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1
acute myeloid leukemia with multilineage dysplasia following myelodysplastic syndrome 2005:2010[pubdate] *count=100
353 results
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Items 1 to 100 of about 353
1.
Quintás-Cardama A, Cortes J:
Omacetaxine mepesuccinate--a semisynthetic formulation of the natural antitumoral alkaloid homoharringtonine, for chronic myelocytic leukemia and other myeloid malignancies.
IDrugs
; 2008 May;11(5):356-72
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[Title]
Omacetaxine mepesuccinate--a semisynthetic formulation of the natural antitumoral alkaloid homoharringtonine, for chronic myelocytic
leukemia
and other
myeloid
malignancies.
ChemGenex Pharmaceuticals Ltd, in collaboration with Stragen Group, is developing omacetaxine mepesuccinate, a semisynthetic formulation of HHT, as a potential treatment for chronic myelocytic
leukemia
(CML),
myelodysplastic syndrome
(
MDS
) and
acute
myelogenous
leukemia
(
AML
).
In preclinical studies, omacetaxine mepesuccinate induced apoptosis in
leukemia
cell lines.
Phase I and II clinical trials for omacetaxine mepesuccinate in the treatment of
AML
and
MDS
are also ongoing; intravenous, subcutaneous and oral formulations of the drug are being developed.
[MeSH-major]
Antineoplastic Agents, Phytogenic / therapeutic use. Harringtonines / therapeutic use.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / drug therapy.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
, Promyelocytic,
Acute
/ drug therapy.
Myelodysplastic
Syndromes / drug therapy
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(PMID = 18465678.001).
[ISSN]
1369-7056
[Journal-full-title]
IDrugs : the investigational drugs journal
[ISO-abbreviation]
IDrugs
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; 0 / Harringtonines; 6FG8041S5B / homoharringtonine
2.
Klymenko S, Trott K, Atkinson M, Bink K, Bebeshko V, Bazyka D, Dmytrenko I, Abramenko I, Bilous N, Misurin A, Zitzelsberger H, Rosemann M:
Aml1 gene rearrangements and mutations in radiation-associated acute myeloid leukemia and myelodysplastic syndromes.
J Radiat Res
; 2005 Jun;46(2):249-55
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[Title]
Aml1 gene rearrangements and mutations in radiation-associated
acute myeloid leukemia
and
myelodysplastic
syndromes.
Several studies suggested a causal link between AML1 gene rearrangements and both radiation-induced
acute myeloid
leukaemia (
AML
) and
myelodysplastic
syndromes (
MDS
).
Fifty-three
AML
samples were analyzed for the presence of AML1 abnormalities using fluorescent in-situ hybridization (FISH) and reverse transcription polymerase chain reaction (RT-PCR).
Of these patients, 24 had experienced radiation exposure due to the Chernobyl accident, and 29 were non-irradiated spontaneous
AML
cases and served as controls.
AML1/ETO translocations were found in 9 of 29 spontaneous
AML
but only in 1 of 24 radiation-associated
AML
cases.
Following
age stratification, the difference becomes less pronounced but remains on borderline significance (p=0.053).
AML1 mutation status was assessed in 5 clean-up workers at Chernobyl NPP with
MDS
, or
AML
following
MDS
, by direct sequencing of genomic DNA from the coding region (exon 3 through 8).
In one patient who developed
MDS
following
an
acute
radiation
syndrome
, a hexanucleotide duplication of CGGCAT in exon 8 was found, inserted after base position 1502.
Our results suggest that AML1 gene translocations are infrequent in radiation-induced leukemogenesis but are consistent with the idea that radiation may contribute to the development of
MDS
through AML1 gene mutation.
[MeSH-major]
Chernobyl Nuclear Accident. DNA-Binding Proteins / genetics.
Leukemia
,
Myeloid
,
Acute
/ epidemiology.
Leukemia
,
Myeloid
,
Acute
/ metabolism.
Myelodysplastic
Syndromes / epidemiology.
Myelodysplastic
Syndromes / metabolism. Neoplasms, Radiation-Induced / epidemiology. Neoplasms, Radiation-Induced / metabolism. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics
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(PMID = 15988144.001).
[ISSN]
0449-3060
[Journal-full-title]
Journal of radiation research
[ISO-abbreviation]
J. Radiat. Res.
[Language]
eng
[Publication-type]
Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Transcription Factors
3.
Tanaka-Harada Y, Kawakami M, Oka Y, Tsuboi A, Katagiri T, Elisseeva OA, Nishida S, Shirakata T, Hosen N, Fujiki F, Murao A, Nakajima H, Oji Y, Kanda Y, Kawase I, Sugiyama H:
Biased usage of BV gene families of T-cell receptors of WT1 (Wilms' tumor gene)-specific CD8+ T cells in patients with myeloid malignancies.
Cancer Sci
; 2010 Mar;101(3):594-600
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[Title]
Biased usage of BV gene families of T-cell receptors of WT1 (Wilms' tumor gene)-specific CD8+ T cells in patients
with myeloid
malignancies.
WT1 (Wilms' tumor gene 1) protein is a potent pan-tumor-associated antigen (TAA) and WT1-specific cytotoxic T lymphocytes (WT1 tetramer(+) CD8(+) T cells) are spontaneously induced in patients
with acute myeloid leukemia
(
AML
) or
myelodysplastic syndrome
(
MDS
).
We conducted a single-cell level comparative analysis of T-cell receptor beta-chain variable region (TCR-BV) gene families of a total of 1242 spontaneously induced WT1 tetramer(+) CD8(+) T cells in HLA-A*2402(+) patients with
AML
or
MDS
and those in healthy donors (HDs).
(ii) that BV4 was commonly biased in HDs and
MDS
patients;.
(iii) that BV19 was commonly biased in the patients; and (iv) that BVs 7 and 28, BVs 9 and 15, and BVs 12 and 29 were specifically biased in HDs,
AML
, and
MDS
patients, respectively.
However, statistical analysis of similarity among HD,
AML
, and
MDS
of individual usage frequencies of 24 kinds of TCR-BV gene families indicated that the usage frequencies of TCR-BV gene families in
AML
and
MDS
patients reflect those in HDs.
[MeSH-major]
CD8-Positive T-Lymphocytes / immunology. Genes, T-Cell Receptor beta.
Leukemia
,
Myeloid
,
Acute
/ immunology.
Myelodysplastic
Syndromes / immunology. WT1 Proteins / immunology
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(PMID = 20132220.001).
[ISSN]
1349-7006
[Journal-full-title]
Cancer science
[ISO-abbreviation]
Cancer Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / CCR7 protein, human; 0 / Receptors, CCR7; 0 / WT1 Proteins; EC 3.1.3.48 / Antigens, CD45
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4.
Watanabe-Okochi N, Oki T, Komeno Y, Kato N, Yuji K, Ono R, Harada Y, Harada H, Hayashi Y, Nakajima H, Nosaka T, Kitaura J, Kitamura T:
Possible involvement of RasGRP4 in leukemogenesis.
Int J Hematol
; 2009 May;89(4):470-81
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To understand the molecular mechanism of leukemogenesis, particularly progression of
myelodysplastic syndrome
(
MDS
) to
acute leukemia
, we made cDNA libraries from the samples of patients and screened them by expression-cloning to detect class I mutations that render HF6 cells factor-independent.
We identified RasGRP4, an activator of Ras, as a candidate for class I mutation from three of six patients (
MDS
/MPD = 1,
MDS
-RA = 1,
MDS
/
AML
= 2, CMMoL/
AML
= 1 and
AML
-M2 = 1).
C57BL/6J mice transplanted with RasGRP4-transduced primary bone marrow cells died of T cell
leukemia
,
myeloid leukemia
, or
myeloid leukemia
with T cell
leukemia
.
The double transduction led to early onset of T cell
leukemia
but not of
AML
in the transplanted mice when compared to transduction of RasGRP4 alone.
[MeSH-major]
Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology.
Leukemia
/ metabolism.
Leukemia
/ pathology. ras Guanine Nucleotide Exchange Factors / metabolism
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18192504.001
]
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[
11369655.001
]
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Proc Natl Acad Sci U S A. 2005 Jan 25;102(4):1104-9
[
15650049.001
]
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Leukemia. 2002 Nov;16(11):2185-9
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12399960.001
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Leukemia. 2005 Oct;19(10 ):1794-805
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Curr Opin Hematol. 2002 Jul;9(4):274-81
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Blood. 2006 Sep 1;108(5):1708-15
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Leukemia. 2005 Dec;19(12):2232-40
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Blood. 2004 Mar 15;103(6):2316-24
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[
11781838.001
]
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Genes Chromosomes Cancer. 2004 Feb;39(2):110-8
[
14695990.001
]
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Leukemia. 2005 Jul;19(7):1153-60
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[
11956218.001
]
[Cites]
J Clin Invest. 2005 Aug;115(8):2159-68
[
16025155.001
]
(PMID = 19350351.001).
[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / RASGRP4 protein, human; 0 / Rasgrp4 protein, mouse; 0 / ras Guanine Nucleotide Exchange Factors
5.
Fabre C, Grosjean J, Tailler M, Boehrer S, Adès L, Perfettini JL, de Botton S, Fenaux P, Kroemer G:
A novel effect of DNA methyltransferase and histone deacetylase inhibitors: NFkappaB inhibition in malignant myeloblasts.
Cell Cycle
; 2008 Jul 15;7(14):2139-45
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Malignant myeloblasts
arising
in high-risk
myelodysplastic syndrome
(
MDS
) and
acute myeloid leukemia
(
AML
) are characterized by the constitutive activation of the anti-apoptotic transcription factor NFkappaB.
We found that DNA methyltransferase (DNMT) inhibitors (such as azacytidine and 5-aza-2'-deoxycytidine) and histone deacetylase (HDAC) inhibitors (such as trichostatin and valproic acid) efficiently induced apoptosis in the P39
MDS
/
AML
cell line, correlating with an inhibition of NFkappaB (which translocated from the nucleus to the cytoplasm).
Finally, circulating myeloblasts
from AML
patients treated with the DNMT inhibitor 5-aza-2'-deoxycytidine manifested a rapid (2 hours post-treatment) inhibition of NFkappaB and IKKalpha/beta.
[MeSH-minor]
Azacitidine / pharmacology. Cell Line, Tumor. Female. Humans. Hydroxamic Acids / pharmacology. I-kappa B Kinase / metabolism.
Leukemia
,
Myeloid
,
Acute
/ metabolism.
Leukemia
,
Myeloid
,
Acute
/ pathology. Male. Middle Aged. Valproic Acid / pharmacology
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(PMID = 18641459.001).
[ISSN]
1551-4005
[Journal-full-title]
Cell cycle (Georgetown, Tex.)
[ISO-abbreviation]
Cell Cycle
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / NF-kappa B; 3X2S926L3Z / trichostatin A; 614OI1Z5WI / Valproic Acid; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.7.11.10 / I-kappa B Kinase; M801H13NRU / Azacitidine
6.
Cataldo VD, Cortes J, Quintás-Cardama A:
Azacitidine for the treatment of myelodysplastic syndrome.
Expert Rev Anticancer Ther
; 2009 Jul;9(7):875-84
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[Title]
Azacitidine for the treatment of
myelodysplastic syndrome
.
The
myelodysplastic
syndromes (
MDS
) encompass a heterogeneous group of malignant hematologic disorders characterized by ineffective hematopoiesis, peripheral cytopenias, frequent karyotypic abnormalities and significant risk for transformation to
acute myeloid leukemia
(
AML
).
The prognosis of patients with intermediate- or high-risk
MDS
is very poor.
Neither autologous stem cell transplantation (SCT) nor chemotherapeutic regimens have been shown to prolong survival in patients with
MDS
.
Allogeneic SCT, while potentially curative, is only available to a selected group of patients and is associated with high morbidity and mortality in elderly patients, which constitute the majority of patients with
MDS
.
Hypermethylation of tumor-suppressor genes has been invoked as an important pathogenetic mechanism in
MDS
.
The pyrimidine nucleoside analog azacitidine, which inhibits DNA methyltransferases, has recently become the first therapeutic to prolong survival in patients with
MDS
, thus changing the natural history of these malignancies.
The activity of azacitidine in
MDS
has spurred the development of combinations of this agent with other epigenetic modifiers for the treatment of
MDS
and
AML
.
[MeSH-major]
Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use.
Myelodysplastic
Syndromes / drug therapy
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.
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.
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(PMID = 19589026.001).
[ISSN]
1744-8328
[Journal-full-title]
Expert review of anticancer therapy
[ISO-abbreviation]
Expert Rev Anticancer Ther
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; M801H13NRU / Azacitidine
[Number-of-references]
55
7.
Bruserud Ø, Reikvam H:
Therapeutic targeting of NF-κB in myelodysplastic syndromes and acute myeloid leukaemia - the biological heterogeneity.
Expert Opin Ther Targets
; 2010 Nov;14(11):1139-42
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[Title]
Therapeutic targeting of NF-κB in
myelodysplastic
syndromes and
acute myeloid
leukaemia - the biological heterogeneity.
This is also true for the malignant cells in
acute myeloid
leukaemia (
AML
) and
myelodysplastic
syndromes (
MDS
), including the malignant stem cells.
However, both
AML
and
MDS
patients are heterogeneous with regard to the effect of pharmacological NF-κB inhibition, and the final effect will probably also depend on the pharmacological agent used for the inhibition, e.g. proteasomal inhibitiors versus specific inhibitors.
[MeSH-major]
Antineoplastic Agents / pharmacology. Drug Design.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Myelodysplastic
Syndromes / drug therapy. NF-kappa B / antagonists & inhibitors
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[CommentOn]
Expert Opin Ther Targets. 2010 Nov;14(11):1157-76
[
20858024.001
]
(PMID = 20942744.001).
[ISSN]
1744-7631
[Journal-full-title]
Expert opinion on therapeutic targets
[ISO-abbreviation]
Expert Opin. Ther. Targets
[Language]
eng
[Publication-type]
Comment; Editorial
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Protease Inhibitors
8.
Hake CR, Graubert TA, Fenske TS:
Does autologous transplantation directly increase the risk of secondary leukemia in lymphoma patients?
Bone Marrow Transplant
; 2007 Jan;39(2):59-70
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[Title]
Does autologous transplantation directly increase the risk of secondary
leukemia
in lymphoma patients?
Patients who undergo autologous stem cell transplantation (ASCT) for lymphoma have a significant risk of therapy-related
acute myeloid leukemia
and myelodysplasia (t-
AML
/
MDS
).
Compared to that seen in other indications such as breast cancer, multiple myeloma or germ cell tumors, there is a substantially increased risk for t-
AML
/
MDS
following
ASCT for lymphoma.
In many of the larger series to date, it has not been possible to directly implicate autologous transplantation itself as a risk factor for t-
AML
/
MDS
.
Although pre-transplant therapy is certainly an important factor in the development of t-
AML
/
MDS
, specific components of the autologous transplantation procedure itself may also contribute to the risk of t-
AML
/
MDS
.
Specifically, priming chemotherapy, total body irradiation, and the extensive cellular proliferation which occurs during engraftment may all play a role in the development of t-
AML
/
MDS
.
Furthermore, there is an increasing body of evidence that certain inherited polymorphisms in genes governing drug metabolism, DNA repair and leukemogenesis may influence susceptibility to t-
AML
/
MDS
.
In this paper, we review the evidence implicating the above risk factors for t-
AML
/
MDS
, present a potential mechanism for t-
AML
/
MDS
and propose interventions to reduce the rate of t-
AML
/
MDS
in lymphoma patients.
[MeSH-major]
Bone Marrow Transplantation / adverse effects.
Leukemia
,
Myeloid
/ etiology. Lymphoma / surgery. Transplantation, Autologous / adverse effects
[MeSH-minor]
Humans. Incidence.
Myelodysplastic
Syndromes / epidemiology.
Myelodysplastic
Syndromes / etiology
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(PMID = 17143301.001).
[ISSN]
0268-3369
[Journal-full-title]
Bone marrow transplantation
[ISO-abbreviation]
Bone Marrow Transplant.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P01 CA101937
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
98
9.
Asou H, Matsui H, Ozaki Y, Nagamachi A, Nakamura M, Aki D, Inaba T:
Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome.
Biochem Biophys Res Commun
; 2009 May 29;383(2):245-51
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[Title]
Identification of a common microdeletion cluster in 7q21.3 subband among patients
with myeloid leukemia
and
myelodysplastic syndrome
.
Monosomy 7 and interstitial deletions in the long arm of chromosome 7 (-7/7q-) is a common nonrandom chromosomal abnormality found frequently in
myeloid
disorders including
acute myeloid leukemia
(
AML
),
myelodysplastic syndrome
(
MDS
), and juvenile myelomonocytic
leukemia
(JMML).
Gene copy number assessment of three genes by real-time PCR revealed heterozygous deletion of these three genes in adult patients with
AML
and
MDS
at high frequency, in addition to JMML patients.
The three genes located to 7q21.3 would be candidates for
myeloid
tumor-suppressor genes on 7q.
[MeSH-major]
Chromosome Aberrations. Chromosomes, Human, Pair 7 / genetics. Genes, Tumor Suppressor.
Leukemia
,
Myeloid
/ genetics.
Myelodysplastic
Syndromes / genetics. Sequence Deletion
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(PMID = 19358830.001).
[ISSN]
1090-2104
[Journal-full-title]
Biochemical and biophysical research communications
[ISO-abbreviation]
Biochem. Biophys. Res. Commun.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Proteins; 0 / SAMD9 protein, human
10.
Swolin B, Rödjer S, Westin J:
Therapy-related patterns of cytogenetic abnormalities in acute myeloid leukemia and myelodysplastic syndrome post polycythemia vera: single center experience and review of literature.
Ann Hematol
; 2008 Jun;87(6):467-74
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[Title]
Therapy-related patterns of cytogenetic abnormalities in
acute myeloid leukemia
and
myelodysplastic syndrome
post polycythemia vera: single center experience and review of literature.
A minor fraction of patients with polycythemia vera (PV) develop a terminal
acute myeloid leukemia
(
AML
) or
myelodysplastic syndrome
(
MDS
).
Analysis of the cytogenetic abnormalities during
AML
or
MDS
may help in understanding if this development is part of the natural course of the disease or induced by myelosuppressive therapy.
Thirty-six cases with
AML
or
MDS
post PV, collected in a single Swedish institution during a 33-year period, are described with special regard to time to development of
AML
or
MDS
, therapy given during active PV, and cytogenetic findings during
AML
or
MDS
.
A further 118 cases of
AML
or
MDS
post PV, in whom type of therapy during active PV and cytogenetic findings during
AML
or
MDS
were reported, were collected from the literature.
AML
or
MDS
developed in our own series after 1-30 years with a fairly constant rate (two cases per year).
The type of therapy given during active PV influences the type of chromosome abnormalities present during terminal
AML
or
MDS
and can also be instrumental in the development of
leukemia
.
[MeSH-major]
Abnormalities, Drug-Induced / genetics.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myelodysplastic
Syndromes / genetics. Polycythemia Vera / complications
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.
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.
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(PMID = 18351338.001).
[ISSN]
0939-5555
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
11.
Zharlyganova D, Harada H, Harada Y, Shinkarev S, Zhumadilov Z, Zhunusova A, Tchaizhunusova NJ, Apsalikov KN, Kemaikin V, Zhumadilov K, Kawano N, Kimura A, Hoshi M:
High frequency of AML1/RUNX1 point mutations in radiation-associated myelodysplastic syndrome around Semipalatinsk nuclear test site.
J Radiat Res
; 2008 Sep;49(5):549-55
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[Title]
High frequency of AML1/RUNX1 point mutations in radiation-associated
myelodysplastic syndrome
around Semipalatinsk nuclear test site.
It is known that bone marrow is a sensitive organ to ionizing radiation, and many patients
with acute myeloid leukemia
(
AML
) or
myelodysplastic syndrome
(
MDS
) have been diagnosed in radiation-treated cases and atomic bomb survivors in Hiroshima and Nagasaki.
The AML1/RUNX1 gene has been known to be frequently mutated in
MDS
/
AML
patients among atomic bomb survivors and radiation therapy-related
MDS
/
AML
patients.
In this study, we investigated the AML1 mutations in radiation-exposed patients with
MDS
/
AML
among the residents near the Semipalatinsk Nuclear Test Site (SNTS), where the risk of solid cancers and leukemias was increased due to the radiation effects.
AML1 mutations were identified in 7 (39%) of 18 radiation-exposed
MDS
/
AML
patients.
In contrast, no AML1 mutation was found in 13 unexposed
MDS
/
AML
cases.
The frequency of AML1 mutations in radiation-exposed patients with
MDS
/
AML
was significantly higher compared with unexposed patients (p < 0.05).We also found a significant correlation between individual estimated doses and AML1 mutations (p < 0.05).
Considering these results, AML1 point mutations might be a useful biomarker that differentiates radio-induced
MDS
/
AML from
spontaneous
MDS
/
AML
.
[MeSH-major]
Core Binding Factor Alpha 2 Subunit / genetics. Environmental Exposure / analysis. Environmental Exposure / statistics & numerical data.
Myelodysplastic
Syndromes / epidemiology.
Myelodysplastic
Syndromes / genetics. Nuclear Warfare. Radiation Injuries / epidemiology. Radiation Injuries / genetics
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(PMID = 18724045.001).
[ISSN]
0449-3060
[Journal-full-title]
Journal of radiation research
[ISO-abbreviation]
J. Radiat. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
12.
Padmanabhan A, Baker JA, Zirpoli G, Sait SN, Ford LA, Moysich KB, Baer MR:
Acute myeloid leukemia and myelodysplastic syndrome following breast cancer: increased frequency of other cancers and of cancers in multiple family members.
Leuk Res
; 2008 Dec;32(12):1820-3
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[Title]
Acute myeloid leukemia
and
myelodysplastic syndrome following
breast cancer: increased frequency of other cancers and of cancers in multiple family members.
Adjuvant chemotherapy and radiation therapy for breast cancer are associated with therapy-related
acute myeloid leukemia
(
AML
)/
myelodysplastic
syndromes (
MDS
), but little is known about additional risk factors.
Thirty-four patients with
AML
(n=26)/
MDS
(n=8)
following
breast cancer (cases) were compared with 2029 breast cancer patients without
AML
/
MDS
(controls).
Thus risk factors for
AML
/
MDS
following
breast cancer include older age, other cancers and multiple first-degree relatives with cancer.
[MeSH-major]
Breast Neoplasms / complications.
Leukemia
,
Myeloid
,
Acute
/ epidemiology.
Myelodysplastic
Syndromes / epidemiology. Neoplasms / complications. Neoplasms, Second Primary / epidemiology
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(PMID = 18468682.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
13.
Slobbe L, Polinder S, Doorduijn JK, Lugtenburg PJ, el Barzouhi A, Steyerberg EW, Rijnders BJ:
Outcome and medical costs of patients with invasive aspergillosis and acute myelogenous leukemia-myelodysplastic syndrome treated with intensive chemotherapy: an observational study.
Clin Infect Dis
; 2008 Dec 15;47(12):1507-12
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[Title]
Outcome and medical costs of patients with invasive aspergillosis and
acute
myelogenous
leukemia
-
myelodysplastic syndrome
treated with intensive chemotherapy: an observational study.
BACKGROUND: Invasive aspergillosis (IA) is a leading cause of mortality in patients
with acute leukemia
.
METHODS: In 269 patients treated for
acute
myelogenous
leukemia
-
myelodysplastic syndrome
(
AML
-
MDS
) during 2002-2007, evidence of IA was collected using high-resolution computed tomography and galactomannan measurement in bronchoalveolar lavage fluid specimens.
[MeSH-major]
Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Aspergillosis / economics. Drug Therapy / economics. Health Care Costs.
Leukemia
,
Myeloid
,
Acute
/ complications
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.
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(PMID = 18990068.001).
[ISSN]
1537-6591
[Journal-full-title]
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
[ISO-abbreviation]
Clin. Infect. Dis.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
14.
Rassool FV, Gaymes TJ, Omidvar N, Brady N, Beurlet S, Pla M, Reboul M, Lea N, Chomienne C, Thomas NS, Mufti GJ, Padua RA:
Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia?
Cancer Res
; 2007 Sep 15;67(18):8762-71
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[Title]
Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in
myeloid leukemia
?
Myelodysplastic
syndromes (
MDS
) comprise a heterogeneous group of disorders characterized by ineffective hematopoiesis, with an increased propensity to develop
acute
myelogenous
leukemia
(
AML
).
The molecular basis for
MDS
progression is unknown, but a key element in
MDS
disease progression is loss of chromosomal material (genomic instability).
Using our two-step mouse model for
myeloid
leukemic disease progression involving overexpression of human mutant NRAS and BCL2 genes, we show that there is a stepwise increase in the frequency of DNA damage leading to an increased frequency of error-prone repair of double-strand breaks (DSB) by nonhomologous end-joining.
Our data link gene abnormalities to constitutive DNA damage and increased DSB repair errors in vivo and provide a mechanism for an increase in the error rate of DNA repair with
MDS
disease progression.
These data suggest treatment strategies that target RAS/RAC pathways and ROS production in human
MDS
/
AML
.
[MeSH-major]
DNA Damage. DNA Repair. Genomic Instability.
Leukemia
,
Myeloid
/ genetics. Reactive Oxygen Species / metabolism
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(PMID = 17875717.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Reactive Oxygen Species
15.
Rund D, Krichevsky S, Bar-Cohen S, Goldschmidt N, Kedmi M, Malik E, Gural A, Shafran-Tikva S, Ben-Neriah S, Ben-Yehuda D:
Therapy-related leukemia: clinical characteristics and analysis of new molecular risk factors in 96 adult patients.
Leukemia
; 2005 Nov;19(11):1919-28
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[Title]
Therapy-related
leukemia
: clinical characteristics and analysis of new molecular risk factors in 96 adult patients.
Therapy-related
leukemia
or myelodysplasia (t-leuk/
MDS
) is a serious problem that is increasing in frequency.
We studied the clinical characteristics of 96 patients (pts) with a mean age of 48 years, and analyzed the molecular parameters that could predispose to t-leuk/
MDS
.
The mean latency until the development of t-
AML
was 45.5 months.
Analysis of drug metabolism and disposition genes showed a protective effect of the CYP3A4 1*B genotype against the development of t-leuk/
MDS
, whereas the CC genotype of MDR1 C3435T and the NAD(P)H:quinone oxidoreductase1 codon 187 polymorphism were both noncontributory.
In conclusion, genetic predisposition as well as epigenetic events contribute to the etiology of t-
AML
/
MDS
.
[MeSH-major]
Genetic Predisposition to Disease.
Leukemia
/ chemically induced.
Myelodysplastic
Syndromes / chemically induced.
Myelodysplastic
Syndromes / genetics. Neoplasms, Second Primary / chemically induced. Neoplasms, Second Primary / genetics
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(PMID = 16167058.001).
[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 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / CYP3A protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A; EC 2.7.11.1 / RPS6KA4 protein, human; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 90-kDa
16.
Martin MG, Uy GL, Procknow E, Stockerl-Goldstein K, Cashen A, Westervelt P, Abboud CN, Augustin K, Luo J, DiPersio JF, Vij R:
Allo-SCT conditioning for myelodysplastic syndrome and acute myeloid leukemia with clofarabine, cytarabine and ATG.
Bone Marrow Transplant
; 2009 Jul;44(1):13-7
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[Title]
Allo-SCT conditioning for
myelodysplastic syndrome
and
acute myeloid leukemia with
clofarabine, cytarabine and ATG.
Given the evidence of activity of clofarabine and cytarabine in
myelodysplastic syndrome
/
acute myeloid leukemia
(
MDS
/
AML
), we explored a novel reduced-intensity conditioning regimen based on this backbone.
Their median age was 54 years; three were with
MDS
and four with
AML
.
Toxicities included hand-foot
syndrome
(57% grade 2), elevated alanine aminotransferase (ALT) (57% grade 3), elevated aspartate aminotransferase (AST) (86% grade 3) and hyperbilirubinemia (29% grade 3-5).
No
acute
GVHD was observed.
[MeSH-major]
Adenine Nucleotides / administration & dosage. Antilymphocyte Serum / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Arabinonucleosides / administration & dosage. Cytarabine / administration & dosage. Immunosuppressive Agents / administration & dosage.
Leukemia
,
Myeloid
,
Acute
/ therapy.
Myelodysplastic
Syndromes / therapy. Stem Cell Transplantation. Transplantation Conditioning / methods
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(PMID = 19139740.001).
[ISSN]
1476-5365
[Journal-full-title]
Bone marrow transplantation
[ISO-abbreviation]
Bone Marrow Transplant.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Adenine Nucleotides; 0 / Antilymphocyte Serum; 0 / Antimetabolites, Antineoplastic; 0 / Arabinonucleosides; 0 / Immunosuppressive Agents; 04079A1RDZ / Cytarabine; 762RDY0Y2H / clofarabine
17.
Thepot S, Itzykson R, Seegers V, Raffoux E, Quesnel B, Chait Y, Sorin L, Dreyfus F, Cluzeau T, Delaunay J, Sanhes L, Eclache V, Dartigeas C, Turlure P, Harel S, Salanoubat C, Kiladjian JJ, Fenaux P, Adès L, Groupe Francophone des Myelodysplasies (GFM):
Treatment of progression of Philadelphia-negative myeloproliferative neoplasms to myelodysplastic syndrome or acute myeloid leukemia by azacitidine: a report on 54 cases on the behalf of the Groupe Francophone des Myelodysplasies (GFM).
Blood
; 2010 Nov 11;116(19):3735-42
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[Title]
Treatment of progression of Philadelphia-negative myeloproliferative neoplasms to
myelodysplastic syndrome
or
acute myeloid leukemia
by azacitidine: a report on 54 cases on the behalf of the Groupe Francophone des Myelodysplasies (GFM).
Transformation of Philadelphia (Ph)-negative myeloproliferative neoplasms (MPNs) to
myelodysplastic syndrome
(
MDS
) or
acute myeloid leukemia
(
AML
) is associated with poor response to chemotherapy and short survival.
Fifty-four patients with Ph-negative MPN (including 21 essential thrombocythemia [ET], 21 polycythemia vera [PV], 7 primary myelofibrosis, and 5 unclassified MPN) who had progressed to
AML
(n = 26) or
MDS
(n = 28) were treated with azacitidine in a patient-named program.
Prognostic factors were for overall response the underlying MPN (71% vs 33% responses in ET and PV, respectively; P = .016); prognostic factors for CR achievement were the underlying MPN (14% CR for PV vs 43% for ET; P = .040) and World Health Organization classification at transformation (36% vs 12% CR in
MDS
and
AML
, respectively, P = .038).
Azacitidine gives encouraging results in Ph-negative MPN having progressed to
AML
or
MDS
, but response duration is short, and consolidation treatments have to be evaluated.
[MeSH-major]
Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ etiology.
Myelodysplastic
Syndromes / drug therapy.
Myelodysplastic
Syndromes / etiology. Myeloproliferative Disorders / complications. Myeloproliferative Disorders / drug therapy
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(PMID = 20664061.001).
[ISSN]
1528-0020
[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]
0 / Antimetabolites, Antineoplastic; M801H13NRU / Azacitidine
18.
Choi SW, Boxer LA, Pulsipher MA, Roulston D, Hutchinson RJ, Yanik GA, Cooke KR, Ferrara JL, Levine JE:
Stem cell transplantation in patients with severe congenital neutropenia with evidence of leukemic transformation.
Bone Marrow Transplant
; 2005 Mar;35(5):473-7
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With appropriate treatment using recombinant human granulocyte-colony-stimulating factor (r-HuG-CSF), SCN patients are now surviving longer, but are at increased risk of developing
myelodysplastic syndrome
(
MDS
)/
acute myeloid leukemia
(
AML
).
We report results for six patients with SCN who underwent HSCT for
MDS
or
AML
between 1997 and 2001 at two transplant centers.
Two patients transplanted for
MDS
survived.
Four patients, who all received induction chemotherapy for
AML
prior to HSCT, died.
Rapid transplantation should be the goal for the SCN patient once the diagnosis of
MDS
/
AML
is established.
SCN patients should be monitored carefully for progression to
MDS
in order to be treated with HSCT as soon as they have progressed and before developing
AML
.
For SCN patients who progress to
AML
, HSCT should still be considered, even though the risks appear to be greater.
[MeSH-major]
Cell Transformation, Neoplastic. Hematopoietic Stem Cell Transplantation / methods.
Leukemia
,
Myeloid
/ therapy. Neutropenia / complications
[MeSH-minor]
Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Bone Marrow Examination. Child. Child, Preschool. Disease Progression. Female. Humans. Infant. Karyotyping. Male.
Myelodysplastic
Syndromes / etiology.
Myelodysplastic
Syndromes / therapy. Retrospective Studies. Survival Rate. Transplantation Conditioning. Treatment Outcome
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(PMID = 15640815.001).
[ISSN]
0268-3369
[Journal-full-title]
Bone marrow transplantation
[ISO-abbreviation]
Bone Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents
19.
Majeed F, Jadko S, Freedman MH, Dror Y:
Mutation analysis of SBDS in pediatric acute myeloblastic leukemia.
Pediatr Blood Cancer
; 2005 Dec;45(7):920-4
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[Title]
Mutation analysis of SBDS in pediatric
acute
myeloblastic
leukemia
.
BACKGROUND: Shwachman-Diamond
syndrome
(SDS) is associated with a high risk of myelodysplasia,
acute myeloid leukemia
(
AML
), and chromosome 7 abnormalities.
Herein, we studied the role of genetic alterations in SBDS in
AML
.
PROCEDURE: DNA was extracted from marrows of SDS patients with
AML
, as well as from children with de novo
AML
.
To study whether SBDS heterozygosity confers a risk for
MDS
/
AML
, data on family members of SDS patients on the Canadian Inherited Marrow Failure Registry (CIMFR) was analyzed.
RESULTS: Of two SDS patients with SDS/
AML
one was homozygous 258 + 2T > C, and one was compound heterozygous 183-184TA > CT/258 + 2T > C.
To determine whether a subset of patients with SDS can present with
AML
, we analyzed 48
AML
samples at remission, but no mutations were identified.
To address whether acquired mutated SBDS gene is associated with leukemic transformation in de novo
AML
, we analyzed 77
AML
samples at diagnosis or relapse (4 with -7 and 7q-) for SBDS mutations; no alterations were detected.
Also, among the relatives of an SDS patient cohort on the registry no cases of
MDS
/
AML
were reported.
CONCLUSIONS: Common mutations occurred in our SDS patients who develop
AML
, and thus,
AML
is not confined to a rare genetic subgroup of SDS.
Newly diagnosed patients with
AML
are unlikely to have an underlying undiagnosed SDS.
Acquired SBDS gene mutations also would appear unlikely to play a mechanistic role in de novo
AML
, and might not be involved in the pathogenesis of chromosome 7 abnormalities as well.
[MeSH-major]
Chromosome Aberrations. Chromosomes, Human, Pair 7 / genetics. Exons.
Leukemia
,
Myeloid
,
Acute
/ genetics. Point Mutation. Proteins / genetics
[MeSH-minor]
Bone Marrow Diseases / complications. Bone Marrow Diseases / genetics. Case-Control Studies. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. Exocrine Pancreatic Insufficiency / complications. Exocrine Pancreatic Insufficiency / genetics. Heterozygote. Humans. Male. Osteochondrodysplasias / complications. Osteochondrodysplasias / genetics.
Syndrome
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[Copyright]
2005 Wiley-Liss, Inc.
(PMID = 16007594.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Proteins; 0 / SBDS protein, human
20.
Barouk-Simonet E, Soenen-Cornu V, Roumier C, Cosson A, Laï JL, Fenaux P, Preudhomme C:
Role of multiplex FISH in identifying chromosome involvement in myelodysplastic syndromes and acute myeloid leukemias with complex karyotypes: a report on 28 cases.
Cancer Genet Cytogenet
; 2005 Mar;157(2):118-26
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[Title]
Role of multiplex FISH in identifying chromosome involvement in
myelodysplastic
syndromes and
acute myeloid
leukemias with complex karyotypes: a report on 28 cases.
Chromosomal abnormalities are found by conventional cytogenetic (CC) analysis in about 50% of
myelodysplastic
syndromes (
MDS
) and 70% of
acute myeloid
leukemias (
AML
).
We studied by M-FISH 28 cases of
MDS
and
AML
with complex chromosomal abnormalities, 10 of them were therapy-related.
[MeSH-major]
Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods.
Leukemia
,
Myeloid
/ genetics.
Myelodysplastic
Syndromes / genetics
[MeSH-minor]
Acute
Disease. Adult. Aged. Female. Humans. Karyotyping. Male. Middle Aged
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(PMID = 15721632.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
21.
Armand P, Kim HT, DeAngelo DJ, Ho VT, Cutler CS, Stone RM, Ritz J, Alyea EP, Antin JH, Soiffer RJ:
Impact of cytogenetics on outcome of de novo and therapy-related AML and MDS after allogeneic transplantation.
Biol Blood Marrow Transplant
; 2007 Jun;13(6):655-64
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[Title]
Impact of cytogenetics on outcome of de novo and therapy-related
AML
and
MDS
after allogeneic transplantation.
Cytogenetics has an important impact on the prognosis of patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) for
acute
myelogenous
leukemia
(
AML
) or
myelodysplastic
syndromes (
MDS
).
In this study, we retrospectively analyzed data on 556 patients with
AML
or
MDS
transplanted at our institution.
After accounting for cytogenetics, patients with therapy-related
AML
or
MDS
had an equivalent outcome to those with de novo disease.
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(PMID = 17531775.001).
[ISSN]
1083-8791
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / U19 AI029530-14; United States / NIAID NIH HHS / AI / U19 AI 29530; United States / NHLBI NIH HHS / HL / P01 HL070149; United States / NCI NIH HHS / CA / T32 CA009172; United States / NIAID NIH HHS / AI / AI029530-14; United States / NHLBI NIH HHS / HL / P01 HL 070149; United States / NIAID NIH HHS / AI / U19 AI029530
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS25237; NLM/ PMC2743535
22.
Fischer T, Stone RM, Deangelo DJ, Galinsky I, Estey E, Lanza C, Fox E, Ehninger G, Feldman EJ, Schiller GJ, Klimek VM, Nimer SD, Gilliland DG, Dutreix C, Huntsman-Labed A, Virkus J, Giles FJ:
Phase IIB trial of oral Midostaurin (PKC412), the FMS-like tyrosine kinase 3 receptor (FLT3) and multi-targeted kinase inhibitor, in patients with acute myeloid leukemia and high-risk myelodysplastic syndrome with either wild-type or mutated FLT3.
J Clin Oncol
; 2010 Oct 01;28(28):4339-45
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[Title]
Phase IIB trial of oral Midostaurin (PKC412), the FMS-like tyrosine kinase 3 receptor (FLT3) and multi-targeted kinase inhibitor, in patients
with acute myeloid leukemia
and high-risk
myelodysplastic syndrome
with either wild-type or mutated FLT3.
PURPOSE: Mutations leading to constitutive activation of the FMS-like tyrosine kinase 3 receptor (FLT3) occur in blasts of 30% of patients
with acute myeloid leukemia
(
AML
).
Midostaurin (PKC412; N-benzoylstaurosporin) is a multitargeted tyrosine kinase inhibitor, with demonstrated activity in patients with
AML
/
myelodysplastic syndrome
(
MDS
) with FLT3 mutations.
PATIENTS AND METHODS: Ninety-five patients with
AML
or
MDS
with either wild-type (n = 60) or mutated (n = 35) FLT3 were randomly assigned to receive oral midostaurin at 50 or 100 mg twice daily.
The degree of clinical activity observed supports additional studies that combine midostaurin and other agents such as chemotherapy especially in FLT3-mutant
AML
.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myelodysplastic
Syndromes / drug therapy.
Myelodysplastic
Syndromes / genetics. Staurosporine / analogs & derivatives. fms-Like Tyrosine Kinase 3 / genetics
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.
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.
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.
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.
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.
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.
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[Cites]
Blood. 2000 Dec 1;96(12):3671-4
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]
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16857987.001
]
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]
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[
19602710.001
]
[Cites]
J Clin Oncol. 2001 Mar 1;19(5):1485-92
[
11230495.001
]
(PMID = 20733134.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P01 CA066996
[Publication-type]
Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; H88EPA0A3N / Staurosporine; ID912S5VON / midostaurin
[Other-IDs]
NLM/ PMC4135183
23.
Paulsson K, Heidenblad M, Strömbeck B, Staaf J, Jönsson G, Borg A, Fioretos T, Johansson B:
High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration.
Leukemia
; 2006 May;20(5):840-6
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[Title]
High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in
AML
and
MDS
cases with trisomy 8 as the sole cytogenetic aberration.
Although trisomy 8 as the sole chromosome aberration is the most common numerical abnormality in
acute myeloid leukemia
(
AML
) and
myelodysplastic
syndromes (
MDS
), little is known about its pathogenetic effects.
Considering that +8 is a frequent secondary change in
AML
/
MDS
, cryptic--possibly primary--genetic aberrations may occur in cases with trisomy 8 as the apparently single anomaly.
We performed a high-resolution genome-wide array-based comparative genome hybridization (array CGH) analysis of 10
AML
/
MDS
cases with isolated +8, utilizing a 32K bacterial artificial chromosome array set, providing >98% coverage of the genome with a resolution of 100 kb.
A 1.8 Mb deletion at 7p14.1, which had occurred prior to the +8, was identified in
MDS
transforming to
AML
.
The present results show that cryptic genetic abnormalities are frequent in trisomy 8-positive
AML
/
MDS
cases and that +8 as the sole cytogenetic aberration is not always the primary genetic event.
[MeSH-major]
Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Genome.
Leukemia
,
Myeloid
/ genetics.
Myelodysplastic
Syndromes / genetics. Nucleic Acid Hybridization / methods. Trisomy / genetics
[MeSH-minor]
Acute
Disease. Adult. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged
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.
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(PMID = 16498392.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
24.
Tong FK, Chow S, Hedley D:
Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and AML/MDS patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells.
Cytometry B Clin Cytom
; 2006 May;70(3):107-14
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[Title]
Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and
AML
/
MDS
patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells.
In this article, we describe its application to phase I trials of BAY 43-9006 in solid tumor and
AML
/
MDS
patients.
A modified whole blood fixation protocol was developed for the
AML
/
MDS
trial, using the c-kit ligand stem cell factor (SCF) to activate ERK as an alternative to PMA, and incorporating immunophenotypic markers to identify leukemic blasts.
A similar effect was seen in the lymphocytes of
AML
/
MDS
patients during treatment with BAY 43-9006.
[MeSH-major]
Benzenesulfonates / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Leukocytes, Mononuclear / drug effects. MAP Kinase Signaling System / drug effects.
Myelodysplastic
Syndromes / drug therapy. Neoplasms / drug therapy. Pyridines / therapeutic use
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[Copyright]
Copyright 2006 International Society for Analytical Cytology.
(PMID = 16498671.001).
[ISSN]
1552-4949
[Journal-full-title]
Cytometry. Part B, Clinical cytometry
[ISO-abbreviation]
Cytometry B Clin Cytom
[Language]
eng
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD3; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Benzenesulfonates; 0 / CD33 protein, human; 0 / Phenylurea Compounds; 0 / Pyridines; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Stem Cell Factor; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.11.2 / Antigens, CD13; NI40JAQ945 / Tetradecanoylphorbol Acetate
25.
Kezuka T, Usui N, Suzuki E, Wakasugi K, Usui M:
Ocular complications in myelodysplastic syndromes as preleukemic disorders.
Jpn J Ophthalmol
; 2005 Sep-Oct;49(5):377-83
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[Title]
Ocular complications in
myelodysplastic
syndromes as preleukemic disorders.
PURPOSE: To identify ocular complications in patients
with myelodysplastic
syndromes (
MDS
), who have a propensity to progress to
acute myeloid leukemia
(
AML
).
METHODS: Forty-one patients with
MDS
were the subjects in this retrospective study, and 21 patients with
AML
were selected as controls.
In this study, the
MDS
patients were classified into those with refractory anemia (RA) and those with refractory anemia with excess blasts (RAEB).
RESULTS: Ocular complications were found in 19 (46.3%) of the 41 patients with
MDS
, comprising corneal ulcer (two cases), iridocyclitis (five), vitreous hemorrhage (one), retinal hemorrhage (ten), cotton wool spots (one), and optic neuritis (two). (Some patients had more than one ocular complication.
) Ocular complications were identified in 12 of the 21 (57.1%) patients with
AML
.
There was no significant difference in frequency of ocular complications between
MDS
and
AML
(P = 0.4892).
In
MDS
, retinal hemorrhage was associated with significantly reduced platelet counts (P = 0.0063).
The frequency of ocular complications was significantly higher in
MDS
-RAEB than in
MDS
-RA (P = 0.0478).
Retinal hemorrhage was significantly more frequent in patients with
MDS
-RAEB than in patients with
MDS
-RA (P = 0.0433).
CONCLUSION: Ocular complications in
MDS
patients should be carefully examined as prognostic factors for progression to
acute leukemia
.
[MeSH-major]
Eye Diseases / complications.
Myelodysplastic
Syndromes / complications. Preleukemia / complications
[MeSH-minor]
Acute
Disease. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans.
Leukemia
,
Myeloid
/ complications.
Leukemia
,
Myeloid
/ diagnosis.
Leukemia
,
Myeloid
/ epidemiology. Male. Middle Aged. Platelet Count. Prevalence. Retrospective Studies
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.
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[Cites]
Blood. 2002 Oct 1;100(7):2292-302
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12239137.001
]
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Am J Ophthalmol. 1995 Mar;119(3):370-2
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[
570847.001
]
(PMID = 16187037.001).
[ISSN]
0021-5155
[Journal-full-title]
Japanese journal of ophthalmology
[ISO-abbreviation]
Jpn. J. Ophthalmol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
26.
de Melo Campos P, Traina F, da Silva Santos Duarte A, Lorand-Metze I, Costa FF, Saad ST:
Reduced expression of FLIP SHORT in bone marrow of low risk myelodysplastic syndrome.
Leuk Res
; 2007 Jun;31(6):853-7
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[Title]
Reduced expression of FLIP SHORT in bone marrow of low risk
myelodysplastic syndrome
.
Apoptosis is dysregulated in patients
with myelodysplastic syndrome
(
MDS
) and
acute
myelogenous leukaemia (
AML
).
Here, we characterize the expression level of FLIP(LONG) and FLIP(SHORT) mRNA in bone marrow aspirates from 61 patients diagnosed with
MDS
or
AML
.
FLIP(SHORT) mRNA expression was significantly lower in low risk
MDS
, compared to high risk
MDS
, according to FAB classification (RA/RARS versus RAEB/RAEBt, P=0.0127) and IPSS (low risk/intermediate-1 versus intermediate-2/high risk, P=0.0345).
Furthermore, FLIP(SHORT) mRNA expression was significantly lower in low risk
MDS
, compared to
MDS
-
AML
/
AML
de novo (P=0.0006), according to FAB classification.
Increased levels of FLIP(SHORT) in RAEB and
AML
may be related to apoptosis resistance in these diseases and to
MDS
progression.
[MeSH-major]
Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. CASP8 and FADD-Like Apoptosis Regulating Protein / biosynthesis. Gene Expression Regulation, Leukemic.
Leukemia
,
Myeloid
,
Acute
/ metabolism.
Myelodysplastic
Syndromes / metabolism
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.
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.
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.
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.
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(PMID = 17270269.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein
27.
Mahmud M, Stebbing J:
Epigenetic modifications in AML and MDS.
Leuk Res
; 2010 Feb;34(2):139-40
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[Title]
Epigenetic modifications in
AML
and
MDS
.
[MeSH-major]
Epigenesis, Genetic.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myelodysplastic
Syndromes / genetics
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[CommentOn]
Leuk Res. 2010 Feb;34(2):148-53
[
19595458.001
]
(PMID = 19665226.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Comment; Editorial; Review
[Publication-country]
England
[Number-of-references]
14
28.
Björk J, Johansson B, Broberg K, Albin M:
Smoking as a risk factor for myelodysplastic syndromes and acute myeloid leukemia and its relation to cytogenetic findings: a case-control study.
Leuk Res
; 2009 Jun;33(6):788-91
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[Title]
Smoking as a risk factor for
myelodysplastic
syndromes and
acute myeloid leukemia
and its relation to cytogenetic findings: a case-control study.
In this case-control study, interview data on smoking habits were available for 179 de novo cases (116 with cytogenetic data) of
acute myeloid leukemia
(
AML
) or
myelodysplastic
syndromes (
MDS
).
Each pack-year of smoking increased the risk of
MDS
with 1.3% (95% CI 0.1-2.6%), corresponding to an estimated excess risk of 71% (95% CI 3-180%) for 40 pack-years.
Associations between smoking and the specific aberrations -5/5q-, -7/7q-, and +8 in
AML
and
MDS
were indicated but the estimates were imprecise.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ etiology.
Myelodysplastic
Syndromes / etiology. Smoking / adverse effects
Genetic Alliance.
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(PMID = 19019430.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
29.
Alencar C, Abramowtiz M, Parekh S, Braunshweig I, Jacobson M, Silverman L, Verma A:
Atypical presentations of Sweet's syndrome in patients with MDS/AML receiving combinations of hypomethylating agents with histone deacetylase inhibitors.
Am J Hematol
; 2009 Oct;84(10):688-9
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[Title]
Atypical presentations of Sweet's
syndrome
in patients with
MDS
/
AML
receiving combinations of hypomethylating agents with histone deacetylase inhibitors.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / adverse effects.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Myelodysplastic
Syndromes / drug therapy. Sweet
Syndrome
/ chemically induced
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.
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(PMID = 19722261.001).
[ISSN]
1096-8652
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0 / Histone Deacetylase Inhibitors; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
30.
See HT, Thomas DA, Bueso-Ramos C, Kavanagh J:
Secondary leukemia after treatment with paclitaxel and carboplatin in a patient with recurrent ovarian cancer.
Int J Gynecol Cancer
; 2006 Jan-Feb;16 Suppl 1:236-40
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[Title]
Secondary
leukemia
after treatment with paclitaxel and carboplatin in a patient with recurrent ovarian cancer.
The occurrence of
myelodysplastic syndrome
(
MDS
) or
acute myeloid leukemia
(
AML
) has been reported after treatment with cytotoxic alkylating agent-based chemotherapy for solid tumors.
We report a patient with metastatic ovarian carcinoma treated with carboplatin and paclitaxel, who developed secondary
acute
erythroid
leukemia
.
Monitoring of the long-term outcome of paclitaxel- and platinum-based regimens is warranted, particularly with regard to monitoring the development of secondary
MDS
and/or
AML
.
The incidence and outcome of secondary
leukemia
in the setting of active ovarian carcinoma is reviewed.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / adverse effects.
Leukemia
, Erythroblastic,
Acute
/ chemically induced. Liver Neoplasms / therapy. Neoplasms, Glandular and Epithelial / therapy. Ovarian Neoplasms / therapy
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TAXOL
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BUSULFAN
.
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.
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(PMID = 16515597.001).
[ISSN]
1048-891X
[Journal-full-title]
International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
[ISO-abbreviation]
Int. J. Gynecol. Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
04079A1RDZ / Cytarabine; BG3F62OND5 / Carboplatin; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; P88XT4IS4D / Paclitaxel; ZRP63D75JW / Idarubicin
31.
Kufner S, Fleischer RP, Kroell T, Schmid C, Zitzelsberger H, Salih H, de Valle F, Treder W, Schmetzer HM:
Serum-free generation and quantification of functionally active Leukemia-derived DC is possible from malignant blasts in acute myeloid leukemia and myelodysplastic syndromes.
Cancer Immunol Immunother
; 2005 Oct;54(10):953-70
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[Title]
Serum-free generation and quantification of functionally active
Leukemia
-derived DC is possible from malignant blasts in
acute myeloid leukemia
and
myelodysplastic
syndromes.
Functional dendritic cells (DC) are professional antigen presenting cells (APC) and can be generated in vitro from leukemic cells from
acute myeloid leukemia
AML
patients, giving rise to APC of leukemic origin presenting leukemic antigens (DC(leu)).
We have already shown that DC can be successfully generated
from AML
and myeloplastic syndromes (
MDS
) cells in serum-free 'standard' medium (X-vivo + GM-CSF + IL-4 +TNFalpha + FL) in 10-14 days.
In this study, we present that DC counts generated from mononuclear cells (MNC) varied between 20% (from 55
MDS
samples), 34% (from 100
AML
samples) and 25% (from 38 healthy MNC samples) medium.
DC harvests were highest in monocytoid FAB types (
AML
-M4/M5,
MDS
-CMML) and independent from cytogenetic risk groups, demonstrating that DC-based strategies can be applied for patients with all cytogenetic risk groups.
Proof of the clonal derivation of DC generated was obtained in five
AML
and four
MDS
cases with a combined FISH/immunophenotype analysis (FISH-IPA): The clonal numerical chromosome aberrations of the diseases were regularly codetectable with DC markers; however, not with all clonal cells being convertible to
leukemia
-derived DC(leu) (on average, 53% of blasts in
AML
or
MDS
).
In 41
AML
and 13
MDS
cases with a suitable antigen expression, we could confirm FISH-IPA data by Flow cytometry: although DC(leu) are regularly detectable, on average only 57% of blasts in
AML
and 64% of blasts in
MDS
were converted to DC(leu).
After coculture with DC in mixed lymphocyte reactions (MLR), autologous T cells
from AML
and
MDS
patients proliferate and upregulate costimulatory receptors.
The specific lysis of leukemic cells by autologous T cells could be demonstrated in three cases with
AML
in a Fluorolysis assay.
(1) the generation of DC is regularly possible in
AML
and also in
MDS
under serum-free conditions. (2) Clonal/
leukemia
-derived DC(leu) can be regularly generated
from MDS
and
AML
-MNC; however, not with all blasts being converted to DC(leu) and not all DC generated carrying leukemic markers.
We recommend to select DC(leu) for vaccinations or ex vivo T-cell activations to avoid contaminations with non-converted blasts and non-
leukemia
-derived DC and to improve the harvest of specific, anti-leukemic T cells.
DC and DC-primed T cells could provide a practical strategy for the immunotherapy of
AML
and
MDS
.
[MeSH-major]
Dendritic Cells / immunology.
Leukemia
,
Myeloid
/ immunology. Leukocytes, Mononuclear / immunology.
Myelodysplastic
Syndromes / immunology
[MeSH-minor]
Acute
Disease. Adult. Aged. Antigen-Presenting Cells. Antigens, CD. Antigens, CD80 / immunology. Antigens, CD80 / metabolism. Blast Crisis. Cell Culture Techniques. Culture Media, Serum-Free. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Immunoglobulins / immunology. Immunoglobulins / metabolism. Interleukin-4 / pharmacology. Lymphocyte Activation. Male. Membrane Glycoproteins / immunology. Membrane Glycoproteins / metabolism. Middle Aged. T-Lymphocytes / immunology. T-Lymphocytes, Cytotoxic. Tumor Necrosis Factor-alpha / pharmacology
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(PMID = 15789235.001).
[ISSN]
0340-7004
[Journal-full-title]
Cancer immunology, immunotherapy : CII
[ISO-abbreviation]
Cancer Immunol. Immunother.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD80; 0 / CD83 antigen; 0 / Culture Media, Serum-Free; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
32.
Watanabe-Okochi N, Kitaura J, Ono R, Harada H, Harada Y, Komeno Y, Nakajima H, Nosaka T, Inaba T, Kitamura T:
AML1 mutations induced MDS and MDS/AML in a mouse BMT model.
Blood
; 2008 Apr 15;111(8):4297-308
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[Title]
AML1 mutations induced
MDS
and
MDS
/
AML
in a mouse BMT model.
Myelodysplastic syndrome
(
MDS
) is a hematopoietic stem-cell disorder characterized by trilineage
dysplasia
and susceptibility to
acute
myelogenous
leukemia
(
AML
).
Analysis of molecular basis of
MDS
has been hampered by the heterogeneity of the disease.
Recently, mutations of the transcription factor AML1/RUNX1 have been identified in 15% to 40% of
MDS
-refractory anemia with excess of blasts (RAEB) and
MDS
/
AML
.
Most mice developed
MDS
and
MDS
/
AML
-like symptoms within 4 to 13 months after BMT.
Interestingly, among integration sites identified, Evi1 seemed to collaborate with an AML1 mutant harboring a point mutation in the Runt homology domain (D171N) to induce
MDS
/
AML
with an identical phenotype characterized by marked hepatosplenomegaly,
myeloid dysplasia
, leukocytosis, and biphenotypic surface markers.
Collaboration between AML1-D171N and Evi1 was confirmed by a BMT model where coexpression of AML1-D171N and Evi1 induced
acute leukemia
of the same phenotype with much shorter latencies.
On the other hand, a C-terminal truncated AML1 mutant (S291fsX300) induced pancytopenia with erythroid
dysplasia
in transplanted mice, followed by progression to
MDS
-RAEB or
MDS
/
AML
.
Thus, we have developed a useful mouse model of
MDS
/
AML
that should help in the understanding of the molecular basis of
MDS
and the progression of
MDS
to overt
leukemia
.
[MeSH-major]
Bone Marrow Transplantation. Core Binding Factor Alpha 2 Subunit / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation / genetics.
Myelodysplastic
Syndromes / genetics
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.
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[CommentIn]
Blood. 2008 Apr 15;111(8):3916-7
[
18434965.001
]
(PMID = 18192504.001).
[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 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Evi1 protein, mouse; 0 / Mutant Proteins; 0 / Transcription Factors
33.
Zatkova A, Schoch C, Speleman F, Poppe B, Mannhalter C, Fonatsch C, Wimmer K:
GAB2 is a novel target of 11q amplification in AML/MDS.
Genes Chromosomes Cancer
; 2006 Sep;45(9):798-807
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[Title]
GAB2 is a novel target of 11q amplification in
AML
/
MDS
.
Chromosome arm 11q amplifications involving the mixed lineage
leukemia
gene (MLL) locus are rare but recurrent aberrations in
acute myeloid leukemia
(
AML
) and
myelodysplastic syndrome
(
MDS
).
Thus, the adaptor molecule GAB2 that has already been shown to enhance oncogenic signaling in other neoplasias appears as a novel target of 11q amplification in
AML
/
MDS
.
[MeSH-major]
Adaptor Proteins, Signal Transducing / genetics. Chromosomes, Human, Pair 11. Gene Amplification / physiology.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myelodysplastic
Syndromes / genetics
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.
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.
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[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 16736498.001).
[ISSN]
1045-2257
[Journal-full-title]
Genes, chromosomes & cancer
[ISO-abbreviation]
Genes Chromosomes Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / GAB2 protein, human
34.
Leleu X, Tamburini J, Roccaro A, Morel P, Soumerai J, Lévy V, Wemeau M, Balkaran S, Poulain S, Hunter ZR, Ghobrial IM, Treon SP, Leblond V:
Balancing risk versus benefit in the treatment of Waldenström's Macroglobulinemia patients with nucleoside analogue-based therapy.
Clin Lymphoma Myeloma
; 2009 Mar;9(1):71-3
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There are sporadic reports on increased incidence of transformation to high grade non-Hodgkin lymphoma (transformation to NHL) and development of therapy related-myelodysplasia/
acute leukemia
(t-
MDS
/
AML
) among WM patients treated with NA.
The incidences of transformation to NHL and t-
MDS
/
AML
ranged from 4.7% to 8%, and from 1.4% to 8.9%, respectively, and demonstrated an increased incidence of these late events among WM patients treated with NA.
[MeSH-minor]
Disease Progression. Humans.
Leukemia
,
Myeloid
,
Acute
/ pathology. Lymphoma, Non-Hodgkin / pathology
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(PMID = 19362978.001).
[ISSN]
1557-9190
[Journal-full-title]
Clinical lymphoma & myeloma
[ISO-abbreviation]
Clin Lymphoma Myeloma
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Nucleosides
35.
Liu TX, Becker MW, Jelinek J, Wu WS, Deng M, Mikhalkevich N, Hsu K, Bloomfield CD, Stone RM, DeAngelo DJ, Galinsky IA, Issa JP, Clarke MF, Look AT:
Chromosome 5q deletion and epigenetic suppression of the gene encoding alpha-catenin (CTNNA1) in myeloid cell transformation.
Nat Med
; 2007 Jan;13(1):78-83
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[Title]
Chromosome 5q deletion and epigenetic suppression of the gene encoding alpha-catenin (CTNNA1) in
myeloid
cell transformation.
Interstitial loss of all or part of the long arm of chromosome 5, or del(5q), is a frequent clonal chromosomal abnormality in human
myelodysplastic syndrome
(
MDS
, a preleukemic disorder) and
acute myeloid leukemia
(
AML
), and is thought to contribute to the pathogenesis of these diseases by deleting one or more tumor-suppressor genes.
We focused our analysis of gene expression on RNA from primitive
leukemia
-initiating cells, which harbor 5q deletions, and analyzed 12 genes within the CDR that are expressed by normal hematopoietic stem cells.
Here we show that the gene encoding alpha-catenin (CTNNA1) is expressed at a much lower level in
leukemia
-initiating stem cells from individuals with
AML
or
MDS
with a 5q deletion than in individuals with
MDS
or
AML
lacking a 5q deletion or in normal hematopoietic stem cells.
Analysis of HL-60 cells, a
myeloid leukemia
line with deletion of the 5q31 region, showed that the CTNNA1 promoter of the retained allele is suppressed by both methylation and histone deacetylation.
Thus, loss of expression of the alpha-catenin tumor suppressor in hematopoietic stem cells may provide a growth advantage that contributes to human
MDS
or
AML
with del(5q).
[MeSH-major]
Cell Transformation, Neoplastic. Chromosome Deletion. Chromosomes, Human, Pair 5 / genetics.
Myeloid
Progenitor Cells / pathology. alpha Catenin / genetics
[MeSH-minor]
Acute
Disease. Blotting, Western. Cell Line. Cell Line, Tumor. DNA Methylation / drug effects. Flow Cytometry. Gene Expression Regulation, Neoplastic / drug effects. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. HL-60 Cells. Humans. Hydroxamic Acids / pharmacology. In Situ Hybridization, Fluorescence / methods. K562 Cells.
Leukemia
,
Myeloid
/ blood.
Leukemia
,
Myeloid
/ genetics.
Leukemia
,
Myeloid
/ pathology. Mutation.
Myelodysplastic
Syndromes / blood.
Myelodysplastic
Syndromes / genetics.
Myelodysplastic
Syndromes / pathology. Reverse Transcriptase Polymerase Chain Reaction. Transfection. U937 Cells
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(PMID = 17159988.001).
[ISSN]
1078-8956
[Journal-full-title]
Nature medicine
[ISO-abbreviation]
Nat. Med.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA104987; United States / NCI NIH HHS / CA / CA108631
[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 / CTNNA1 protein, human; 0 / Hydroxamic Acids; 0 / alpha Catenin; 147336-22-9 / Green Fluorescent Proteins; 3X2S926L3Z / trichostatin A
36.
Chen BA, Gao C, Ding J, Ding JH, Sun YY, Zhao G, Cheng J, Wang J, Bao W, Song HH, Xia GH, Ma JL, Wu LL:
[Analysis on laboratory and clinical characteristics in 65 cases of myelodysplastic syndrome].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2009 Dec;17(6):1472-6
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[Title]
[Analysis on laboratory and clinical characteristics in 65 cases of
myelodysplastic syndrome
].
The aim of this study was to gain more insight into the understanding of
myelodysplastic syndrome
in the clinical and laboratory features.
The clinical data of 65 patients with
MDS
were reviewed and analysed.
The median age of them was 66 years old (range 19-89 years), and 6 patients had a history of toxic exposure (secondary
MDS
).
The results showed that
dysplasia
was found in 64 patients examined with bone marrow smears (98.5%), among them trilineage
dysplasia
in 21 patients (32.3%), bilineage
dysplasia
in 33 patients (50.8%), only erythroid
dysplasia
in 8 cases (12.3%) and 2 patients (3.1%) only
with myeloid dysplasia
.
The abnormal chromosome was the major cytogenetic abnormality, which occurred more often in secondary
MDS
and the patients with RAEB or RAEB-T.
Among the 49 patients who had received cytogenetic examination, 15 patients transformed into
AML
with the incidence of 30.61%, but only 3 out of 20 patients in the group of normal chromosome transformed into
AML
(15%), while 12 out of 29 patients in the group of abnormal karyotypes transformed into
AML
(41.4%).
The median time of
following
up was 35 months (range 2 - 106 months).
In conclusion, the incidence of
MDS
in our country is younger than that in Western countries, the rate of abnormal chromosome in high risk
MDS
is higher than that in low risk
MDS
.
Meanwhile, those who have the change of chromosome are related to the transformation of
MDS
into
AML
and have shorter survival time than those
MDS
patients with normal karyotypes.
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(PMID = 20030929.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
CHI
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
37.
Andersson BS, de Lima M, Thall PF, Wang X, Couriel D, Korbling M, Roberson S, Giralt S, Pierre B, Russell JA, Shpall EJ, Jones RB, Champlin RE:
Once daily i.v. busulfan and fludarabine (i.v. Bu-Flu) compares favorably with i.v. busulfan and cyclophosphamide (i.v. BuCy2) as pretransplant conditioning therapy in AML/MDS.
Biol Blood Marrow Transplant
; 2008 Jun;14(6):672-84
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[Title]
Once daily i.v. busulfan and fludarabine (i.v. Bu-Flu) compares favorably with i.v. busulfan and cyclophosphamide (i.v. BuCy2) as pretransplant conditioning therapy in
AML
/
MDS
.
To account for improved supportive care and other unidentified factors that may affect outcome ("period" effects), 78
acute
myelogenous
leukemia
(
AML
) patients receiving Melphalan-Flu (MF), treated in parallel during this time (1997-2004) were used to estimate the period effect.
These results support replacing BuCy +/- ATG with Bu-Flu +/- rabbit-antithymocyte globulin (ATG), and warrant a prospective comparison between allogeneic HSCT and conventional induction/consolidation chemotherapy for
AML
in CR1.
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(PMID = 18489993.001).
[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
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / P01 CA055164-160020; United States / NCI NIH HHS / CA / 2P30CA16672-26; United States / NCI NIH HHS / CA / P01 CA055164
[Publication-type]
Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Myeloablative Agonists; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
[Other-IDs]
NLM/ NIHMS52878; NLM/ PMC4230823
38.
Yagasaki H, Mugishima H:
[Hereditary diseases with propensity to myeloid malignancy].
Nihon Rinsho
; 2009 Oct;67(10):1884-8
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[Title]
[Hereditary diseases with propensity to
myeloid
malignancy].
Hematological malignancy is known to be associated with Down
syndrome
(DS), neurofibromatosis type 1 (NF1) and congenital bone marrow failure syndromes (CBMFS).
Although many responsible germ-cell mutations have been identified, the secondary mutations that are responsible for the development of
myelodysplastic syndrome
and
acute
myelogenous
leukemia
(
MDS
/
AML
) have not been determined.
Additional chromosomal abnormalities such as monosomy 7 and trisomy 21 are often observed in the progression to
MDS
/
AML
, and the critical genes for monosomy 7 have recently been reported.
In this review, we briefly present recent findings regarding DS, NF1 and CBMFS with a tendency for malignant transformation; Fanconi anemia, familial platelet disorder with propensity to
myeloid
malignancy and congenital severe neutropenia.
[MeSH-major]
Blood Platelet Disorders / genetics. Down
Syndrome
/ genetics. Fanconi Anemia / genetics.
Leukemia
,
Myeloid
/ genetics. Neurofibromatosis 1 / genetics. Neutropenia / genetics
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(PMID = 19860184.001).
[ISSN]
0047-1852
[Journal-full-title]
Nihon rinsho. Japanese journal of clinical medicine
[ISO-abbreviation]
Nippon Rinsho
[Language]
jpn
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Japan
[Number-of-references]
15
39.
Montoto S, Canals C, Rohatiner AZ, Taghipour G, Sureda A, Schmitz N, Gisselbrecht C, Fouillard L, Milpied N, Haioun C, Slavin S, Conde E, Fruchart C, Ferrant A, Leblond V, Tilly H, Lister TA, Goldstone AH, EBMT Lymphoma Working Party:
Long-term follow-up of high-dose treatment with autologous haematopoietic progenitor cell support in 693 patients with follicular lymphoma: an EBMT registry study.
Leukemia
; 2007 Nov;21(11):2324-31
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Thirty-nine patients developed secondary
myelodysplastic syndrome
/
acute myeloid
leukaemia (
MDS
/
AML
), in 34 cases having received TBI as the conditioning regimen.
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(PMID = 17637813.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
40.
Wilking N, Lidbrink E, Wiklund T, Erikstein B, Lindman H, Malmström P, Kellokumpu-Lehtinen P, Bengtsson NO, Söderlund G, Anker G, Wist E, Ottosson S, Salminen E, Ljungman P, Holte H, Nilsson J, Blomqvist C, Bergh J:
Long-term follow-up of the SBG 9401 study comparing tailored FEC-based therapy versus marrow-supported high-dose therapy.
Ann Oncol
; 2007 Apr;18(4):694-700
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Ten patients in the tailored FEC regimen developed
acute myeloid
leukaemia (
AML
)/myelodysplasia (
MDS
).
CONCLUSION: The update of this study shows an improved outcome linked to the tailored FEC treatment in relation to breast cancer relapse, but also an increased incidence of
AML
/
MDS
.
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.
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.
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(PMID = 17301072.001).
[ISSN]
0923-7534
[Journal-full-title]
Annals of oncology : official journal of the European Society for Medical Oncology
[ISO-abbreviation]
Ann. Oncol.
[Language]
ENG
[Publication-type]
Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
143011-72-7 / Granulocyte Colony-Stimulating Factor; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; U3P01618RT / Fluorouracil
41.
Tanvetyanon T, Stiff PJ:
Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations.
Leuk Lymphoma
; 2005 Jan;46(1):151-4
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[Title]
Recurrent steroid-responsive pancreatitis associated
with myelodysplastic syndrome
and transformations.
Several paraneoplastic inflammatory conditions, particularly autoimmune diseases, have been described in association
with myelodysplastic
syndromes (
MDS
).
However, to date, recurrent
acute
pancreatitis has never been described in association with
MDS
.
Aortitis and pericarditis were diagnosed simultaneously with
MDS
, refractory anemia with excess blast type 2.
The vasculitic
syndrome
responded rapidly to corticosteroids, but soon after tapering of corticosteroids,
acute
pancreatitis developed.
Finally, his
MDS
transformed into
acute myeloid leukemia
(
AML
); severe
acute
pancreatitis closely accompanied.
A subsequent pancreatitis attack with pseudocyst formation occurred, but again was controlled with corticosteroids, although this was followed closely by another relapse of
AML
.
All etiologies for recurrent
acute
pancreatitis were ruled out.
The dramatic response of his pancreatitis attacks to immunosuppression suggested its autoimmune origin, while the close relationship in both the timing and severity of
acute
pancreatitis and
MDS
/
AML
suggested that the autoimmune pancreatitis was a paraneoplastic phenomenon related to
MDS
.
[MeSH-major]
Myelodysplastic
Syndromes / complications.
Myelodysplastic
Syndromes / pathology. Pancreatitis / drug therapy. Pancreatitis / pathology. Steroids / therapeutic use
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(PMID = 15621795.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Steroids
42.
Boehrer S, Adès L, Braun T, Galluzzi L, Grosjean J, Fabre C, Le Roux G, Gardin C, Martin A, de Botton S, Fenaux P, Kroemer G:
Erlotinib exhibits antineoplastic off-target effects in AML and MDS: a preclinical study.
Blood
; 2008 Feb 15;111(4):2170-80
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[Title]
Erlotinib exhibits antineoplastic off-target effects in
AML
and
MDS
: a preclinical study.
Erlotinib, an inhibitor of the epidermal growth factor receptor (EGFR), induces differentiation, cell-cycle arrest, and apoptosis of EGFR-negative myeloblasts of patients
with myelodysplastic syndrome
(
MDS
) and
acute myeloid leukemia
(
AML
), as well as in EGFR-negative cell lines representing these diseases (P39, KG-1, and HL 60).
In apoptosis-sensitive
AML
cells, erlotinib caused a rapid (within less than 1 hour) nucleocytoplasmic translocation of nucleophosmin-1 (NPM-1) and p14(ARF).
Moreover, erlotinib reduced the growth of xenografted human
AML
cells in vivo.
Erlotinib also killed CD34(+) bone marrow blasts
from MDS
and
AML
patients while sparing normal CD34(+) progenitors.
One patient afflicted with both
MDS
and non-small cell lung cancer manifested hematologic improvement in response to erlotinib.
In summary, we here provide novel evidence in vitro, ex vivo, and in vivo for the potential therapeutic efficacy of erlotinib in the treatment of high-risk
MDS
and
AML
.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Myelodysplastic
Syndromes / drug therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use
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(PMID = 17925489.001).
[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 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride
43.
Shimoni A, Hardan I, Shem-Tov N, Yerushalmi R, Nagler A:
Allogeneic hematopoietic stem-cell transplantation in AML and MDS using myeloablative versus reduced-intensity conditioning: long-term follow-up.
Leukemia
; 2010 May;24(5):1050-2
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[Title]
Allogeneic hematopoietic stem-cell transplantation in
AML
and
MDS
using myeloablative versus reduced-intensity conditioning: long-term follow-up.
[MeSH-major]
Hematopoietic Stem Cell Transplantation.
Leukemia
,
Myeloid
,
Acute
/ therapy. Myeloablative Agonists / therapeutic use.
Myelodysplastic
Syndromes / therapy. Transplantation Conditioning
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(PMID = 20147978.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Comparative Study; Letter
[Publication-country]
England
[Chemical-registry-number]
0 / Myeloablative Agonists
44.
Carvalho G, Fabre C, Braun T, Grosjean J, Ades L, Agou F, Tasdemir E, Boehrer S, Israel A, Véron M, Fenaux P, Kroemer G:
Inhibition of NEMO, the regulatory subunit of the IKK complex, induces apoptosis in high-risk myelodysplastic syndrome and acute myeloid leukemia.
Oncogene
; 2007 Apr 5;26(16):2299-307
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[Title]
Inhibition of NEMO, the regulatory subunit of the IKK complex, induces apoptosis in high-risk
myelodysplastic syndrome
and
acute myeloid leukemia
.
In high-risk
myelodysplastic
syndromes (
MDS
) and
acute myeloid leukemia
(
AML
), blasts constitutively activate the antiapoptotic transcription factor nuclear factor-kappaB (NF-kappaB).
A cell-permeable peptide that mimics the leucine zipper subdomain of IKKgamma, thus preventing its oligomerization, inhibited the constitutive NF-kappaB activation and induced apoptotic cell death in a panel of human
MDS
and
AML
cell lines (P39, MOLM13, THP1 and MV4-11).
Primary bone marrow CD34(+) cells from high-risk
MDS
and
AML
patients also succumbed to the IKKgamma/NEMO-antagonistic peptide, but not to a mutated control peptide.
Altogether, these data indicate that malignant cells in high-risk
MDS
and
AML
cells critically depend on IKKgamma/NEMO to survive.
[MeSH-major]
I-kappa B Kinase / antagonists & inhibitors.
Leukemia
,
Myeloid
/ pathology.
Myelodysplastic
Syndromes / pathology
[MeSH-minor]
Acute
Disease. Amino Acid Sequence. Apoptosis. Cell Line, Tumor. Humans. Molecular Sequence Data. NF-kappa B / physiology. Peptide Fragments / chemistry. Protein Subunits. RNA, Small Interfering / genetics. Transfection
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(PMID = 17043643.001).
[ISSN]
0950-9232
[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 / IKBKG protein, human; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Protein Subunits; 0 / RNA, Small Interfering; EC 2.7.11.10 / I-kappa B Kinase
45.
Niimi H, Harada H, Harada Y, Ding Y, Imagawa J, Inaba T, Kyo T, Kimura A:
Hyperactivation of the RAS signaling pathway in myelodysplastic syndrome with AML1/RUNX1 point mutations.
Leukemia
; 2006 Apr;20(4):635-44
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[Title]
Hyperactivation of the RAS signaling pathway in
myelodysplastic syndrome
with AML1/RUNX1 point mutations.
AML1/RUNX1 mutations have been reported frequently in
myelodysplastic syndrome
(
MDS
) patients, especially those diagnosed with refractory anemia with excess blast (RAEB), RAEB in transformation (RAEBt), or
AML
following
MDS
(these categories are defined as
MDS
/
AML
).
Although AML1 mutations are suspected to play a pivotal role in the development of
MDS
/
AML
, acquisition of additional genetic alterations is also necessary.
We analyzed gene alterations in
MDS
/
AML
patients with AML1 mutations, comparing them to alterations in those without an AML1 mutation.
AML1 mutations were significantly associated with -7/7q-, whereas
MDS
/
AML
patients without AML1 mutations showed a high frequency of -5/5q- and a complex karyotype.
Patients with AML1 mutations showed more mutations of their FLT3, N-RAS, PTPN11, and NF1 genes, resulting in a significantly higher mutation frequency for receptor tyrosine kinase (RTK)-RAS signaling pathways in AML1-mutated
MDS
/
AML
patients compared to AML1-wild-type
MDS
/
AML
patients (38% versus 6.3%, P < 0.0001).
Furthermore, blast cells of the AML1-mutated patients expressing surface c-KIT, and SHP-2 mutants contributed to prolonged and enhanced extracellular signal-regulated kinase activation
following
stem cell factor stimulation.
Our results suggest that
MDS
/
AML arising
from AML1/RUNX1 mutations has a significant association with -7/7q- alteration, and frequently involves RTK-RAS signaling pathway activation.
[MeSH-major]
Core Binding Factor Alpha 2 Subunit / genetics. Genes, ras.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myelodysplastic
Syndromes / genetics.
Myelodysplastic
Syndromes / metabolism. Point Mutation. Signal Transduction
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(PMID = 16467864.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / Intracellular Signaling Peptides and Proteins; 0 / Ligands; 0 / RUNX1 protein, human; 62229-50-9 / Epidermal Growth Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases
46.
Alter BP, Giri N, Savage SA, Peters JA, Loud JT, Leathwood L, Carr AG, Greene MH, Rosenberg PS:
Malignancies and survival patterns in the National Cancer Institute inherited bone marrow failure syndromes cohort study.
Br J Haematol
; 2010 Jul;150(2):179-88
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Fanconi anaemia (FA), dyskeratosis congenita (DC), Diamond-Blackfan anaemia (DBA), and Shwachman-Diamond
syndrome
(SDS) comprise major inherited bone marrow failure syndromes (IBMFS).
Adverse events include severe bone marrow failure (BMF),
myelodysplastic syndrome
(
MDS
),
acute myeloid
leukaemia (
AML
), and solid tumours (ST).
Most patients in each
syndrome
survived to young adulthood.
While FA and DC patients had markedly increased risks of cancer,
AML
and
MDS
, there were no cases of leukaemia in DBA or SDS patients.
[MeSH-minor]
Adolescent. Adult. Age Distribution. Anemia, Diamond-Blackfan / complications. Anemia, Diamond-Blackfan / genetics. Child. Child, Preschool. Dyskeratosis Congenita / complications. Dyskeratosis Congenita / genetics. Epidemiologic Methods. Fanconi Anemia / complications. Fanconi Anemia / genetics. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Prognosis.
Syndrome
. Young Adult
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[ISSN]
1365-2141
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CP / N02CP31003; United States / NCI NIH HHS / CP / N02CP65501; United States / NCI NIH HHS / CP / N02CP65504; United States / Intramural NIH HHS / / ZIA CP010144-12; United States / NCI NIH HHS / CP / N02CP11019
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
[Publication-country]
England
[Other-IDs]
NLM/ NIHMS298716; NLM/ PMC3125983
47.
Warlick ED, O'Donnell PV, Borowitz M, Grupka N, Decloe L, Garrett-Mayer E, Borrello I, Brodsky R, Fuchs E, Huff CA, Luznik L, Matsui W, Ambinder R, Jones RJ, Smith BD:
Myeloablative allogeneic bone marrow transplant using T cell depleted allografts followed by post-transplant GM-CSF in high-risk myelodysplastic syndromes.
Leuk Res
; 2008 Sep;32(9):1439-47
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[Title]
Myeloablative allogeneic bone marrow transplant using T cell depleted allografts followed by post-transplant GM-CSF in high-risk
myelodysplastic
syndromes.
Allogeneic blood and marrow transplantation (alloBMT) remains the only curative treatment for patients
with myelodysplastic
syndromes (
MDS
), but its application has been limited by the older age range of patients with this disease.
Myeloid
growth factors have been used to speed engraftment
following
alloBMT, but data suggest that they may also have anti-tumor properties.
We treated 43 patients (median age 56) with
MDS
/
AML
with high-risk features using a myeloablative T cell depleted alloBMT followed by prolonged systemic GM-CSF.
These results suggest that it is possible to maintain treatment intensity while minimizing toxicity in older, high-risk
MDS
patients.
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[CommentIn]
Leuk Res. 2008 Sep;32(9):1354-5
[
18346785.001
]
(PMID = 18261793.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA015396-33; United States / NCI NIH HHS / CA / P01 CA015396; United States / NCI NIH HHS / CA / P01 CA015396-33; United States / NCI NIH HHS / CA / P01CA15396
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
[Other-IDs]
NLM/ NIHMS53499; NLM/ PMC2719785
48.
Andersen MK, Christiansen DH, Pedersen-Bjergaard J:
Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML.
Leukemia
; 2005 Feb;19(2):197-200
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[Title]
Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related
MDS
and
AML
.
Amplification or duplication of the AML1 gene at chromosome band 21q22 was detected by FISH using a locus-specific probe in three out of 171 unselected patients with therapy-related myelodysplasia (t-
MDS
) or t-
AML
(1.7%).
The results support a pivotal role of impaired TP53 function in the development of gene amplification or duplication in t-
MDS
and t-
AML
.
[MeSH-major]
Chromosomes, Human, Pair 21 / genetics. DNA-Binding Proteins / genetics. Gene Amplification / genetics. Gene Duplication. Genes, p53.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myelodysplastic
Syndromes / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics
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(PMID = 15618958.001).
[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 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Transcription Factors
49.
Corey SJ, Minden MD, Barber DL, Kantarjian H, Wang JC, Schimmer AD:
Myelodysplastic syndromes: the complexity of stem-cell diseases.
Nat Rev Cancer
; 2007 Feb;7(2):118-29
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[Title]
Myelodysplastic
syndromes: the complexity of stem-cell diseases.
The prevalence of patients
with myelodysplastic
syndromes (
MDS
) is increasing owing to an ageing population and increased awareness of these diseases.
MDS
represent many different conditions, not just a single disease, that are grouped together by several clinical characteristics.
A striking feature of
MDS
is genetic instability, and a large proportion of cases result in
acute myeloid
leukaemia (
AML
).
We Review three emerging principles of
MDS
biology: stem-cell dysfunction and the overlap with
AML
, genetic instability and the deregulation of apoptosis, in the context of inherited bone marrow-failure syndromes, and treatment-related
MDS
and
AML
.
[MeSH-major]
Myelodysplastic
Syndromes / pathology. Stem Cells / pathology
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(PMID = 17251918.001).
[ISSN]
1474-175X
[Journal-full-title]
Nature reviews. Cancer
[ISO-abbreviation]
Nat. Rev. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents
[Number-of-references]
114
50.
Gupta G, Singh R, Kotasthane DS, Kotasthane VD:
Myelodysplastic syndromes/neoplasms: recent classification system based on World Health Organization Classification of Tumors - International Agency for Research on Cancer for Hematopoietic and Lymphoid Tissues.
J Blood Med
; 2010;1:171-82
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[Title]
Myelodysplastic
syndromes/neoplasms: recent classification system based on World Health Organization Classification of Tumors - International Agency for Research on Cancer for Hematopoietic and Lymphoid Tissues.
The
myelodysplastic
Syndromes (
MDS
) are a group of clonal hematopoietic stem cell diseases characterized by cytopenia(s),
dysplasia
in one or more of the major
myeloid
cell lines, ineffective hematopoiesis, and increased risk of development of
acute myeloid leukemia
.
The
myelodysplastic
syndromes are now classified into the
following
categories - refractory cytopenia with unilineage
dysplasia
, refractory anemia with ring sideroblasts, refractory cytopenia
with multilineage dysplasia
, refractory anemia with excess blasts,
myelodysplastic syndrome
associated with isolated del (5q),
myelodysplastic syndrome
- unclassifiable, and childhood
myelodysplastic syndrome
.
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(PMID = 22282696.001).
[ISSN]
1179-2736
[Journal-full-title]
Journal of blood medicine
[ISO-abbreviation]
J Blood Med
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
New Zealand
[Other-IDs]
NLM/ PMC3262332
[Keywords]
NOTNLM ; leukemia / myelodysplastic syndromes
51.
Brethon B, Auvrignon A, Galambrun C, Yakouben K, Leblanc T, Bertrand Y, Leverger G, Baruchel A:
Efficacy and tolerability of gemtuzumab ozogamicin (anti-CD33 monoclonal antibody, CMA-676, Mylotarg) in children with relapsed/refractory myeloid leukemia.
BMC Cancer
; 2006;6:172
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[Title]
Efficacy and tolerability of gemtuzumab ozogamicin (anti-CD33 monoclonal antibody, CMA-676, Mylotarg) in children with relapsed/refractory
myeloid leukemia
.
BACKGROUND: Gemtuzumab ozogamicin (GO) is a cytotoxic anti-CD33 monoclonal antibody that has given promising preliminary results in adult
myeloid
CD33+
AML
.
Three patients (2
MDS
/
AML
, 1 JMML) were refractory to first-line treatment, 8 patients with de novo
AML
were in refractory first relapse, and one patient with de novo
AML
was in 2nd relapse after stem cell transplantation (SCT).
No case of sinusoidal obstruction
syndrome
occurred.
CONCLUSION: These results warrant a prospective trial of GO in a larger population of children with
AML
.
[MeSH-major]
Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Immunotoxins / therapeutic use.
Leukemia
,
Myeloid
/ drug therapy
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[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
England
[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 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
[Other-IDs]
NLM/ PMC1523361
52.
Voso MT, D'Alò F, Greco M, Fabiani E, Criscuolo M, Migliara G, Pagano L, Fianchi L, Guidi F, Hohaus S, Leone G:
Epigenetic changes in therapy-related MDS/AML.
Chem Biol Interact
; 2010 Mar 19;184(1-2):46-9
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[Title]
Epigenetic changes in therapy-related
MDS
/
AML
.
Therapy-related
Myelodysplastic
Syndromes/
Acute Myeloid
Leukemias (t-
MDS
/
AML
) are one of the most compelling long term adverse events occurring in cancer survivors treated with chemo-radiotherapy regimes.
Gene promoter methylation is a common finding in t-
MDS
/
AML
and has been associated to a shorter latency period from the treatment of the primary tumor.
We found frequent methylation of DAPK in the t-
MDS
/
AML
group, especially in patients with a
previous
lymphoproliferative disease.
In patients studied for concurrent methylation of several promoters, t-
MDS
/
AML
were significantly more frequently hypermethylated in 2 or more promoter regions than de novo
MDS
or
AML
suggesting that promoter hypermethylation of genes involved in cell cycle control, apoptosis and DNA repair pathways is a frequent finding in t-
MDS
/
AML
and may contribute to secondary leukemogenesis.
[MeSH-major]
Epigenesis, Genetic. Gene Expression Regulation, Neoplastic.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myelodysplastic
Syndromes / genetics
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[Copyright]
Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
(PMID = 19874806.001).
[ISSN]
1872-7786
[Journal-full-title]
Chemico-biological interactions
[ISO-abbreviation]
Chem. Biol. Interact.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
53.
Pulliam-Leath AC, Ciccone SL, Nalepa G, Li X, Si Y, Miravalle L, Smith D, Yuan J, Li J, Anur P, Orazi A, Vance GH, Yang FC, Hanenberg H, Bagby GC, Clapp DW:
Genetic disruption of both Fancc and Fancg in mice recapitulates the hematopoietic manifestations of Fanconi anemia.
Blood
; 2010 Oct 21;116(16):2915-20
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Fanconi anemia (FA) is an inherited chromosomal instability
syndrome
characterized by bone marrow failure, myelodysplasia (
MDS
), and
acute myeloid leukemia
(
AML
).
Here we show that double-mutant Fancc(-/-);Fancg(-/-) mice develop spontaneous hematologic sequelae including bone marrow failure,
AML
,
MDS
and complex random chromosomal abnormalities that the single-mutant mice do not.
Importantly, this model closely recapitulates the phenotypes found in FA patients and may be useful as a preclinical platform to evaluate the molecular pathogenesis of spontaneous bone marrow failure,
MDS
and
AML
in FA.
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]
(PMID = 20606166.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / T32 HL007910; United States / NCI NIH HHS / CA / R01 CA138287-01; United States / NHLBI NIH HHS / HL / P01 HL053586; United States / NHLBI NIH HHS / HL / T32 HL07910-09; United States / NHLBI NIH HHS / HL / P01 HL053586-14
[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 / Fancc protein, mouse; 0 / Fancg protein, mouse; 0 / Fanconi Anemia Complementation Group C Protein; 0 / Fanconi Anemia Complementation Group G Protein
[Other-IDs]
NLM/ PMC2974601
54.
Pagel JM, Gooley TA, Rajendran J, Fisher DR, Wilson WA, Sandmaier BM, Matthews DC, Deeg HJ, Gopal AK, Martin PJ, Storb RF, Press OW, Appelbaum FR:
Allogeneic hematopoietic cell transplantation after conditioning with 131I-anti-CD45 antibody plus fludarabine and low-dose total body irradiation for elderly patients with advanced acute myeloid leukemia or high-risk myelodysplastic syndrome.
Blood
; 2009 Dec 24;114(27):5444-53
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[Title]
Allogeneic hematopoietic cell transplantation after conditioning with 131I-anti-CD45 antibody plus fludarabine and low-dose total body irradiation for elderly patients with advanced
acute myeloid leukemia
or high-risk
myelodysplastic syndrome
.
Fifty-eight patients older than 50 years with advanced
acute myeloid leukemia
(
AML
) or high-risk
myelodysplastic syndrome
(
MDS
) were treated with (131)I-BC8 Ab and fludarabine plus 2 Gy total body irradiation.
Eighty-six percent of patients had
AML
or
MDS
with greater than 5% marrow blasts at the time of transplantation.
These results show that CD45-targeted radiotherapy can be safely combined with a reduced-intensity conditioning regimen to yield encouraging overall survival for older, high-risk patients with
AML
or
MDS
.
[MeSH-major]
Hematopoietic Stem Cell Transplantation / methods.
Leukemia
,
Myeloid
/ therapy.
Myelodysplastic
Syndromes / therapy. Transplantation Conditioning / methods
[MeSH-minor]
Acute
Disease. Aged. Antibodies / administration & dosage. Antibodies / immunology. Antigens, CD45 / immunology. Combined Modality Therapy. Female. Humans. Iodine Radioisotopes / pharmacokinetics. Male. Middle Aged. Risk Factors. Survival Analysis. Survival Rate. Tissue Distribution. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Whole-Body Irradiation
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[CommentIn]
Blood. 2009 Dec 24;114(27):5410-1
[
20035041.001
]
(PMID = 19786617.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00008177
[Grant]
United States / NCI NIH HHS / CA / K08 CA095448; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / R01 CA109663; United States / NCI NIH HHS / CA / P01 CA044991; United States / NCI NIH HHS / CA / P01 CA078902
[Publication-type]
Clinical Trial, Phase II; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies; 0 / Iodine Radioisotopes; EC 3.1.3.48 / Antigens, CD45; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
[Other-IDs]
NLM/ PMC2798861
55.
Park CH, Kimler BF, Yi SY, Park SH, Kim K, Jung CW, Kim SH, Lee ER, Rha M, Kim S, Park MH, Lee SJ, Park HK, Lee MH, Yoon SS, Min YH, Kim BS, Kim JA, Kim WS:
Depletion of L-ascorbic acid alternating with its supplementation in the treatment of patients with acute myeloid leukemia or myelodysplastic syndromes.
Eur J Haematol
; 2009 Aug;83(2):108-18
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[Title]
Depletion of L-ascorbic acid alternating with its supplementation in the treatment of patients
with acute myeloid leukemia
or
myelodysplastic
syndromes.
PURPOSE: L-ascorbic acid (LAA) modifies the in vitro growth of leukemic cells from approximately 50% of patients
with acute myeloid leukemia
(
AML
) or
myelodysplastic
syndromes (
MDS
).
Experimental results: During depletion phase, patients with refractory
AML
or
MDS
were placed on a diet deficient in LAA; during supplementation phase, patients received daily intravenous administration of LAA.
[MeSH-major]
Ascorbic Acid / metabolism. Ascorbic Acid / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ diet therapy.
Myelodysplastic
Syndromes / diet therapy
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(PMID = 19284416.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00329498
[Grant]
United States / NCI NIH HHS / CA / KO4 CA00534; United States / NCI NIH HHS / CA / R01 CA20717
[Publication-type]
Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
PQ6CK8PD0R / Ascorbic Acid
56.
Rudd E, Göransdotter Ericson K, Zheng C, Uysal Z, Ozkan A, Gürgey A, Fadeel B, Nordenskjöld M, Henter JI:
Spectrum and clinical implications of syntaxin 11 gene mutations in familial haemophagocytic lymphohistiocytosis: association with disease-free remissions and haematopoietic malignancies.
J Med Genet
; 2006 Apr;43(4):e14
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Two of the six patients harbouring STX11 gene defects developed
myelodysplastic syndrome
(
MDS
) or
acute
myelogenous leukaemia (
AML
).
These results suggest that STX11 gene mutations may be associated with secondary malignancies (
MDS
/
AML
), and that there is segregation of specific clinical features in FHL patients with an underlying genotype.
[MeSH-major]
Leukemia
,
Myeloid
/ genetics. Lymphohistiocytosis, Hemophagocytic / diagnosis. Lymphohistiocytosis, Hemophagocytic / genetics. Mutation.
Myelodysplastic
Syndromes / genetics. Qa-SNARE Proteins / genetics
[MeSH-minor]
Acute
Disease. Adult. Aged, 80 and over. Child. Child, Preschool. DNA Mutational Analysis. Female. Genotype. Humans. Infant. Male. Pedigree. Phenotype. Psychomotor Disorders / complications. Psychomotor Disorders / genetics. Remission, Spontaneous
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SciCrunch.
OMIM: Data: Gene Annotation
.
SciCrunch.
Clinical Genomic Database: Data: Gene Annotation
.
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[ISSN]
1468-6244
[Journal-full-title]
Journal of medical genetics
[ISO-abbreviation]
J. Med. Genet.
[Language]
eng
[Publication-type]
Letter; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Qa-SNARE Proteins
[Other-IDs]
NLM/ PMC2563216
57.
Bacher U, Haferlach T, Kern W, Haferlach C, Schnittger S:
A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia.
Haematologica
; 2007 Jun;92(6):744-52
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[Title]
A comparative study of molecular mutations in 381 patients
with myelodysplastic syndrome
and in 4130 patients
with acute myeloid leukemia
.
BACKGROUND AND OBJECTIVES: The precise relationship between
myelodysplastic syndrome
(
MDS
) and
acute myeloid leukemia
(
AML
) is unclear and the role of molecular mutations in leukemic transformation in
MDS
is controversial.
The aim of this study was to clarify the relationship between
AML
and
MDS
by comparing the frequency of molecular mutations in the two conditions.
DESIGN AND METHODS: We compared the frequency of FLT3-length mutations (FLT3-LM), FLT3-TKD, MLL-partial tandem duplications (MLL-PTD), NRAS, and KITD816 in 381 patients with
MDS
refractory anemia with excess blasts [RAEB] n=49; with ringed sideroblasts [RARS] n=310; chronic monomyelocytic
leukemia
[CMML] n=22) and in 4130 patients with
AML
(de novo: n=3139; secondary
AML
[s-
AML
]
following
MDS
: n=397; therapy-related [t-
AML
]: n=233; relapsed: n=361).
RESULTS: All mutations were more frequent in s-
AML
than in
MDS
and all but the FLT3-TKD were more frequent in RAEB than in RA/RARS.
The higher incidences in s-
AML
were significant for FLT3-TKD (p=0.032), MLL-PTD (p=0.034), and FLT3-LM (RA/RARS: 0/45; RAEB: 8/293; 2.7%; s-
AML
: 45/389; 11.6%; p<0.0001).
The incidence of NRAS-mutations increased from 17/272 (6.3%) in
MDS
to 41/343 in s-
AML
(12.0%) and that of KITD816-mutations from 2/290 (0.7%) to 5/341 (1.5%) (p=n.s.).
FLT3-LM-acquisition occurred in 3/22 cases (13.6%) during
MDS
transformation; NRAS-acquisition occurred in 1/24 (4.2%).
FLT3-LM and MLL-PTD were more frequent in
AML
relapse than in de novo
AML
or s-
AML
(p<0.0001).
INTERPRETATION AND CONCLUSIONS: The increase of molecular mutations from low- to high-risk
MDS
, to s-
AML
, and to relapsed
AML
emphasizes the value of these mutations as markers of progressing disease.
Finally, we found a low rate of 5q- in the molecularly mutated cases in
MDS
which might explain the stability of this subtype.
[MeSH-major]
Leukemia
,
Myeloid
/ genetics. Mutation.
Myelodysplastic
Syndromes / genetics
[MeSH-minor]
Acute
Disease. Disease Progression. Gene Frequency. Histone-Lysine N-Methyltransferase. Humans. Molecular Epidemiology.
Myeloid
-Lymphoid
Leukemia
Protein / genetics. Proto-Oncogene Proteins c-kit / genetics. fms-Like Tyrosine Kinase 3 / genetics. ras Proteins / genetics
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[CommentIn]
Haematologica. 2007 Jun;92(6):723-7
[
17550842.001
]
(PMID = 17550846.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / ras Proteins
58.
McVey M, Cserti-Gazdewich CM:
Platelet transfusion refractoriness responding preferentially to single donor aphaeresis platelets compatible for both ABO and HLA.
Transfus Med
; 2010 Oct;20(5):346-53
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Patient 1, age 59 years, group O,
with myelodysplastic syndrome
/
acute
myelogenous
leukemia
(
MDS
/
AML
), was unresponsive to either fresh ABO-m or HLA-m platelets.
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[Copyright]
© 2010 The Authors. Transfusion Medicine © 2010 British Blood Transfusion Society.
(PMID = 20492602.001).
[ISSN]
1365-3148
[Journal-full-title]
Transfusion medicine (Oxford, England)
[ISO-abbreviation]
Transfus Med
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / ABO Blood-Group System; 0 / HLA Antigens
59.
Li X, Wu LY, Ying SX, Chang CK, He Q, Song LQ, Pu Q:
[Preliminary study of biological characteristics of myelodysplastic syndromes clonal cells].
Zhonghua Xue Ye Xue Za Zhi
; 2007 Jul;28(7):478-83
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[Title]
[Preliminary study of biological characteristics of
myelodysplastic
syndromes clonal cells].
OBJECTIVE: To investigate the biological difference of clonal cells between
myelodysplastic
syndromes (
MDS
) and
acute myeloid leukemia
(
AML
).
METHOD: Bone marrow (BM) clonal cells (which had cytogenetic markers detected by FISH assay) and blasts were quantitatively analysed in 51
MDS
and 11
AML
patients.
The biological functions for phagocytosis and oxidation of
MDS
peripheral blood (PB) neutrophils were compared with that of normal controls.
RESULTS: Almost all
MDS
patients BM had a higher clonal cell percentage (mean 48.2%) than blasts percentage (mean 6.7%) (P < 0.01), but with the subtype of
MDS
advancing this percentage gap was closing up, and in 11
AML
patients no such gap was observed.
This gap in
MDS
patients with + 8 abnormality was smaller than in those with 5q -.
In
MDS
BM, clonal cells were detected in segmented granulocytes (mean 45.9%), orthochromatic normoblasts (mean 46.0%) and mature megakaryocytes (mean 38.0%).
In Addition, an approximate amount of clonal cells with the same karyotype abnormality in BM were detected in
MDS
PB (mean 37.3% in blood vs 48.6% in marrow).
Functional analysis showed that the neutrophils in
MDS
PB could exert nearly normal physiological functions (P > 0.05), but those
from AML
could not as compared to healthy donors (P < 0.01).
CONCLUSION: There is a significant difference in the biological features between
MDS
and
AML
clonal cells.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ pathology.
Myelodysplastic
Syndromes / pathology
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(PMID = 18072633.001).
[ISSN]
0253-2727
[Journal-full-title]
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
[ISO-abbreviation]
Zhonghua Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
60.
Iwai M, Kiyoi H, Ozeki K, Kinoshita T, Emi N, Ohno R, Naoe T:
Expression and methylation status of the FHIT gene in acute myeloid leukemia and myelodysplastic syndrome.
Leukemia
; 2005 Aug;19(8):1367-75
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[Title]
Expression and methylation status of the FHIT gene in
acute myeloid leukemia
and
myelodysplastic syndrome
.
To clarify the role of fragile histidine triad (FHIT) in hematological malignancies, we examined the methylation status and the expression level of the FHIT gene in
myelodysplastic syndrome
(
MDS
) and
acute myeloid leukemia
(
AML
) cells in comparison with the methylation of the p15(INK4B) gene.
The FHIT methylation was found in 13 of 94 (13.8%)
AML
and 22 of 40 (55.0%)
MDS
cases, but not in normal mononuclear cells (MNCs).
Both the frequency and density of methylation increased in the advanced-stages
MDS
and the relapsed
AML
cases.
Although FHIT and p15(INK4B) methylations were not correlated in
MDS
and
AML
, increased FHIT methylation at the relapse in
AML
was associated with p15(INK4B) methylation.
The median expression level in
AML
was significantly higher than in normal MNCs, although the median expression level in those with methylation was significantly lower than in those without methylation.
Furthermore, the methylation level at relapse was significantly higher than at diagnosis in
AML
.
These results suggested that FHIT methylation was accumulated through the disease progression of
MDS
and
AML
, and the role of the FHIT gene as a tumor suppressor seemed different in
AML
and
MDS
.
[MeSH-major]
Acid Anhydride Hydrolases / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic.
Leukemia
,
Myeloid
/ genetics.
Myelodysplastic
Syndromes / genetics. Neoplasm Proteins / genetics
[MeSH-minor]
Acute
Disease. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Bone Marrow / pathology. Cell Cycle Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p15. Genes, Tumor Suppressor. Humans. RNA, Messenger / analysis. Recurrence. Tumor Suppressor Proteins / genetics
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[Copyright]
Leukemia (2005) 19, 1367-1375.
(PMID = 15902282.001).
[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 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 0 / fragile histidine triad protein; 776B62CQ27 / decitabine; EC 3.6.- / Acid Anhydride Hydrolases; M801H13NRU / Azacitidine
61.
Reindl C, Quentmeier H, Petropoulos K, Greif PA, Benthaus T, Argiropoulos B, Mellert G, Vempati S, Duyster J, Buske C, Bohlander SK, Humphries KR, Hiddemann W, Spiekermann K:
CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion acute myeloid leukemia/myelodysplastic syndrome subtypes.
Clin Cancer Res
; 2009 Apr 1;15(7):2238-47
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[Title]
CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion
acute myeloid leukemia
/
myelodysplastic syndrome
subtypes.
In this study, we determined the frequency of CBL mutations in
acute
leukemias and evaluated the oncogenic potential of mutant CBL.
EXPERIMENTAL DESIGN: The cDNA of 300
acute myeloid leukemia
(
AML
)/
myelodysplastic syndrome
(
MDS
) and
acute
lymphoblastic
leukemia
(ALL) patients and 82 human leukemic cell lines was screened for aberrations in the linker and RING finger domain of CBL.
RESULTS: We identified 3 of 279
AML
/
MDS
patients expressing CBL exon 8/9 deletion mutants.
One of 116 sequenced
AML
/
MDS
cases carried a R420G missense mutation.
All
AML
/
MDS
patients with identified CBL mutants belonged to the core binding factor and 11q deletion
AML
subtypes.
CONCLUSION: CBL exon8/9 mutants occur in genetically defined
AML
/
MDS
subtypes and transform hematopoietic cells by constitutively activating the FLT3 pathway.
This phenotype resembles the one of mutated RTKs and suggests that CBL mutant
AML
patients might benefit from treatment with FLT3 PTK inhibitors.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics. Mutation.
Myelodysplastic
Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics. fms-Like Tyrosine Kinase 3 / metabolism
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(PMID = 19276253.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
62.
Cashen AF, Shah AK, Todt L, Fisher N, DiPersio J:
Pharmacokinetics of decitabine administered as a 3-h infusion to patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
Cancer Chemother Pharmacol
; 2008 Apr;61(5):759-66
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[Title]
Pharmacokinetics of decitabine administered as a 3-h infusion to patients
with acute myeloid leukemia
(
AML
) or
myelodysplastic syndrome
(
MDS
).
PURPOSE: In this study, pharmacokinetics (PK) of decitabine administered as a 3-h intravenous infusion of 15 mg/m2 every 8 h for 3 days (cycles repeated every 6 weeks) was evaluated in patients with
MDS
or
AML
.
METHODS: The PK of this dosing regimen was evaluated in sixteen patients with
MDS
or
AML
.
CONCLUSIONS: Decitabine dosed at 15 mg/m2 iv every 8 h for 3 days resulted in a predictable and manageable toxicity profile in patients with
MDS
/
AML
.
[MeSH-major]
Antimetabolites, Antineoplastic / pharmacokinetics. Azacitidine / analogs & derivatives.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Myelodysplastic
Syndromes / drug therapy
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.
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(PMID = 17564707.001).
[ISSN]
0344-5704
[Journal-full-title]
Cancer chemotherapy and pharmacology
[ISO-abbreviation]
Cancer Chemother. Pharmacol.
[Language]
eng
[Publication-type]
Clinical Trial, Phase I; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
63.
Epling-Burnette PK, Loughran TP Jr:
Suppression of farnesyltransferase activity in acute myeloid leukemia and myelodysplastic syndrome: current understanding and recommended use of tipifarnib.
Expert Opin Investig Drugs
; 2010 May;19(5):689-98
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[Title]
Suppression of farnesyltransferase activity in
acute myeloid leukemia
and
myelodysplastic syndrome
: current understanding and recommended use of tipifarnib.
IMPORTANCE OF THE FIELD:
Acute myeloid leukemia
(
AML
) and
myelodysplastic syndrome
(
MDS
) incidence in the United States increases with age.
There is an
acute
need for therapeutic developments because of the poor prognosis of these diseases.
Since the knowledge of molecular genetics in
AML
and
MDS
has expanded recently, targeted therapeutics should offer an exciting new frontier for advancement.
AREAS COVERED IN THIS REVIEW: Described in this review are the molecular targets of tipifarnib, safety and tolerability of the drug, chemistry, and clinical efficacy in
AML
.
WHAT THE READER WILL GAIN: The reader will gain a thorough understanding of tipifarnib as it relates to the current and future use of the drug in
AML
.
TAKE HOME MESSAGE: The future of tipifarnib, along with other molecularly-targeted drugs, lies in achieving a better understanding of
leukemia
biology and harnessing the activity of this agent using predictive biomarkers for improved patient selection.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Myelodysplastic
Syndromes / drug therapy. Quinolones / therapeutic use
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(PMID = 20402600.001).
[ISSN]
1744-7658
[Journal-full-title]
Expert opinion on investigational drugs
[ISO-abbreviation]
Expert Opin Investig Drugs
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA112112; United States / NCI NIH HHS / CA / R01 CA112112-01A1
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Quinolones; EC 2.5.1.29 / Farnesyltranstransferase; MAT637500A / tipifarnib
[Number-of-references]
58
[Other-IDs]
NLM/ NIHMS302278; NLM/ PMC3252817
64.
Pan F, Peng S, Fleurence R, Linnehan JE, Knopf K, Kim E:
Economic analysis of decitabine versus best supportive care in the treatment of intermediate- and high-risk myelodysplastic syndromes from a US payer perspective.
Clin Ther
; 2010 Dec;32(14):2444-56
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[Title]
Economic analysis of decitabine versus best supportive care in the treatment of intermediate- and high-risk
myelodysplastic
syndromes from a US payer perspective.
BACKGROUND:
Myelodysplastic
syndromes (
MDS
) are blood and bone marrow disorders that occur primarily in the elderly population, with 30% of all cases progressing to
acute myeloid leukemia
(
AML
).
Red blood cell transfusions--a conventional treatment of
MDS
--have been associated with high costs and decreased quality of life compared with transfusion independence.
Phase III clinical trial data suggest that decitabine may offer an improved
AML
-free survival versus best supportive care (BSC), which consists of red blood cell transfusions, deferoxamine, erythropoiesis-stimulating agents, platelet transfusions, and colony-stimulating factors.
OBJECTIVE: The aim of this study was to assess the cost-effectiveness of 5-day dosing of decitabine versus BSC in US patients with intermediate- and high-risk
MDS from
a US payer perspective.
METHODS: A Markov model with 3 health states (
MDS
,
AML
, and death) was constructed to simulate natural disease progression.
Drug and
AML
costs were obtained from published sources.
RESULTS: In the base-case model, decitabine yielded 0.276 additional year of
AML
-free survival and 0.052 more quality-adjusted life-year (QALY) compared with BSC.
CONCLUSION: In this study, decitabine administered on a 5-day dosing schedule was likely a cost-effective treatment option in patients with intermediate- and high-risk
MDS from
a US payer perspective.
[MeSH-major]
Antimetabolites, Antineoplastic / economics. Azacitidine / analogs & derivatives. Drug Costs. Models, Economic.
Myelodysplastic
Syndromes / drug therapy. Patient Care / economics
[MeSH-minor]
Clinical Trials, Phase III as Topic. Cost-Benefit Analysis. Disease-Free Survival. Drug Administration Schedule. Humans.
Leukemia
,
Myeloid
,
Acute
/ economics.
Leukemia
,
Myeloid
,
Acute
/ mortality.
Leukemia
,
Myeloid
,
Acute
/ prevention & control. Markov Chains. Randomized Controlled Trials as Topic. Risk. United States
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[Copyright]
Copyright © 2010 Elsevier HS Journals, Inc. All rights reserved.
(PMID = 21353113.001).
[ISSN]
1879-114X
[Journal-full-title]
Clinical therapeutics
[ISO-abbreviation]
Clin Ther
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
65.
Hasserjian RP, Zuo Z, Garcia C, Tang G, Kasyan A, Luthra R, Abruzzo LV, Kantarjian HM, Medeiros LJ, Wang SA:
Acute erythroid leukemia: a reassessment using criteria refined in the 2008 WHO classification.
Blood
; 2010 Mar 11;115(10):1985-92
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[Title]
Acute
erythroid
leukemia
: a reassessment using criteria refined in the 2008 WHO classification.
Acute
erythroid
leukemia
(AEL) is a rare type of
acute myeloid leukemia
(
AML
) for which diagnostic criteria have been refined in the 2008 World Health Organization (WHO) classification of
AML
.
The relationship of AEL to
myelodysplastic
syndromes (MDSs) and to
AML
with myelodysplasia-related changes (
AML
-MRC) is not clearly defined.
We conducted a retrospective, multi-institutional study of patients with AEL and compared them with patients with
MDS
or
AML
-MRC with erythroid hyperplasia (> or = 50% erythroid cells).
Among a total of 124 patients with AEL, 32% had a history of
MDS
or chronic cytopenia, 32% had therapy-related disease, and 35% had de novo disease.
Sixty-four percent of patients had unfavorable
AML
risk-group karyotypes.
The median overall survival (OS) of all AEL patients was 8 months, comparable with that of patients with
MDS
or
AML
-MRC with erythroid hyperplasia.
The OS was related to cytogenetic risk group, but not blast count or morphologic
dysplasia
.
Our findings suggest that AEL is in the continuum of
MDS
and
AML
with erythroid hyperplasia, where karyotype rather than an arbitrary blast cutoff represents the most important prognostic factor.
[MeSH-major]
Classification / methods.
Leukemia
, Erythroblastic,
Acute
/ classification. World Health Organization
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[Cites]
Leukemia. 2002 Aug;16(8):1399-401
[
12145675.001
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]
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[
16049515.001
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Cancer Genet Cytogenet. 2005 Dec;163(2):113-22
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16938665.001
]
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17210514.001
]
[Cites]
Blood. 2007 Dec 15;110(13):4385-95
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]
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]
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Mod Pathol. 2008 Nov;21(11):1394-402
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]
[Cites]
Blood. 2009 Feb 26;113(9):1906-8
[
19131546.001
]
[Cites]
Mod Pathol. 2009 Aug;22(8):1023-31
[
19430420.001
]
[Cites]
Blood. 2002 Nov 1;100(9):3135-40
[
12384410.001
]
(PMID = 20040759.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Grant]
United States / NCRR NIH HHS / RR / UL1 RR024153
[Publication-type]
Evaluation Studies; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2942006
66.
Greiner RA, Meier Y, Papadopoulos G, O'Sullivan AK, Imhof A:
Cost-effectiveness of posaconazole compared with standard azole therapy for prevention of invasive fungal infections in patients at high risk in Switzerland.
Oncology
; 2010;78(3-4):172-80
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METHODS: Decision tree models based on the results of two registration trials and subsequent Markov models over patient lifetimes were developed for patients
with acute
myelogenous
leukemia
(
AML
) or
myelodysplastic syndrome
(
MDS
) with neutropenia and for hematopoietic stem cell transplant recipients with graft-versus-host disease (GVHD).
RESULTS: By reducing IFIs in
AML
/
MDS
patients with posaconazole prophylaxis, the contained IFI-related treatment costs more than compensated for the incremental cost of posaconazole, resulting in savings of CHF 1,118 per patient.
[MeSH-minor]
Cost-Benefit Analysis. Decision Support Techniques. Graft vs Host Disease / therapy. Hematopoietic Stem Cell Transplantation. Humans.
Leukemia
,
Myeloid
,
Acute
/ complications.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Markov Chains. Models, Theoretical.
Myelodysplastic
Syndromes / complications.
Myelodysplastic
Syndromes / drug therapy. Neutropenia / complications. Neutropenia / drug therapy. Risk. Switzerland. Treatment Outcome
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[Copyright]
Copyright 2010 S. Karger AG, Basel.
(PMID = 20414005.001).
[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 / Triazoles; 6TK1G07BHZ / posaconazole
67.
Grant S:
New agents for AML and MDS.
Best Pract Res Clin Haematol
; 2009 Dec;22(4):501-7
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[Title]
New agents for
AML
and
MDS
.
The heterogeneity of
acute myeloid
leukaemia (
AML
) and
myelodysplastic
syndromes (
MDS
) has led to a multiplicity of treatments, from cytotoxic agents to signal transduction modulators, cell-cycle inhibitors and epigenetic therapies.
While some have shown promising initial results, the outlook for
AML
patients, particularly older and relapsed patients, as well as patients whose cells exhibit certain adverse chromosomal abnormalities or mutant oncoproteins, continues to be grim.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Myelodysplastic
Syndromes / drug therapy
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[Cites]
J Clin Invest. 2008 Sep;118(9):3003-6
[
18725993.001
]
[Cites]
Blood. 2008 Sep 1;112(5):1638-45
[
18565853.001
]
[Cites]
J Clin Oncol. 2008 Oct 1;26(28):4603-9
[
18559876.001
]
[Cites]
Leukemia. 2008 Nov;22(11):2091-6
[
18685609.001
]
[Cites]
Cancer Cell. 2008 Dec 9;14(6):485-93
[
19061839.001
]
[Cites]
Clin Cancer Res. 2008 Dec 15;14(24):8102-11
[
19088025.001
]
[Cites]
Ann Hematol. 2009 Mar;88(3):213-9
[
18696067.001
]
[Cites]
Lancet Oncol. 2009 Mar;10(3):223-32
[
19230772.001
]
[Cites]
Cancer Res. 2009 Apr 1;69(7):3032-41
[
19318574.001
]
[Cites]
Blood. 2009 Apr 23;113(17):3938-46
[
19029442.001
]
[Cites]
Expert Opin Investig Drugs. 2007 Jul;16(7):1111-20
[
17594194.001
]
[Cites]
Cancer Res. 2007 Jul 15;67(14):6916-24
[
17638903.001
]
[Cites]
Blood. 2007 Oct 1;110(7):2302-8
[
17596541.001
]
[Cites]
Chem Biol. 2007 Oct;14(10):1186-97
[
17961830.001
]
[Cites]
Blood. 2007 Dec 15;110(13):4427-35
[
17804695.001
]
[Cites]
Blood. 2008 Feb 1;111(3):1060-6
[
17962510.001
]
[Cites]
Leuk Res. 2008 May;32(5):771-80
[
18031811.001
]
[Cites]
Cell. 2003 Dec 12;115(6):727-38
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14675537.001
]
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Invest New Drugs. 2005 Jan;23(1):31-7
[
15528978.001
]
[Cites]
Blood. 2005 Jun 1;105(11):4163-9
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15687234.001
]
[Cites]
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[
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]
[Cites]
Cancer Res. 2006 Jun 15;66(12):6361-9
[
16778214.001
]
[Cites]
Leukemia. 2006 Jul;20(7):1254-60
[
16642049.001
]
[Cites]
Blood. 2006 Nov 15;108(10):3271-9
[
16882711.001
]
[Cites]
Hematology Am Soc Hematol Educ Program. 2006;:178-84
[
17124058.001
]
[Cites]
J Clin Oncol. 2007 Jan 1;25(1):25-31
[
17146105.001
]
[Cites]
Blood. 2007 Feb 15;109(4):1387-94
[
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]
[Cites]
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[
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]
[Cites]
Clin Cancer Res. 2008 May 15;14(10):3077-82
[
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]
[Cites]
Blood. 2008 Aug 15;112(4):981-9
[
18495956.001
]
[Cites]
Cancer Control. 2008 Oct;15 Suppl:40-9
[
18813208.001
]
(PMID = 19959100.001).
[ISSN]
1532-1924
[Journal-full-title]
Best practice & research. Clinical haematology
[ISO-abbreviation]
Best Pract Res Clin Haematol
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R21 CA115260-01; United States / NCI NIH HHS / CA / P50 CA130805-02; United States / NCI NIH HHS / CA / CA63753; United States / NCI NIH HHS / CA / RC2 CA148431-01; United States / NCI NIH HHS / CA / R01 CA063753-13; United States / NCI NIH HHS / CA / R01 CA100866; United States / NCI NIH HHS / CA / R01 CA063753; United States / NCI NIH HHS / CA / R01 CA100866-04; United States / NCI NIH HHS / CA / P50CA130805; United States / NCI NIH HHS / CA / R01 CA093738; United States / CCR NIH HHS / RC / RC2 CA148431-01; United States / NCI NIH HHS / CA / CA100866; United States / NCI NIH HHS / CA / P50 CA130805; United States / NCI NIH HHS / CA / RC2 CA148431; United States / NCI NIH HHS / CA / R01 CA093738-05A2; United States / NCI NIH HHS / CA / CA93738; United States / NCI NIH HHS / CA / R21 CA115260
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Cytotoxins; 0 / Protein Kinase Inhibitors
[Number-of-references]
38
[Other-IDs]
NLM/ NIHMS157911; NLM/ PMC2793080
68.
Graubert T:
AML1 and Evi1: coconspirators in MDS/AML?
Blood
; 2008 Apr 15;111(8):3916-7
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[Title]
AML1 and Evi1: coconspirators in
MDS
/
AML
?
In this issue of Blood, Watanabe-Okochi and colleagues use a mouse bone marrow transplantation model to demonstrate that mutant alleles of AML1 (RUNX1) can initiate a
myelodysplastic syndrome
(
MDS
) that progresses to
acute
myelogenous
leukemia
(
AML
) in association with overexpression of Evi1.
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[CommentOn]
Blood. 2008 Apr 15;111(8):4297-308
[
18192504.001
]
(PMID = 18434965.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Comment; Journal Article
[Publication-country]
United States
69.
Park MJ, Park YH, Ahn HJ, Choi W, Paik KH, Kim JM, Chang YH, Ryoo BY, Yang SH:
Secondary hematological malignancies after breast cancer chemotherapy.
Leuk Lymphoma
; 2005 Aug;46(8):1183-8
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According to several reports, the 10 year incidence of secondary
acute
myelogenous
leukemia
(
AML
) or
myelodysplastic syndrome
(
MDS
) after systemic chemotherapy is approximately 1.5%.
We detected 2 cases of secondary
AML
and 1 case of
MDS
, 19, 52 and 12 months, respectively, after systemic chemotherapy for breast cancer.
Published data on the occurrence of secondary hematological malignancies other than
AML
or
MDS
in this setting are scarce.
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(PMID = 16085560.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
70.
Balleisen S, Kuendgen A, Hildebrandt B, Haas R, Germing U:
Prognostic relevance of achieving cytogenetic remission in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome following induction chemotherapy.
Leuk Res
; 2009 Sep;33(9):1189-93
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[Title]
Prognostic relevance of achieving cytogenetic remission in patients
with acute
myelogenous
leukemia
or high-risk
myelodysplastic syndrome following
induction chemotherapy.
Cytogenetic findings at diagnosis have influence on prognosis in patients
with acute
myelogenous leukaemia (
AML
) or
MDS
who undergo induction chemotherapy.
Median survival (excluding patients with
AML
M3) of the CCR group was 37 months, as compared to 11 months in patients with persistence of abnormal karyotype (p < 0.0001).
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Myelodysplastic
Syndromes / drug therapy. Remission Induction
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(PMID = 19428106.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents
71.
Harada H, Harada Y, Kimura A:
Implications of somatic mutations in the AML1/RUNX1 gene in myelodysplastic syndrome (MDS): future molecular therapeutic directions for MDS.
Curr Cancer Drug Targets
; 2006 Sep;6(6):553-65
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[Title]
Implications of somatic mutations in the AML1/RUNX1 gene in
myelodysplastic syndrome
(
MDS
): future molecular therapeutic directions for
MDS
.
Myelodysplastic syndrome
(
MDS
) is a clonal disorder of hematopoietic stem cells characterized by ineffective and inadequate hematopoiesis.
MDS
is also a susceptibility to
acute myeloid leukemia
(
AML
) and shown to be extremely resistant to current therapeutic strategies.
MDS
in a subset of 10-20% of patients arise after
previous
chemotherapy or radiation exposure for other malignancies.
Because
MDS
is a heterogeneous disorder, specific gene abnormalities playing a role in the
myelodysplastic
process have been difficult to identify.
Cytogenetic abnormalities are seen in half of
MDS
patients, and generally consist of partial or complete chromosome deletion or addition, whereas balanced translocations are rare.
Genes more frequently implicated in the pathogenesis of
MDS
remain unknown.
Although point mutations of critical genes have been demonstrated to contribute to the development
MDS
, there was no strong correlation between these mutations and clinical features.
Recently, we reported the high incidence of somatic mutations in the AML1/RUNX1 gene, which is a critical regulator of definitive hematopoiesis and the most frequent target for translocation of
AML
, in
MDS
, especially refractory anemia with excess blasts (RAEB), RAEB in transformation (RAEBt) and
AML
following
MDS
(defined here as
MDS
/
AML
).
The
MDS
/
AML
patients with AML1 mutations had a significantly worse prognosis than those without AML1 mutations.
Most of AML1/RUNX1 mutants lose trans-activation potential, which leads to a loss of AML1 function indicating that AML1/RUNX1 dysfunction is one of the major pathogenesis of
MDS
/
AML
.
[MeSH-major]
Core Binding Factor Alpha 2 Subunit / genetics. Genetic Therapy / trends. Mutation.
Myelodysplastic
Syndromes / genetics.
Myelodysplastic
Syndromes / therapy
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(PMID = 17017876.001).
[ISSN]
1873-5576
[Journal-full-title]
Current cancer drug targets
[ISO-abbreviation]
Curr Cancer Drug Targets
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
[Number-of-references]
83
72.
Wang XL, Shao ZH, Yao C, He GS, Liu H, Shi J, Bai J, Cao YR, Tu MF, Wang HQ, Xing LM, Sun J, Jia HR, Yang CL:
[Study of Th cell subsets in bone marrow of myelodysplastic syndromes patients].
Zhonghua Xue Ye Xue Za Zhi
; 2005 Dec;26(12):743-5
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[Title]
[Study of Th cell subsets in bone marrow of
myelodysplastic
syndromes patients].
OBJECTIVE: To study the quantity and ratio of Th1, Th2 cells in the bone marrow of
myelodysplastic
syndromes (
MDS
) patients, and to evaluate the correlation between the ratio of the blast cells and the number of the Th1 cells in the bone marrow of
MDS
patients.
METHODS: By FACS, the quantity and ratio of IFN-gamma producing CD4(+) T cell (Th1) and IL-4 producing CD4(+) T cell (Th2) cells in the bone marrow were detected in 21
MDS
patients, 18 normal controls and 13 severe aplastic anemia (SAA) patients respectively.
The karyotypes of 18
MDS
patients and 15 normal controls were assayed.
The correlation between the ratio of the blast cells in the bone marrow and the number of the Th1 cells in the
MDS
patients were analyzed.
RESULTS: The percentages of Th1 cells, Th2 cells and ratio of Th1/Th2 in the bone marrow of normal controls were (0.48 +/- 0.10)%, (0.24 +/- 0.19)% and 2.31 +/- 0.76 respectively, while those of the
MDS
patients were (0.36 +/- 0.11)%, (0.76 +/- 0.35)% and 0.51 +/- 0.13.
The percentage of Th1 cells of patients with
MDS
was reduced and the Th1/Th2 ratio was significantly lower than that of normal controls (P < 0.01).
In all of the 15 normal controls the karyotypes were normal, but that of
MDS
patients was (50.00 +/- 0.10)%.
The lower ratio of the Th1 cells in the bone marrow of the patients with
MDS
and the
AML
which progressed
from MDS
was negatively correlated with the higher percentage of the blast cells (r = -0.563, P < 0.01). CONCLUSIONS:.
(1) The immune function of T lymphocytes in
MDS
is abnormal: the balance between Th1 and Th2 cells is broken. (2) With descending of the number of Th1 cells in the bone marrow of the
MDS
patients, the disease is progressing to
leukemia
.
[MeSH-major]
Bone Marrow / immunology.
Myelodysplastic
Syndromes / immunology. T-Lymphocytes, Helper-Inducer / immunology
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(PMID = 16620580.001).
[ISSN]
0253-2727
[Journal-full-title]
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
[ISO-abbreviation]
Zhonghua Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
73.
Andersson BS, de Lima M, Thall PF, Madden T, Russell JA, Champlin RE:
Reduced-toxicity conditioning therapy with allogeneic stem cell transplantation for acute leukemia.
Curr Opin Oncol
; 2009 Jun;21 Suppl 1:S11-5
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[Title]
Reduced-toxicity conditioning therapy with allogeneic stem cell transplantation for
acute leukemia
.
We hypothesized that standardized systemic drug delivery would improve treatment safety and provide better
leukemia
control.
We used a Bayesian method to compare the outcomes of 67
acute myeloid leukemia
(
AML
)/
myelodysplastic syndrome
(
MDS
) patients who received intravenous busulfan-cyclophosphamide (BuCy2) with 148 subsequent
AML
/
MDS
patients who received busulfan-fludarabine (Bu-Flu).
Overall, the data support replacing BuCy2 with or without antithymocyte globulin (ATG) with Bu-Flu with or without rabbit-ATG for
AML
or
MDS
.
The extremely low one-year treatment-related mortality as well as high overall and event-free survival of patients in the Bu-Flu group indicate that it is time to revisit the value of alloSCT compared with conventional maintenance chemotherapy for patients in first complete remission of
AML
/
MDS
.
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[Cites]
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N Engl J Med. 1997 Mar 27;336(13):897-904
[
9070469.001
]
(PMID = 19561406.001).
[ISSN]
1531-703X
[Journal-full-title]
Current opinion in oncology
[ISO-abbreviation]
Curr Opin Oncol
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / 2P30CA16672-26
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
[Other-IDs]
NLM/ NIHMS588342; NLM/ PMC4037323
74.
Babicka L, Ransdorfova S, Brezinova J, Zemanova Z, Sindelarova L, Siskova M, Maaloufova J, Cermak J, Michalova K:
Analysis of complex chromosomal rearrangements in adult patients with MDS and AML by multicolor FISH.
Leuk Res
; 2007 Jan;31(1):39-47
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[Title]
Analysis of complex chromosomal rearrangements in adult patients with
MDS
and
AML
by multicolor FISH.
We analyzed complex chromosomal aberrations in 37 adult patients
with myelodysplastic syndrome
(
MDS
) and
acute myeloid leukemia
(
AML
) using classical cytogenetic method, FISH with locus-specific probes, multicolor FISH (mFISH) and multicolor banding (mBAND).
[MeSH-major]
Chromosome Aberrations. Chromosomes, Human / genetics. Gene Rearrangement / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myelodysplastic
Syndromes / genetics
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(PMID = 16687173.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Historical Article; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
75.
Bernasconi P, Klersy C, Boni M, Cavigliano PM, Giardini I, Rocca B, Zappatore R, Dambruoso I, Calvello C, Caresana M, Lazzarino M:
Does cytogenetic evolution have any prognostic relevance in myelodysplastic syndromes? A study on 153 patients from a single institution.
Ann Hematol
; 2010 Jun;89(6):545-51
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[Title]
Does cytogenetic evolution have any prognostic relevance in
myelodysplastic
syndromes? A study on 153 patients from a single institution.
The present study was designed to establish the incidence of cytogenetic evolution (CE), defined as the acquisition of chromosomal defects during the course of
MDS
, in order to correlate it with the WHO classification and IPSS score, and to assess its impact on overall survival (OS) and risk of
MDS
/
AML
evolution (progression-free interval, PFI) by means of Cox models for time-dependent covariates.
The study was carried out in 153
MDS
patients who were followed for a median period of 45.2 months.
Our study shows that (1) CE was more common in advanced than in early
MDS
, and advanced
MDS
presented secondary chromosomal defects distinct from those of early
MDS
;.
[MeSH-major]
Myelodysplastic
Syndromes / diagnosis.
Myelodysplastic
Syndromes / genetics
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(PMID = 20217086.001).
[ISSN]
1432-0584
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
Germany
76.
Teng Y, Liu Q, Ma J, Liu F, Han Z, Wang Y, Wang W:
Cloning, expression and characterization of a novel human CAP10-like gene hCLP46 from CD34(+) stem/progenitor cells.
Gene
; 2006 Apr 12;371(1):7-15
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A novel human gene, named as human CAP10-like protein 46 kDa (hCLP46), was isolated and identified from human
acute myeloid leukemia
transformed from
myelodysplastic syndrome
(
MDS
-
AML
) CD34(+) cells. hCLP46 (3q13.33) contains 11 exons encoding a putative protein of 392 amino acids, with a highly conserved CAP10 domain, a hydrophobic signal peptide at its N-terminus, and an endoplasmic reticulum (ER) retention signal motif KTEL at the C-terminus.
[MeSH-major]
Antigens, CD34. Chromosomes, Human, Pair 3 / genetics. Gene Expression Regulation, Leukemic / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Neoplasm Proteins / genetics. Neoplastic Stem Cells. Proteins / genetics
[MeSH-minor]
Amino Acid Sequence. Endoplasmic Reticulum / genetics. Glucosyltransferases. Humans. Molecular Sequence Data.
Myelodysplastic
Syndromes / genetics.
Myelodysplastic
Syndromes / metabolism.
Myelodysplastic
Syndromes / pathology. Organ Specificity / genetics. Protein Structure, Tertiary / genetics. Sequence Homology, Amino Acid. U937 Cells
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HGNC: Data: Gene Annotation
.
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OMIM: Data: Gene Annotation
.
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(PMID = 16524674.001).
[ISSN]
0378-1119
[Journal-full-title]
Gene
[ISO-abbreviation]
Gene
[Language]
eng
[Databank-accession-numbers]
GENBANK/ AY298903
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Neoplasm Proteins; 0 / Proteins; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.- / POGLUT1 protein, human
77.
Buchmann I, Meyer RG, Herr W, Helisch A, Bartenstein P:
[Radioimmunotherapy for treatment of acute myeloid leukaemia and myelodysplastic syndrome: conceptual chances].
Nuklearmedizin
; 2005;44(3):107-17; quiz N21-2
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[Title]
[Radioimmunotherapy for treatment of
acute myeloid
leukaemia and
myelodysplastic syndrome
: conceptual chances].
The prognosis of patients
with acute myeloid
leukaemia (
AML
) has improved considerably by introduction of aggressive consolidation chemotherapy and haematopoietic stem cell transplantation (SCT).
Nevertheless, only 20-30% of patients with
AML
achieve long-term disease-free survival after SCT.
Including radioimmunotherapies in the treatment of
AML
and myelodyplastic
syndrome
(
MDS
) allows for the achievement of a pronounced antileukaemic effect for the reduction of relapse rates on the one hand.
On the other hand, no increase of
acute
toxicity and later complications should be induced.
This paper provides a systematic and critical review of the currently used radionuclides and immunoconjugates for the treatment of
AML
and
MDS
and summarizes the literature on primary tumour cell reductive radioimmunotherapies on the one hand and conditioning radioimmunotherapies before SCT on the other hand.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ radiotherapy.
Myelodysplastic
Syndromes / radiotherapy. Radioimmunotherapy
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(PMID = 15968419.001).
[ISSN]
0029-5566
[Journal-full-title]
Nuklearmedizin. Nuclear medicine
[ISO-abbreviation]
Nuklearmedizin
[Language]
ger
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Germany
[Number-of-references]
49
78.
Liu YC, Miyazawa K, Sashida G, Kodama A, Ohyashiki K:
Deletion (20q) as the sole abnormality in Waldenström macroglobulinemia suggests distinct pathogenesis of 20q11 anomaly.
Cancer Genet Cytogenet
; 2006 Aug;169(1):69-72
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The deletion of the long arm of chromosome 20, or del(20q), is a common cytogenetic abnormality in various
myeloid
disorders but is less commonly seen in lymphoid neoplasms.
Reviewing all 11 reported cases of plasma cell dyscrasia possessing sole del(20q), including our case, none of 4 cases with del(20q) as an initial anomaly developed
myelodysplastic syndrome
-
acute myeloid leukemia
(
MDS
/
AML
), but at least 3 cases with del(20q) appearing after chemotherapy developed
MDS
/
AML
at or after the time of del(20q).
We propose that the del(20q) may have different clinical significance in plasma cell dyscrasia: one is when del(20q) appears at diagnosis and may involve the initial event of oncogenesis, and the other is when del(20q) appears after treatment and is associated with therapy-related and potential
MDS
/
AML
risk.
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(PMID = 16875940.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
79.
Mihara K, Chowdhury M, Nakaju N, Hidani S, Ihara A, Hyodo H, Yasunaga S, Takihara Y, Kimura A:
Bmi-1 is useful as a novel molecular marker for predicting progression of myelodysplastic syndrome and patient prognosis.
Blood
; 2006 Jan 1;107(1):305-8
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[Title]
Bmi-1 is useful as a novel molecular marker for predicting progression of
myelodysplastic syndrome
and patient prognosis.
The International Prognostic Scoring System (IPSS) has been widely used to predict the prognosis of patients
with myelodysplastic syndrome
(
MDS
).
Here, we analyzed the expression of Bmi-1, which is required to regulate the self-renewal in CD34+ cells from 51 patients with cases of
MDS
and
acute myeloid leukemia
preceded by
MDS
(
MDS
-
AML
).
Higher positivity rate of Bmi-1 was preferentially seen in refractory anemia with excess blasts (RAEB), RAEB in transformation (RAEB-T), and
MDS
-
AML
compared with refractory anemia (RA) and RA with ringed sideroblasts (RARS).
Here, we propose Bmi-1 as a novel molecular marker to predict the progression and prognosis of
MDS
.
[MeSH-major]
Myelodysplastic
Syndromes / diagnosis. Nuclear Proteins / analysis. Proto-Oncogene Proteins / analysis. Repressor Proteins / analysis
[MeSH-minor]
Aged. Aged, 80 and over. Anemia, Refractory / diagnosis. Antigens, CD34. Biomarkers / analysis. Bone Marrow / chemistry. Bone Marrow / pathology. Case-Control Studies. Cell Proliferation. Disease Progression. Female. Humans.
Leukemia
,
Myeloid
. Male. Middle Aged. Polycomb Repressive Complex 1. Prognosis
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(PMID = 16160010.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD34; 0 / BMI1 protein, human; 0 / Biomarkers; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; EC 6.3.2.19 / Polycomb Repressive Complex 1
81.
Sun Y, Cook JR:
Fluorescence in situ hybridization for del(5q) in myelodysplasia/acute myeloid leukemia: comparison of EGR1 vs. CSF1R probes and diagnostic yield over metaphase cytogenetics alone.
Leuk Res
; 2010 Mar;34(3):340-3
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[Title]
Fluorescence in situ hybridization for del(5q) in myelodysplasia/
acute myeloid leukemia
: comparison of EGR1 vs. CSF1R probes and diagnostic yield over metaphase cytogenetics alone.
To determine the clinical utility of FISH for del(5q) in
MDS
/
AML
, we first compared FISH for 5q31 (EGR1) and 5q33 (CSF1R) in 51
myeloid
neoplasms containing del(5q) by metaphase cytogenetics.
Next, EGR1 FISH was compared to metaphase cytogenetics alone in 269 cases of known or suspected
MDS
/
AML
.
EGR1 FISH detects del(5q) in a broad variety of
myeloid
neoplasms, including at least most cases of 5q-
syndrome
, while studies for CSF1R add little to the diagnostic yield.
[MeSH-major]
Cytogenetics / methods. In Situ Hybridization, Fluorescence / methods.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myelodysplastic
Syndromes / genetics. Receptors, Colony-Stimulating Factor / genetics
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[Copyright]
Copyright (c) 2009 Elsevier Ltd. All rights reserved.
(PMID = 19608274.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / EGR1 protein, human; 0 / Early Growth Response Protein 1; 0 / Receptors, Colony-Stimulating Factor
82.
Ma W, Kantarjian H, Bekele B, Donahue AC, Zhang X, Zhang ZJ, O'Brien S, Estey E, Estrov Z, Cortes J, Keating M, Giles F, Albitar M:
Proteasome enzymatic activities in plasma as risk stratification of patients with acute myeloid leukemia and advanced-stage myelodysplastic syndrome.
Clin Cancer Res
; 2009 Jun 1;15(11):3820-6
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[Title]
Proteasome enzymatic activities in plasma as risk stratification of patients
with acute myeloid leukemia
and advanced-stage
myelodysplastic syndrome
.
PURPOSE: Cytogenetic abnormalities are currently the most important predictors of response and clinical outcome for patients
with acute myeloid leukemia
(
AML
) or advanced-stage
myelodysplastic syndrome
(
MDS
).
EXPERIMENTAL DESIGN: We assessed the utility of measuring pretreatment proteasome chymotrypsin-like, caspase-like, and trypsin-like activities in plasma to predict response and survival of patients with
AML
(n = 174) or advanced-stage
MDS
(n = 52).
RESULTS: All three enzymatic activities were significantly (P < 0.001) increased in the plasma of patients with
AML
and
MDS
compared with normal controls.
CONCLUSIONS: Measuring plasma chymotrypsin-like activity may provide a powerful biomarker for risk stratification in patients with
AML
and advanced-stage
MDS
, including those with normal karyotype.
[MeSH-major]
Leukemia
,
Myeloid
/ blood.
Myelodysplastic
Syndromes / blood. Proteasome Endopeptidase Complex / blood
[MeSH-minor]
Acute
Disease. Adolescent. Adult. Aged. Aged, 80 and over. Caspases / blood. Caspases / metabolism. Chymotrypsin / blood. Chymotrypsin / metabolism. Female. Humans. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Prognosis. Risk Factors. Survival Analysis. Trypsin / blood. Trypsin / metabolism. Young Adult
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[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.4.21.1 / Chymotrypsin; EC 3.4.21.4 / Trypsin; EC 3.4.22.- / Caspases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
[Other-IDs]
NLM/ NIHMS592798; NLM/ PMC4091712
83.
Ebihara Y, Manabe A, Tsuruta T, Ishikawa K, Hasegawa D, Ohtsuka Y, Kawasaki H, Ogami K, Wada Y, Kanda T, Tsuji K:
The effect of donor leukocyte infusion on refractory pure red blood cell aplasia after allogeneic stem cell transplantation in a patient with myelodysplastic syndrome developing from Kostmann syndrome.
Int J Hematol
; 2007 Dec;86(5):446-50
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[Title]
The effect of donor leukocyte infusion on refractory pure red blood cell aplasia after allogeneic stem cell transplantation in a patient
with myelodysplastic syndrome
developing from Kostmann
syndrome
.
We describe the clinical course of a patient who experienced refractory pure red cell aplasia (PRCA) after undergoing HLA-matched allogeneic peripheral blood stem cell transplantation (allo-PBSCT) for refractory anemia with an excess of blasts in transformation that had evolved from Kostmann
syndrome
.
The treatment for patients
with myelodysplastic syndrome
(
MDS
) or
acute myeloid leukemia
(
AML
) developing from Kostmann
syndrome
has not been standardized.
Myeloid
and platelet recoveries were achieved rapidly.
The results indicate that the conditioning regimen we describe seems safe and effective for those who have
MDS
/
AML
and that DLI might be a valuable approach for refractory PRCA after ABO-incompatible SCT.
[MeSH-major]
Leukocyte Transfusion. Living Donors.
Myelodysplastic
Syndromes / therapy. Myelopoiesis. Peripheral Blood Stem Cell Transplantation. Red-Cell Aplasia, Pure / therapy
[MeSH-minor]
Child. Cyclophosphamide / administration & dosage. Graft Survival. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Immunosuppressive Agents / administration & dosage. Infant. Male. Myeloablative Agonists / administration & dosage. Recombinant Proteins. Remission Induction.
Syndrome
. Transplantation, Homologous. Whole-Body Irradiation
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(PMID = 18192114.001).
[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 / Immunosuppressive Agents; 0 / Myeloablative Agonists; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8N3DW7272P / Cyclophosphamide
84.
Stone R, Sekeres M, Garcia-Manero G:
Evolving strategies in the treatment of MDS and AML.
Clin Adv Hematol Oncol
; 2009 Aug;7(8):1-14; quiz 2 p following 14
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[Title]
Evolving strategies in the treatment of
MDS
and
AML
.
Myelodysplastic syndrome
(
MDS
) is a clonal hematopoietic disorder characterized by a hyperproliferative bone marrow, cellular
dysplasia
, and ineffective hematopoiesis.
The treatment of
MDS
involves improving patient survival and quality of life while decreasing the likelihood of progression to
acute
myelogenous
leukemia
(
AML
).
In addition to supportive care with transfusions and hematopoietic growth factors as well as stem cell transplantation, three chemotherapeutic agents have been approved to treat
MDS
--lenalidomide, azacitidine, and decitabine.
In addition, multiple agents and novel combinations are currently in development to treat both
MDS AML
.
Several clinical studies which have investigated these therapeutic approaches, as well as the incorporation of new tools used in the diagnosis of
MDS
, have been published since the 2008 American Society of Hematology (ASH) Annual Meeting and Exposition, and are discussed here.
[MeSH-major]
Education, Medical, Continuing.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Myelodysplastic
Syndromes / drug therapy
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(PMID = 19927982.001).
[ISSN]
1543-0790
[Journal-full-title]
Clinical advances in hematology & oncology : H&O
[ISO-abbreviation]
Clin Adv Hematol Oncol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
85.
Kuendgen A, Knipp S, Fox F, Strupp C, Hildebrandt B, Steidl C, Germing U, Haas R, Gattermann N:
Results of a phase 2 study of valproic acid alone or in combination with all-trans retinoic acid in 75 patients with myelodysplastic syndrome and relapsed or refractory acute myeloid leukemia.
Ann Hematol
; 2005 Dec;84 Suppl 1:61-6
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[Title]
Results of a phase 2 study of valproic acid alone or in combination with all-trans retinoic acid in 75 patients
with myelodysplastic syndrome
and relapsed or refractory
acute myeloid leukemia
.
Valproic acid (VPA) inhibits histone deacetylase activity and induces differentiation of
acute myeloid leukemia
(
AML
) blasts in vitro.
We observed clinical responses to VPA in patients
with myelodysplastic syndrome
(
MDS
) and
AML
.
Hematological improvement, according to international working group criteria for
MDS
, was observed in 18 patients (24%).
We found a response rate of 52% in
MDS
patients with a normal blast count (refractory sideroblastic anemia, refractory cytopenia
with multilineage dysplasia
, and refractory sideroblastic cytopenia
with multilineage dysplasia
).
The response rate was 6% in refractory anemia with excess blasts (I + II), 16% in
AML
, and 0% in chronic myelomonocytic
leukemia
.
We conclude that VPA is clinically useful in low-risk
MDS
.
For patients with high-risk
MDS
, VPA may be combined with chemotherapy or demethylating drugs.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Histone Deacetylase Inhibitors.
Leukemia
,
Myeloid
/ drug therapy.
Myelodysplastic
Syndromes / drug therapy. Valproic Acid / therapeutic use
[MeSH-minor]
Acute
Disease. Adult. Aged. Aged, 80 and over. Cell Differentiation / drug effects. Female. Histone Deacetylases / drug effects. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Remission Induction. Treatment Outcome. Tretinoin / administration & dosage
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(PMID = 16270213.001).
[ISSN]
1432-0584
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Comparative Study; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Histone Deacetylase Inhibitors; 5688UTC01R / Tretinoin; 614OI1Z5WI / Valproic Acid; EC 3.5.1.98 / Histone Deacetylases
86.
Tabata R, Tabata C, Omori K, Nagai T:
Disappearing myelodysplastic syndrome-associated hemolytic anemia in leukemic transformation.
Int Arch Allergy Immunol
; 2010;152(4):407-12
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[Title]
Disappearing
myelodysplastic syndrome
-associated hemolytic anemia in leukemic transformation.
BACKGROUND: Here we report 2 rare cases of
acute myeloid leukemia
(
AML
) complicated with hemolytic anemia limited to the
myelodysplastic syndrome
(
MDS
) stage, and disappearing in leukemic transformation.
METHODS/RESULTS: A 66-year-old man with
MDS
-RAEB-2 was admitted to hospital for severe anemia with increased reticulocyte counts.
In another case, a 68-year-old man was admitted to hospital when laboratory findings showed a white blood cell count of 24,800/microl with increased myeloblasts (62.5%), leading to the diagnosis of
AML
with multilineage dysplasia
.
Following
a decrease in blasts due to anti-cancer drugs, supporting the
MDS
-RAEB-2 status, severe anemia with increased reticulocytes and positive direct antiglobulin test was diagnosed, suggesting the existence of autoimmune hemolytic anemia, which was then ameliorated by steroid therapy.
[MeSH-major]
Anemia, Hemolytic, Autoimmune / diagnosis.
Leukemia
,
Myeloid
,
Acute
/ diagnosis.
Myelodysplastic
Syndromes / diagnosis
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[Copyright]
Copyright 2010 S. Karger AG, Basel.
(PMID = 20197683.001).
[ISSN]
1423-0097
[Journal-full-title]
International archives of allergy and immunology
[ISO-abbreviation]
Int. Arch. Allergy Immunol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Glucocorticoids; X4W7ZR7023 / Methylprednisolone
87.
Li LJ, Fu R, Shao ZH, Wang HQ, Yue LZ, Ruan EB, Liu H, Wang J, Wang HL:
[Abnormalities of CD34+ cells differentiation and bone marrow cell cycle in myelodysplastic syndrome].
Zhonghua Nei Ke Za Zhi
; 2010 Nov;49(11):963-6
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[Title]
[Abnormalities of CD34+ cells differentiation and bone marrow cell cycle in
myelodysplastic syndrome
].
OBJECTIVES: To detect the abnormalities of CD(34)(+) cells differentiation and bone marrow cell cycle in
myelodysplastic syndrome
(
MDS
).
METHODS: Fifty newly diagnosed
MDS
(17 in low risk and 33 in high risk), 8
acute myeloid leukemia
preceded by
MDS
(
MDS
-
AML
) and 25 normal controls were enrolled into this study.
RESULTS: The mean percentages of CD(34)(+) cells in bone marrow karyocyte of high risk [(2.29 ± 2.17)%] and
MDS
-
AML
groups [(18.69 ± 17.47)%] were significantly higher than that of control group [(0.36 ± 0.49)%, P < 0.05].
The mean percentages of CD(34)(+)CD(38)(+) cells were significantly lower in low risk, high risk and
MDS
-
AML
groups [(86.09 ± 7.79)%, (81.68 ± 11.82)% and (82.88 ± 2.60)%, respectively] than that in control group [(92.21 ± 3.85)%, P < 0.05], thus the percentages of CD(34)(+)CD(38)(-) cells were significantly higher in either
MDS
(low risk and high risk) or
MDS
-
AML
groups [(13.91 ± 7.79)%, (18.32 ± 11.82)% or (17.13 ± 2.60)%, respectively] than that in control group [(7.79 ± 3.85)%, P < 0.05].
The percentages of CD(34)(+)CD(38)(-) cells of
MDS
cases correlated directly with their International Prognostic Scoring System (IPSS) (r = 0.493, P = 0.001) and WHO Adapted Prognostic Scoring System (WPSS) (r = 0.586, P = 0.000) scores.
The percentages of bone marrow mononuclear cells (BMMNCs) in G(0)/G(1) phase of in low risk, high risk and
MDS
-
AML
groups [(94.52 ± 4.32)%, (96.07 ± 3.88)% and (94.65 ± 4.55)%, respectively] were significantly higher than that in control group [(88.94 ± 7.30)%, P < 0.01], thus the percentages of BMMNCs in S and G(2)/M phase were significantly lower in either
MDS
(low risk and high risk) or
MDS
-
AML
groups than that in control group (P < 0.05).
MDS
patients with low percentages of CD(34)(+)CD(38)(-) cells presented higher therapeutic efficacy than those with high percentages of CD(34)(+)CD(38)(-) cells, while without significant differences (P > 0.05).
CONCLUSIONS: There are abnormalities of differentiation of CD(34)(+) bone marrow cells and high proportion of G(0)/G(1) cells which indicates a G(1) phase arrest in
MDS
that might be involved in the pathogenesis of
MDS
.
So the examination of CD(34)(+) bone marrow cells and cell cycle might be helpful for
MDS
diagnosis and assessment of prognosis and therapeutic effects.
[MeSH-major]
Bone Marrow Cells / cytology. Cell Cycle.
Myelodysplastic
Syndromes / diagnosis
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(PMID = 21211213.001).
[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]
0 / Antigens, CD34
88.
Nand S, Godwin J, Smith S, Barton K, Michaelis L, Alkan S, Veerappan R, Rychlik K, Germano E, Stiff P:
Hydroxyurea, azacitidine and gemtuzumab ozogamicin therapy in patients with previously untreated non-M3 acute myeloid leukemia and high-risk myelodysplastic syndromes in the elderly: results from a pilot trial.
Leuk Lymphoma
; 2008 Nov;49(11):2141-7
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[Title]
Hydroxyurea, azacitidine and gemtuzumab ozogamicin therapy in patients with previously untreated non-M3
acute myeloid leukemia
and high-risk
myelodysplastic
syndromes in the elderly: results from a pilot trial.
Elderly patients
with acute myeloid leukemia
(
AML
) and high-risk
myelodysplastic
syndromes (
MDS
) have a poor prognosis due to low response rates (26-46%) to standard chemotherapy and high treatment-related mortality (11-31%).
Twenty patients with non-M3
AML
and
MDS
were treated with this regimen.
The combination of HU, azacitdine and GO appears to be a safe and effective regimen in the treatment of
AML
and high risk
MDS
in the elderly.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ therapy.
Myelodysplastic
Syndromes / therapy
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(PMID = 19021057.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / gemtuzumab; M801H13NRU / Azacitidine; X6Q56QN5QC / Hydroxyurea
89.
Krishna G, AbuTarif M, Xuan F, Martinho M, Angulo D, Cornely OA:
Pharmacokinetics of oral posaconazole in neutropenic patients receiving chemotherapy for acute myelogenous leukemia or myelodysplastic syndrome.
Pharmacotherapy
; 2008 Oct;28(10):1223-32
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[Title]
Pharmacokinetics of oral posaconazole in neutropenic patients receiving chemotherapy for
acute
myelogenous
leukemia
or
myelodysplastic syndrome
.
STUDY OBJECTIVE: To analyze the pharmacokinetics of posaconazole administered as prophylaxis for invasive fungal infection (IFI) in neutropenic patients receiving chemotherapy for
acute
myelogenous
leukemia
(
AML
) or
myelodysplastic syndrome
(
MDS
).
PATIENTS: One hundred ninety-four patients with
AML
or
MDS
who received posaconazole oral suspension 200 mg 3 times/day with meals or a nutritional supplement for a minimum of 7 days to achieve steady state and for a maximum of 12 weeks.
MEASUREMENTS AND MAIN RESULTS: The effects of the
following
covariates on average (Cav) and maximum (Cmax) posaconazole plasma concentrations at steady state were explored: age, sex, and race-ethnicity; proven or probable IFI; baseline body weight and body surface area; and baseline (on or before day 7) increases in liver enzyme levels, mucositis, neutropenia, diarrhea, vomiting, or use of an H2-receptor antagonist or proton pump inhibitor.
[MeSH-major]
Antifungal Agents / pharmacokinetics. Antineoplastic Agents / adverse effects.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Mycoses / prevention & control.
Myelodysplastic
Syndromes / drug therapy. Neutropenia / chemically induced. Triazoles / pharmacokinetics
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(PMID = 18823218.001).
[ISSN]
0277-0008
[Journal-full-title]
Pharmacotherapy
[ISO-abbreviation]
Pharmacotherapy
[Language]
eng
[Publication-type]
Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial
[Publication-country]
United States
[Chemical-registry-number]
0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Triazoles; 6TK1G07BHZ / posaconazole
90.
Bhatia R, Van Heijzen K, Palmer A, Komiya A, Slovak ML, Chang KL, Fung H, Krishnan A, Molina A, Nademanee A, O'Donnell M, Popplewell L, Rodriguez R, Forman SJ, Bhatia S:
Longitudinal assessment of hematopoietic abnormalities after autologous hematopoietic cell transplantation for lymphoma.
J Clin Oncol
; 2005 Sep 20;23(27):6699-711
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PURPOSE: Autologous hematopoietic cell transplantation (HCT) is being increasingly used as an effective treatment strategy for patients with relapsed or refractory Hodgkin's lymphoma (HL) or non-Hodgkin's lymphoma (NHL) but is associated with therapy-related myelodysplasia and
acute myeloid leukemia
(t-
MDS
/
AML
) as a major cause of nonrelapse mortality.
The phenomenon of hematopoietic reconstitution after autologous HCT and the role of proliferative stress in the pathogenesis of t-
MDS
/
AML
are poorly understood.
Patients within this cohort who developed t-
MDS
/
AML
had reduced recovery of committed progenitors and poorer telomere recovery, possibly indicating a functional defect in primitive hematopoietic cells.
Increased proliferative stress on stem cells bearing genotoxic damage could contribute to the pathogenesis of t-
MDS
/
AML
.
Extended follow-up of a larger number of patients is required to confirm whether alterations in progenitor and telomere recovery predict for increased risk of t-
MDS
/
AML
.
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(PMID = 16170178.001).
[ISSN]
0732-183X
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Grant]
United States / NCRR NIH HHS / RR / 5M01 RR00043; United States / NCI NIH HHS / CA / P01 CA30206
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
91.
La Starza R, Aventin A, Matteucci C, Crescenzi B, Romoli S, Testoni N, Pierini V, Ciolli S, Sambani C, Locasciulli A, Di Bona E, Lafage-Pochitaloff M, Martelli MF, Marynen P, Mecucci C:
Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia.
Leukemia
; 2006 Jun;20(6):958-64
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[Title]
Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary
myelodysplastic syndrome
and
acute myeloid leukemia
.
Fluorescence in situ hybridization and comparative genomic hybridization characterized 6p rearrangements in eight primary and in 10 secondary
myeloid
disorders (including one patient with Fanconi anemia) and found different molecular lesions in each group.
In the 10 patients with secondary
acute myeloid leukemia
/
myelodysplastic syndrome
(
AML
/
MDS
), the short arm of chromosome 6 was involved in unbalanced translocations in 7.
Consequently, in secondary
AML
/
MDS
, we hypothesize that 6p gains are major pathogenetic events
arising from
acquired and/or congenital genomic instability.
[MeSH-major]
Chromosomes, Human, Pair 6 / genetics.
Leukemia
,
Myeloid
/ genetics.
Myelodysplastic
Syndromes / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic / genetics
[MeSH-minor]
Acute
Disease. Adult. Aged. Aged, 80 and over. Cytogenetic Analysis. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Sensitivity and Specificity
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(PMID = 16617324.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
92.
Chakraborty S, Sun CL, Francisco L, Sabado M, Li L, Chang KL, Forman S, Bhatia S, Bhatia R:
Accelerated telomere shortening precedes development of therapy-related myelodysplasia or acute myelogenous leukemia after autologous transplantation for lymphoma.
J Clin Oncol
; 2009 Feb 10;27(5):791-8
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[Title]
Accelerated telomere shortening precedes development of therapy-related myelodysplasia or
acute
myelogenous
leukemia
after autologous transplantation for lymphoma.
PURPOSE: Therapy-related myelodysplasia or
acute
myelogenous
leukemia
(t-
MDS
/
AML
) is a lethal complication of autologous hematopoietic stem-cell transplantation (aHCT) for Hodgkin's lymphoma (HL) and non-Hodgkin's lymphoma (NHL).
Here, we investigated the hypothesis that accelerated telomere shortening after aHCT could contribute to the development of t-
MDS
/
AML
.
PATIENTS AND METHODS: A prospective longitudinal cohort was constructed to investigate the sequence of cellular and molecular abnormalities leading to development of t-
MDS
/
AML
after aHCT for HL/NHL.
This cohort formed the sampling frame for a nested case-control study to compare changes in telomere length in serial blood samples from patients who developed t-
MDS
/
AML
with matched controls who did not develop t-
MDS
/
AML
.
RESULTS: An initial increase in telomere length at day 100 after aHCT was followed by an accelerated telomere shortening in t-
MDS
/
AML
patients when compared with controls.
These telomere alterations preceded the onset of t-
MDS
and were independent of other known risk factors associated with development of t-
MDS
/
AML
on multivariate analysis.
Additionally, we observed reduced generation of committed progenitors in patients who developed t-
MDS
/
AML
, indicating that these telomere alterations were associated with reduced regenerative capacity of hematopoietic stem cells.
CONCLUSION: The development of t-
MDS
/
AML
after aHCT is associated with and preceded by markedly altered telomere dynamics in hematopoietic cells.
Accelerated telomere loss in patients developing t-
MDS
/
AML
may reflect increased clonal proliferation and/or altered telomere regulation in premalignant cells.
Genetic instability associated with shortened telomeres may contribute to leukemic transformation in t-
MDS
/
AML
.
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