A, Hjerming M, Moser C, Kjeldsen L:
Safe and feasible outpatient treatment following induction and consolidation chemotherapy for patients with acute leukaemia.
Eur J Haematol
; 2010 Apr;84(4):316-22
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[Title]
Safe and feasible outpatient treatment following induction and consolidation chemotherapy for patients with
acute leukaemia
.
Traditionally, patients with
acute leukaemia
are admitted to hospital during chemotherapy-induced pancytopenia, although a few recent reports have reported the feasibility and safety of outpatient treatment.
We have developed an outpatient treatment programme for patients with
acute leukaemia
incorporating comprehensive patient education for self-care management at home during pancytopenia and involvement of patients in care of their tunnelled central venous catheter (CVC).
Herein, we report the results of outpatient treatment of 60 patients with
acute leukaemia
(54 with
acute
myeloid
leukaemia
) followed prospectively in the period from March 2004 to 2007.
We conclude that outpatient treatment of patients with
acute leukaemia
is feasible and safe.
[MeSH-major]
Ambulatory Care / methods. Anti-Infective Agents / administration & dosage.
Leukemia
/ drug therapy. Neutropenia / drug therapy. Pancytopenia / drug therapy
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Prospective Studies
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(PMID = 20002732.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Anti-Infective Agents
10.
Palmisano M, Grafone T, Renzulli M, Ottaviani E, Testoni N, Paolini S, Papayannidis C, Baccarani M, Martinelli G:
Molecular and chromosomal alterations: new therapies for relapsed acute myeloid leukemia.
Hematology
; 2008 Feb;13(1):1-12
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[Title]
Molecular and chromosomal alterations: new therapies for relapsed
acute
myeloid leukemia
.
Acute
myeloid leukemia
(
AML
) remains the most common form
of leukemia
and the most common cause
of leukemia
death.
Although conventional chemotherapy can cure between 25 and 45%
of AML
patients, the majority of patients die after relapse or of complications associated with treatment.
Thus, more specific and less toxic treatments
for AML
patients are needed, especially for elderly patients.
An indispensable prerequisite to investigate tailored approaches
for AML
is the recent progress in the understanding the molecular features that distinguish
leukemia
progenitors from normal hematopoietic counterparts and the identification
of a
variety of dysregulated molecular pathways.
In this review, we describe some of the signaling pathways that are aberrantly regulated in
AML
, with a specific focus on their pathogenetic and therapeutic significance, and we examine some recent therapies directed against these targets, used in clinical trial for relapsed patients or unfit for conventional chemotherapy.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Signal Transduction / drug effects
[MeSH-minor]
Antineoplastic Agents / pharmacology. Drug Design. Genetic Predisposition to
Disease
/ genetics. Humans. Immunologic Factors / pharmacology. Remission Induction. Translocation, Genetic
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(PMID = 18534059.001).
[ISSN]
1607-8454
[Journal-full-title]
Hematology (Amsterdam, Netherlands)
[ISO-abbreviation]
Hematology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Immunologic Factors; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
[Number-of-references]
126
11.
Kang HJ, Hong SH, Kim IH, Park BK, Han KS, Cho HI, Shin HY, Ahn HS:
Prognostic significance of FLT3 mutations in pediatric non-promyelocytic acute myeloid leukemia.
Leuk Res
; 2005 Jun;29(6):617-23
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[Title]
Prognostic significance of FLT3 mutations in pediatric
non
-promyelocytic
acute
myeloid leukemia
.
This is the first study of FLT3 mutations in pediatric
non
-promyelocytic
AML
patients that received the same treatment scheme in single institute.
Patients with FLT3/TKD remain alive after autologous stem
cell
transplantation.
The
disease
-free survival (DFS) of patients with FLT3/ITD (0%) was significantly lower than that of the others (52%).
New therapeutic scheme such as stem
cell
transplantation with more intensive conditioning just after complete remission could be applied in pediatric
non
-promyelocytic
AML
patients with the FLT3/ITD mutation.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics
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(PMID = 15863200.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
12.
Madlambayan GJ, Meacham AM, Hosaka K, Mir S, Jorgensen M, Scott EW, Siemann DW, Cogle CR:
Leukemia regression by vascular disruption and antiangiogenic therapy.
Blood
; 2010 Sep 2;116(9):1539-47
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[Title]
Leukemia
regression by vascular disruption and antiangiogenic therapy.
Acute
myelogenous leukemias
(
AMLs
) and endothelial cells depend on each other for survival and proliferation.
Monotherapy antivascular strategies such as targeting vascular endothelial growth factor (VEGF) has limited efficacy in treating
AML
.
Thus, in search
of a
multitarget antivascular treatment strategy
for AML
, we tested a novel vascular disrupting agent, OXi4503, alone and in combination with the anti-VEGF antibody, bevacizumab.
Using xenotransplant animal models, OXi4503 treatment of human
AML
chloromas led to vascular disruption in
leukemia
cores that displayed increased
leukemia cell
apoptosis.
However, viable rims
of leukemia
cells remained and were richly vascular with increased VEGF-A expression.
To target this peripheral reactive angiogenesis, bevacizumab was combined with OXi4503 and abrogated viable vascular rims, thereby leading to enhanced
leukemia
regression.
In a systemic model of primary human
AML
, OXi4503 regressed
leukemia
engraftment alone and in combination with bevacizumab.
Differences in blood vessel density alone could
not
account for the observed regression, suggesting that OXi4503 also exhibited direct cytotoxic effects on
leukemia
cells.
Together, these data show that OXi4503 alone is capable of regressing
AML
by a multitargeted mechanism and that the addition of bevacizumab mitigates reactive angiogenesis.
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gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
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Mouse Genome Informatics (MGI)
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[CommentIn]
Blood. 2010 Sep 2;116(9):1389-90
[
20813902.001
]
(PMID = 20472832.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / K08 DK067359; United States / NCI NIH HHS / CA / CA084408; United States / NCI NIH HHS / CA / CA089655; United States / NCI NIH HHS / CA / R01 CA089655; United States / NHLBI NIH HHS / HL / R01 HL070738; United States / NCI NIH HHS / CA / R01 CA084408
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Diphosphates; 0 / Il2rg protein, mouse; 0 / Interleukin Receptor Common gamma Subunit; 0 / Oxi 4503; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Stilbenes; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab
[Other-IDs]
NLM/ PMC2938842
13.
Preudhomme C, Renneville A, Bourdon V, Philippe N, Roche-Lestienne C, Boissel N, Dhedin N, André JM, Cornillet-Lefebvre P, Baruchel A, Mozziconacci MJ, Sobol H:
High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder.
Blood
; 2009 May 28;113(22):5583-7
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[Title]
High frequency of RUNX1 biallelic alteration in
acute
myeloid leukemia
secondary to familial platelet
disorder
.
Familial platelet
disorder
(FPD), a rare autosomal dominant
disorder
characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to
acute
myeloid leukemia
(
AML
).
So far, monoallelic RUNX1 germline mutations have been found in 19 of 20 families with reported FPD, and the analysis of blast cells from only 5 patients at
acute
leukemia
(AL) stage has shown no additional RUNX1
abnormality
.
In addition to the germline RUNX1 mutation, we identified a second RUNX1 alteration in 6
AML
cases (acquired point mutations in 4 cases and duplication of the altered RUNX1 allele associated with acquired trisomy 21 in 2 other cases).
Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to
AML
.
[MeSH-major]
Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Platelet Disorders
.
SciCrunch.
OMIM: Data: Gene Annotation
.
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Clinical Genomic Database: Data: Gene Annotation
.
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(PMID = 19357396.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
14.
Petersen WC, Schlis KD, Braverman RS, Carlson I, Liang X, Wang M:
Pseudohypopyon: Extramedullary relapse of acute myelogenous leukemia with poor prognosis.
Pediatr Blood Cancer
; 2009 Jul;52(7):885-7
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[Title]
Pseudohypopyon: Extramedullary relapse of
acute
myelogenous leukemia
with poor prognosis.
She was diagnosed with
acute
myelogenous leukemia
.
[MeSH-major]
Anterior Chamber / pathology. Eye
Diseases
/
diagnosis
.
Leukemia
, Myelomonocytic,
Acute
/
diagnosis
. Neoplasm Recurrence, Local /
diagnosis
[MeSH-minor]
Antimetabolites, Antineoplastic / therapeutic use. Cytarabine / therapeutic use. Female. Humans. Infant. Injections, Spinal. Prognosis. Suppuration /
diagnosis
Genetic Alliance.
consumer health - Acute Myeloid Leukemia, Adult
.
MedlinePlus Health Information.
consumer health - Eye Diseases
.
Hazardous Substances Data Bank.
CYTARABINE
.
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[Copyright]
(c) 2008 Wiley-Liss, Inc.
(PMID = 19090546.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine
15.
Papamanthos MK, Kolokotronis AE, Skulakis HE, Fericean AM, Zorba MT, Matiakis AT:
Acute myeloid leukaemia diagnosed by intra-oral myeloid sarcoma. A case report.
Head Neck Pathol
; 2010 Jun;4(2):132-5
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[Title]
Acute
myeloid
leukaemia
diagnosed by intra-oral
myeloid
sarcoma. A case report.
Myeloid
sarcoma (MS) is a rare extramedullary malignant tumor composed of immature
myeloid
cells.
It is strongly associated with a well known or covert
acute
myeloid
leukaemia
, chronic myeloproliferative
diseases
or myelodysplastic syndromes.
An unusual case of
acute
myeloid
leukaemia
, which was diagnosed by mandibular MS that was developed in the alveolar socket after a dental extraction, is reported.
The histological examination (including immunohistochemical analysis)
of a
subsequent biopsy showed infiltration of the oral mucosa by neoplastic cells.
This
lesion
was therefore classified as
acute
myeloid
leukaemia
.
The patient was referred to oncologists that confirmed the initial
diagnosis
.
Forty days later, a relapse of the
disease
, which appeared as a great-ulcerated
lesion
, was developed in the hard palate.
Review of the literature shows no report of intraoral relapse and particularly multiple relapse
of a
MS that involves the oral cavity.
Even though MS is encountered infrequently in the oral cavity, it should be considered in the differential
diagnosis of
conditions (especially tumors) with a similar clinical appearance.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/
diagnosis
. Neoplasms, Multiple Primary /
diagnosis
. Sarcoma,
Myeloid
/
diagnosis
[MeSH-minor]
Aged. Antineoplastic Agents / therapeutic use. Biopsy.
Diagnosis
, Differential. Etoposide / therapeutic use. Fatal Outcome. Female. Humans. Mouth Mucosa / pathology. Mouth Neoplasms
Genetic Alliance.
consumer health - Myeloid sarcoma
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
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[Cites]
J Oral Maxillofac Surg. 1990 Jul;48(7):748-52
[
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Leuk Res. 2004 Jan;28(1):25-34
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Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008 Jan;105(1):e34-6
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Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007 Jun;103(6):e44-8
[
17428693.001
]
(PMID = 20512638.001).
[ISSN]
1936-0568
[Journal-full-title]
Head and neck pathology
[ISO-abbreviation]
Head Neck Pathol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide
[Other-IDs]
NLM/ PMC2878628
16.
Coppage M, Belanger T, Zauderer M, Sahasrabudhe D:
In vitro generation of tumor specific T cells that recognize a shared antigen of AML: molecular characterization of TCR genes.
Leuk Res
; 2007 Feb;31(2):195-202
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[Title]
In vitro generation of tumor specific T cells that recognize a shared antigen
of AML
: molecular characterization of TCR genes.
We present data demonstrating in vitro induction of autologous
acute
myelogenous leukemia
(
AML
)-specific CTL.
The specific T
cell
receptor has been identified and cloned.
The CTL demonstrated specific lysis to autologous tumor blasts, but
not
to autologous BLCL or the NK-sensitive target K562.
The clone secreted GM-CSF, TNFa, and IFNg when stimulated with
AML
blasts from 3 of 11 patients or
cell
lines tested, but
not
with K562 or autologous B-LCL.
These three
AML
samples share a single HLA Class I antigen, HLA-A24.
The T
cell
receptor genes identified by molecular methods are Vbeta7.9-J2.3-Cbeta2 and Valpha17-J49-Calpha.
[MeSH-major]
Antigens, Neoplasm / immunology. HLA Antigens / immunology.
Leukemia
,
Myeloid
/ immunology. Receptors, Antigen, T-
Cell
/ genetics. T-Lymphocytes, Cytotoxic / immunology
[MeSH-minor]
Acute
Disease
. Amino Acid Sequence. CD8-Positive T-Lymphocytes / immunology.
Cell
Line, Tumor. Humans. Molecular Sequence Data
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[CommentIn]
Leuk Res. 2007 Feb;31(2):127-8
[
17137625.001
]
(PMID = 16750565.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / HLA Antigens; 0 / Receptors, Antigen, T-Cell
17.
Renneville A, Boissel N, Zurawski V, Llopis L, Biggio V, Nibourel O, Philippe N, Thomas X, Dombret H, Preudhomme C:
Wilms tumor 1 gene mutations are associated with a higher risk of recurrence in young adults with acute myeloid leukemia: a study from the Acute Leukemia French Association.
Cancer
; 2009 Aug 15;115(16):3719-27
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[Title]
Wilms tumor 1 gene mutations are associated with a higher risk of recurrence in young adults with
acute
myeloid leukemia
: a study from the
Acute
Leukemia
French Association.
BACKGROUND: Wilms tumor 1 (WT1) is a transcription factor that is overexpressed in most
acute
myeloid leukemias
(
AMLs
).
Recently, 2 groups reported that WT1 mutations occur in approximately 10% of normal karyotype
AMLs
and are an independent predictor of poor outcome in this subgroup of patients with
AML
.
METHODS: The authors studied a cohort of 268 young adults (ages 15-50 years) with
AML
who were treated on the
Acute
Leukemia
French Association 9802 trial.
Within the subgroup of patients who had normal karyotype
AML
(n = 106), WT1 mutation was identified as an independent adverse prognostic factor for the risk of recurrence.
CONCLUSIONS: The current results indicted that WT1 mutations represent an adverse prognostic factor in young adults with
AML
.
Prospective trials should confirm the clinical relevance of WT1 mutations in relation to other prognostic factors in patients with
AML
.
[MeSH-major]
Genes, Wilms Tumor.
Leukemia
,
Myeloid
,
Acute
/ genetics
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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.
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(PMID = 19536888.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
18.
El-Shemy HA, Aboul-Enein AM, Aboul-Enein KM, Fujita K:
Willow leaves' extracts contain anti-tumor agents effective against three cell types.
PLoS One
; 2007;2(1):e178
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[Title]
Willow leaves' extracts contain anti-tumor agents effective against three
cell
types.
Many
non
-natural, synthetic drugs cause severe side effects that were
not
acceptable except as treatments of last resort for terminal
diseases
such as cancer.
In vitro the willow extract could kill the majority (75%-80%) of abnormal cells among primary cells harvested from seven patients with
acute
lymphoblastic leukemia
(ALL) and 13 with
AML
(
acute
myeloid leukemia
).
DNA fragmentation patterns within treated cells inferred targeted
cell
death by apoptosis had occurred.
The metabolites within the willow extract may act as tumor inhibitors that promote apoptosis, cause DNA damage, and affect
cell
membranes and/or denature proteins.
[MeSH-major]
Antineoplastic Agents, Phytogenic / pharmacology.
Cell
Line, Tumor / drug effects. Plant Extracts / pharmacology. Plant Leaves / chemistry. Salix
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(PMID = 17264881.001).
[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; 0 / Benzyl Alcohols; 0 / Glucosides; 0 / Plant Extracts; 4649620TBZ / salicin; FA1N0842KB / salicyl alcohol
[Other-IDs]
NLM/ PMC1779808
[General-notes]
NLM/ Original DateCompleted: 20070723
19.
Rawat VP, Thoene S, Naidu VM, Arseni N, Heilmeier B, Metzeler K, Petropoulos K, Deshpande A, Quintanilla-Martinez L, Bohlander SK, Spiekermann K, Hiddemann W, Feuring-Buske M, Buske C:
Overexpression of CDX2 perturbs HOX gene expression in murine progenitors depending on its N-terminal domain and is closely correlated with deregulated HOX gene expression in human acute myeloid leukemia.
Blood
; 2008 Jan 1;111(1):309-19
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[Title]
Overexpression of CDX2 perturbs HOX gene expression in murine progenitors depending on its N-terminal domain and is closely correlated with deregulated HOX gene expression in human
acute
myeloid leukemia
.
The mechanisms underlying deregulation of HOX gene expression in
AML
are poorly understood.
Deletion of the N-terminal domain of Cdx2 abrogated its ability to perturb Hox gene expression and to cause
acute
myeloid leukemia
(
AML
) in mice.
In contrast inactivation of the putative Pbx interacting site of Cdx2 did
not
change the leukemogenic potential of the gene.
In an analysis of 115 patients with
AML
, expression levels of CDX2 were closely correlated with deregulated HOX gene expression.
All patients with
AML
with normal karyotype tested were negative for CDX1 and CDX4 expression.
They furthermore correlate the level of CDX2 expression with HOX gene expression in human
AML
and support a potential role of CDX2 in the development of human
AML
with aberrant Hox gene expression.
[MeSH-major]
Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Transcription Factors / genetics
[MeSH-minor]
Adult. Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / physiology. Bone Marrow Transplantation.
Cell
Line, Tumor. Gene Expression Profiling. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Humans. Karyotyping. Mice. Mutagenesis. NIH 3T3 Cells. Protein Structure, Tertiary. Translocation, Genetic. Up-Regulation / physiology
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(PMID = 17855634.001).
[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 / CDX2 protein, human; 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors
20.
O'Brien MM, Lacayo NJ, Lum BL, Kshirsagar S, Buck S, Ravindranath Y, Bernstein M, Weinstein H, Chang MN, Arceci RJ, Sikic BI, Dahl GV:
Phase I study of valspodar (PSC-833) with mitoxantrone and etoposide in refractory and relapsed pediatric acute leukemia: a report from the Children's Oncology Group.
Pediatr Blood Cancer
; 2010 May;54(5):694-702
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[Title]
Phase I study of valspodar (PSC-833) with mitoxantrone and etoposide in refractory and relapsed pediatric
acute
leukemia
: a report from the Children'
s Oncology
Group.
BACKGROUND: Valspodar,
a non
-immunosuppressive analog of cylosporine, is a potent P-glycoprotein (MDR1) inhibitor.
As MDR1-mediated efflux of chemotherapeutic agents from leukemic blasts may contribute to drug resistance, a phase 1 study of valspodar combined with mitoxantrone and etoposide in pediatric patients with relapsed or refractory
leukemias
was performed.
Three of 11 patients with
acute
lymphoblastic leukemia
(ALL) had complete responses while no patient with
acute
myeloid leukemia
(
AML
) had an objective response.
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.
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ETOPOSIDE
.
Hazardous Substances Data Bank.
NOVANTRONE
.
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Curr Opin Oncol. 2000 Sep;12(5):450-8
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]
(PMID = 20209646.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA052168-12S1; United States / NCI NIH HHS / CA / U10 CA98413; United States / PHS HHS / / R01 52168; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCRR NIH HHS / RR / M01 RR 00070; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R01 CA052168; United States / NCRR NIH HHS / RR / M01 RR000070; United States / NCI NIH HHS / CA / U10 CA98543
[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 / Cyclosporins; 0 / P-Glycoprotein; 121584-18-7 / valspodar; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone
[Other-IDs]
NLM/ NIHMS155713; NLM/ PMC2838930
21.
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
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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
22.
Mann C, Parkinson N, Bleetman A:
Endotracheal tube and laryngeal mask airway cuff volume changes with altitude: a rule of thumb for aeromedical transport.
Emerg Med J
; 2007 Mar;24(3):165-7
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Most of these patients are ventilated through endotracheal tubes (ETTs), others through laryngeal mask airways (
LMAs
).
The cuffs of both ETTs and
LMAs
inflate with increases in altitude as barometric pressure decreases (30 mbar/1000 feet).
METHODS: The change in dimensions of the inflated cuffs
of a
size 8 ETT and a size 5
LMA
were measured with digital callipers at 1000 feet intervals in the unpressurised cabin of an Agusta 109 helicopter used by the Warwickshire and Northamptonshire Air Ambulance.
RESULTS:
A linear
expansion in cuff dimensions as a function of altitude increase was identified.
CONCLUSION: The data
for LMA
cuff expansion failed to show significant correlation with altitude change.
Further work is required to determine a similar rule of thumb
for LMA
cuff deflation.
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Emerg Med J. 2007 Aug;24(8):605
[
17652705.001
]
(PMID = 17351218.001).
[ISSN]
1472-0213
[Journal-full-title]
Emergency medicine journal : EMJ
[ISO-abbreviation]
Emerg Med J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2660019
23.
Beluffi G, Bernardo ME, Meloni G, Spinazzola A, Locatelli F:
Spinal osteomyelitis due to Aspergillus flavus in a child: a rare complication after haematopoietic stem cell transplantation.
Pediatr Radiol
; 2008 Jun;38(6):709-12
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[Title]
Spinal osteomyelitis due to Aspergillus flavus in a child: a rare complication after haematopoietic stem
cell
transplantation.
We report the case
of a
child affected by
acute
myeloid
leukaemia
who was treated with allogeneic haematopoietic stem
cell
transplantation and developed cervicothoracic spinal osteomyelitis due to Aspergillus flavus.
The
diagnosis
was difficult on a clinical basis, but made possible by conventional radiography and MRI.
[MeSH-major]
Aspergillosis / complications. Hematopoietic Stem
Cell
Transplantation / adverse effects. Osteomyelitis / microbiology. Spinal
Diseases
/ microbiology
[MeSH-minor]
Aspergillus flavus / isolation & purification. Bronchoalveolar Lavage.
Diagnosis
, Differential. Fatal Outcome. Fever / etiology. Humans. Hydrocephalus / etiology. Infant.
Leukemia
,
Myeloid
,
Acute
/ surgery. Magnetic Resonance Imaging. Male. Radiography. Rare
Diseases
. Recurrence. Spine / diagnostic imaging. Spine / pathology
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0301-0449
[Journal-full-title]
Pediatric radiology
[ISO-abbreviation]
Pediatr Radiol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
24.
Ye Y, McDevitt MA, Guo M, Zhang W, Galm O, Gore SD, Karp JE, Maciejewski JP, Kowalski J, Tsai HL, Gondek LP, Tsai HC, Wang X, Hooker C, Smith BD, Carraway HE, Herman JG:
Progressive chromatin repression and promoter methylation of CTNNA1 associated with advanced myeloid malignancies.
Cancer Res
; 2009 Nov 1;69(21):8482-90
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[Title]
Progressive chromatin repression and promoter methylation of CTNNA1 associated with advanced
myeloid
malignancies.
Complete loss or deletion of the long arm of chromosome 5 is frequent in myelodysplastic syndrome (MDS) and
acute
myelogenous leukemia
(
AML
).
This study is a comprehensive analysis of previously implicated and novel genes for epigenetic inactivation in
AML
and MDS.
In 146
AML
cases, methylation of CTNNA1 was frequent, and more common in
AML
patients with 5q deletion (31%) than those without 5q deletion (14%), whereas no methylation of other 5q genes was observed.
In 31 MDS cases, CTNNA1 methylation was only found in high-risk MDS (>or=RAEB2), but
not
in low-risk MDS (<RAEB2), indicating that CTNNA1 methylation might be important in the transformation of MDS to
AML
.
CTNNA1 expression was lowest in
AML
/MDS patients with CTNNA1 methylation, although reduced expression was found in some patients without promoter methylation.
Repressive chromatin marks (H3K27me3) at the promoter were identified in CTNNA1-repressed
AML cell
lines and primary
leukemias
, with the most repressive state correlating with DNA methylation.
These results suggest progressive, acquired epigenetic inactivation at CTNNA1, including histone modifications and promoter CpG methylation, as a component
of leukemia
progression in patients with both 5q- and
non
-5q-
myeloid
malignancies.
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(PMID = 19826047.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA058184-090013; United States / NCI NIH HHS / CA / P50 CA058184; United States / NCI NIH HHS / CA / P50 CA058184-090013
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / CTNNA1 protein, human; 0 / Chromatin; 0 / RNA, Messenger; 0 / alpha Catenin; EC 1.13.12.- / Luciferases
[Other-IDs]
NLM/ NIHMS142652; NLM/ PMC3081599
25.
Kohlschütter J, Michelfelder S, Trepel M:
Drug delivery in acute myeloid leukemia.
Expert Opin Drug Deliv
; 2008 Jun;5(6):653-63
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[Title]
Drug delivery in
acute
myeloid leukemia
.
BACKGROUND:
Acute
myeloid leukemia
was among the first malignancies to be cured by drug therapy alone, but overall survival rates remain unsatisfactory and have changed little over the past 20 years.
OBJECTIVE: We have chosen
acute
myeloid leukemia
as
a disease
prototype to review established and novel targeted approaches in
leukemia
treatment.
CONCLUSION: While the toxicity profile of chemotherapeutics has been improved by liposomal formulations and antibody conjugation
for leukemia
-directed uptake, their efficacy has probably
not
changed significantly.
Further improvements may result from the characterization of novel
acute
myeloid leukemia
(
AML
)
cell
surface receptors and of leukemic stem cells, as well as from the design
of leukemia
-targeted gene therapy vectors.
[MeSH-minor]
Antibodies, Monoclonal / administration & dosage. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Drug Delivery Systems. Genetic Therapy. Humans. Integrin alpha4beta1 / antagonists & inhibitors.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Liposomes. Neoplastic Stem Cells / drug effects. Sialic Acid Binding Ig-like Lectin 3
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(PMID = 18532921.001).
[ISSN]
1742-5247
[Journal-full-title]
Expert opinion on drug delivery
[ISO-abbreviation]
Expert Opin Drug Deliv
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Integrin alpha4beta1; 0 / Liposomes; 0 / Sialic Acid Binding Ig-like Lectin 3
[Number-of-references]
114
26.
Vyas HK, Pal R, Vishwakarma R, Lohiya NK, Talwar GP:
Selective killing of leukemia and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit.
Oncology
; 2009;76(2):101-11
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[Title]
Selective killing
of leukemia
and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit.
EXPERIMENTAL DESIGN: The study was carried out on MOLT-4 and U-937 cells expressing hCGbeta and on peripheral blood leukocytes of
acute
myeloid leukemia
(
AML
) patients.
RESULTS: The antibody did
not
impair the growth of MOLT-4 and U-937 cells in culture.
Its conjugate with curcumin, however, was lethal to both
cell
lines.
The immunoconjugate killed tumor cells bearing the CD33 marker of an
AML
patient expressing hCGbeta but did
not
have a similar action on cells of another
AML
patient with the CD13 marker but who was negative for hCGbeta.
[MeSH-major]
Chorionic Gonadotropin, beta Subunit, Human / metabolism. Curcumin / metabolism.
Leukemia
/ drug therapy. Lymphoma / drug therapy
[MeSH-minor]
Aged. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis.
Cell
Separation. Drug Design. Female. Humans.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Sialic Acid Binding Ig-like Lectin 3. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. U937 Cells
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.
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METHYLTHIAZOLETETRAZOLIUM
.
Hazardous Substances Data Bank.
CURCUMIN
.
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(PMID = 19127081.001).
[ISSN]
1423-0232
[Journal-full-title]
Oncology
[ISO-abbreviation]
Oncology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; IT942ZTH98 / Curcumin
27.
O'Sullivan AK, Pandya A, Papadopoulos G, Thompson D, Langston A, Perfect J, Weinstein MC:
Cost-effectiveness of posaconazole versus fluconazole or itraconazole in the prevention of invasive fungal infections among neutropenic patients in the United States.
Value Health
; 2009 Jul-Aug;12(5):666-73
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METHODS: We used modeling techniques to assess the cost-effectiveness of posaconazole versus FLU or ITRA in the prevention of IFIs among patients with
acute
myelogenous leukemia
(
AML
) or myelodysplastic syndromes (MDS) and chemotherapy-induced neutropenia.
CONCLUSIONS: We conclude that posaconazole is very likely to be a cost-effective alternative to FLU or ITRA in the prevention of IFIs among neutropenic patients with
AML
and MDS, and may result in cost savings.
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.
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(PMID = 19508661.001).
[ISSN]
1524-4733
[Journal-full-title]
Value in health : the journal of the International Society for Pharmacoeconomics and Outcomes Research
[ISO-abbreviation]
Value Health
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antifungal Agents; 304NUG5GF4 / Itraconazole; 8VZV102JFY / Fluconazole
28.
Raffegerst SH, Hoelzlwimmer G, Kunder S, Mysliwietz J, Quintanilla-Martinez L, Schendel DJ:
Diverse hematological malignancies including hodgkin-like lymphomas develop in chimeric MHC class II transgenic mice.
PLoS One
; 2009;4(12):e8539
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The majority of malignancies were distributed equally between T and B
cell
neoplasms and included
lymphoblastic
T
cell
lymphoma (LTCL),
lymphoblastic
B
cell
lymphoma (LBCL), diffuse large B
cell
lymphoma (DLBCL), the histiocyte/T
cell
rich variant of DLBCL (DLBCL-HA/T
cell
rich DLBCL), splenic marginal zone lymphoma (SMZL), follicular B
cell
lymphoma (FBL) and plasmacytoma (PCT).
Most of these neoplasms were highly similar to human
diseases
.
Also, some
non
-lymphoid malignancies such as
acute
myeloid leukemia
(
AML
) and histiocytic sarcoma were found.
Interestingly, composite lymphomas, including Hodgkin-like lymphomas, were also detected that had CD30(+) Hodgkin/Reed-Sternberg (H/RS)-like cells, representing a tumor type
not
previously described in mice.
Thus, this DR4 line is a useful model to investigate common molecular mechanisms that may contribute to important neoplastic
diseases
in man.
[MeSH-major]
Chimerism. Hematologic Neoplasms / immunology. Hematologic Neoplasms / pathology. Histocompatibility Antigens Class II / immunology. Hodgkin
Disease
/ immunology. Hodgkin
Disease
/ pathology
[MeSH-minor]
Animals. Antigens, CD30 / metabolism. Base Sequence. Lymphoma, B-
Cell
/ pathology. Lymphoma, T-
Cell
/ pathology. Mice. Mice, Transgenic. Molecular Sequence Data. Reed-Sternberg Cells / pathology. Survival Analysis. Transgenes / genetics
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(subscription/membership/fee required).
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.
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[Cites]
Blood. 2002 Jul 1;100(1):238-45
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Blood. 2002 Jul 1;100(1):246-58
[
12070034.001
]
(PMID = 20046882.001).
[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 / Antigens, CD30; 0 / Histocompatibility Antigens Class II
[Other-IDs]
NLM/ PMC2796171
29.
Calvo D, Cariddi LN, Grosso M, Demo MS, Maldonado AM:
Achyrocline satureioides (LAM.) DC (Marcela): antimicrobial activity on Staphylococcus spp. and immunomodulating effects on human lymphocytes.
Rev Latinoam Microbiol
; 2006 Jul-Dec;48(3-4):247-55
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[Title]
Achyrocline satureioides (
LAM
.) DC (Marcela): antimicrobial activity on Staphylococcus spp. and immunomodulating effects on human lymphocytes.
Achyrocline satureioides (
LAM
.
They were isolated from 18 patients with acne
lesions
and from 7 patients infected with Staphylococcus spp. (5 strains were taken from catheters and 2 from wounds).
On the other hand, cultures of lymphocytes were made from those patients who displayed infections caused by Staphylococcus spp. and from 12 control
non
-infected individuals.
The A. satureiodes decoction inhibited 95% of the isolated Staphylococcus spp. strains and stimulated the
lymphocyte
expansion, of which 40% were CD8+ T cells.
[MeSH-minor]
Acne Vulgaris / microbiology. Adolescent. Adult. Bacteremia / microbiology. Catheterization. Cells, Cultured / drug effects. Drug Evaluation, Preclinical. Humans.
Lymphocyte
Activation / drug effects. Phytohemagglutinins / pharmacology. Plant Leaves / chemistry. Staphylococcal Infections / microbiology. Staphylococcal Skin Infections / microbiology. Wound Infection / microbiology
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(PMID = 18293658.001).
[ISSN]
0187-4640
[Journal-full-title]
Revista latinoamericana de microbiología
[ISO-abbreviation]
Rev. Latinoam. Microbiol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Mexico
[Chemical-registry-number]
0 / Adjuvants, Immunologic; 0 / Anti-Bacterial Agents; 0 / Phytohemagglutinins; 0 / Plant Extracts
30.
Senatore F, Arnold NA, Bruno M:
Volatile components of Centaurea eryngiodes Lam. and Centaurea iberica Trev.var. hermonis Bois. Lam.,two Asteraceae growing wild in Lebanon.
Nat Prod Res
; 2005 Dec;19(8):749-54
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[Title]
Volatile components of Centaurea eryngiodes
Lam
. and Centaurea iberica Trev.var. hermonis Bois.
Lam
.,two Asteraceae growing wild in Lebanon.
The volatile components of the flowerheads of Centaurea eryngioides
Lam
. and Centaurea iberica Trev. var. hermonis Boiss.
Lam
. were obtained by hydrodistillation and identified by GC and GC-MS.
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(PMID = 16317829.001).
[ISSN]
1478-6419
[Journal-full-title]
Natural product research
[ISO-abbreviation]
Nat. Prod. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Oils, Volatile; 0 / Plant Oils
31.
Konoplev S, Huang X, Drabkin HA, Koeppen H, Jones D, Kantarjian HM, Garcia-Manero G, Chen W, Medeiros LJ, Bueso-Ramos CE:
Cytoplasmic localization of nucleophosmin in bone marrow blasts of acute myeloid leukemia patients is not completely concordant with NPM1 mutation and is not predictive of prognosis.
Cancer
; 2009 Oct 15;115(20):4737-44
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[Title]
Cytoplasmic localization of nucleophosmin in bone marrow blasts of
acute
myeloid leukemia
patients is
not
completely concordant with NPM1 mutation and is
not
predictive of prognosis.
BACKGROUND: Nucleophosmin (NPM1) gene mutations are reported to predict a favorable prognosis in
acute
myeloid leukemia
(
AML
) patients.
RESULTS: The study included 252
AML
patients: 192
de
novo
AML
, 33
AML
preceded by either myelodysplastic syndrome or chronic myelomonocytic
leukemia
, and 27 therapy-related
AML
.
Cytoplasmic NPM was detected in 59 of 252 (23%) patients, including 48 of 192 (25%)
de
novo
AML
and 33 of 94 (35%) with a normal karyotype.
CONCLUSIONS: IHC assessment for NPM localization did
not
predict prognosis in this patient cohort.
[MeSH-major]
Bone Marrow / metabolism. Cytoplasm / metabolism.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Nuclear Proteins / genetics. Nuclear Proteins / metabolism
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[Copyright]
Copyright (c) 2009 American Cancer Society.
[Cites]
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[
11764078.001
]
(PMID = 19637342.001).
[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 / U54 CA096300
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
[Other-IDs]
NLM/ NIHMS633932; NLM/ PMC4199225
32.
Kim HW, Choi SJ, Lee JH, Lee JH, Kim TS, Kim YG, Kang JM, Huh J, Park KM, Lee KH:
Nonleukemic granulocytic sarcoma in the bile duct: a case report.
J Korean Med Sci
; 2006 Aug;21(4):745-8
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[Title]
Nonleukemic
granulocytic
sarcoma in the bile duct: a case report.
Granulocytic
sarcoma (GS) is an extramedullary tumor composed of immature
myeloid
cells, typically occurring during the course of
acute
myelogenous leukemia
.
Non
-leukemic GS, that is, GS with no evidence of overt
leukemia
and no previous history
of leukemia
, is very rare, and even more unusual is nonleukemic GS of the bile duct.
The patient was initially misdiagnosed as a bile duct carcinoma arising in the hilum of the
liver
(so-called Klatskin tumor), and received a right lobectomy of the
liver
.
Histological examination of the tumor yielded the
diagnosis of
GS, and the bone marrow biopsy did
not
show any evidence
of leukemia
.
Considering the risk of subsequent development of overt
leukemia
, the patient was treated with two cycles of combination chemotherapy as used in the cases of
acute
myelogenous leukemia
.
To date, he has remained free
of disease
15 months after treatment.
[MeSH-major]
Bile Duct Neoplasms / chemically induced. Sarcoma,
Myeloid
/
diagnosis
[MeSH-minor]
Adult. Antigens, CD45 / analysis. Bile Ducts / chemistry. Bile Ducts / pathology.
Diagnosis
, Differential. Humans. Immunohistochemistry. Male. Peroxidase / analysis. Radiography, Abdominal. Tomography, X-Ray Computed / methods
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[Cites]
Cancer. 2002 Mar 15;94(6):1739-46
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(PMID = 16891824.001).
[ISSN]
1011-8934
[Journal-full-title]
Journal of Korean medical science
[ISO-abbreviation]
J. Korean Med. Sci.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Korea (South)
[Chemical-registry-number]
EC 1.11.1.7 / Peroxidase; EC 3.1.3.48 / Antigens, CD45
[Other-IDs]
NLM/ PMC2729902
33.
Kuchenbauer F, Kern W, Schoch C, Kohlmann A, Hiddemann W, Haferlach T, Schnittger S:
Detailed analysis of FLT3 expression levels in acute myeloid leukemia.
Haematologica
; 2005 Dec;90(12):1617-25
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[Title]
Detailed analysis of FLT3 expression levels in
acute
myeloid leukemia
.
BACKGROUND AND OBJECTIVES: FLT3 mutations are found in up to 30% of cases of
acute
myeloid leukemia
(
AML
).
DESIGN AND METHODS: To further evaluate the role of FLT3 in
AML
we investigated FLT3 expression levels in 207 adult
AML
patients and 8 healthy donors by real-time polymerase chain reaction (PCR).
RESULTS: FLT3 expression levels were different in certain FAB types with increasing levels in the following order: M3<M3v<M6<
M2
<M4eo<M4<
M0
<
M1
<M5a<M5b.
Independent analysis of FLT3 expression in cytogenetic
AML
subgroups showed the lowest levels in t(15;17) and the highest in the t(11q23) positive
AML
.
On the molecular level, no differences in FLT3 expression levels were detected between
AML
with and without any FLT3 mutation as well as for FAB M5 with or without MLL abnormalities (p=0.495).
In patients with normal cytogenetics no impact or overall survival or event-free survival could be detected (p=0.128 and p=0.305, respectively) regardless of FLT3 muatation status, whereas investigating the group of patients with normal cytogenetics and wild-type FLT3, a clear tendency
for a
worse overall (p=0.059) and event free (p=0.087) survival was found.
[MeSH-major]
Gene Expression Regulation, Leukemic.
Leukemia
,
Myeloid
/ enzymology. Neoplasm Proteins / biosynthesis. fms-Like Tyrosine Kinase 3 / biosynthesis
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Marrow / pathology. Chromosome Aberrations.
Disease
-Free Survival. Enzyme Induction. Female. Gene Duplication. Humans. Karyotyping.
Leukemia
, Monocytic,
Acute
/ genetics.
Leukemia
, Monocytic,
Acute
/ pathology. Leukocyte Count. Life Tables. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Proportional Hazards Models. RNA, Messenger / biosynthesis. RNA, Messenger / metabolism. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / metabolism. Survival Analysis. Tandem Repeat Sequences
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[CommentIn]
Haematologica. 2005 Dec;90(12):1586
[
16330422.001
]
(PMID = 16330434.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
34.
Ohsaka A, Otsubo K, Yokota H, Hisa T, Saito H, Kozaki T:
Spectral karyotyping and fluorescence in situ hybridization analyses identified a novel three-way translocation involving inversion 16 in therapy-related acute myeloid leukemia M4eo.
Cancer Genet Cytogenet
; 2008 Jul 15;184(2):113-8
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[Title]
Spectral karyotyping and fluorescence in situ hybridization analyses identified a novel three-way translocation involving inversion 16 in therapy-related
acute
myeloid leukemia
M4eo.
We report a novel three-way translocation involving inversion 16 and chromosome 12 at bands 16p13, 16q22, and 12q24 in a patient with therapy-related
acute
myeloid leukemia
(
AML
)-M4eo.
Conventional G-banding of bone marrow cells at
diagnosis
was suggestive of inv(16)(p13q22) and a translocation of chromosomes 12 and 16.
Although we could
not
establish that this complex chromosomal aberration occurred either as a one-step, three-way event, or a sequential event with inv(16)(p13q22) followed by t(12;16)(q24;q22), SKY in combination with FISH and RT-PCR analyses successfully detected this complex chromosome
abnormality
in the patient.
[MeSH-major]
Chromosome Inversion. Chromosomes, Human, Pair 16. In Situ Hybridization, Fluorescence.
Leukemia
,
Myeloid
,
Acute
/ genetics. Neoplasms, Second Primary / genetics. Spectral Karyotyping. Translocation, Genetic
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(PMID = 18617061.001).
[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
35.
Sahu GR, Mishra R, Nagpal JK, Das BR:
Notice of retraction. Alteration of p73 in acute myelogenous leukemia.
Am J Hematol
; 2008 Aug;83(8):691
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[Title]
Notice of retraction. Alteration of p73 in
acute
myelogenous leukemia
.
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[RetractionOf]
Sahu GR, Mishra R, Nagpal JK, Das BR. Am J Hematol. 2005 May;79(1):1-7
[
15849769.001
]
(PMID = 18615454.001).
[ISSN]
1096-8652
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Retraction of Publication
[Publication-country]
United States
36.
Parikh SA, Kadia T, Jabbour E:
Peripheral blasts on day 21 of induction chemotherapy in a patient with core binding factor acute myeloid leukemia: more than meets the eye.
Clin Lymphoma Myeloma Leuk
; 2010 Aug;10(4):301-2
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[Title]
Peripheral blasts on day 21 of induction chemotherapy in a patient with core binding factor
acute
myeloid leukemia
: more than meets the eye.
The combination of fludarabine, high-dose cytarabine, gemtuzumab ozogamicin, and granulocyte colony-stimulating factor (G-CSF), the FLAG-GO protocol, has resulted in excellent response rates and superior relapse-free survival as first-line therapy for patients with core binding factor
acute
myeloid leukemia
(
AML
).
A side effect of administration
of G
-CSF is an increase in peripheral white blood
cell
count and blast
cell
percentage during the recovery phase of the bone marrow after induction chemotherapy.
A 60-year-old man with inversion 16
AML
was admitted for induction chemotherapy with the FLAG-GO protocol at our institution.
Our case report underscores the importance of recognizing this phenomenon associated with the administration
of G
-CSF, and waiting for 5-7 days before administering
re
-induction therapy or classifying the
disease
as primary refractory
AML
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy
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CYTARABINE
.
Hazardous Substances Data Bank.
VIDARABINE
.
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(PMID = 20709669.001).
[ISSN]
2152-2669
[Journal-full-title]
Clinical lymphoma, myeloma & leukemia
[ISO-abbreviation]
Clin Lymphoma Myeloma Leuk
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factors; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; FLAG protocol
37.
Kessler T, Fehrmann F, Bieker R, Berdel WE, Mesters RM:
Vascular endothelial growth factor and its receptor as drug targets in hematological malignancies.
Curr Drug Targets
; 2007 Feb;8(2):257-68
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With regard to hematological malignancies a stimulating effect of VEGF for proliferation, survival and migration
of leukemia
cells could be demonstrated.
Bone marrow
of leukemia
patients shows an increased microvessel density as well as VEGF expression.
Complete remissions in
acute
myeloid leukemia
(
AML
) have been reported by targeting the receptor tyrosine kinase system of VEGF.
While the pathophysiology behind the contribution of VEGF to
leukemia
progression is
not
yet completely understood, VEGF and its receptors may provide promising targets
not
only in solid tumors but also hematological malignancies such as
AML
.
[MeSH-minor]
Cell
Proliferation.
Cell
Survival.
Disease
Progression. Humans
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(PMID = 17305503.001).
[ISSN]
1873-5592
[Journal-full-title]
Current drug targets
[ISO-abbreviation]
Curr Drug Targets
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
[Number-of-references]
226
38.
Rickerts V, Atta J, Herrmann S, Jacobi V, Lambrecht E, Bialek R, Just-Nübling G:
Successful treatment of disseminated mucormycosis with a combination of liposomal amphotericin B and posaconazole in a patient with acute myeloid leukaemia.
Mycoses
; 2006;49 Suppl 1:27-30
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[Title]
Successful treatment of disseminated mucormycosis with a combination of liposomal amphotericin B and posaconazole in a patient with
acute
myeloid
leukaemia
.
[MeSH-major]
Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ complications. Liposomes / therapeutic use. Mucormycosis / drug therapy. Rhizomucor / isolation & purification. Triazoles / therapeutic use
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AMPHOTERICIN B
.
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(PMID = 16961579.001).
[ISSN]
0933-7407
[Journal-full-title]
Mycoses
[ISO-abbreviation]
Mycoses
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antifungal Agents; 0 / Liposomes; 0 / Triazoles; 0 / liposomal amphotericin B; 6TK1G07BHZ / posaconazole; 7XU7A7DROE / Amphotericin B
39.
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.
The
cell
cycle was examined by flow cytometric analysis.
(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
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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
40.
Zhou Q, Bucher C, Munger ME, Highfill SL, Tolar J, Munn DH, Levine BL, Riddle M, June CH, Vallera DA, Weigel BJ, Blazar BR:
Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-cell immunotherapy in murine acute myeloid leukemia.
Blood
; 2009 Oct 29;114(18):3793-802
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[Title]
Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-
cell
immunotherapy in murine
acute
myeloid leukemia
.
To elucidate host factors contributing to the poor response of adoptively transferred tumor-reactive cytotoxic T lymphocytes (CTLs), we used a systemic model of murine
acute
myeloid leukemia
(
AML
).
AML
progression resulted in a progressive regulatory T-
cell
(Treg) accumulation in
disease
sites.
The adoptive transfer of in vitro-generated, potently lytic anti-
AML
-reactive CTLs failed to reduce
disease
burden or extend survival.
Compared with
non
-
AML
-bearing hosts, transferred CTLs had reduced proliferation in
AML
sites of metastases.
Treg depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced
AML disease
burden but did
not
permit long-term survival.
In contrast, IL-2DT prevented anti-
AML
CTL hypoproliferation, increased the number of transferred CTLs at
AML disease
sites, reduced
AML
tumor burden, and resulted in long-term survivors that sustained an anti-
AML memory
response.
These data demonstrated that Tregs present at
AML disease
sites suppress adoptively transferred CTL proliferation, limiting their in vivo expansion, and Treg depletion before CTL transfer can result in therapeutic efficacy in settings of substantial pre-existing tumor burden in which antitumor reactive CTL infusion alone has proven ineffective.
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[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA120409-03; United States / NCI NIH HHS / CA / CA120409-03; United States / NCI NIH HHS / CA / R01 CA120409; United States / NCI NIH HHS / CA / R01 CA72669; United States / NHLBI NIH HHS / HL / R01 HL056067; United States / NCI NIH HHS / CA / R01 CA072669
[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 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 0 / interleukin 2-diphtheria toxin
[Other-IDs]
NLM/ PMC2773484
41.
Löwenberg B, Delwel HR, Valk PJ:
[The diagnosis of acute myeloid leukaemia enhanced by using DNA microarrays].
Ned Tijdschr Geneeskd
; 2005 Mar 19;149(12):623-5
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[Title]
[The
diagnosis of
acute
myeloid
leukaemia
enhanced by using DNA microarrays].
[Transliterated title]
Diagnostiek van
acute
myeloïde
leukemie
in een stroomversnelling door toepassing van DNA-microarrays.
Recently, two studies have shown that the use ofgene-expression profiling using DNA microarrays or DNA chips may improve the
classification of
acute
myeloid
leukaemia
(
AML
).
In both studies, cluster analyses based on the molecular signatures defined known subgroups as well as novel subgroups
of AML
.
Chromosomal
lesions
, mutations, and abnormal gene expression with prognostic value determined the clustering.
In fact, gene-expression profiling recognized
leukaemias
with certain chromosomal aberrations that had been missed by routine cytogenetics.
Thus, gene-expression profiling allows a comprehensive
classification of AML
that includes previously-identified genetically-defined as well as novel prognostically-relevant subgroups.
[MeSH-major]
Chromosome Aberrations. Gene Expression Profiling / methods.
Leukemia
,
Myeloid
/
diagnosis
.
Leukemia
,
Myeloid
/ genetics. Oligonucleotide Array Sequence Analysis
[MeSH-minor]
Acute
Disease
. Cluster Analysis. Cytogenetic Analysis. Humans
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[CommentIn]
Ned Tijdschr Geneeskd. 2005 Mar 19;149(12):618-22
[
15813427.001
]
(PMID = 15813428.001).
[ISSN]
0028-2162
[Journal-full-title]
Nederlands tijdschrift voor geneeskunde
[ISO-abbreviation]
Ned Tijdschr Geneeskd
[Language]
dut
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Netherlands
42.
Sorror ML, Giralt S, Sandmaier BM, De Lima M, Shahjahan M, Maloney DG, Deeg HJ, Appelbaum FR, Storer B, Storb R:
Hematopoietic cell transplantation specific comorbidity index as an outcome predictor for patients with acute myeloid leukemia in first remission: combined FHCRC and MDACC experiences.
Blood
; 2007 Dec 15;110(13):4606-13
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[Title]
Hematopoietic
cell
transplantation specific comorbidity index as an outcome predictor for patients with
acute
myeloid leukemia
in first remission: combined FHCRC and MDACC experiences.
A new hematopoietic
cell
transplantation-specific comorbidity index (HCT-CI) was effective in predicting outcomes among patients with hematologic malignancies who underwent HCT at Fred Hutchinson Cancer Research Center (FHCRC).
Here, we compared the performance of the HCT-CI to 2 other indices and then tested its capacity to predict outcomes among 2 cohorts of patients diagnosed with a single
disease
entity,
acute
myeloid leukemia
in first complete remission, who underwent transplantation at either FHCRC or M. D.
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(PMID = 17873123.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA78902; United States / NHLBI NIH HHS / HL / R00 HL088021; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / P01 CA078902; United States / NHLBI NIH HHS / HL / K99 HL088021; United States / NHLBI NIH HHS / HL / HL088021
[Publication-type]
Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2234788
43.
Jädersten M, Montgomery SM, Dybedal I, Porwit-MacDonald A, Hellström-Lindberg E:
Long-term outcome of treatment of anemia in MDS with erythropoietin and G-CSF.
Blood
; 2005 Aug 1;106(3):803-11
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The
International
Prognostic Scoring System (IPSS) groups Low/Intermediate-1 (Low/Int-1) had longer response duration than Int-2/High (25 versus 7 months, P = .002).
The time until 25% developed
acute
myeloid leukemia
(
AML
) was longer in the good and intermediate predictive groups for erythroid response compared with the poor predictive group (52 versus 13 months, P = .008).
Only 1 of 20 long-term responders developed
AML
.
There was no difference in survival (odds ratio [OR], 0.9; 95% confidence interval [CI], 0.7-1.2; P = .55) or risk
of AML
evolution (OR, 1.3; 95% CI, 0.7-2.2; P = .40) between treated and untreated patients.
Patients with high/intermediate probability of response and with IPSS Low/Int-1 show frequent and durable responses without adverse effects on outcome, while other patients should
not
be considered candidates for this treatment.
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Analysis of Variance.
Cell
Transformation, Neoplastic. Female. Humans.
Leukemia
,
Myeloid
/ etiology. Male. Middle Aged. Predictive Value of Tests. Prognosis. Survival Analysis. Treatment Outcome
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(PMID = 15840690.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor
44.
van der Straaten HM, Fijnheer R, Nieuwenhuis HK, van de Winkel JG, Verdonck LF:
The FcgammaRIIa-polymorphic site as a potential target for acute graft-versus-host disease in allogeneic stem cell transplantation.
Biol Blood Marrow Transplant
; 2005 Mar;11(3):206-12
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[Title]
The FcgammaRIIa-polymorphic site as a potential target for
acute
graft-versus-host
disease
in allogeneic stem
cell
transplantation.
Graft-versus-host
disease
(GVHD) is a serious complication of allogeneic stem
cell
transplantation for hematologic
diseases
.
Polymorphisms are known for FcgammaRIIa, and this
molecule
is present on endothelial, dendritic, and Langerhans cells.
Donor cells reacting against the patient as GVHD can also react against the malignancy of the patient, and this is known as the graft-versus-
leukemia
(GVL) effect.
Because the FcgammaRIIa
molecule
is also present on
acute
myeloid leukemia
(
AML
) cells, an FcgammaRIIa mismatch could be a target for both GVHD and GVL.
We retrospectively studied 73
AML
patients and analyzed the differences in GVHD and relapse incidence between patients with and without a pro-GVHD/GVL FcgammaRIIa allotype mismatch.
Univariate and multivariate analyses demonstrated the pro-GVHD mismatch to be a significant risk factor for the development of
acute
GVHD.
The relapse incidence was
not
significantly different for patients with or without the pro-GVL mismatch, although there was a trend for fewer relapses in standard-risk
AML
patients with the pro-GVL mismatch.
We conclude that the polymorphism of the FcgammaRIIa receptor may be a candidate target for
acute
GVHD.
[MeSH-major]
Antigens, CD / genetics. Graft vs Host
Disease
/ genetics. Hematopoietic Stem
Cell
Transplantation / adverse effects. Polymorphism, Genetic. Receptors, IgG / genetics
[MeSH-minor]
Acute
Disease
. Adult. Aged. Analysis of Variance. Cohort Studies. Female. Graft vs
Leukemia
Effect / genetics. Graft vs
Leukemia
Effect / immunology. Humans. Incidence.
Leukemia
,
Myeloid
/ complications.
Leukemia
,
Myeloid
/ therapy. Male. Middle Aged. Recurrence. Retrospective Studies. Transplantation Immunology. Transplantation, Homologous
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(PMID = 15744239.001).
[ISSN]
1083-8791
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Fc gamma receptor IIA; 0 / Receptors, IgG
45.
Dheda K, Davids V, Lenders L, Roberts T, Meldau R, Ling D, Brunet L, van Zyl Smit R, Peter J, Green C, Badri M, Sechi L, Sharma S, Hoelscher M, Dawson R, Whitelaw A, Blackburn J, Pai M, Zumla A:
Clinical utility of a commercial LAM-ELISA assay for TB diagnosis in HIV-infected patients using urine and sputum samples.
PLoS One
; 2010 Mar 24;5(3):e9848
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[Title]
Clinical utility
of a
commercial
LAM
-ELISA assay for TB
diagnosis
in HIV-infected patients using urine and sputum samples.
BACKGROUND: The accurate
diagnosis of
TB in HIV-infected patients, particularly with advanced immunosuppression, is difficult.
Recent studies indicate that a lipoarabinomannan (
LAM
) assay (Clearview-TB(R)-ELISA) may have some utility for the
diagnosis of
TB in HIV-infected patients; however, the precise subgroup that may benefit from this technology requires clarification.
The utility
of LAM
in sputum samples has, hitherto,
not
been evaluated.
METHODS:
LAM
was measured in sputum and urine samples obtained from 500 consecutively recruited ambulant patients, with suspected TB, from 2 primary care clinics in South Africa.
Culture positivity
for M
. tuberculosis was used as the reference standard for TB
diagnosis
.
Urine-
LAM
positivity was associated with HIV positivity (p = 0.007) and test sensitivity, although low, was significantly higher in HIV-infected compared to uninfected patients (21% versus 6%; p<0.001), and also in HIV-infected participants with a CD4 <200 versus >200 cells/mm(3) (37% versus 0%; p = 0.003).
Urine-
LAM
remained highly specific in all 3 subgroups (95%-100%).
25% of smear-negative but culture-positive HIV-infected patients with a CD4 <200 cells/mm(3) were positive for urine-
LAM
.
Sputum-
LAM
had good sensitivity (86%) but poor specificity (15%) likely due to test cross-reactivity with several mouth-residing organisms including actinomycetes and nocardia species.
CONCLUSIONS: These preliminary data indicate that in a high burden primary care setting the diagnostic usefulness of urine-
LAM
is limited, as a rule-in test, to a specific patient subgroup i.e. smear-negative HIV-infected TB patients with a CD4 count <200 cells/mm(3), who would
otherwise
have required further investigation.
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(PMID = 20352098.001).
[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
ENG
[Grant]
None / None / / 89918; Canada / Canadian Institutes of Health Research / / 89918; Canada / Canadian Institutes of Health Research / / MOP-89918; United Kingdom / Medical Research Council / /
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2844421
46.
Paschka P:
Core binding factor acute myeloid leukemia.
Semin Oncol
; 2008 Aug;35(4):410-7
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[Title]
Core binding factor
acute
myeloid leukemia
.
Core binding factor (CBF)
acute
myeloid leukemia
(
AML
) is cytogenetically defined by the presence of t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), which are found in approximately 15% of all adult
de
novo
AML
cases.
Despite this molecular commonality, recent studies have demonstrated differences in genetic, clinical, and prognostic features between t(8;21) and inv(16)/t(16;16)
AML
, thereby supporting the notion that they represent two distinct biologic and clinical entities.
Furthermore, despite being considered as a more favorable
AML
risk group, only approximately half of the CBF
AML
patients are cured with current therapy, indicating the need for improved therapeutic approaches.
This review summarizes the most recent laboratory and clinical discoveries relevant to this subset
of AML
and how they are being applied for in an effort to improve the cure rate in patients with the
disease
.
[MeSH-major]
Chromosome Inversion. Core Binding Factors / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ therapy. Translocation, Genetic
[MeSH-minor]
Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Neoplasm, Residual /
diagnosis
. Prognosis
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(PMID = 18692691.001).
[ISSN]
0093-7754
[Journal-full-title]
Seminars in oncology
[ISO-abbreviation]
Semin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factors
[Number-of-references]
76
47.
Shim H, Chi HS, Jang S, Seo EJ, Park CJ, Lee JH, Lee JH, Lee KH:
Therapy-related acute leukemia in breast cancer patients: twelve cases treated with a topoisomerase inhibitor.
Korean J Hematol
; 2010 Sep;45(3):177-82
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[Title]
Therapy-related
acute
leukemia
in breast cancer patients: twelve cases treated with a topoisomerase inhibitor.
BACKGROUND: Therapy-related
myeloid
neoplasm (t-MN) is a distinct class of
acute
myeloid leukemia
(
AML
) in the World Health Organization (WHO)
classification
.
Both
AML
and
acute
lymphoblastic leukemia
(ALL) may develop after treatment for primary cancer.
Topoisomerase inhibitors are commonly used to treat breast cancer patients and are well-known for their effect on leukemogenesis of therapy-related
acute
leukemias
(t-AL).
METHODS: We retrospectively evaluated bone marrow test results, chromosomal findings, and clinical characteristics of 12 patients who received topoisomerase inhibitors for breast cancer treatment and later developed
acute
leukemia
.
Among them, 9 patients (75%, 9/12) were diagnosed with therapy-related
AML
(t-
AML
) and 3 patients (25%, 3/12) with therapy-related ALL (t-ALL).
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(PMID = 21120206.001).
[ISSN]
2092-9129
[Journal-full-title]
The Korean journal of hematology
[ISO-abbreviation]
Korean J Hematol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Korea (South)
[Other-IDs]
NLM/ PMC2983048
[Keywords]
NOTNLM ; 11q23 / Breast cancer / Therapy-related acute myeloid leukemia / Topoisomerase inhibitors
48.
Edwards DB, Tempelman RJ, Bates RO:
Evaluation of Duroc- vs. Pietrain-sired pigs for growth and composition.
J Anim Sci
; 2006 Feb;84(2):266-75
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Body weight, 10th rib backfat (BF10), last rib backfat (LRF), and loin muscle
area
(
LMA
) were serially measured at 10, 13, 16, 19, 22, 24, and 26 wk of age.
At 26 wk of age, Duroc-sired progeny were heavier (143.4 vs. 132.7 kg, P < 0.001), had more BF10 (27.1 vs. 23.7 mm, P < 0.001) and LRF (21.2 vs. 19.2 mm, P < 0.001), but had similar
LMA
(46.4 vs. 47.1 cm2) compared with Pietrain-sired progeny.
Mean feed efficiency did
not
differ between breed of sire in any period of the study.
Random regression animal models with polynomial regression on week on-test were fitted to BW, BF10, LRF,
LMA
, FFTOLN, TOFAT, EBPRO, and EBLIPID from 10 to 26 wk of age.
Serial heritability estimates generally increased from 10 to 26 wk of age with ranges as follows: BW (0.05 to 0.39), BF10 (0.13 to 0.76), LRF (0.11 to 0.79),
LMA
(0.05 to 0.73), FFTOLN (0.07 to 0.16), TOFAT (0.19 to 0.45), EBPRO (0.02 to 0.55), and EBLIPID (0.12 to 0.60).
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(PMID = 16424252.001).
[ISSN]
1525-3163
[Journal-full-title]
Journal of animal science
[ISO-abbreviation]
J. Anim. Sci.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
49.
Ozhak-Baysan B, Alastruey-Izquierdo A, Saba R, Ogunc D, Ongut G, Timuragaoglu A, Arslan G, Cuenca-Estrella M, Rodriguez-Tudela JL:
Aspergillus alliaceus and Aspergillus flavus co-infection in an acute myeloid leukemia patient.
Med Mycol
; 2010 Nov;48(7):995-9
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[Title]
Aspergillus alliaceus and Aspergillus flavus co-infection in an
acute
myeloid leukemia
patient.
We report a case
of a
pulmonary infection caused by Aspergillus flavus and Aspergillus alliaceus in an
acute
myeloid leukemia
patient.
[MeSH-major]
Aspergillosis / complications. Aspergillosis / microbiology. Aspergillus / isolation & purification. Aspergillus flavus /
classification
.
Leukemia
,
Myeloid
,
Acute
/ complications. Lung
Diseases
, Fungal / complications. Lung
Diseases
, Fungal / microbiology
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(PMID = 20392148.001).
[ISSN]
1460-2709
[Journal-full-title]
Medical mycology
[ISO-abbreviation]
Med. Mycol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA, Intergenic; 0 / Fungal Proteins; 0 / Tubulin
50.
Nahimana A, Attinger A, Aubry D, Greaney P, Ireson C, Thougaard AV, Tjørnelund J, Dawson KM, Dupuis M, Duchosal MA:
The NAD biosynthesis inhibitor APO866 has potent antitumor activity against hematologic malignancies.
Blood
; 2009 Apr 2;113(14):3276-86
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Intracellular NAD is essential
for cell
survival, and NAD depletion resulting from APO866 treatment elicits tumor
cell
death.
Here, we determine the in vitro and in vivo sensitivities of hematologic cancer cells to APO866 using a panel
of cell
lines (n = 45) and primary cells (n = 32).
Most cancer cells (
acute
myeloid leukemia
[
AML
],
acute
lymphoblastic leukemia
[ALL], mantle
cell
lymphoma [MCL], chronic
lymphocytic leukemia
[CLL], and T-
cell
lymphoma), but
not
normal hematopoietic progenitor cells, were sensitive to low concentrations of APO866 as measured in cytotoxicity and clonogenic assays.
The NAD depletion led to
cell
death.
At 96 hours, APO866-mediated
cell
death occurred in a caspase-independent mode, and was associated with mitochondrial dysfunction and autophagy.
Further, in vivo administration of APO866 as a single agent prevented and abrogated tumor growth in animal models of human
AML
,
lymphoblastic
lymphoma, and
leukemia
without significant toxicity to the animals.
[MeSH-minor]
Animals.
Cell
Death / drug effects. Dose-Response Relationship, Drug. HL-60 Cells. Humans. Jurkat Cells. K562 Cells. Mice. Mice, Inbred BALB C. Mice, Nude. Tumor Cells, Cultured. U937 Cells. Xenograft Model Antitumor Assays
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[CommentIn]
Blood. 2009 Jun 4;113(23):6035-7; author reply 6037-8
[
19498032.001
]
(PMID = 19196867.001).
[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 / Acrylamides; 0 / Antineoplastic Agents; 0 / Cytokines; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / Piperidines; 0U46U6E8UK / NAD; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human
51.
Chowdhury T, Brady HJ:
Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.
Blood Cells Mol Dis
; 2008 Mar-Apr;40(2):192-9
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[Title]
Insights from clinical studies into the role of the MLL gene in infant and childhood
leukemia
.
Translocations involving the Mixed Lineage
Leukemia
(MLL) gene at 11q23 are found in both
acute
lymphoblastic leukemia
(ALL) and
acute
myeloblastic leukemia
(
AML
), but have different prognostic implications depending on the phenotype of the
leukemia
in
de
novo pediatric cases.
Rearrangements of the MLL gene are found in most cases of infant
AML
and regardless of age confer an intermediate risk.
The treatment of MLL-rearranged ALL in children involves increased intensification of chemotherapy, and infants with ALL are treated with an intensive regimen of ALL- and
AML
-like chemotherapy, with the proportion of MLL-rearranged cases being responsible for the poor outcome in this age group.
The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged
leukemias
is shedding light on the molecular mechanisms and potential therapeutic targets of these
leukemias
.
It may also prove to have a useful role in both
diagnosis
and prognosis.
[MeSH-major]
Gene Rearrangement.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myeloid
-Lymphoid
Leukemia
Protein / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics
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(PMID = 17905612.001).
[ISSN]
1079-9796
[Journal-full-title]
Blood cells, molecules & diseases
[ISO-abbreviation]
Blood Cells Mol. Dis.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
149025-06-9 / Myeloid-Lymphoid Leukemia Protein
[Number-of-references]
82
52.
Czibere A, Grall F, Aivado M:
Perspectives of proteomics in acute myeloid leukemia.
Expert Rev Anticancer Ther
; 2006 Nov;6(11):1663-75
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[Title]
Perspectives of proteomics in
acute
myeloid leukemia
.
Acute
myeloid leukemia
(
AML
) is a frequent hematological malignancy.
Despite enormous therapeutic efforts that range from various cytotoxic agents to allogeneic stem
cell
transplantation, overall survival of patients with
AML
remains unsatisfying.
There is hope that elucidation of the
AML
-specific proteome will prompt the discovery of novel therapeutic targets and biomarkers in
AML
.
Modern mass-spectrometry instrumentation has achieved excellent performance in terms of sensitivity, resolution and mass accuracy; however, so far, the contribution of proteomics to the care of patients with
AML
is virtually zero.
Since mass-spectrometry instruments are very intricate devices, their successful operation will hinge on the willingness and ability of mass-spectrometry experts and clinical researchers to adopt new views, learn from each other and cooperate in order to ultimately benefit the patient suffering from
AML
.
This review highlights some clinical problems circumventing the treatment of patients with
AML
.
Furthermore, it provides a brief overview of the technical background of standard proteomics approaches and describes opportunities, challenges and pitfalls of proteomic studies with regards to
AML
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ therapy. Proteomics
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(PMID = 17134369.001).
[ISSN]
1744-8328
[Journal-full-title]
Expert review of anticancer therapy
[ISO-abbreviation]
Expert Rev Anticancer Ther
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
[Number-of-references]
99
53.
Ayala F, Dewar R, Kieran M, Kalluri R:
Contribution of bone microenvironment to leukemogenesis and leukemia progression.
Leukemia
; 2009 Dec;23(12):2233-41
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[Title]
Contribution of bone microenvironment to leukemogenesis and
leukemia
progression.
Both BM stroma and leukemic blasts promote angiogenesis, which is increased in
acute
lymphoblastic leukemia
and
acute
myeloid leukemia
.
Growth factors like vascular endothelial growth factor (VEGF), basic fibroblast growth factor and angiopoietins are the main proangiogenic mediators in
acute
leukemia
.
Interactions of stromal cells and extracellular matrix with leukemic blasts can also generate antiapoptotic signals that contribute to neoplastic progression and persistence of treatment-resistant minimal residual
disease
.
High expression of CXC chemokine ligand 4 (CXCR4) by leukemic blasts and activation of the CXCR4-CXCL12 axis is involved in
leukemia
progression and disruption of normal hematopoiesis.
Leukemia
-associated bone microenvironment markers could be used as prognostic or predictive indicators
of disease
progression and/or treatment outcome.
Studies related to bone microenvironment would likely provide a better understanding of the treatment resistance associated with
leukemia
therapy and design of new treatments.
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(PMID = 19727127.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK61688; United States / NIDDK NIH HHS / DK / DK55001; United States / NIAAA NIH HHS / AA / R01 AA013913; United States / NIDDK NIH HHS / DK / R01 DK061688; United States / NIDDK NIH HHS / DK / R01 DK062987; United States / NCI NIH HHS / CA / R01 CA125550; United States / NCI NIH HHS / CA / CA125550; United States / NIDDK NIH HHS / DK / R01 DK055001; United States / NIDDK NIH HHS / DK / DK62987; United States / NIAAA NIH HHS / AA / AA13913
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
99
[Other-IDs]
NLM/ NIHMS590537; NLM/ PMC4313556
54.
Schlenk RF, Döhner K, Kneba M, Götze K, Hartmann F, Del Valle F, Kirchen H, Koller E, Fischer JT, Bullinger L, Habdank M, Späth D, Groner S, Krebs B, Kayser S, Corbacioglu A, Anhalt A, Benner A, Fröhling S, Döhner H, German-Austrian AML Study Group (AMLSG):
Gene mutations and response to treatment with all-trans retinoic acid in elderly patients with acute myeloid leukemia. Results from the AMLSG Trial AML HD98B.
Haematologica
; 2009 Jan;94(1):54-60
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[Title]
Gene mutations and response to treatment with all-trans retinoic acid in elderly patients with
acute
myeloid leukemia
. Results from the AMLSG Trial
AML
HD98B.
BACKGROUND: In a previous randomized trial,
AML
HD98B, we showed that administration of all-trans retinoic acid in addition to intensive chemotherapy improved the outcome of older patients with
acute
myeloid leukemia
.
DESIGN AND METHODS: Data from mutation analyses of the NPM1, CEBPA, FLT3, and MLL genes were correlated with outcome in patients 61 years and older treated within the
AML
HD98B trial.
The genotype mutant NPM1 was positively and adverse cytogenetics as well as higher white blood
cell
count negatively correlated with achievement of complete remission.
Other significant factors for survival were age, adverse cytogenetics, and logarithm of white
cell
count.
CONCLUSIONS: In elderly patients with
acute
myeloid leukemia
, NPM1 mutations are associated with achievement of complete remission, and the genotype 'mutant NPM1 without FLT3-ITD' appears to be a predictive marker for response to all-trans retinoic acid given as an adjunct to intensive chemotherapy (ClinicalTrials.gov Identifier: NCT00151242).
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation / genetics. Tretinoin / therapeutic use
[MeSH-minor]
Aged. Aged, 80 and over. Biomarkers / metabolism.
Disease
-Free Survival. Female. Humans. Male. Middle Aged. Pilot Projects. Survival Rate. Treatment Outcome
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.
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.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Hazardous Substances Data Bank.
ALL-TRANS-RETINOIC ACID
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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.
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]
[CommentIn]
Haematologica. 2009 Jan;94(1):10-6
[
19118375.001
]
(PMID = 19059939.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00151242
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Biomarkers; 5688UTC01R / Tretinoin
[Other-IDs]
NLM/ PMC2625424
[Investigator]
Glasmacher A; Mergenthaler HG; Nerl C; Pralle H; Hensel M; Preiss J; Salwender H; Biedermann HG; Kremers S; Griesinger F
55.
Griessinger E, Imbert V, Lagadec P, Gonthier N, Dubreuil P, Romanelli A, Dreano M, Peyron JF:
AS602868, a dual inhibitor of IKK2 and FLT3 to target AML cells.
Leukemia
; 2007 May;21(5):877-85
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[Title]
AS602868, a dual inhibitor of IKK2 and FLT3 to target
AML
cells.
Acute
myeloid leukemia
(
AML
) cells carry molecular defects that promote their leukemic proliferation, resistance to apoptosis and defect in differentiation.
Pharmacological targeting of the nuclear factor kappaB (NF-kappaB) pathway has been shown to promote apoptosis of primary
AML
cells and to sensitize blasts to neoplastic drugs (Frelin, Blood 2005, 105, 804).
The Fms-like tyrosine kinase 3 (FLT3), which sustains proliferation of normal hematopoietic progenitors is frequently overexpressed or mutated in
AML
patients.
Using Ba/F3 murine pre-B cells transfected with various mutants of FLT3 (ITD, D835V, D835Y) and the MV4-11 human
AML
line, we show that normal or oncogenic stimulation of FLT3 led to activation of NF-kappaB.
Pharmacological inhibition of either FLT3 with AG1296 or NF-kappaB with the small
molecule
inhibitor of IkappaB kinase-2 AS602868 reduced viability and triggered
cell
death.
AS602868 thus appears to target two different kinases that play a crucial role in the pathogenesis
of AML
, making it particularly attractive as a new therapeutical approach
for AML
.
[MeSH-major]
I-kappa B Kinase / antagonists & inhibitors.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors
[MeSH-minor]
Animals. Annexin A5 / analysis. Caspase 3 / metabolism.
Cell
Line.
Cell
Proliferation. Child. Humans. Male. Mice. NF-kappa B / metabolism. Poly(ADP-ribose) Polymerases / metabolism. bcl-X Protein / analysis
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NCI CPTAC Assay Portal
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(PMID = 17330097.001).
[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 / AS602868; 0 / Annexin A5; 0 / NF-kappa B; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / bcl-X Protein; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.10 / I-kappa B Kinase; EC 3.4.22.- / Caspase 3
56.
Siegler U, Meyer-Monard S, Jörger S, Stern M, Tichelli A, Gratwohl A, Wodnar-Filipowicz A, Kalberer CP:
Good manufacturing practice-compliant cell sorting and large-scale expansion of single KIR-positive alloreactive human natural killer cells for multiple infusions to leukemia patients.
Cytotherapy
; 2010 Oct;12(6):750-63
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[Title]
Good manufacturing practice-compliant
cell
sorting and large-scale expansion of single KIR-positive alloreactive human natural killer cells for multiple infusions to
leukemia
patients.
The introduction of NK
cell
-based immunotherapy to current treatment options in
acute
myeloid leukemia
(
AML
) requires NK
cell
products with high anti-leukemic efficacy optimized for clinical use.
METHODS: We describe a good manufacturing practice (GMP)-compliant protocol of large-scale ex vivo expansion of alloreactive NK cells suitable for multiple donor
lymphocyte
infusions (NK-DLI) in
AML
.
NK
cell
numbers increased 117.0 ± 20.0-fold in 19 days.
To reduce the culture volume associated with expansion of bulk NK cells and to expand selectively the alloreactive NK
cell
subsets, GMP-certified
cell
sorting was introduced to obtain cells with single killer immunoglobulin-like receptor (KIR) specificities.
The subsequent GMP-compliant expansion of single KIR+ cells was 268.3 ± 66.8-fold, with a contaminating T-
cell
content of only 0.006 ± 0.002%.
The single KIR-expressing NK cells were cytotoxic against HLA-mismatched primary
AML
blasts in vitro and effectively reduced tumor
cell
load in vivo in NOD/SCID mice transplanted with human
AML
.
CONCLUSIONS: The approach to generating large numbers of GMP-grade alloreactive NK cells described here provides the basis for clinical efficacy trials of NK-DLI to complement and advance therapeutic strategies against human
AML
.
[MeSH-major]
Cell
Culture Techniques / methods.
Cell
Proliferation. Immunotherapy, Adoptive. Killer Cells, Natural / metabolism.
Leukemia
,
Myeloid
,
Acute
/ therapy
[MeSH-minor]
Animals. Antineoplastic Protocols.
Cell
Line, Tumor. Cytotoxicity, Immunologic. Guideline Adherence. Humans. Infusions, Intravenous. Isoantigens / immunology. Mice. Mice, SCID. Neoplasm Transplantation. Receptors, KIR / metabolism. Tumor Burden
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(PMID = 20491532.001).
[ISSN]
1477-2566
[Journal-full-title]
Cytotherapy
[ISO-abbreviation]
Cytotherapy
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Isoantigens; 0 / Receptors, KIR
57.
Liu XM, Chen YZ, Huang MJ, Liu X, Guo JR:
[The potential prognostic influence of granulocyte-colony stimulating factor in acute leukemia].
Zhonghua Nei Ke Za Zhi
; 2005 Jul;44(7):518-21
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[Title]
[The potential prognostic influence of granulocyte-colony stimulating factor in
acute
leukemia
].
OBJECTIVE: To investigate the potential influence of granulocyte-colony stimulating factor (G-CSF) on the prognosis of patients with
acute
leukemia
(AL).
METHODS: In 171 evaluable cases with AL, the complete remission (CR) rate post first course of chemotherapy, CR rate, effective rate, duration of leucopenia post chemotherapy, CR duration, lifespan and the relationship between the dosage
of G
-CSF and CR duration or lifespan were retrospectively analyzed with Chi-square test, paired t-test, Cox regression, Kaplan-Meier and rank correlation method.
For remission induction and postremission therapy, the cases with
acute
myeloid leukemia
(
AML
) received chemotherapy regimes based on daunorubicin + ara-C (DA), homoharringtonine + ara-C (HA) or mitoxantrone + ara-C (MA).
The patients with
acute
lymphocyte leukemia
(ALL) were treated with regimes based on vinblastine + daunorubicin + prednisone (VDP), vinblastine + adriamycin + prednisone (VAP), vinblastine + mitoxantrone + prednisone (VMP) or cyclophosphamide + vinblastine + daunorubicin + prednisone(CODP).
However, there was no statistical difference between the two groups in the CR rate post first course of chemotherapy, CR rate and the effective rate of treatment. (2) Use
of G
-CSF did
not
affect CR durations of ALL patients, but shortened that
of AML
patients. (3) The application
of G
-CSF had little effect on the lifespan of ALL patients.
By contrast, it showed clearly negative effects on that
of AML
patients. (4) No relationship between the dosage
of G
-CSF and CR duration or lifespan in
AML
patients.
CONCLUSION: With
AML
patients, the administration
of G
-CSF must be very cautious.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Granulocyte Colony-Stimulating Factor / administration & dosage.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy
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(PMID = 16080844.001).
[ISSN]
0578-1426
[Journal-full-title]
Zhonghua nei ke za zhi
[ISO-abbreviation]
Zhonghua Nei Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
143011-72-7 / Granulocyte Colony-Stimulating Factor
58.
Cilloni D, Messa E, Messa F, Carturan S, Defilippi I, Arruga F, Rosso V, Catalano R, Bracco E, Nicoli P, Saglio G:
Genetic abnormalities as targets for molecular therapies in myelodysplastic syndromes.
Ann N Y Acad Sci
; 2006 Nov;1089:411-23
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Recent advances in molecular genetics have increased knowledge regarding the mechanisms leading to myelodysplastic syndrome (MDS), secondary
acute
myeloid leukemia
(
AML
), and therapy-induced MDS.
Many genetic defects underlying MDS and
AML
have been identified thereby allowing the development of new molecular-targeted therapies.
These agents have been tested in patients with solid tumors and hematologic malignancies such as
AML
and MDS.
The DNA hypomethylating compounds azacytidine and decitabine may reduce hypermethylation and induce
re
-expression of key tumor suppressor genes in MDS.
Future therapies will attempt to resolve cytopenias in MDS, eliminate malignant clones, and allow differentiation by attacking specific mechanisms of the
disease
.
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(PMID = 17261784.001).
[ISSN]
0077-8923
[Journal-full-title]
Annals of the New York Academy of Sciences
[ISO-abbreviation]
Ann. N. Y. Acad. Sci.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / MECOM protein, human; 0 / Transcription Factors; 0 / WT1 Proteins; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
[Number-of-references]
76
59.
Yang L, Dong ZR, Wen SP, Pan L, Zhang XJ, Luo JM, Xu SR:
[Relationship between VEGF and MMP-2, MMP-9 in 82 patients with acute myeloid leukemia].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2006 Feb;14(1):15-20
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[Title]
[Relationship between VEGF and MMP-2, MMP-9 in 82 patients with
acute
myeloid leukemia
].
In order to investigate the relationship between VEGF and matrix metalloproteinase (MMP)-2, -9 in
acute
myeloid leukemia
patients, and evaluate the significance of them in extramedullary leukemic invasion, the expressions of MMP-2 mRNA, MMP-9 mRNA, VEGF mRNA in bone marrow from 86 patients with
acute
myeloid leukemia
(
AML
), as well as human hematopoietic
cell
lines were analyzed by reverse transcription-polymerase chain reaction (RT-PCR).
But no such correlation was demonstrated in the
AML
(CR) and normal control (NC) groups.
More extramedullary infiltration occurred in VEGF positive groups than that in VEGF negative groups
of AML
.
It is concluded that there are significantly positive correlations between the expression of MMP-2 and MMP-9 with VEGF mRNA or protein levels in
AML
patients.
VEGF and MMP-2, MMP-9 may participate in the extramedullary leukemic invasion
of AML
patients.
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(PMID = 16584583.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
CHI
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
60.
Racay P, Hatok J, Hudecek J, Chudej J, Jurecekova J, Dobrota D:
Transcription of genes of p53-dependent apoptosis in acute leukaemia.
Int J Mol Med
; 2008 Dec;22(6):833-9
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[Title]
Transcription of genes of p53-dependent apoptosis in
acute leukaemia
.
We demonstrated that
acute leukaemia
,
myeloblastic
(
AML
) and
lymphoblastic
(ALL), is associated with significantly elevated levels of p53 and Bax mRNA in leukaemic cells.
Altered alternative processing of Bcl-x and
myeloid cell
leukaemia
-1 (MCL1) primary transcripts were observed in the case
of AML
and
AML
and ALL, respectively.
We assumed that increased glyceraldehyde-3-phosphate dehydrogenase (gapdh) transcription and decreased MCL1s mRNA were
not
fully responsible for the dysregulation of p53-dependent apoptosis in the case
of AML
.
In addition, transcription of hsp70.1 and Bcl-2 producing anti-apoptotic proteins was
not
affected in
acute leukaemia
.
[MeSH-major]
Apoptosis.
Leukemia
,
Myeloid
,
Acute
/ genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Transcription, Genetic. Tumor Suppressor Protein p53 / genetics
[MeSH-minor]
Actins / genetics. Actins / metabolism. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Glyceraldehyde-3-Phosphate Dehydrogenases / metabolism. HSP70 Heat-Shock Proteins / genetics. HSP70 Heat-Shock Proteins / metabolism. Humans. Leukocytes, Mononuclear / metabolism.
Myeloid Cell Leukemia
Sequence 1 Protein. Polymorphism, Single-Stranded Conformational. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism. bcl-X Protein / genetics. bcl-X Protein / metabolism
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(PMID = 19020783.001).
[ISSN]
1107-3756
[Journal-full-title]
International journal of molecular medicine
[ISO-abbreviation]
Int. J. Mol. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Actins; 0 / BCL2L1 protein, human; 0 / HSP70 Heat-Shock Proteins; 0 / MCL1 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
61.
Crapanzano JP:
Fine-needle aspiration of renal angiomyolipoma: cytological findings and diagnostic pitfalls in a series of five cases.
Diagn Cytopathol
; 2005 Jan;32(1):53-7
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Diagnosis of
renal angiomyolipoma (
AML
) by fine-needle aspiration (FNA) may be difficult because cytological and radiological findings sometimes overlap with renal
cell
carcinoma (RCC) and liposarcoma.
Five FNAs
of AMLs
were studied.
Corresponding surgical material showed typical features
of AML
.
In FNA, bland chromatin and inconspicuous nucleoli distinguish renal
AML
from RCC and liposarcoma.
Adipose tissue is
not
universally present.
Immunocytochemical (ICC) stains may elucidate the correct
diagnosis
.
[MeSH-minor]
Adenoma, Oxyphilic /
diagnosis
. Adult. Aged. Carcinoma, Renal
Cell
/
diagnosis
.
Diagnosis
, Differential. Epithelioid Cells / pathology. Female. Humans. Liposarcoma /
diagnosis
. Male. Middle Aged. Retroperitoneal Neoplasms /
diagnosis
. Stromal Cells / pathology
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[Copyright]
(c) 2005 Wiley-Liss, Inc.
(PMID = 15584043.001).
[ISSN]
8755-1039
[Journal-full-title]
Diagnostic cytopathology
[ISO-abbreviation]
Diagn. Cytopathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
62.
Wang Z, Xu HX, Xie XY, Xie XH, Kuang M, Xu ZF, Liu GJ, Chen LD, Lin MX, Lu MD:
Imaging features of hepatic angiomyolipomas on real-time contrast-enhanced ultrasound.
Br J Radiol
; 2010 May;83(989):411-8
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The aim of this study was to evaluate the imaging features of hepatic angiomyolipoma (
AML
) on contrast-enhanced ultrasound (CEUS).
The imaging features of 12 pathologically proven hepatic
AML lesions
in 10 patients who had undergone baseline ultrasound (BUS) and CEUS examinations were evaluated retrospectively.
The results showed that 75% (9/12) of the
AML lesions
exhibited mixed echogenicity on BUS and most showed remarkable hyperechogenicity in combination with a hypoechoic or anechoic portion.
Arterial flow signals were detected in 75% (9/12) of the
lesions
on colour Doppler imaging.
On CEUS, 66.7% (n = 8) of the 12
lesions
exhibited hyperenhancement in the arterial phase, slight hyperenhancement (n = 2) or isoenhancement (n = 6) in the portal phase, and slight hyperenhancement (n = 1) or isoenhancement (n = 7) in the late phase.
Three (25%)
lesions
exhibited hyperenhancement in the arterial phase and hypoenhancement in both portal and late phases.
One (8.3%)
lesion
exhibited hypoenhancement throughout the CEUS process.
Before pathological examination with BUS, only 3 (25%)
lesions
were correctly diagnosed as hepatic
AML
.
Conversely, on CEUS, correct diagnoses were made for 66.8% (8/12) of hepatic
AMLs
.
Therefore, arterial hyperenhancement and subsequent sustained enhancement on CEUS were found in the majority of hepatic
AMLs
.
The combination of BUS and CEUS leads to the correct
diagnosis
in the majority of hepatic
AMLs
, and is higher than the success rate achieved by BUS alone.
[MeSH-major]
Angiomyolipoma / ultrasonography.
Liver
Neoplasms / ultrasonography
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[ISSN]
1748-880X
[Journal-full-title]
The British journal of radiology
[ISO-abbreviation]
Br J Radiol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Contrast Media
[Other-IDs]
NLM/ PMC3473573
63.
Wihlidal P, Varga F, Pfeilstöcker M, Karlic H:
Expression and functional significance of osteocalcin splicing in disease progression of hematological malignancies.
Leuk Res
; 2006 Oct;30(10):1241-8
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[Title]
Expression and functional significance of osteocalcin splicing in
disease
progression of hematological malignancies.
We analysed bone marrow obtained from two patients with chronic
myeloid leukemia
(CML), seven patients with other myeloproliferative
diseases
(MPD) and four patients with
acute
myeloid leukemia
(
AML
).
[MeSH-minor]
Bone Marrow Cells / pathology. DNA Primers.
Disease
Progression. Humans.
Leukemia
,
Myelogenous
, Chronic, BCR-ABL Positive / genetics. Myeloproliferative Disorders / genetics. Protein Biosynthesis. Proto-Oncogene Proteins c-kit / genetics. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / pathology. Transcription, Genetic
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(PMID = 16387359.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA Primers; 0 / RNA, Messenger; 104982-03-8 / Osteocalcin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
64.
Fernandes MS, Reddy MM, Croteau NJ, Walz C, Weisbach H, Podar K, Band H, Carroll M, Reiter A, Larson RA, Salgia R, Griffin JD, Sattler M:
Novel oncogenic mutations of CBL in human acute myeloid leukemia that activate growth and survival pathways depend on increased metabolism.
J Biol Chem
; 2010 Oct 15;285(42):32596-605
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[Title]
Novel oncogenic mutations of CBL in human
acute
myeloid leukemia
that activate growth and survival pathways depend on increased metabolism.
Acute
myeloid leukemia
(
AML
) is characterized by multiple mutagenic events that affect proliferation, survival, as well as differentiation.
Recently, gain-of-function mutations in the α helical structure within the linker sequence of the E3 ubiquitin ligase CBL have been associated with
AML
.
We identified four novel CBL mutations, including a point mutation (Y371H) and a putative splice site mutation in
AML
specimens.
Overall, our data demonstrate that mutations of CBL alter cellular biology at multiple levels and require
not
only the activation of receptor proximal signaling events but also an increase in cellular glucose metabolism.
Pathways that are activated by CBL gain-of-function mutations can be efficiently targeted by small
molecule
drugs.
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[
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Nature. 2009 Aug 13;460(7257):904-8
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J Clin Oncol. 2009 Dec 20;27(36):6109-16
[
19901108.001
]
[Cites]
Oncogene. 2002 Feb 21;21(9):1423-33
[
11857085.001
]
(PMID = 20622007.001).
[ISSN]
1083-351X
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA087986; United States / NCI NIH HHS / CA / 5R01CA134660-02; United States / NCI NIH HHS / CA / CA099163-11; United States / NCI NIH HHS / CA / 5R01CA87986-12; United States / NCI NIH HHS / CA / R01 CA099163-09; United States / NCI NIH HHS / CA / 5R01CA105489-06; United States / NCI NIH HHS / CA / CA099163-10; United States / NCI NIH HHS / CA / 5R01CA125541-04; United States / NCI NIH HHS / CA / 5R01CA129501-02; United States / NCI NIH HHS / CA / R01 CA125541; United States / NCI NIH HHS / CA / 5R01CA116552-04; United States / NCI NIH HHS / CA / R01 CA116552; United States / NCI NIH HHS / CA / CA099163-09; United States / NCI NIH HHS / CA / R01 CA105489; United States / NCI NIH HHS / CA / 5R01CA99163-09; United States / NCI NIH HHS / CA / R01 CA099163-11; United States / NCI NIH HHS / CA / 5R01CA100750-06; United States / NCI NIH HHS / CA / R01 CA129501; United States / NCI NIH HHS / CA / R01 CA099163-10; United States / NCI NIH HHS / CA / R01 CA061593; United States / NCI NIH HHS / CA / R01 CA099163; United States / NCI NIH HHS / CA / R01 CA100750; United States / NCI NIH HHS / CA / R01 CA134660
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / STAT5 Transcription Factor; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.1.- / GTP-Binding Proteins; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl; IY9XDZ35W2 / Glucose
[Other-IDs]
NLM/ PMC2952262
65.
Ngo N, Lampert IA, Naresh KN:
Bone marrow trephine findings in acute myeloid leukaemia with multilineage dysplasia.
Br J Haematol
; 2008 Feb;140(3):279-86
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[Title]
Bone marrow trephine findings in
acute
myeloid
leukaemia
with multilineage dysplasia.
Acute
myeloid
leukaemia
(
AML
) with multilineage dysplasia (MD) is one of the four main categories
of AML
in the World Health Organization (WHO)
classification
.
The role of bone marrow trephine biopsy (BMTB) histology and immunohistochemistry in the
diagnosis of AML
-MD is currently unclear.
BMTBs were studied in 11 cases
of AML
-MD and two cases of myelodysplasia that subsequently transformed to
AML
.
With respect to conforming to the WHO definition
of AML
, documentation of an increased proportion of immature
myeloid
cells was possible on morphology and counting of immature cells following immunostaining with CD34, CD117 or HLA-DR antibodies.
Based on this relatively small series of cases we show the utility of BMTB and immunohistochemistry as an aid to the
diagnosis of AML
-MD.
This has to be seen
not
just in light of its utility at
diagnosis
, but also the role the diagnostic BMTB would play for purposes of comparison when follow-up BMTBs are submitted in this group of patients.
[MeSH-major]
Bone Marrow Cells / pathology.
Leukemia
,
Myeloid
,
Acute
/ pathology. Myelodysplastic Syndromes / pathology
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Antigens, CD34 / analysis. Biomarkers / analysis. Biopsy / methods. Bone Marrow Examination / methods. Cytogenetics.
Disease
Progression. Erythroblasts / pathology. Female. Humans. Immunohistochemistry. Immunophenotyping. Male. Megakaryocytes / pathology. Middle Aged.
Myeloid
Cells / pathology. Proto-Oncogene Proteins c-kit / analysis
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(PMID = 17973948.001).
[ISSN]
1365-2141
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Biomarkers; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
66.
Huang XF, Luo SK, Xu J, Li J, Xu DR, Wang LH, Yan M, Wang XR, Wan XB, Zheng FM, Zeng YX, Liu Q:
Aurora kinase inhibitory VX-680 increases Bax/Bcl-2 ratio and induces apoptosis in Aurora-A-high acute myeloid leukemia.
Blood
; 2008 Mar 1;111(5):2854-65
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[Title]
Aurora kinase inhibitory VX-680 increases Bax/Bcl-2 ratio and induces apoptosis in Aurora-A-high
acute
myeloid leukemia
.
In this study, we found that expression of Aur-A was markedly elevated in bone marrow mononuclear cells (BMMCs) obtained from a significant portion
of de
novo
acute
myeloid leukemia
(
AML
) patients.
Targeting human primary
AML
cells with Aur-A kinase inhibitory VX-680 led to apoptotic
cell
death in a dose-dependent manner.
Importantly, VX-680-induced
cell
death was preferentially higher in Aur-A-high primary leukemic blasts compared with Aur-A-low
AML
(P < .001) or normal BMMCs (P < .001), suggesting the possible pharmacologic window in targeting Aurora kinase among Aur-A-high VX-680-sensitive
leukemia
patients.
VX-680-induced
cell
death in
AML cell
lines was accompanied by formation of monopolar mitotic spindles, G(2)/M phase arrest, decreased phosphorylated(p)-Akt-1, and increased proteolytic cleavage of procaspase-3 and poly(ADP)ribose polymerase.
Notably, VX-680 increased Bax/Bcl-2 expression ratio, a favorable proapoptotic predictor for drug response and survival in
AML
.
Lastly, VX-680 enhanced the cytotoxic effect of the chemotherapeutic agent etoposide (VP16) on
AML
cells.
Together, we concluded that Aurora kinases were potentially therapeutic targets
for AML
and that Aur-A-high expression may serve as a differential marker for selective treatment.
[MeSH-major]
Apoptosis / drug effects.
Leukemia
,
Myeloid
,
Acute
/ enzymology.
Leukemia
,
Myeloid
,
Acute
/ pathology. Piperazines / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. bcl-2-Associated X Protein / metabolism
[MeSH-minor]
Adolescent. Adult. Aged. Antineoplastic Agents / pharmacology. Aurora Kinases. Bone Marrow Cells / drug effects. Bone Marrow Cells / enzymology. Bone Marrow Cells / pathology. Caspases / metabolism.
Cell
Division / drug effects.
Cell
Line, Tumor. Child. Drug Screening Assays, Antitumor. Drug Synergism. Enzyme Activation / drug effects. Etoposide / pharmacology. Female. G2 Phase / drug effects. Humans. Male. Middle Aged. Mutation / genetics. fms-Like Tyrosine Kinase 3 / metabolism
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(PMID = 18160664.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Piperazines; 0 / bcl-2-Associated X Protein; 639089-54-6 / VX680; 6PLQ3CP4P3 / Etoposide; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.4.22.- / Caspases
67.
Anagnostopoulos C, Jadwat Y, Wood NH, Meyerov R, Lemmer J, Bouckaert M, Feller L:
A report of oral extramedullary acute myeloid leukaemia (AML) in an 8-year-old girl with newly diagnosed AML-M4Eo.
SADJ
; 2007 Oct;62(9):390, 392-3
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[Title]
A report of oral extramedullary
acute
myeloid
leukaemia
(
AML
) in an 8-year-old girl with newly diagnosed
AML
-M4Eo.
Acute
myeloid
leukaemia
(
AML
), characterized by proliferation of immature neoplastic
myeloid
cells, is uncommon in childhood.
We present a case of an 8-year-old girl with
AML
-M4Eo who had an extramedullary leukaemic tumour in the oral cavity.
[MeSH-major]
Leukemia
, Myelomonocytic,
Acute
/ pathology. Mouth Neoplasms / pathology
[MeSH-minor]
Bone Marrow Neoplasms / pathology. Child.
Diagnosis
, Differential. Eosinophilia / pathology. Fatal Outcome. Female. Humans. Immunophenotyping / methods. Sepsis / drug therapy
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consumer health - Oral Cancer
.
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(PMID = 18260548.001).
[ISSN]
1029-4864
[Journal-full-title]
SADJ : journal of the South African Dental Association = tydskrif van die Suid-Afrikaanse Tandheelkundige Vereniging
[ISO-abbreviation]
SADJ
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
South Africa
68.
Andersen MH, Svane IM, Kvistborg P, Nielsen OJ, Balslev E, Reker S, Becker JC, Straten PT:
Immunogenicity of Bcl-2 in patients with cancer.
Blood
; 2005 Jan 15;105(2):728-34
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B-
cell
lymphoma 2 (Bcl-2) is a pivotal regulator of apoptotic
cell
death and it is overexpressed in many cancers.
Consequently, the Bcl-2 protein is an attractive target for drug design, and Bcl-2-specific antisense oligonucleotides or small-
molecule
Bcl-2 inhibitors have shown broad anticancer activities in preclinical models and are currently in several clinical trials.
The clinical application of immunotherapy against cancer is rapidly moving forward in multiple
areas
, including the adoptive transfer of anti-tumor-reactive T cells and the use of "therapeutic" vaccines.
Herein, we describe spontaneous T-
cell
reactivity against Bcl-2 in peripheral blood from patients suffering from unrelated tumor types (ie, pancreatic cancer, breast cancer,
acute
myeloid leukemia
[
AML
], and chronic
lymphocytic leukemia
[CLL]).
[MeSH-minor]
Acute
Disease
. Breast Neoplasms / immunology. Granzymes. HLA-A2 Antigen / metabolism. Humans.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ immunology.
Leukemia
,
Myeloid
/ immunology. Peptide Fragments / metabolism. Protein Binding. Serine Endopeptidases. T-Lymphocytes, Cytotoxic / immunology. Tumor Cells, Cultured
The Lens.
Cited by Patents in
.
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(PMID = 15367432.001).
[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 / Antigens, Neoplasm; 0 / HLA-A2 Antigen; 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins c-bcl-2; EC 3.4.21.- / GZMB protein, human; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Serine Endopeptidases
69.
Petrovici K, Graf M, Hecht K, Reif S, Pfister K, Schmetzer H:
Use of NG2 (7.1) in AML as a tumor marker and its association with a poor prognosis.
Cancer Genomics Proteomics
; 2010 Jul-Aug;7(4):173-80
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[Title]
Use of NG2 (7.1) in
AML
as a tumor marker and its association with a poor prognosis.
We analyzed 70 bone marrow (BM) samples from
acute
myeloid leukemia
(
AML
) patients for 11q23 aberrations and reactivity with the monoclonal antibody NG2.
We detected NG2(+) cells in
AML
cases with normal karyotype, however,
not
in healthy BM cells.
This means that NG2 qualifies as a reliable
AML
blast tumor marker, enabling monitoring of the course
of AML
independently of, although often associated with, 11q23-aberrations.
While 31% of the patients with NG2(+) cells responded to chemotherapy, 58% of the group with NG2(+) cells did
not
respond (p=0.047).
In conclusion, NG2 detects many, but
not
all 11q23 aberrations and other cases without 11q23 aberrations.
However, it does
not
react with healthy BM cells, thereby contributing to the detection of patients with poor prognosis.
[MeSH-major]
Antigens / analysis. Biomarkers, Tumor / analysis.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Proteoglycans / analysis
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(PMID = 20656983.001).
[ISSN]
1790-6245
[Journal-full-title]
Cancer genomics & proteomics
[ISO-abbreviation]
Cancer Genomics Proteomics
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antigens; 0 / Biomarkers, Tumor; 0 / Proteoglycans; 0 / chondroitin sulfate proteoglycan 4
70.
Hoshino T, Matsushima T, Saitoh Y, Yamane A, Takizawa M, Irisawa H, Saitoh T, Handa H, Tsukamoto N, Karasawa M, Murakami H, Nojima Y:
Sacroiliitis as an initial manifestation of acute myelogenous leukemia.
Int J Hematol
; 2006 Dec;84(5):421-4
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[Title]
Sacroiliitis as an initial manifestation of
acute
myelogenous leukemia
.
We herein report a 28-year-old female patient who presented with sacroiliitis as an initial manifestation of
acute
myelogenous leukemia
(
AML
).
Although she was initially diagnosed with myelodysplastic syndrome (MDS), blasts rapidly increased and
AML
developed 1 month after the
diagnosis of
MDS with Sacroiliitis.
Induction chemotherapy failed to induce a complete remission
of AML
, but it did effectively treat the sacroiliitis.
However, the sacroiliitis relapsed when the
leukemia
cells progressed thereafter.
The close relationship between the occurrence of sacroiliitis and
AML
suggested that autoimmune sacroiliitis was a paraneoplastic phenomenon
of AML
in this patient.
Although autoimmune disorders develop in a substantial number of MDS patients, they are rarely observed in
de
novo
AML
.
No previous report has described sacroiliitis as the initial manifestation
of de
novo
AML
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
. Sacroiliac Joint. Spondylitis, Ankylosing
[MeSH-minor]
Adrenal Cortex Hormones / therapeutic use. Adult. Blast Crisis /
diagnosis
. Blast Crisis / diagnostic imaging. Blast Crisis / therapy. Bone Marrow Transplantation. Fatal Outcome. Female. Humans. Radiography. Recurrence. Transplantation, Homologous
Genetic Alliance.
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.
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[Cites]
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[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Adrenal Cortex Hormones
71.
McGrath P, Suppiah R, Patton MA:
Re-entering life: paediatric acute myeloid leukaemia at one year post treatment.
Aust J Holist Nurs
; 2005 Oct;12(2):23-34
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[Title]
Re
-entering life: paediatric
acute
myeloid
leukaemia
at one year post treatment.
To date, there is scant psychosocial research on the experience of childhood
AML
.
The findings highlight challenges associated with
re
-entering life post-treatment with an emphasis on the ongoing sense of uncertainty, the changed sense of normalcy, and the difficulty of returning to the hospital for check-ups.
A number of recommendations are made including the desirability of providing hospital space for check-ups away from the treatment
area
and the need for ongoing reassurance and support.
[MeSH-major]
Attitude to Health. Holistic Health.
Leukemia
, Myelomonocytic,
Acute
/ psychology. Parent-Child Relations. Parenting / psychology
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(PMID = 19175261.001).
[ISSN]
1322-8803
[Journal-full-title]
The Australian journal of holistic nursing
[ISO-abbreviation]
Aust J Holist Nurs
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Australia
72.
Liu Z, Liu S, Xie Z, Blum W, Perrotti D, Paschka P, Klisovic R, Byrd J, Chan KK, Marcucci G:
Characterization of in vitro and in vivo hypomethylating effects of decitabine in acute myeloid leukemia by a rapid, specific and sensitive LC-MS/MS method.
Nucleic Acids Res
; 2007;35(5):e31
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[Title]
Characterization of in vitro and in vivo hypomethylating effects of decitabine in
acute
myeloid leukemia
by a rapid, specific and sensitive LC-MS/MS method.
DNA hypermethylation is a common
finding
in malignant cells and has been explored as a therapeutic target for hypomethylating agents (e.g., decitabine).
The assay was validated in
a linear
range from 40 fmol to 200 pmol 5mdC.
This method was initially applied for characterization of decitabine-induced GDM changes in in-vitro-treated
leukemia
cells.
The clinical applicability of this method was then demonstrated in bone marrow samples from patients with
acute
myeloid leukemia
treated with decitabine.
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(PMID = 17264127.001).
[ISSN]
1362-4962
[Journal-full-title]
Nucleic acids research
[ISO-abbreviation]
Nucleic Acids Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / CA102031
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Validation Studies
[Publication-country]
England
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 776B62CQ27 / decitabine; B200GV71QM / 5-methyldeoxycytidine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA (cytosine-5-)-methyltransferase 1; G9481N71RO / Deoxyguanosine; M801H13NRU / Azacitidine
[Other-IDs]
NLM/ PMC1865075
73.
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
74.
ZHANG LW, WANG Y, ZHANG CH:
[A case with severity stenosis of left main artery manifested with recurrent syncope].
Zhonghua Xin Xue Guan Bing Za Zhi
; 2010 Sep;38(9):844-5
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[MeSH-major]
Aortic Valve Stenosis /
diagnosis
. Syncope /
diagnosis
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(PMID = 21092658.001).
[ISSN]
0253-3758
[Journal-full-title]
Zhonghua xin xue guan bing za zhi
[ISO-abbreviation]
Zhonghua Xin Xue Guan Bing Za Zhi
[Language]
chi
[Publication-type]
Case Reports; Journal Article
[Publication-country]
China
75.
Glienke W, Chow KU, Bauer N, Bergmann L:
Down-regulation of wt1 expression in leukemia cell lines as part of apoptotic effect in arsenic treatment using two compounds.
Leuk Lymphoma
; 2006 Aug;47(8):1629-38
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[Title]
Down-regulation of wt1 expression in
leukemia cell
lines as part of apoptotic effect in arsenic treatment using two compounds.
Arsenic trioxide (As2O3) induces remission in patients with
acute
promyelocytic
leukemia
(APL).
The Wilms' tumor gene (wt1) is up-regulated in
acute
myeloid leukemia
(
AML
) and a variety
of leukemia cell
lines.
Low concentrations of 0.1 microM arsenic induced expression of the anti-apoptotic bcl-2 gene in both
cell
lines HL-60 and K562.
After arsenic treatment of the
leukemia cell
lines HL-60 and K562 the up-regulation of par-4 may contribute to the induction of apoptosis rather than down-regulation of bcl-2.
[MeSH-major]
Apoptosis / drug effects. Arsenicals / pharmacology. Carrier Proteins / genetics.
Leukemia
/ drug therapy. WT1 Proteins / genetics
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.
Hazardous Substances Data Bank.
ARSENIC TRIOXIDE
.
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(PMID = 16966277.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / Arsenicals; 0 / Arsenites; 0 / Carrier Proteins; 0 / Oxides; 0 / Sodium Compounds; 0 / WT1 Proteins; 0 / WTIP protein, human; 48OVY2OC72 / sodium arsenite; S7V92P67HO / arsenic trioxide
76.
Shen Q, Chen Z, Liu XP, Xing HY, Wang M, Wang JX:
[Expression of PTEN mRNA in acute leukemia and its clinical significance].
Zhonghua Xue Ye Xue Za Zhi
; 2005 Aug;26(8):493-6
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[Title]
[Expression of PTEN mRNA in
acute
leukemia
and its clinical significance].
OBJECTIVE: To explore PTEN gene expression and its clinical significance in
acute
leukemia
.
METHODS: The expression levels of PTEN mRNA in 5
leukemia cell
lines, 87 patients with
acute
leukemias
(AL), including 59
acute
myeloid leukemia
(
AML
), 26
acute
lymphoblastic leukemia
(ALL), and 2
acute
hybrid
leukemia
, 21 AL in complete remission (AL-CR), 31 chronic
myelogenous leukemia
(CML) and 14 normal controls were assayed by RT-PCR.
RESULTS: PTEN mRNA was detected in K562
cell
line, but
not
in Kasumi-1, HL-60, U937, Nalm-6
cell
lines.
The decreased level of PTEN mRNA had a positive correlation with poor-prognostic factors (high white blood
cell
count of > or = 20 x 10(9)/L and chromosome
abnormality
).
[MeSH-major]
Leukemia
/ metabolism. PTEN Phosphohydrolase / metabolism
[MeSH-minor]
Cell
Line, Tumor. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction
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(PMID = 16383243.001).
[ISSN]
0253-2727
[Journal-full-title]
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
[ISO-abbreviation]
Zhonghua Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / RNA, Messenger; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
77.
Rahmani M, Anderson A, Habibi JR, Crabtree TR, Mayo M, Harada H, Ferreira-Gonzalez A, Dent P, Grant S:
The BH3-only protein Bim plays a critical role in leukemia cell death triggered by concomitant inhibition of the PI3K/Akt and MEK/ERK1/2 pathways.
Blood
; 2009 Nov 12;114(20):4507-16
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[Title]
The BH3-only protein Bim plays a critical role in
leukemia cell
death triggered by concomitant inhibition of the PI3K/Akt and MEK/ERK1/2 pathways.
Mechanisms underlying apoptosis induced by concomitant interruption of the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase 1/2 (MEK/ERK1/2) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways were investigated in human
leukemia
cells.
Inhibition of these pathways using the MEK inhibitor PD184352 or U0126 and the PI3K/Akt inhibitor perifosine strikingly induced apoptosis in multiple malignant human hematopoietic cells, and substantially reduced the colony-forming capacity of primary
acute
myeloblastic leukemia
, but
not
normal CD34+ cells.
These events were associated with pronounced Bim up-regulation, Mcl-1 down-regulation, marked Bak/Bax conformational change accompanied by Bax
membrane
translocation, and a pronounced increase in Bax/Bak association.
Notably, knockdown of Bim, but
not
Bad, blocked Bak and Bax conformational change, inhibited Bax
membrane
translocation, diminished Bax/Bak binding, and sharply attenuated perifosine/PD184352-induced apoptosis.
Collectively, these findings suggest that Bim, and Mcl-1, but
not
Bad, integrate death signaling triggered by concomitant disruption of the PI3K/Akt and MEK1/2/ERK1/2 pathways in human
leukemia
cells.
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(PMID = 19773546.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA63753; United States / NCI NIH HHS / CA / R01 CA100866; United States / NCI NIH HHS / CA / R01 CA063753; United States / NCI NIH HHS / CA / P50CA130805; United States / NCI NIH HHS / CA / R01 CA093738; United States / NCI NIH HHS / CA / CA100866; United States / NCI NIH HHS / CA / P50 CA130805; United States / NCI NIH HHS / CA / R01 CA141703; United States / NCI NIH HHS / CA / CA93738; United States / NIDDK NIH HHS / DK / R01 DK052825; United States / NCI NIH HHS / CA / R01 CA150214
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / BAD protein, human; 0 / Bcl-2-like protein 11; 0 / Enzyme Inhibitors; 0 / Membrane Proteins; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-Associated Death Protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases
[Other-IDs]
NLM/ PMC2777129
78.
Vrbanus L, Sucić M, Marković-Glamocak M, Ries S, Gjadrov-Kuvezdić K, Fabijanić I, Antulov J, Petrik J, Labar B:
Apoptosis of leukemic cells: a case report.
Coll Antropol
; 2010 Jun;34(2):705-11
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However, some studies have revealed that Fas (CD95/APO1) which mediates apoptotic signal and decrease of anti-apoptotic Bcl-2 are frequently observed in
acute
myeloid leukemia
(
AML
) M4/M5 leukemic cells.
The aim of the study was to compare cytomorphology and cytochemistry of bone marrow (BM) apoptotic leukemic cells to preserved peripheral blood (PB) leukemic cells in our patient, a 76-year-old man with
AML
-M5b treated at Zagreb University Hospital Center.
BM and PB of the AL patient were analyzed after Pappenheim and cytochemical stainings, and leukemic cells were classified according to FAB and WHO
classification
.
Thus, cytomorphology of PB leukemic cells pointed to proliferation of immature monocytic cells, and cytomorphology of BM to
cell
apoptosis.
Cytochemistry of PB monocytic cells and BM apoptotic cells confirmed monocytic
cell
lineage because esterase was strongly positive in almost all BM apoptotic leukemic cells and PB leukemic cells, and esterase was completely inhibited with sodium fluoride.
On the basis of these findings,
AML
-M5b was diagnosed in our patient.
There are many possible explanations for our observation of BM leukemic
cell
apoptosis in a patient with
AML
-M5.
Mass BM leukemic
cell
apoptosis that was recorded in contrast to numerous preserved leukemic cells in PK could be probably connected to unfavorable ratio of relatively low concentration of cytokines in relation to high leukemic
cell
number in BM aspirated cytologic specimen.
[MeSH-major]
Apoptosis.
Leukemia
,
Myeloid
,
Acute
/ pathology
[MeSH-minor]
Aged. Antigens, CD95 / analysis. Blood Cells / pathology. Bone Marrow / pathology.
Cell
Nucleus / pathology.
Cell
Size. Humans. Male. Megakaryocytes / pathology. Monocytes / pathology
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(PMID = 20698159.001).
[ISSN]
0350-6134
[Journal-full-title]
Collegium antropologicum
[ISO-abbreviation]
Coll Antropol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Croatia
[Chemical-registry-number]
0 / Antigens, CD95
79.
Tang HR, Wang FC, Jiang YW, Fei X, Jiang Q, Xu WL, Lin J:
[CD36 expression in leukemia cells checked with multi-parameter flow cytometry and its significance].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2007 Feb;15(1):29-34
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[Title]
[CD36 expression in
leukemia
cells checked with multi-parameter flow cytometry and its significance].
The aim of study was to investigate the expression of CD36 in
leukemia
cells and to explore its significance in
diagnosis
and differential
diagnosis for leukemia
in patients.
Blood samples from 133 cases
of leukemias
were analyzed by CD45/SSC double parameters and multi-color flow cytometry in order to determine the CD36 and other leukocyte differentiation antigens.
The results show that the CD36 positive rate was 21.8% (29/133) in 133 cases
of leukemia
, 41.9% (26/62) in 62 cases
of AML
(
acute
myeloid leukemia
), and none of the 54 cases
of lymphocytic leukemia
was positive for this antigen.
A significantly negative regression was found between CD36 and CD117 in
AML
(r = -0.751, P = 0.005).
In monocyte lineage involved
leukemia
(MLIL), the positive rate of CD36 (92.6%, 25/27) was significantly higher than that of CD14 (48.1%, 13/27)(P = 0.001).
None of the 7 cases with M(5a) was positive for CD14, but 4 of 5 cases
of M
(5b) were positive.
It is concluded that the combination of CD36 with lymphoid and
myeloid
antigens is helpful to the
diagnosis
and differential
diagnosis of
lymphoid,
myeloid
and MLIL.
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(PMID = 17490515.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
CHI
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD14; 0 / Antigens, CD36; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
80.
Bhagwat N, Levine RL:
Metabolic syndromes and malignant transformation: where the twain shall meet.
Sci Transl Med
; 2010 Oct 20;2(54):54ps50
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Recurrent somatic mutations in the isocitrate dehydrogenase 1 (IDH1) and IDH2 genes that result in the accumulation
of D
-2-hydroxyglutarate (D-2-HG) have been identified in malignant gliomas and in
acute
myeloid leukemia
(
AML
).
A report in the current issue of Science describes a germline IDH2 mutation in a subset of patients with a rare metabolic
disorder
--D-2-hydroxyglutaric aciduria-that is similar to mutations seen in cancer patients.
[MeSH-major]
Cell
Transformation, Neoplastic. Glioma / complications. Glutarates / metabolism.
Leukemia
,
Myeloid
,
Acute
/ complications. Metabolism, Inborn Errors / complications
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(PMID = 20962328.001).
[ISSN]
1946-6242
[Journal-full-title]
Science translational medicine
[ISO-abbreviation]
Sci Transl Med
[Language]
eng
[Grant]
United States / Howard Hughes Medical Institute / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Glutarates; 2889-31-8 / alpha-hydroxyglutarate; EC 1.1.1.41 / Isocitrate Dehydrogenase
81.
Hiramatsu A, Miwa H, Shikami M, Ikai T, Tajima E, Yamamoto H, Imai N, Hattori A, Kyo T, Watarai M, Miura K, Satoh A, Itoh M, Imamura A, Mihara H, Katoh Y, Nitta M:
Disease-specific expression of VEGF and its receptors in AML cells: possible autocrine pathway of VEGF/type1 receptor of VEGF in t(15;17) AML and VEGF/type2 receptor of VEGF in t(8;21) AML.
Leuk Lymphoma
; 2006 Jan;47(1):89-95
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[Title]
Disease
-specific expression of VEGF and its receptors in
AML
cells: possible autocrine pathway of VEGF/type1 receptor of VEGF in t(15;17)
AML
and VEGF/type2 receptor of VEGF in t(8;21)
AML
.
Various angiogenic factors, such as vascular endothelial growth factor (VEGF) and an associated
molecule
, placenta growth factor (PlGF), are thought to be important for normal and malignant hematopoiesis.
This study examined mRNA expression of VEGF, PlGF and receptors for these
molecules
in
AML
cells and identified the
disease
-specific patterns of expression.
AML
M3 having t(15;17)
abnormality
showed highest expression of VEGF and VEGF receptor type 1 (VEGFR1), suggesting the autocrine pathway of VEGF-VEGFR1.
Then, t(8;21)
AML
demonstrated augmented expression of VEGF and VEGF receptor type 2 (VEGFR2), suggesting VEGF-VEGFR2 autocrine pathway.
Then, addition of VEGFR2 kinase inhibitor in Kasumi-1, a t(8;21)
AML cell
line, resulted in marked inhibition
of cell
growth, although growth inhibitory effect of R2 kinase inhibitor to HL-60 was marginal.
In addition,
cell
cycle analysis study showed S-phase
cell
population reduction by R2 kinase inhibitor in Kasumi-1, but
not
in HL-60.
This observation is thought to be the rationale for novel molecular target therapy directed to angiogenic
molecules
.
[MeSH-major]
Autocrine Communication / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Translocation, Genetic / genetics. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor Receptor-1 / genetics. Vascular Endothelial Growth Factor Receptor-2 / genetics
[MeSH-minor]
Adult. Aged.
Cell
Cycle / drug effects.
Cell
Cycle / physiology.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Chromosome Aberrations. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics.
Disease
. Enzyme Inhibitors / pharmacology. Gene Expression Regulation, Leukemic / genetics. HL-60 Cells. Humans. Middle Aged. Pregnancy Proteins / biosynthesis. Pregnancy Proteins / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured
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(PMID = 16465716.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Enzyme Inhibitors; 0 / Pregnancy Proteins; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 144589-93-5 / placenta growth factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
82.
Piloto O, Wright M, Brown P, Kim KT, Levis M, Small D:
Prolonged exposure to FLT3 inhibitors leads to resistance via activation of parallel signaling pathways.
Blood
; 2007 Feb 15;109(4):1643-52
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To study resistance to TKIs targeting FLT3, a receptor tyrosine kinase that is frequently mutated in
acute
myelogenous leukemia
(
AML
), we developed resistant human
cell
lines through prolonged coculture with FLT3 TKIs.
FLT3 TKI-resistant
cell
lines and primary samples still exhibit inhibition of FLT3 phosphorylation on FLT3 TKI treatment.
However, FLT3 TKI-resistant
cell
lines and primary samples often show continued activation of downstream PI3K/Akt and/or Ras/MEK/MAPK signaling pathways as well as continued expression of genes involved in FLT3-mediated cellular transformation.
Mutational screening of FLT3 TKI-resistant
cell
lines revealed activating N-Ras mutations in 2
cell
lines that were
not
present in the parental FLT3 TKI-sensitive
cell
line.
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[Cites]
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(PMID = 17047150.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA090668; United States / NCI NIH HHS / CA / P01 CA070970; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / CA111728; United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA90668; United States / NCI NIH HHS / CA / CA95600-03; United States / NCI NIH HHS / CA / K08 CA095600
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / ras Proteins
[Other-IDs]
NLM/ PMC1794049
83.
Chang PH, Lai YH, Shun SC, Lin LY, Chen ML, Yang Y, Tsai JC, Huang GS, Cheng SY:
Effects of a walking intervention on fatigue-related experiences of hospitalized acute myelogenous leukemia patients undergoing chemotherapy: a randomized controlled trial.
J Pain Symptom Manage
; 2008 May;35(5):524-34
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[Title]
Effects
of a
walking intervention on fatigue-related experiences of hospitalized
acute
myelogenous leukemia
patients undergoing chemotherapy: a randomized controlled trial.
The purpose of this randomized, controlled clinical trial was to preliminarily examine the effects
of a
three-week walking exercise program (WEP) on fatigue-related experiences of
acute
myelogenous leukemia
(
AML
) patients receiving chemotherapy.
Eligible
AML
patients were randomly assigned to either an experimental group (n=11), which received 12 minutes of WEP per day, five days per week for three consecutive weeks, or to a control group (n=11), which received standard ward care.
Data were analyzed by Generalized Estimating Equation and revealed that
AML
patients in the three-week WEP group had a significantly greater increase in 12-minute walking distance than the control group.
Although preliminary, our results strongly suggest that three weeks of systematic walking exercise is clinically feasible
for AML
patients undergoing chemotherapy and can effectively improve their fatigue-related experiences.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / adverse effects. Exercise Therapy. Fatigue / etiology. Fatigue / therapy.
Leukemia
,
Myeloid
,
Acute
/ complications. Walking / physiology
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(PMID = 18280104.001).
[ISSN]
0885-3924
[Journal-full-title]
Journal of pain and symptom management
[ISO-abbreviation]
J Pain Symptom Manage
[Language]
eng
[Publication-type]
Journal Article; Randomized Controlled Trial
[Publication-country]
United States
84.
Forestier E, Izraeli S, Beverloo B, Haas O, Pession A, Michalová K, Stark B, Harrison CJ, Teigler-Schlegel A, Johansson B:
Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study.
Blood
; 2008 Feb 1;111(3):1575-83
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[Title]
Cytogenetic features of
acute
lymphoblastic
and
myeloid leukemias
in pediatric patients with Down syndrome: an iBFM-SG study.
Children with Down syndrome (DS) have a markedly increased risk of
acute
lymphoblastic leukemia
(ALL) and
acute
myeloid leukemia
(
AML
).
To identify chromosomal changes cooperating with +21 that may provide information on the pathogenesis of these
leukemias
, we analyzed 215 DS-ALLs and 189 DS-
AMLs
.
Unlike previous smaller series, a significant proportion of DS-ALLs had the typical B-
cell
precursor ALL abnormalities high hyperdiploidy (HeH; 11%) and t(12;21)(p13;q22) (10%).
The HeH DS-ALLs were characterized by gains of the same chromosomes as
non
-DS-HeH, suggesting the same etiology/pathogenesis.
Unlike DS-ALL, the common translocations associated with
non
-DS-
AML
were rare in DS-
AML
, which instead were characterized by the frequent presence of dup(1q), del(6q), del(7p), dup(7q), +8, +11, del(16q), and +21.
This series of DS
leukemias
-the largest to date-reveals that DS-ALL is a heterogeneous
disorder
that comprises both t(12;21) and HeH as well as DS-related abnormalities.
Furthermore, this analysis confirms that DS-
AML
is a distinct entity, originating through other genetic pathways than do
non
-DS-
AMLs
, and suggests that unbalanced changes such as dup(1q), +8, and +21 are involved in the leukemogenic process.
[MeSH-major]
Down Syndrome / complications. Down Syndrome / genetics.
Leukemia
,
Myeloid
,
Acute
/ complications.
Leukemia
,
Myeloid
,
Acute
/ genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / complications. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics
[MeSH-minor]
Adolescent. Adult. Child. Child, Preschool. Chromosome Aberrations /
classification
. Chromosomes, Human / genetics. Cytogenetics. Female. Genome, Human / genetics. Humans. Infant. Infant, Newborn. Karyotyping. Male
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(PMID = 17971484.001).
[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
85.
Chehensse C, Braun T, Morin AS, Stirnemann J, Agranat P, Boukari L, Aras N, Kiladjian JJ, Ziol M, Fenaux P, Fain O:
[Extramedullary blastic transformation revealed by a prolonged fever during the course of a 5q- syndrome].
Rev Med Interne
; 2009 Oct;30(10):886-9
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[Title]
[Extramedullary blastic transformation revealed by a prolonged fever during the course
of a
5q- syndrome].
INTRODUCTION: Fever during a myelodysplastic syndrome can be due to infectious complications, systemic
disease
or
acute
transformation with clonal evolution.
Neither bone marrow nor blood blasts were detected, but
liver
biopsy demonstrated significant blast infiltration compatible with the
diagnosis of
acute
myeloid
leukaemia
(
AML
).
CONCLUSION: The absence of blasts in blood or bone marrow does
not
exclude the malignant transformation
of a
myelodysplastic syndrome to
AML
.
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.
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.
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(PMID = 19748163.001).
[ISSN]
0248-8663
[Journal-full-title]
La Revue de medecine interne
[ISO-abbreviation]
Rev Med Interne
[Language]
FRE
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
86.
Unal S, Cakir M, Kuşkonmaz B, Cetin M, Tuncer AM:
Successful treatment with gemtuzumab ozogamicin monotherapy in a pediatric patient with resistant relapse of acute myeloid leukemia.
Turk J Pediatr
; 2009 Jan-Feb;51(1):69-71
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[Title]
Successful treatment with gemtuzumab ozogamicin monotherapy in a pediatric patient with resistant relapse of
acute
myeloid leukemia
.
There are few therapeutic options in relapsed or refractory
acute
myeloid leukemia
patients.
Herein, we present a 15-year-old
acute
myeloid leukemia
patient who was resistant at relapse and could achieve remission with gemtuzumab ozogamicin at a total dose of 9 mg/
m2
, divided into three doses and delivered to hematopoietic stem-
cell
transplantation; however, the patient relapsed in a short time without application of transplantation.
[MeSH-major]
Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy
[MeSH-minor]
Adolescent. Antibodies, Monoclonal, Humanized. Antigens, CD / blood. Antigens, Differentiation, Myelomonocytic / blood. Hematopoietic Stem
Cell
Transplantation. Humans. Leukocyte Count. Male. Sialic Acid Binding Ig-like Lectin 3
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(PMID = 19378895.001).
[ISSN]
0041-4301
[Journal-full-title]
The Turkish journal of pediatrics
[ISO-abbreviation]
Turk. J. Pediatr.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Turkey
[Chemical-registry-number]
0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
87.
Walter K, Cockerill PN, Barlow R, Clarke D, Hoogenkamp M, Follows GA, Richards SJ, Cullen MJ, Bonifer C, Tagoh H:
Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5.
Oncogene
; 2010 May 20;29(20):2927-37
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[Title]
Aberrant expression of CD19 in
AML
with t(8;21) involves a poised chromatin structure and PAX5.
Co-expression of lymphoid and
myeloid molecules
is a well-known feature of
acute
myeloblastic leukemia
(
AML
) with t(8;21).
These cells consistently express the B-
cell
-specific transcription factor PAX5, and the B-
cell
-specific
cell
surface protein CD19.
We show that CD19 chromatin exists in a poised configuration in
myeloid
progenitors and that this poised chromatin structure facilitates PAX5-dependent CD19 activation.
Our results also show a positive correlation between PAX5 and CD19 expression in t(8;21)-positive
AML
cells and demonstrate that PAX5 binds to the promoter and enhancer of CD19 gene and remodels chromatin structure at the promoter.
This study shows that expression of PAX5 in leukemic cells has functional consequences and points to an important role
of a
progenitor-specific chromatin configuration in
myeloid leukemia
.
[MeSH-major]
Antigens, CD19 / genetics. B-
Cell
-Specific Activator Protein / genetics. Chromatin / chemistry. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Translocation, Genetic / genetics
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(PMID = 20208555.001).
[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD19; 0 / B-Cell-Specific Activator Protein; 0 / Chromatin; 0 / PAX5 protein, human
88.
Scholl S, Theuer C, Scheble V, Kunert C, Heller A, Mügge LO, Fricke HJ, Höffken K, Wedding U:
Clinical impact of nucleophosmin mutations and Flt3 internal tandem duplications in patients older than 60 yr with acute myeloid leukaemia.
Eur J Haematol
; 2008 Mar;80(3):208-15
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[Title]
Clinical impact of nucleophosmin mutations and Flt3 internal tandem duplications in patients older than 60 yr with
acute
myeloid
leukaemia
.
BACKGROUND: Nucleophosmin (NPM1) and Flt3 internal tandem duplications (Flt3-ITD mutations) represent the most frequent molecular aberrations in patients with
acute
myeloid leukemia
(
AML
).
While NPM1 mutations are associated with favourable prognosis in younger
AML
patients, Flt3-ITD mutations reflect an unfavourable prognostic factor in these patients.
So far, especially NPM1 mutations have
not
yet been evaluated exclusively in older patients.
PATIENTS AND METHODS: We retrospectively analysed the prevalence of NPM1 and Flt3-ITD mutations and its association with complete remission (CR), and survival in 99 elderly patients (median age 71 yr, range 60-85 yr) newly diagnosed
for AML
.
Interestingly, there is no significant difference in overall survival between group 1 and group 2 (
Log
-rank test P = 0.22, median 440 d vs. 1125 d).
In contrast, patients carrying a Flt3-ITD mutation had a significant worse overall survival compared to wildtype patients (P = 0.03, median 210
d for
group 3 + 4 vs. 634
d for
group 1 + 2) while no difference of CR rate could be observed (42.8% vs. 48.9%, P = 0.91).
CONCLUSION: As elderly but medically fit patients with
AML
carrying a NPM1 mutation have a high CR rate, age itself should
not
be a barrier for induction treatment.
However, new therapeutic concepts of postremission therapy (e.g. allogeneic stem
cell
transplantation after dose-reduced conditioning) should be considered for these patients in first CR.
[MeSH-major]
Gene Duplication.
Leukemia
,
Myeloid
,
Acute
/ genetics. Nuclear Proteins / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
[MeSH-minor]
Aged. Aged, 80 and over. Cohort Studies.
Disease
-Free Survival. Female. Gene Frequency. Humans. Male. Middle Aged. Prognosis. Remission Induction. Retrospective Studies
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(PMID = 18081718.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
89.
Di Cataldo A, La Spina M, Bertuna G, Lo Nigro L, Branciforte F, Castagnola E:
Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with acute non-lymphoblastic leukemia.
Pediatr Blood Cancer
; 2006 Feb;46(2):266
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[Title]
Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with
acute
non
-
lymphoblastic leukemia
.
[MeSH-major]
Acinetobacter Infections / drug therapy. Acinetobacter calcoaceticus. Anti-Infective Agents / administration & dosage. Ciprofloxacin / administration & dosage.
Leukemia
,
Myeloid
,
Acute
/ complications
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.
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(PMID = 16078222.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Infective Agents; 5E8K9I0O4U / Ciprofloxacin
90.
Ishikawa T, Kakumu S:
Combination therapy with lamivudine and HB vaccine on chronic hepatitis B.
Hepatol Res
; 2007 Jul;37(s1):S62-6
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BACKGROUND AND AIM: Lamivudine (
LAM
) has problems of breakthrough hepatitis (BTH) and post-treatment relapse despite its significant effect for suppressing hepatitis B virus (HBV) replication.
In order to find solutions for the problems, the efficacy of combination therapy
of LAM
plus hepatitis B (HB) vaccine in patients with chronic HBV infection was assessed.
PATIENTS AND METHODS: Fifty-three patients with chronic hepatitis B, 33 hepatitis B e-antigen positive (HBeAg+), and 20 HBeAg negative (HBeAg-) patients, were enrolled in the study, and randomized to receive either
LAM
monotherapy or combination therapy
of LAM
and HB vaccine.
In the combination therapy group, 100 mg/day
of LAM
was administered as a baseline therapy, and 10 mug of HB vaccine was injected subcutaneously every month starting at 2 months after
LAM
administration, six times in total.
RESULTS: HBeAg negative patients responded well to
LAM
therapy, and there were no significant differences in short-term effects between the two therapy groups.
Regardless of HBeAg serologic status or therapy protocols, post-treatment relapse was seen in most patients when the administrations
of LAM
were discontinued.
CONCLUSION: Combination therapy
of LAM
and HB vaccine is a safe and effective way to control HBV replication and prevent the development of BTH especially in patients with high viral load.
However, further study is required in order to achieve the continuous suppression of HBV replication even after cessation
of LAM
.
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(PMID = 17627638.001).
[ISSN]
1386-6346
[Journal-full-title]
Hepatology research : the official journal of the Japan Society of Hepatology
[ISO-abbreviation]
Hepatol. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
91.
Seyama K, Kumasaka T, Souma S, Sato T, Kurihara M, Mitani K, Tominaga S, Fukuchi Y:
Vascular endothelial growth factor-D is increased in serum of patients with lymphangioleiomyomatosis.
Lymphat Res Biol
; 2006;4(3):143-52
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BACKGROUND: Lymphangioleiomyomatosis (
LAM
) is a rare destructive lung
disease
characterized by an abnormal proliferation of smooth muscle-like cells (
LAM
cells) in the lung and along the axial lymphatics.
LAM
demonstrates a heterogeneous clinical course, but there is no serum surrogate marker available for assessing the
disease
severity or predicting the
disease
progression.
Since the authors have recently demonstrated the extensive
LAM
-associated lymphangiogenesis and its potential role in progression and metastasis
of LAM
cells, they hypothesized that serum levels of lymphangiogenic growth factors might be increased in
LAM
and become a surrogate marker
for disease
severity.
METHODS AND RESULTS: VEGF-A, VEGF-C, and VEGF-D in serum of 44 patients with
LAM
were measured by enzyme-linked immunosorbant assay.
Only VEGF-D was significantly increased in
LAM
patients as compared with age- and gender-matched healthy volunteers (n=24) (
LAM
vs. control, geometric mean 95% CI; 1069.3 pg/mL (809.4 approximately 1412.6) vs. 295.9 pg/mL (262.6 approximately 333.5), p<0.0001).
Immunohistochemical examination of lung specimens demonstrated the positive immunoreactivity
of LAM
cells for VEGF-D.
CONCLUSION: Serum VEGF-D levels may be a valuable surrogate marker for evaluating the
disease
severity in
LAM
.
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(PMID = 17034294.001).
[ISSN]
1539-6851
[Journal-full-title]
Lymphatic research and biology
[ISO-abbreviation]
Lymphat Res Biol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Hormones; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 0 / Vascular Endothelial Growth Factor D
92.
Tan L, Xu B, Liu R, Liu H, Tan H, Huang W:
Gene therapy for acute myeloid leukemia using Sindbis vectors expressing a fusogenic membrane glycoprotein.
Cancer Biol Ther
; 2010 Mar 1;9(5):350-7
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[Title]
Gene therapy for
acute
myeloid leukemia
using Sindbis vectors expressing a fusogenic
membrane
glycoprotein.
AML
has a dismal prognosis.
It was previously shown that the expression of gene coding for the hyperfusogenic gibbon ape
leukemia
virus envelope glycoprotein (GALV.fus) can efficiently kill leukemic cells.
However, target killing effect of GALV.fus on
leukemia
cells may be limited.
Viral vectors, such as retroviruses and adenoviruses, have been developed to deliver heterologous genes into tumors in vivo, but these vectors have some limitations for gene therapy
of leukemia
.
We found that Laminin-R was obviously expressed in HL-60 and primary human
AML
cells, but weakly expressed in K562 cells and blood samples of normal human.
So we reasoned that Sindbis-virus-based vectors might be ideal for target gene transfer of GALV.fus to
acute
myeloid
leukemic
cell
.
It was shown that Sindbis virus efficiently transduced human
acute
myeloid
leukemic cells with high expression of Laminin-R and exhibited potent cytopathic potential.
What is more, we found that CFU-GMs were significantly reduced after Sindbis virus carrying GALV.fus transduced human primary
AML
cells.
Sindbis virus carrying GALV.fus was active against human
AML
xenografts in vivo.
Taken together, we concluded that Sindbis virus carrying GALV.fus may be an useful strategy for gene therapy of
acute
myeloid leukemia
.
[MeSH-minor]
Adenoviridae / genetics. Granulocyte-Macrophage Progenitor Cells. Humans.
Leukemia
Virus, Gibbon Ape / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ therapy.
Membrane
Glycoproteins / genetics
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[CommentIn]
Cancer Biol Ther. 2010 Mar 1;9(5):358-61
[
20104027.001
]
(PMID = 20061812.001).
[ISSN]
1555-8576
[Journal-full-title]
Cancer biology & therapy
[ISO-abbreviation]
Cancer Biol. Ther.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Membrane Glycoproteins
93.
Rheingold SR:
Acute myeloid leukemia in a child with hereditary thrombocytopenia.
Pediatr Blood Cancer
; 2007 Jan;48(1):105-7
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[Title]
Acute
myeloid leukemia
in a child with hereditary thrombocytopenia.
A child with a known
diagnosis of
an autosomal dominant macrothrombocytopenia, Fechtner Syndrome, developed
acute
myeloid leukemia
(
AML
).
Recently the
disease
gene for the inherited macrothrombocytopenias has been identified as MYH9, encoding
for non
-muscle myosin heavy chain-A.
MYH9 has never been associated with the development of
acute
leukemia
, but MYH11 is disrupted in the M4 eosinophilia sub-type
of AML
(inv16).
The patients leukemic blasts did carry the common t(8;21) which yields an AML1-ETO fusion protein that inhibits
AML
-1.
[MeSH-major]
Blood Coagulation Disorders, Inherited / genetics. Chromosome Disorders / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Thrombocytopenia / genetics
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[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 16276527.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MYH9 protein, human; 0 / Molecular Motor Proteins; 0 / Oncogene Proteins, Fusion; EC 3.6.4.1 / Myosin Heavy Chains
94.
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
95.
Abdel Alim A, Youssef SR, Farouk HM:
The prognostic potential of bone marrow cyclin E and P27, in Egyptian patients with acute myeloid leukemia.
Egypt J Immunol
; 2010;17(1):9-18
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[Title]
The prognostic potential of bone marrow cyclin E and P27, in Egyptian patients with
acute
myeloid leukemia
.
Aberrations in the
cell
cycle control are often observed in tumors and might even be mandatory in tumor development.
There are few molecular biologic determinants that may be prognostic for patients with
acute
myeloid leukemia
(
AML
).
To investigate the importance
of cell
cycle defects in
AML
, the cellular levels of cyclin E and the cyclin-dependent kinase inhibitor P27 (Kip 1) were evaluated in thirty
AML
patients (11 males and 19 females) diagnosed by standard clinical, morphological and immunophenotypic criteria and staged according to the FAB
classification
.
Using immunoblot analysis, cyclin E and P27 were detected in blast cells
of AML
patients who were then treated by the standard
AML
chemotherapeutic protocol and were followed up.
With respect to cyclin E, it was detected in 9/30(30%)
AML
cases among them 13.3% (4/30 cases) exhibited very strong bands while 16.6% (5/30 cases) showed faint bands.
Cyclin E was high among M4/M5 cases and low among M3 cases and showed a statistically significant positive correlation with percentage of blast cells, aberrant phenotype and abnormal karyotype at
diagnosis
.
All our
AML
cases exhibited P27 at low and high levels as seen in 19/30 (63.4%) and 11/30 (36.6%) cases, respectively.
P27 showed a statistically significant negative correlation to the percentage of blasts at
diagnosis
and a significant positive correlation with achievement of CR.
The present study suggested that levels
of cell
cycle regulators cyclin E and P27 can be used as a useful prognostic molecular markers in
AML
patients.
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(PMID = 22053605.001).
[ISSN]
1110-4902
[Journal-full-title]
The Egyptian journal of immunology
[ISO-abbreviation]
Egypt J Immunol
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
Egypt
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cyclin E; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
96.
Rytting M, Ravandi F, Estey E, Cortes J, Faderl S, Garcia-Manero G, Jeha S, Ouzounian S, Pierce S, Kantarjian H:
Intensively timed combination chemotherapy for the induction of adult patients with acute myeloid leukemia: long-term follow-up of a phase 2 study.
Cancer
; 2010 Nov 15;116(22):5272-8
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[Title]
Intensively timed combination chemotherapy for the induction of adult patients with
acute
myeloid leukemia
: long-term follow-up
of a
phase 2 study.
BACKGROUND: Despite advances in therapy, the majority of adult patients diagnosed with
acute
myeloid leukemia
(
AML
) develop
disease
recurrence and die of their
disease
.
Early intensification of treatment
for AML
using timed sequential therapy (TST) has been proposed as a means of improving the survival outcome in children.
The Children's Cancer Group demonstrated that children with
AML
who were randomized to receive 2 courses of daunorubicin, cytarabine, thioguanine, etoposide, and dexamethasone (the DCTER regimen) given 10 days apart had an improved event-free survival (EFS) and
disease
-free survival (DFS) (42% ± 7% and 55% ± 9%, respectively, at 2 years).
Reports have suggested an improved outcome in adult patients with
AML
using TST (at the cost of increased toxicity).
The current study was conducted to evaluate the feasibility and effectiveness of the intensively timed DCTER regimen
for non
-core-binding factor
AML
in adult patients aged <50 years.
The timed sequential DCTER regimen had a lower complete remission (CR) rate when compared with the IA combination,, (71% vs 80%, respectively), but this appeared to be counterbalanced by a higher long-term
leukemia
-free survival rate using the intensified regimen (48% vs 30%, respectively) in patients who achieved a CR (P = .06).
CONCLUSIONS: The intensively timed regimen of DCTER was found to induce durable remissions in adult patients with
AML
, including those patients with high-risk
disease
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / administration & dosage.
Leukemia
,
Myeloid
,
Acute
/ drug therapy
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.
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.
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author profiles
.
Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
THIOGUANINE
.
Hazardous Substances Data Bank.
DAUNORUBICIN
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
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[Copyright]
Copyright © 2010 American Cancer Society.
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Blood. 1989 Jan;73(1):24-30
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Cancer. 2006 Jul 1;107(1):116-24
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16721819.001
]
(PMID = 20665501.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Clinical Trial, Phase II; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin; DCTER protocol
97.
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
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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
98.
Fischbach NA, Rozenfeld S, Shen W, Fong S, Chrobak D, Ginzinger D, Kogan SC, Radhakrishnan A, Le Beau MM, Largman C, Lawrence HJ:
HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo.
Blood
; 2005 Feb 15;105(4):1456-66
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[Title]
HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem
cell
expansion and
acute
myeloid leukemia
in vivo.
Dysregulated HOX gene expression profoundly effects the proliferation and differentiation of hematopoietic stem cells (HSCs) and committed progenitors, and aberrant activation of HOX genes is a common event in human
myeloid leukemia
.
HOXB6 is frequently overexpressed in human
acute
myeloid leukemia
(
AML
).
We also explored structure-function relationships using mutant HOXB6 proteins unable to bind to DNA or a key HOX-binding partner, pre-B-
cell leukemia
transcription factor-1 (PBX1).
Additionally, we investigated the potential cooperative interaction with
myeloid
ecotropic viral integration site 1 homolog (MEIS1).
In vivo, HOXB6 expanded HSCs and
myeloid
precursors while inhibiting erythropoiesis and lymphopoiesis.
Overexpression of HOXB6 resulted in
AML
with a median latency of 223 days.
Coexpression of MEIS1 dramatically shortened the onset
of AML
.
Cytogenetic analysis
of a
subset of HOXB6-induced
AMLs
revealed recurrent deletions of chromosome bands 2D-E4, a region frequently deleted in HOXA9-induced
AMLs
.
In vitro, HOXB6 immortalized a factor-dependent myelomonocytic precursor capable
of granulocytic
and monocytic differentiation.
[MeSH-major]
Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology.
Cell
Transformation, Neoplastic / pathology. Homeodomain Proteins / biosynthesis. Homeodomain Proteins / genetics.
Leukemia
,
Myeloid
/ blood.
Myeloid
Progenitor Cells / metabolism.
Myeloid
Progenitor Cells / pathology
[MeSH-minor]
Acute
Disease
. Animals.
Cell
Differentiation / genetics.
Cell
Line, Transformed.
Cell
Proliferation. Erythropoiesis / genetics. Female. Karyotyping. Lymphopoiesis / genetics. Mice. Mice, Congenic. Mice, Inbred C57BL. Neoplasm Proteins / physiology. Phenotype. Time Factors
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PMID 15522959 (Special Collections)
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(PMID = 15522959.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / DK48642
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / Hoxb6 protein, mouse; 0 / Neoplasm Proteins; 0 / myeloid ecotropic viral integration site 1 protein
99.
Ferrara F, D'Arco AM, De Simone M, Mele G, Califano C, Pocali B, Danise P, Palmieri S:
Fludarabine and cytarabine as continuous sequential infusion for elderly patients with acute myeloid leukemia.
Haematologica
; 2005 Jun;90(6):776-84
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[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Fludarabine and cytarabine as continuous sequential infusion for elderly patients with
acute
myeloid leukemia
.
BACKGROUND AND OBJECTIVES: A phase II study was conducted to investigate the effects
of a
therapeutic program based on the combination of fludarabine and cytarabine (ARA-C) administered as a sequential continuous infusion in untreated elderly patients with
acute
myeloid leukemia
(
AML
).
DESIGN AND METHODS: Sixty-three patients with
non
-M3
AML
, median age 69 years (range 61-81), were accrued.
Twenty-four patients (38%) had
AML
secondary to myelodysplastic syndrome.
Patients achieving complete remission (CR) were intended to receive an additional course, followed by autologous stem
cell
transplantation (ASCT).
The median overall and
disease
-free survival were both 10 months.
Results in terms of CR achievement, CD34+
cell
collection and ASCT feasibility.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Vidarabine / analogs & derivatives
[MeSH-minor]
Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis.
Disease
-Free Survival. Female. Humans. Male. Middle Aged. Myelodysplastic Syndromes / complications. Stem
Cell
Transplantation. Treatment Outcome
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
FLUDARABINE
.
Hazardous Substances Data Bank.
VIDARABINE
.
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