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1
acute biphenotypic leukemia 2005:2010[pubdate] *count=100
196 results
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Items 1 to 100 of about 196
1.
Murase K, Iyama S, Sato T, Takimoto R, Kobune M, Kato J:
[Therapeutic results in patients with biphenotypic acute leukemia at Sapporo Medical University Hospital].
Gan To Kagaku Ryoho
; 2010 Oct;37(10):2011-3
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[Title]
[Therapeutic results in patients with
biphenotypic acute leukemia
at Sapporo Medical University Hospital].
We reviewed the results of 6 patients with
biphenotypic acute leukemia
(BAL) which the diagnostic standard of the European Group for the Immunological Characterization of
Leukemia
(EGIL) at Sapporo Medical University Hospital between 2006 and 2008.
Among them, 4 were
B lymphoid and myeloid
, 2 were
T lymphoid and myeloid
, and one was T/
B lymphoid
.
Two of 4 patients did not attain complete remission, and two relapsed after first treatment with
acute
myeloblastic
leukemia
(AML) protocol.
On the other hand, two showed complete remission after the
acute
lymphoblastic
leukemia
(ALL) protocol.
One of 4 patients survived who had been treated with hematopoietic stem
cell
transplantation as a post-remission therapy.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/ drug therapy
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.
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(PMID = 20948276.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
2.
Bueno C, Montes R, Martín L, Prat I, Hernandez MC, Orfao A, Menendez P:
NG2 antigen is expressed in CD34+ HPCs and plasmacytoid dendritic cell precursors: is NG2 expression in leukemia dependent on the target cell where leukemogenesis is triggered?
Leukemia
; 2008 Aug;22(8):1475-8
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[Title]
NG2 antigen is expressed in CD34+ HPCs and plasmacytoid dendritic
cell
precursors: is NG2 expression in
leukemia
dependent on the target
cell
where leukemogenesis is triggered?
[MeSH-major]
Antigens / immunology. Antigens, CD34 / immunology. Dendritic Cells / immunology.
Leukemia
,
Biphenotypic
,
Acute
/ immunology. Proteoglycans / immunology
[MeSH-minor]
Cell
Line, Tumor. Flow Cytometry. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics
The Lens.
Cited by Patents in
.
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(PMID = 18698324.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Editorial; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens; 0 / Antigens, CD34; 0 / MLL protein, human; 0 / Proteoglycans; 0 / chondroitin sulfate proteoglycan 4; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
3.
Alvarado Y, Welch MA, Swords R, Bruzzi J, Schlette E, Giles FJ:
Nelarabine activity in acute biphenotypic leukemia.
Leuk Res
; 2007 Nov;31(11):1600-3
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[Title]
Nelarabine activity in
acute biphenotypic leukemia
.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use.
Leukemia
/ drug therapy
[MeSH-minor]
Acute
Disease
. Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cyclophosphamide / administration & dosage. Dexamethasone / administration & dosage. Doxorubicin / administration & dosage. Flow Cytometry. Humans. Middle Aged. Phenotype. Vincristine / administration & dosage
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MedlinePlus Health Information.
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.
MedlinePlus Health Information.
consumer health - Leukemia
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
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(PMID = 17512588.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Arabinonucleosides; 5J49Q6B70F / Vincristine; 60158CV180 / nelarabine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
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4.
Tsutsumi Y, Tanaka J, Minami H, Musashi M, Fukushima A, Ehira N, Kanamori H, Yamato H, Sasaki J, Funaki C, Hasegawa S, Obara S, Ogura N, Asaka M, Imamura M, Masauzi N:
Acute biphenotypic leukemia and an acquired X chromosome.
Cancer Genet Cytogenet
; 2005 Feb;157(1):94-5
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[Title]
Acute biphenotypic leukemia
and an acquired X chromosome.
[MeSH-major]
Chromosomes, Human, X.
Leukemia
/ genetics. Sex Chromosome Aberrations
[MeSH-minor]
Acute
Disease
. Aged. Humans. Male
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.
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.
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(PMID = 15676158.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
5.
Suh B, Song J, Kim J, Park TS, Choi JR:
Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous leukemia.
Korean J Lab Med
; 2010 Jun;30(3):218-23
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[Title]
Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous
leukemia
.
BACKGROUND: Although the pericentric inversion of chromosome 9, inv(9)(p11q13), is generally considered a normal variation, it is also associated with solid tumors and several hematologic malignancies such as
biphenotypic acute leukemia
, ALL, AML, and myeloproliferative neoplasms.
The purpose of this retrospective study was to investigate the frequency and clinical features of CML patients with concomitant inv(9)
and t
(9;22)(q34;q11.2) variation at our institution.
METHODS: We reviewed the bone marrow chromosome database entries between October 2006 and December 2008 to identify patients with concomitant inv(9)
and t
(9;22) variations.
RESULTS: Among the 51 CML patients, 4 (7.8%) had concomitant inv(9)
and t
(9;22) variations.
[MeSH-major]
Asian Continental Ancestry Group / genetics. Chromosome Inversion. Chromosomes, Human, Pair 9.
Leukemia
,
Myeloid
,
Acute
/ genetics
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(PMID = 20603579.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Korea (South)
6.
He GS, Zhang X, Wu DP, Sun AN, Jin ZM, Qiu HY, Miao M, Tang XW, Fu ZZ, Han Y:
Outcomes of CAG regimen for refractory biphenotypic acute leukemia patients.
Chin Med Sci J
; 2009 Sep;24(3):178-81
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[Title]
Outcomes of CAG regimen for refractory
biphenotypic acute leukemia
patients.
OBJECTIVE: To evaluated the efficiency of low-dose cytosine arabinoside plus aclarubicin with concurrent administration of granulocyte colony-stimulating factor (CAG) regimen for refractory
biphenotypic acute leukemia
(BAL).
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.
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CYTARABINE
.
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(PMID = 19848320.001).
[ISSN]
1001-9294
[Journal-full-title]
Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
[ISO-abbreviation]
Chin. Med. Sci. J.
[Language]
ENG
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 74KXF8I502 / Aclarubicin
7.
Boatsman EE, Fu CH, Song SX, Moore TB:
Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation.
J Pediatr Hematol Oncol
; 2010 Mar;32(2):e57-60
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[Title]
Graft-versus-
leukemia
effect on infant
lymphoblastic
leukemia
relapsed after sibling hematopoietic stem
cell
transplantation.
INTRODUCTION: Infant
acute
lymphoblastic
leukemia
(ALL) is considered a high-risk entity.
By morphology, infant ALL is classified as
a lymphoid lineage
leukemia
; however, its physiologic behavior has brought many to consider it a pathologic
hybrid
between
lymphoid
leukemia
and myeloid leukemias
.
As such, standard of care currently employs the use of chemotherapeutic agents used commonly in ALL protocols and agents typically reserved for the treatment of myelogenous
lineage leukemias
.
The role of hematopoietic stem
cell
transplantation and graft-versus-
leukemia
effect in these patients has not been well studied.
CASE PRESENTATION: An earlier healthy 9-week-old Hispanic male diagnosed with precursor B-
cell lymphoblastic
leukemia
was treated with protocol P9407 and matched sibling hematopoietic stem
cell
transplantation.
The sole antigraft-versus-host
disease
(GVHD) agent, cyclosporine, was discontinued.
He remains
disease
free more than 2 years posttransplant.
CONCLUSION: Traditionally, graft-versus-
leukemia
effect was thought to contribute therapeutically little to the treatment of ALL by hematopoietic stem
cell
transplantation (HSCT).
The effects of graft-versus-
leukemia
immunologic phenomenon in our patient with infant
acute
lymphoblastic
leukemia
underscore the potential that infant ALL may not be entirely the same biologic entity as standard pediatric ALL and may be more responsive than understood earlier.
Therapeutic response and appearance of GVHD after the withdrawal of immunosuppression in this patient provides evidence that graft-versus-
leukemia
effect may play a role in
disease
control in infant ALL after HSCT.
This suggests that other immunotherapeutic interventions in the context of relapse may offer potential clinical benefit in this
disease
.
[MeSH-major]
Graft vs
Leukemia
Effect. Hematopoietic Stem
Cell
Transplantation. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / therapy
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(PMID = 20168246.001).
[ISSN]
1536-3678
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
8.
Mulloy JC, Wunderlich M, Zheng Y, Wei J:
Transforming human blood stem and progenitor cells: a new way forward in leukemia modeling.
Cell Cycle
; 2008 Nov 1;7(21):3314-9
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[Title]
Transforming human blood stem and progenitor cells: a new way forward in
leukemia
modeling.
MLL-AF9 (MA9) is a
leukemia
fusion gene formed upon translocation of the AF9 gene on chromosome 9 and the MLL gene on chromosome 11.
MA9 is commonly found in
acute
myeloid
leukemia
(AML) and occasionally in
acute
lymphoid
leukemia
and is associated with intermediate to poor outcome.
We have recently described a model system whereby we expressed the MA9 fusion gene in human CD34(+) Umbilical Cord Blood (UCB) cells and showed that these cells transformed to
acute
myeloid
or
lymphoid
leukemia
when injected into immunodeficient mice.
The
Mixed Lineage
Leukemia
(MLL) oncogenes are unique in this model system in that they promote full transformation of primary human blood cells, while all other
leukemia
-associated oncogenes tested thus far have induced only partial phenotypes.
Here we provide an update on the use of this system for modeling human
leukemia
and its potential application for therapeutic testing of novel compounds to treat the
disease
.
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[Cites]
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Leukemia. 2003 Apr;17(4):760-3
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]
(PMID = 18948748.001).
[ISSN]
1551-4005
[Journal-full-title]
Cell cycle (Georgetown, Tex.)
[ISO-abbreviation]
Cell Cycle
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA118319; United States / NCI NIH HHS / CA / K01 CA090370; United States / NCRR NIH HHS / RR / M01 RR 08084; United States / NCRR NIH HHS / RR / M01 RR008084; United States / NCI NIH HHS / CA / CA118319-04; United States / NCI NIH HHS / CA / R01 CA118319-04; United States / NCI NIH HHS / CA / CA118319; United States / NCI NIH HHS / CA / CA90370
[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 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.6.5.2 / rac GTP-Binding Proteins
[Other-IDs]
NLM/ NIHMS169825; NLM/ PMC2812025
9.
Bastida Vilá P, Palacio García C, Solsona Riera M, Ortega Aramburu JJ, Sánchez de Toledo Codina J:
[Minimal residual disease in acute lymphoblastic leukemia: a new concept of complete remission].
An Pediatr (Barc)
; 2005 Nov;63(5):390-5
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[Title]
[Minimal residual
disease
in
acute
lymphoblastic
leukemia
: a new concept of complete remission].
[Transliterated title]
Leucemia
mínima residual: nuevo concepto
de
remisión completa.
INTRODUCTION: Early response to induction treatment is one of the most important prognostic factors in children with
acute
lymphoblastic
leukemia
(ALL).
More sensitive techniques are required to measure residual
leukemia
and establish a new definition of complete remission.
OBJECTIVE: To identify minimal residual
disease
(MRD) by immunological techniques and define its prognostic impact in children with ALL.
All the children achieved complete cytological remission (< 5 %) with the induction treatment and had at least one useful phenotype for follow-up: 11 % were T phenotype, one was
biphenotypic
and the remainder were
B cell leukemias
.
Elimination was slower in patients with
a T
phenotype and in high-risk patients according to the traditional classification.
[MeSH-major]
Neoplasm, Residual / epidemiology. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / epidemiology
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(PMID = 16266612.001).
[ISSN]
1695-4033
[Journal-full-title]
Anales de pediatría (Barcelona, Spain : 2003)
[ISO-abbreviation]
An Pediatr (Barc)
[Language]
spa
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Spain
10.
Scolnik MP, Aranguren PN, Cuello MT, Palacios MF, Sanjurjo J, Giunta M, Bracco MM, Acevedo S:
Biphenotypic acute leukemia with t(15;17).
Leuk Lymphoma
; 2005 Apr;46(4):607-10
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[Title]
Biphenotypic acute leukemia
with t(15;17).
Biphenotypic acute
leukemias
(BAL) represent 5% of all
acute
leukemias
.
Immunophenotype revealed the compromise of
myeloid and
B-
lymphoid
lineages.
This report describes a BAL case with an unfrequent cytogenetic
abnormality
, and highlights the importance of correlating the results of multiple diagnostic methods in order to establish a correct
diagnosis and
treatment in BAL patients.
[MeSH-major]
Chromosome Inversion. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics.
Leukemia
/ genetics
[MeSH-minor]
Acute
Disease
. Child. Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Female. Flow Cytometry / methods. Gene Rearrangement. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence / methods. Neoplasm, Residual /
diagnosis
. Neoplasm, Residual / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Trisomy
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(PMID = 16019491.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
11.
Zheng C, Wu J, Liu X, Ding K, Cai X, Zhu W:
What is the optimal treatment for biphenotypic acute leukemia?
Haematologica
; 2009 Dec;94(12):1778-80; author reply 1780
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[Title]
What is the optimal treatment for
biphenotypic acute leukemia
?
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Biphenotypic
,
Acute
/ drug therapy
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[Cites]
Blood. 1992 Oct 15;80(8):2066-73
[
1327288.001
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[CommentOn]
Haematologica. 2009 Jul;94(7):919-27
[
19454497.001
]
(PMID = 19996120.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Comment; Letter
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antigens, CD34; EC 1.11.1.7 / Peroxidase
[Other-IDs]
NLM/ PMC2791943
12.
Gerr H, Zimmermann M, Schrappe M, Dworzak M, Ludwig WD, Bradtke J, Moericke A, Schabath R, Creutzig U, Reinhardt D:
Acute leukaemias of ambiguous lineage in children: characterization, prognosis and therapy recommendations.
Br J Haematol
; 2010 Apr;149(1):84-92
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[Title]
Acute
leukaemias
of ambiguous
lineage
in children: characterization, prognosis and therapy recommendations.
Acute
leukaemias
of ambiguous
lineage
(ALAL) represent a rare type of
leukaemia
, expressing both
myeloid and lymphoid
markers.
This study retrospectively analyzed data from 92 children (
biphenotypic
n = 78, bilineal n = 6,
lineage
switch n = 8) with ALAL registered in the Berlin-Frankfürt-Münster (BFM)
acute
myeloid leukaemia
(AML) and
acute
lymphoblastic leukaemia
(ALL) studies between 1998 and 2006 (2.4% of all cases with
acute
leukaemia
).
Our cohort of ALAL patients was characterized by comparatively high median age (8.9 years), high median white blood
cell
count (14.9 x 10(9)/l), as well as frequent hyperleucocytosis (18.5%) and central nervous system involvement (24.1%).
Our data suggest that an intensive therapy regimen including stem
cell
transplantation may be favourable for bilineal or
lineage
switch cases, whereas patients with ETV6/RUNX1 fusion,
lymphoid
morphology and patients with expression of cyCD22 and cyCD79a should be treated with an ALL-directed therapy.
[MeSH-major]
Leukemia
/
diagnosis
[MeSH-minor]
Acute
Disease
. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Chromosome Aberrations. Hematopoietic Stem
Cell
Transplantation. Humans. Immunophenotyping. Infant. Prognosis. Retrospective Studies. Survival Analysis. Treatment Outcome
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(PMID = 20085575.001).
[ISSN]
1365-2141
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
13.
Naghashpour M, Lancet J, Moscinski L, Zhang L:
Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report.
Am J Hematol
; 2010 Jun;85(6):451-4
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[Title]
Mixed
phenotype
acute leukemia
with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-
lymphoid
type: A first case report.
The majority of cases of
acute leukemia
belong to a specific
lineage
origin, either
lymphoid
or
myeloid
, and therefore are classified as
acute
lymphoblastic
leukemia
(ALL) or
acute
myelogenous
leukemia
(AML), based on
morphologic
features and cytochemical and immunophenotypic profile of the blast cells.
A minority of
acute
leukemias
however, show no clear evidence of differentiation along a single
lineage
.
These are now classified under
acute
leukemias
of ambiguous
lineage
by the most recent WHO classification and account for <4% of all cases of
acute leukemia
[1].
They include
leukemias
with no
lineage
specific antigens (
acute
undifferentiated
leukemias
) and those with blasts that express antigens of more than one
lineage
to such degree that it is not possible to assign the
leukemia
to any one particular
lineage
with certainty (
mixed
phenotype
acute
leukemias
).
The latter can either be
leukemias
with two distinct populations of blasts, each expressing antigens of a different
lineage
(historically referred to as "bilineal"
leukemias
) or a single blast population expressing antigens of multiple lineages (historically referred to as "
biphenotypic
"
acute
leukemias
) [2].
Acute
leukemias
of ambiguous
lineage
may harbor a variety of genetic lesions.
Those with t(9;22)(q34;q11) or translocations associated with
mixed lineage leukemias
(MLL) gene, i.e., t(11;V)(q23;V), occur frequently enough and are associated with distinct features, that are considered as separate entities according to the recent WHO classification.
Co-expression of
myeloid and
B-
lymphoid
antigens is most common in
mixed
phenotype
acute leukemia
(MPAL), followed by co-expression of
myeloid and
T-
lymphoid
antigens, accounting for 66-70% and 23-24% of MLLs, respectively.
Coexpression of B-
and T
-
lineage
associated antigens or antigens of all three lineages is exceedingly rare, accounting for <5% of MLLs [3,4].
The requirements for assigning more than one
lineage
to a single blast population has been established by current WHO classification [1].
[MeSH-major]
Antigens, Neoplasm / blood. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Immunophenotyping.
Leukemia
/ classification.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
[MeSH-minor]
Acute
Disease
. Adult. Antigens, CD / analysis. Bone Marrow / pathology.
Cell Lineage
. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics
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(PMID = 20513125.001).
[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 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / MLL-ENL oncoprotein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
14.
Iacobucci I, Storlazzi CT, Cilloni D, Lonetti A, Ottaviani E, Soverini S, Astolfi A, Chiaretti S, Vitale A, Messa F, Impera L, Baldazzi C, D'Addabbo P, Papayannidis C, Lonoce A, Colarossi S, Vignetti M, Piccaluga PP, Paolini S, Russo D, Pane F, Saglio G, Baccarani M, Foà R, Martinelli G:
Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP).
Blood
; 2009 Sep 3;114(10):2159-67
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[Title]
Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive
acute
lymphoblastic
leukemia
patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto
Acute Leukemia
Working Party (GIMEMA AL WP).
The BCR-ABL1 fusion gene defines the subgroup of
acute
lymphoblastic
leukemia
(ALL) with the worst clinical prognosis.
The IKZF1 deletion also was identified in the progression of chronic
myeloid
leukemia
to
lymphoid
blast crisis (66%) but never in
myeloid
blast crisis or chronic-phase chronic
myeloid
leukemia
or in patients with
acute
myeloid
leukemia
.
[MeSH-major]
Base Sequence / genetics. Chromosomes, Human, Pair 7 / genetics. Fusion Proteins, bcr-abl / genetics. Ikaros Transcription Factor / genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Sequence Deletion
[MeSH-minor]
Adolescent. Adult. Aged. Blast Crisis / genetics. Blast Crisis / metabolism.
Cell
Line, Tumor. Codon, Initiator / genetics. Codon, Initiator / metabolism. Cohort Studies. Exons / genetics. Female. Gene Expression Regulation, Leukemic / genetics. Humans.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / genetics.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / metabolism.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Male. Microarray Analysis. Middle Aged. Polymorphism, Single Nucleotide
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[ErratumIn]
Blood. 2010 Sep 23;116(12):2196
(PMID = 19589926.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Codon, Initiator; 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Fusion Proteins, bcr-abl
15.
Gozzetti A, Calabrese S, Raspadori D, Crupi R, Tassi M, Bocchia M, Fabbri A, Lauria F:
Concomitant t(4;11) and t(1;19) in a patient with biphenotypic acute leukemia.
Cancer Genet Cytogenet
; 2007 Aug;177(1):81-2
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[Title]
Concomitant t(4;11)
and t
(1;19) in a patient with
biphenotypic acute leukemia
.
[MeSH-major]
Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 4 / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Translocation, Genetic
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(PMID = 17693199.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
16.
Choi HW, Shin MG, Kim HJ, Lee IK, Yun JH, Kim HR, Kim YK, Yun HK, Cho D, Kee SJ, Shin JH, Suh SP, Ryang DW:
[Biphenotypic Acute Leukemia with BCR-ABL mRNA Transcript b3a2 Type: A Case Report with Review of the Literature.].
Korean J Lab Med
; 2006 Aug;26(4):249-54
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[Title]
[
Biphenotypic Acute Leukemia
with BCR-ABL mRNA Transcript b3a2 Type: A Case Report with Review of the Literature.].
Biphenotypic acute leukemia
(BAL) is a subtype of
leukemia
of ambiguous
lineage
in the World Health Organization classification system.
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(PMID = 18156734.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
kor
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Korea (South)
17.
Weinberg OK, Arber DA:
Mixed-phenotype acute leukemia: historical overview and a new definition.
Leukemia
; 2010 Nov;24(11):1844-51
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[Title]
Mixed
-phenotype
acute leukemia
: historical overview
and a
new definition.
Acute leukemia
with
a mixed
phenotype is a rare
disease and
comprises 2-5% of all
acute
leukemias
.
These disorders have been known historically by a variety of names, such as
mixed lineage
leukemia
, bilineal
leukemia
and
biphenotypic leukemia
, and the criteria for
diagnosis
have often been arbitrary.
The scoring criteria proposed by the European Group for the Immunological Characterization of
Leukemias
represented a major attempt to define this
disorder
.
However, the relative weight given to some markers and the lack of
lineage
specificity of most markers have raised questions regarding the significance of this approach.
In 2008, the World Health Organization classification of hematopoietic
and lymphoid
tumors proposed a simpler diagnostic algorithm, which relies on fewer and more
lineage
-specific markers to define
mixed
-phenotype
acute leukemia
(MPAL).
Several studies have suggested that patients with
acute leukemia
of
mixed
phenotype have a worse clinical outcome when compared with matched controls with
acute
myeloid
leukemia
or
acute
lymphoblastic
leukemia
.
Further studies are needed to confirm the significance of MPAL as currently defined, to determine a standardized treatment approach and to better understand the biological and clinical aspects of this
disease
.
[MeSH-major]
Leukemia
/ genetics
[MeSH-minor]
Acute
Disease
. Antigens, CD / analysis. Biomarkers, Tumor / analysis. Blast Crisis / pathology. Gene Rearrangement. Humans.
Leukemia
, B-
Cell
/ classification.
Leukemia
, B-
Cell
/ genetics.
Leukemia
, T-
Cell
/ classification.
Leukemia
, T-
Cell
/ genetics. Phenotype
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(PMID = 20844566.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD; 0 / Biomarkers, Tumor
18.
Alsayed H, Owaidah T, Al Rawas F:
Validation of a modified cryopreservation method for leukemic blasts for flow cytometry assessment.
Hematol Oncol Stem Cell Ther
; 2008 Apr-Jun;1(2):94-7
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BACKGROUND: Cryopreservation, a common method for storing human cells, has advantages when cells are used in retrospective studies of selected
cell
populations.
Frozen lymphocytes can be used for tissue typing, for monitoring
cell
-mediated immunity, and for various immunological tests.
Our report describes an efficient, simple and inexpensive method for cryopreservation of human
acute leukemia
cells.
METHODS:
Leukemia
cells from 20 newly diagnosed cases were frozen at -80 degrees C after cryopreservation with 5% dimethysulfoxide and then assayed by flow cytometry for antigen expression determined by monoclonal antibodies at different time intervals.
After 4 weeks, 91% of pre-B ALL, 88% of T-ALL, 100% of AML, and 100% of
biphenotypic
aliquots had viability over 75%.
CONCLUSION: We confirm that the method does not significantly alter the viability of cells and it preserved the antigenic expression of
leukemia
cells.
[MeSH-major]
Antigens, Neoplasm / biosynthesis. Cryopreservation / methods. Immunophenotyping / methods.
Leukemia
/
diagnosis
[MeSH-minor]
Cell
Survival. Flow Cytometry. Humans
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(PMID = 20063537.001).
[ISSN]
1658-3876
[Journal-full-title]
Hematology/oncology and stem cell therapy
[ISO-abbreviation]
Hematol Oncol Stem Cell Ther
[Language]
eng
[Publication-type]
Journal Article; Validation Studies
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, Neoplasm
19.
Lee HR, Kang SH, Kang HJ, Shin HY, Ahn HS, Kim HK, Park MH, Cho HI, Lee DS:
Lineage switch from acute myeloid leukemia to biphenotypic acute leukemia with acquisition of Philadelphia chromosome.
Cancer Genet Cytogenet
; 2008 Jul 15;184(2):124-6
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[Title]
Lineage
switch from
acute
myeloid
leukemia
to
biphenotypic acute leukemia
with acquisition of Philadelphia chromosome.
[MeSH-major]
Cell Lineage
/ genetics.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / pathology.
Leukemia
,
Myeloid
,
Acute
/ genetics. Philadelphia Chromosome
[MeSH-minor]
Cell
Transdifferentiation / genetics. Child.
Disease
Progression. Humans. Male. Phenotype
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(PMID = 18617064.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
20.
Pérez-Campos-Mayoral L, Ruiz-Argüelles A, Pérez-Romano B, Zenteno E, Hernández-Cruz P, Martínez-Cruz R, Martínez-Cruz M, Pina-Canseco S, Pérez-Campos E:
Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia.
Tohoku J Exp Med
; 2008 Jan;214(1):11-6
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[Title]
Potential use of the Macrobrachium rosenbergii lectin for
diagnosis
of T-
cell
acute
lymphoblastic
leukemia
.
T-
cell
acute
lymphoblastic
leukemia
is the most common form of cancer in children.
Lectins are proteins or glycoproteins from plants or animals that recognize oligossacharides on the
cell
surface and have been used to characterize the structural changes of oligosaccharides in
leukemias
.
In this study, we used the lectin from the freshwater prawn Macrobrachium (M. rosenbergii), specific for acetyl groups in sialylated glycans, because increased sialylation of glycoproteins and glycolipids has been identified in
lymphoblastic leukemias
.
We compared the specificity of the M. rosenbergii lectin for
lymphoblastic leukemias
with the specificities of the lectins from Triticum vulgaris, Solanum tuberosum, Arachis hipogaea, and Phytolacca americana.
By
morphologic and
phenotype characterization with a panel of monoclonal antibodies, we identified four types of
leukemias
from 106
leukemia
patients: 11 cases of T-
cell
acute
lymphoblastic
leukemia
, 61 cases of B-
cell
acute
lymphoblastic
leukemia
, 24 cases of
acute
myeloblastic
leukemia
, and 10 cases of
acute biphenotypic leukemia
.
As determined by cytofluorometric assays, nine of the eleven cases with T-
cell
acute
lymphoblastic
leukemia
(8 +/- 3 years old) were specifically identified with the lectin from M. rosenbergii.
In contrast, only six cases of B-
cell
leukemia
, one case of myeloblastic
leukemia
, and 2 cases of
biphenotypic leukemia
were identified with this M. rosenbergii lectin.
The other lectins tested showed no capacity to differentiate, in a significant manner, any of the four types of
leukemias
tested.
Thus, the lectin from M. rosenbergii could be considered a useful tool for the
diagnosis and
study of T-
cell
acute
lymphoblastic
leukemia
.
[MeSH-major]
Lectins.
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
. Palaemonidae / chemistry
[MeSH-minor]
Animals. Antibodies, Monoclonal. Antigens, CD45 / analysis. Antigens, Neoplasm / immunology. Child.
Diagnosis
, Differential. Flow Cytometry. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Phenotype
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(PMID = 18212483.001).
[ISSN]
0040-8727
[Journal-full-title]
The Tohoku journal of experimental medicine
[ISO-abbreviation]
Tohoku J. Exp. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Lectins; EC 3.1.3.48 / Antigens, CD45
21.
Coche D, Bergues B, Harrivel V, Guillaume N:
[Biphenotypic acute leukaemia with Burkitt-like cytology].
Ann Biol Clin (Paris)
; 2009 Jul-Aug;67(4):437-40
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[Title]
[
Biphenotypic acute
leukaemia
with Burkitt-like cytology].
[Transliterated title]
Leucémie aiguë biphénotypique avec aspect cytologique
de
type Burkitt.
Biphenotypic acute
leukaemia
(BAL) represents about 5% of adult
acute
leukaemia
.
Based on a previously described scoring system, the European Group for Immunologic Classification of
Leukaemia
(EGIL) proposed a set of diagnostic criteria for BAL.
This scoring system is based on the number and degree of the specificity of several markers for
myeloid
or T/
B lymphoid
blasts.
Here, we report the case of a BAL with Burkitt-like cytology, corresponding to "the
acute
lymphoblastic leukaemia
, Burkitt type" L3 for the FAB classification.
By flow cytometry, the blasts showed a positivity for
B lymphoid
cytoplasmic (CD79a and mu) and membrane (CD19, CD22, CD24, IgM) markers
AND a
positivity for the
myeloid
(CD13, CD33, CD65, CD15) markers.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/ genetics
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(PMID = 19654084.001).
[ISSN]
0003-3898
[Journal-full-title]
Annales de biologie clinique
[ISO-abbreviation]
Ann. Biol. Clin. (Paris)
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
22.
Buckley O, Reardon M:
A young male with bone pain.
Eur J Intern Med
; 2005 Sep;16(5):366-8
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Bone marrow biopsy and peripheral blood film confirmed the
diagnosis
of an
acute biphenotypic
leukaemia
.
This case report highlights the fact that bone pain associated with a normal peripheral blood count may be the presentation of an
acute
haematological
disorder
in both adults and children.
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(PMID = 16137555.001).
[ISSN]
0953-6205
[Journal-full-title]
European journal of internal medicine
[ISO-abbreviation]
Eur. J. Intern. Med.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
23.
Horton TM, Ames MM, Reid JM, Krailo MD, Pendergrass T, Mosher R, Reaman GH, Seibel NL, Children's Oncology Group:
A Phase 1 and pharmacokinetic clinical trial of paclitaxel for the treatment of refractory leukemia in children: a Children's Oncology Group study.
Pediatr Blood Cancer
; 2008 Apr;50(4):788-92
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[Title]
A Phase 1 and pharmacokinetic clinical trial of paclitaxel for the treatment of refractory
leukemia
in children: a Children's Oncology Group study.
BACKGROUND: This report summarizes a phase 1 study conducted by the Children's Cancer Group (CCG) to determine the maximum tolerated dose (MTD), dose-limiting toxicities (DLTs), pharmacokinetics, and anti-
leukemia
activity of paclitaxel in children with advanced stage
leukemias
.
Doses ranged from 250 to 500 mg/m(2) every 21 days in schedule
A and
105 to 200 mg/m(2) weekly x 3 every 28 days in schedule B.
RESULTS: Sixty-three patients (median 10 years) with refractory or relapsed
leukemia
(ALL) (n = 39),
acute
myeloid
leukemia
(AML) (n = 19),
biphenotypic
(n = 4), and JCML (n = 1)) were enrolled.
Among 54 evaluable patients, there was one complete response (CR), three partial responses (PR), and five patients with stable
disease
(SD).
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[Copyright]
(c) 2008 Wiley-Liss, Inc.
(PMID = 17668866.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / K23 CA113775; United States / NCI NIH HHS / CA / U01 CA097452; United States / NCRR NIH HHS / RR / M01 RR000188; United States / NCI NIH HHS / CA / U01-CA97452; United States / NCI NIH HHS / CA / K23-CA113775; United States / NCI NIH HHS / CA / K12-CA90433; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCRR NIH HHS / RR / MO1 RR00108
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; P88XT4IS4D / Paclitaxel
24.
Formankova R, Sedlacek P, Keslová P, Sramkova L, Zizkova H, Stary J:
Adoptive immunotherapy, chemotherapy, and second allogeneic transplant in the treatment of post-transplant relapse of acute leukemia in children: a single center experience.
Leuk Lymphoma
; 2010 Oct;51(10):1936-40
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[Title]
Adoptive immunotherapy, chemotherapy, and second allogeneic transplant in the treatment of post-transplant relapse of
acute leukemia
in children: a single center experience.
[MeSH-major]
Drug Therapy / methods. Hematopoietic Stem
Cell
Transplantation / methods. Immunotherapy, Adoptive / methods.
Leukemia
/ therapy
[MeSH-minor]
Acute
Disease
. Adolescent. Child. Child, Preschool. Humans.
Leukemia
,
Biphenotypic
,
Acute
/ therapy.
Leukemia
,
Myeloid
/ therapy. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / therapy. Survival Analysis. Transplantation, Homologous. Treatment Outcome
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(PMID = 20846093.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Letter; Research Support, Non-U.S. Gov't
[Publication-country]
England
25.
Nishiuchi T, Ohnishi H, Kamada R, Kikuchi F, Shintani T, Waki F, Kitanaka A, Kubota Y, Tanaka T, Ishida T:
Acute leukemia of ambiguous lineage, biphenotype, without CD34, TdT or TCR-rearrangement.
Intern Med
; 2009;48(16):1437-41
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[Title]
Acute leukemia
of ambiguous
lineage
, biphenotype, without CD34, TdT or TCR-rearrangement.
Biphenotypic acute leukemia
(BAL) is a rare entity that comprises 0.5-3% of all
acute
leukemias and
probably arises from multipotent progenitor cells.
We report the case of a 41-year-old man with BAL having
myeloid and
T-
lymphoid lineage
phenotypes.
This pattern is rarely encountered and suggests that the blast cells were possibly considered immature with aspects of differentiation indicating
myeloid lineage
, rather than T-
lymphoid lineage
.
[MeSH-major]
Antigens, CD34 / genetics.
Cell Lineage
/ genetics. DNA Nucleotidylexotransferase / genetics. Gene Rearrangement / genetics.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Receptors, Antigen, T-
Cell
. Receptors, Antigen, T-
Cell
, alpha-beta / genetics. Receptors, Antigen, T-
Cell
, gamma-delta / genetics
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(PMID = 19687594.001).
[ISSN]
1349-7235
[Journal-full-title]
Internal medicine (Tokyo, Japan)
[ISO-abbreviation]
Intern. Med.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; EC 2.7.7.31 / DNA Nucleotidylexotransferase
26.
Matsumoto Y, Taki T, Fujimoto Y, Taniguchi K, Shimizu D, Shimura K, Uchiyama H, Kuroda J, Nomura K, Inaba T, Shimazaki C, Horiike S, Taniwaki M:
Monosomies 7p and 12p and FLT3 internal tandem duplication: possible markers for diagnosis of T/myeloid biphenotypic acute leukemia and its clonal evolution.
Int J Hematol
; 2009 Apr;89(3):352-8
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[Title]
Monosomies 7p and 12p and FLT3 internal tandem duplication: possible markers for
diagnosis
of T/
myeloid
biphenotypic acute leukemia
and its clonal evolution.
Biphenotypic acute leukemia
co-expressing T-
lymphoid and myeloid
markers is rare, accounting for less than 1% of
acute
leukemias
.
Recurrence of monosomies 7p and/or 12p in T/
myeloid
biphenotypic acute leukemia
has been reported.
We treated a patient with T/
myeloid
biphenotypic acute leukemia
showing clonal chromosomal and genetic abnormalities including dic(7;12)(p11;p11) and Fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication.
Cytogenetic analysis of both bone marrow and lymph node cells disclosed that the patient's lymph node
leukemia
cells had chromosomal abnormalities in addition to dic(7;12).
Our findings suggest that the
leukemia
cells of systemic lymphadenopathy had evolved as secondary cells from marrow
leukemia
cells.
The patient was successfully treated with induction chemotherapy for
acute
myeloid
leukemia
followed by allogeneic bone marrow transplantation.
[MeSH-major]
Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Duplication.
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
.
Leukemia
,
Biphenotypic
,
Acute
/ enzymology. fms-Like Tyrosine Kinase 3 / metabolism
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[ISSN]
1865-3774
[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 / Biomarkers, Tumor; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
27.
Imataki O, Ohnishi H, Yamaoka G, Arai T, Kitanaka A, Kubota Y, Kushida Y, Ishida T, Tanaka T:
Lineage switch from precursor B cell acute lymphoblastic leukemia to acute monocytic leukemia at relapse.
Int J Clin Oncol
; 2010 Feb;15(1):112-5
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[Title]
Lineage
switch from precursor
B cell
acute
lymphoblastic
leukemia
to
acute
monocytic
leukemia
at relapse.
A lineage
switch in
leukemia
, in which the leukemic
cell lineage
at onset converts to another
lineage
at a later time, is an uncommon type of
hybrid
(
mixed
)
leukemia
regarded as a variation of bilineage
leukemia
.
We present a case of a 60-year-old female diagnosed with precursor
B cell
acute
lymphoblastic
leukemia
(ALL), whose markers in flow cytometry shifted from their original status of CD19+, 22+, 79a+, 13+, HLA-DR+, and TdT+.
Residual
disease
was proved by biopsy and pathologically shown to have an immature phenotype of CD5+, CD10-, CD20-, CD79a- and myeloperoxidase negativity.
Two weeks after liver biopsy, blast cells progressively appeared in the peripheral blood; these cells had a monocytoid morphology and phenotype (CD13, 14) but were accompanied by
myeloid
(CD33)
and lymphoid
(CD2, 4, 20) cells.
This phenotypical conversion from B-ALL to
hybrid
leukemia
featuring monocytoid characteristics is known as
a lineage
switch.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/ pathology.
Leukemia
, Monocytic,
Acute
/ pathology. Precursor B-
Cell Lymphoblastic
Leukemia
-Lymphoma / pathology
[MeSH-minor]
Biomarkers, Tumor / blood. Bone Marrow / pathology.
Cell Lineage
. Female. Humans. Immunophenotyping. Middle Aged. Recurrence
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[ISSN]
1437-7772
[Journal-full-title]
International journal of clinical oncology
[ISO-abbreviation]
Int. J. Clin. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers, Tumor
28.
Oka S, Yokote T, Akioka T, Hara S, Kobayashi K, Hirata Y, Hiraoka N, Tsuji M, Hanafusa T:
Trisomy 21 as the sole acquired karyotypic abnormality in biphenotypic acute leukemia.
Int J Hematol
; 2007 Apr;85(3):270-2
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[Title]
Trisomy 21 as the sole acquired karyotypic
abnormality
in
biphenotypic acute leukemia
.
[MeSH-major]
Chromosome Aberrations. Down Syndrome / blood. Down Syndrome / pathology.
Leukemia
/ genetics
[MeSH-minor]
Acute
Disease
/ classification.
Acute
Disease
/ therapy. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Dexamethasone / therapeutic use. Doxorubicin / therapeutic use. Humans. Male. Treatment Outcome. Vincristine / therapeutic use
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.
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.
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.
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DOXORUBICIN
.
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DEXAMETHASONE
.
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.
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VINCRISTINE
.
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[Cites]
Blood. 1998 Jul 15;92(2):596-9
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[Cites]
J Clin Oncol. 1998 Dec;16(12):3803-9
[
9850025.001
]
(PMID = 17483067.001).
[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
Japan
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
29.
Ramamoorthy SK, Pandita R, Prakash A, Ramaswamy NV, Al Bahar S:
Safety of imatinib in chronic myeloid leukemia in blastic crisis presenting as cholestatic jaundice.
Acta Haematol
; 2007;118(3):141-5
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[Title]
Safety of imatinib in chronic
myeloid
leukemia
in blastic crisis presenting as cholestatic jaundice.
Acute leukemia
presenting as cholestatic jaundice is rare.
It can occur due to granulocytic sarcoma compressing the bile ducts in case of
acute
myeloid
leukemia
.
We report a case of chronic
myeloid
leukemia
in
lymphoid
blast
cell
crisis presenting with severe cholestatic jaundice due to diffuse infiltration of the liver sinusoids with lymphoblasts.
[MeSH-major]
Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Jaundice, Obstructive / drug therapy.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Liver Neoplasms / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
[MeSH-minor]
Adult. Benzamides.
Diagnosis
, Differential. Drug-Related Side Effects and Adverse Reactions. Humans. Imatinib Mesylate. Male
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.
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.
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[Copyright]
2007 S. Karger AG, Basel
(PMID = 17804901.001).
[ISSN]
1421-9662
[Journal-full-title]
Acta haematologica
[ISO-abbreviation]
Acta Haematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
30.
Chou ST, Opalinska JB, Yao Y, Fernandes MA, Kalota A, Brooks JS, Choi JK, Gewirtz AM, Danet-Desnoyers GA, Nemiroff RL, Weiss MJ:
Trisomy 21 enhances human fetal erythro-megakaryocytic development.
Blood
; 2008 Dec 1;112(12):4503-6
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Children with Down syndrome exhibit 2 related hematopoietic diseases: transient myeloproliferative
disorder
(TMD) and
acute
megakaryoblastic
leukemia
(AMKL).
Both exhibit clonal expansion of blasts with
biphenotypic
erythroid and megakaryocytic features and contain somatic GATA1 mutations.
Our findings indicate that trisomy 21 itself is associated with
cell
-autonomous expansion of erythro-megakaryocytic progenitors.
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[Cites]
Blood. 2004 Jan 15;103(2):399-406
[
14512321.001
]
[Cites]
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]
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]
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[
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]
[Cites]
Blood. 2004 Apr 1;103(7):2480-9
[
14656875.001
]
(PMID = 18812473.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK061692; United States / NCRR NIH HHS / RR / UL1 RR024134; United States / NCRR NIH HHS / RR / UL1-RR-024134
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2597125
31.
Zekri AR, Ahmed H, Ismail M, El-Nashar AT, El-Mokadem T, Hassan A:
Genetic profiling of non-Hodgkin's lymphoma with or without hepatitis C virus infection.
Egypt J Immunol
; 2010;17(2):81-90
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Hepatitis C virus (HCV) which is one of the endemic viral infections in Egypt is not only hepatotropic, but also a lymphotropic virus and has many extrahepatic manifestations as
mixed
cryoglobulinemia and non-Hodgkin's lymphoma.
We studied gene expression profile of 20 B-
cell
non-Hodgkin's lymphoma with HCV infection and 20 B-
cell
non-Hodgkin's lymphoma without HCV infection as a control group by c-DNA microarray.
Also, HCV was associated with overexpression of the genes related to
myeloid
/
lymphoid
leukemia
and B
lymphoma as MLLT3, BAL, influences the overexpression of transcription regulator genes as TATA box binding protein (TBP) and may influence the overexpression of some immunoglobulin genes as immunoglobulin superfamily containing leucine gene in B cells resulting in overproduction of immunoglobulins in B-lymphocyte disorders.
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(PMID = 23082489.001).
[ISSN]
1110-4902
[Journal-full-title]
The Egyptian journal of immunology
[ISO-abbreviation]
Egypt J Immunol
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
Egypt
[Chemical-registry-number]
0 / Immunoglobulins; 0 / MLLT3 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / PARP9 protein, human; 0 / TATA-Box Binding Protein; 0 / TBP protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP4 protein, human; EC 3.4.22.- / Caspases, Initiator; EC 3.4.22.36 / Caspase 1
32.
Teuffel O, Betts DR, Thali M, Eberle D, Meyer C, Schneider B, Marschalek R, Trakhtenbrot L, Amariglio N, Niggli FK, Schäfer BW:
Clonal expansion of a new MLL rearrangement in the absence of leukemia.
Blood
; 2005 May 15;105(10):4151-2
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[Title]
Clonal expansion of a new MLL rearrangement in the absence of
leukemia
.
[MeSH-major]
Cell Lineage
. Clone Cells / cytology. Clone Cells / metabolism.
Leukemia
,
Biphenotypic
,
Acute
/ genetics.
Leukemia
,
Myeloid
/ genetics.
Leukemia
,
Myeloid
/ pathology
[MeSH-minor]
Acute
Disease
. Bone Marrow Cells / metabolism. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans
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(PMID = 15867425.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
33.
Sun JX, Zhang WG, Chen YX, Zhao WH, Tian W, Yang Y, Liu SH:
Indoleamine 2, 3-dioxygenase expression in cells of human acute monocyte leukemia (M(5)) and acute lymphocyte leukemia and therapeutic effect of its inhibitor 1-methyl tryptophan.
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2007 Jun;15(3):478-82
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[Title]
Indoleamine 2, 3-dioxygenase expression in cells of human
acute
monocyte
leukemia
(M(5)) and
acute
lymphocyte
leukemia
and therapeutic effect of its inhibitor 1-methyl tryptophan.
The objective of this study was to investigate the expression and function of indoleamine 2, 3-dioxygenase (IDO) in
leukemia
.
The IDO expressions in human
acute
monocyte
leukemia
(M(5)) and
acute
lymphocyte
leukemia
(ALL) were detected by immunofluorescence staining.
Constructed
leukemia
mouse model was used to observe whether the IDO inhibitor, 1-methyl tryptophan (1-MT), has any effect in treating
leukemia
.
After statistical test, IDO expression level in
leukemia
cells was significantly higher than that of normal mononuclear cells.
Some of the
leukemia
mice in the experimental group long-term survived without tumor (more than three months after vaccination).
It is concluded that human
acute
monocyte
leukemia
(M(5)) and
acute
lymphocyte
leukemia
(ALL) express IDO, and both can be treated by 1-MT in mice.
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(PMID = 17605849.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
ENG
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / 1-methyltryptophan; 0 / Indoleamine-Pyrrole 2,3,-Dioxygenase; 8DUH1N11BX / Tryptophan
34.
Bursen A, Schwabe K, Rüster B, Henschler R, Ruthardt M, Dingermann T, Marschalek R:
The AF4.MLL fusion protein is capable of inducing ALL in mice without requirement of MLL.AF4.
Blood
; 2010 Apr 29;115(17):3570-9
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The chromosomal translocation t(4;11)(q21;q23) is the most frequent genetic aberration of the human MLL gene, resulting in high-risk
acute
lymphoblastic
leukemia
(ALL).
Recipients of AF4.MLL- or double-transduced LSPCs developed pro-B ALL, B/T
biphenotypic acute leukemia
, or
mixed lineage
leukemia
.
Transplantation of MLL.AF4- or mock-transduced LSPCs did not result in
disease
development during an observation period of 13 months.
These findings indicate that the expression of the AF4.MLL fusion protein is capable of inducing
acute
lymphoblastic
leukemia
even in the absence of the MLL.AF4 fusion protein.
In view of recent findings, these results may imply that t(4;11)
leukemia
is based on 2 oncoproteins, providing an explanation for the very early onset of
disease
in humans.
[MeSH-major]
Cell
Transformation, Neoplastic / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Leukemic.
Myeloid
-
Lymphoid
Leukemia
Protein / metabolism. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Precursor B-
Cell Lymphoblastic
Leukemia
-Lymphoma / metabolism
SciCrunch.
ArrayExpress: Data: Microarray
.
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(PMID = 20194896.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Aff1 protein, mouse; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse
35.
Hayette S, Chabane K, Tchirkov A, Berger MG, Nicolini FE, Tournilhac O:
Detection of twelve nucleotides insertion in the BCR-ABL kinase domain in an imatinib-resistant but dasatinib-sensitive patient with bi-phenotypic acute leukemia.
Haematologica
; 2009 Sep;94(9):1324-6
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[Title]
Detection of twelve nucleotides insertion in the BCR-ABL kinase domain in an imatinib-resistant but dasatinib-sensitive patient with bi-phenotypic
acute leukemia
.
[MeSH-major]
Base Sequence / genetics. Fusion Proteins, bcr-abl / genetics.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Piperazines / administration & dosage. Protein Kinase Inhibitors / administration & dosage. Protein-Tyrosine Kinases / genetics. Pyrimidines / administration & dosage. Sequence Deletion. Thiazoles / administration & dosage
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[Cites]
Blood. 2003 Jul 1;102(1):276-83
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Blood. 2006 Jul 1;108(1):28-37
[
16522812.001
]
(PMID = 19734429.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Case Reports; Letter; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
[Other-IDs]
NLM/ PMC2738731
36.
Andreeff M, Ruvolo V, Gadgil S, Zeng C, Coombes K, Chen W, Kornblau S, Barón AE, Drabkin HA:
HOX expression patterns identify a common signature for favorable AML.
Leukemia
; 2008 Nov;22(11):2041-7
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Deregulated HOX expression, by chromosomal translocations
and myeloid
-
lymphoid
leukemia
(MLL) rearrangements, is causal in some types of
leukemia
.
Using real-time reverse transcription-PCR, we examined the expression of 43 clustered HOX, polycomb, MLL and FLT3 genes in 119 newly diagnosed adult
acute
myeloid leukemias
(AMLs) selected from all major cytogenetic groups.
We also observed that HOXA9 levels were significantly inversely correlated with survival and that BMI-1 was overexpressed in cases with 11q23 rearrangements, suggesting that p19(ARF) suppression may be involved in MLL-associated
leukemia
.
These results underscore the close relationship between HOX expression patterns and certain forms of AML and emphasize the need to determine whether these differences play a role in the
disease
process.
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[
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[
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]
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]
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]
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[
9052833.001
]
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Mol Cell Biol. 1998 Jan;18(1):322-33
[
9418879.001
]
(PMID = 18668134.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA97710; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA097710-04; United States / NCI NIH HHS / CA / R21 CA097710; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / R33 CA097710-04; United States / NCI NIH HHS / CA / R33 CA097710; United States / NCI NIH HHS / CA / P01 CA055164
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Polycomb-Group Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Repressor Proteins; 0 / myeloid ecotropic viral integration site 1 protein; 117896-08-9 / nucleophosmin; 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 / fms-Like Tyrosine Kinase 3; EC 6.3.2.19 / Polycomb Repressive Complex 1
[Other-IDs]
NLM/ NIHMS104075; NLM/ PMC2676170
37.
Ru YX, Wang HJ, Yang BX, Liu JH, Li ZQ, Li CW, Wang JX, Mi YC:
The ultrastructure of hybrid acute leukemia: a study of 15 cases.
Ultrastruct Pathol
; 2005 Sep-Oct;29(5):341-7
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[Title]
The ultrastructure of
hybrid
acute leukemia
: a study of 15 cases.
The objective of this study was to investigate the ultrastructural characteristics of
hybrid
acute leukemia
(HAL).
By TEM, 5 out 15 cases of HAL were consistent with immunophenotyping (3 cases of
biphenotypic
type, and 2 cases of biclonal type with granulocytes and lymphocytes); 2 cases were suspected as HAL.
Most of the blast cells of
biphenotypic
HAL showed
lymphoid
features, except some cases containing MPO positive granules in blasts, while a few cases exhibited monocytic or nonspecific features.
TEM offers advantages in the
diagnosis
of biclonal type HAL and
biphenotypic
HAL positive for MPO.
However, it is difficult to differentiate MPO-negative cases of
biphenotypic
HAL from ALL
and a
few cases may be misinterpreted as M5 by TEM.
[MeSH-major]
Granulocyte Precursor Cells / ultrastructure.
Leukemia
,
Myeloid
,
Acute
/
diagnosis
. Lymphocytes / ultrastructure. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma /
diagnosis
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(PMID = 16257860.001).
[ISSN]
0191-3123
[Journal-full-title]
Ultrastructural pathology
[ISO-abbreviation]
Ultrastruct Pathol
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 1.11.1.7 / Peroxidase
38.
Ikezoe T, Nishioka C, Tasaka T, Yang Y, Komatsu N, Togitani K, Koeffler HP, Taguchi H:
The antitumor effects of sunitinib (formerly SU11248) against a variety of human hematologic malignancies: enhancement of growth inhibition via inhibition of mammalian target of rapamycin signaling.
Mol Cancer Ther
; 2006 Oct;5(10):2522-30
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We studied antitumor effects of receptor tyrosine kinase inhibitor sunitinib (formerly SU11248) against a variety of hematologic malignancies including the following
leukemias
: eosinophilic (EOL-1),
acute
myeloid
(THP-1, U937, Kasumi-1),
biphenotypic
(MV4-11),
acute
lymphoblastic
(NALL-1, Jurkat, BALL-2, PALL-1, PALL-2), blast crisis of chronic
myeloid
(KU812, Kcl-22, K562), and adult T-
cell
(MT-1, MT-2, MT-4), as well as non-Hodgkin's lymphoma (KS-1, Dauji, Akata) and multiple myeloma (U266).
Thymidine uptake studies showed that sunitinib was active against EOL-1, MV4-11, and Kasumi-1 cells, which possessed activating mutations of the PDGFRalpha, FLT-3,
and c
-KIT genes, respectively, with IC(50)s of <30 nmol/L.
In addition, sunitinib inhibited the proliferation of freshly isolated
leukemia
cells from patients possessing mutations in FLT3 gene.
Interestingly, rapamycin analogue RAD001 enhanced the ability of sunitinib to inhibit the proliferation of
leukemia
cells and down-regulate levels of mammalian target of rapamycin effectors p70 S6 kinase and eukaryotic initiation factor 4E-binding protein 1 in these cells.
Taken together, sunitinib may be useful for treatment of individuals with
leukemias
possessing activation mutation of tyrosine kinase, and the combination of sunitinib and RAD001 represents a promising novel treatment strategy.
[MeSH-minor]
Adaptor Proteins, Signal Transducing / antagonists & inhibitors. Adaptor Proteins, Signal Transducing / biosynthesis. Apoptosis.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Drug Synergism. Everolimus. Humans.
Leukemia
/ metabolism.
Leukemia
/ pathology. Mutation. Phosphoproteins / antagonists & inhibitors. Phosphoproteins / biosynthesis. Receptor Protein-Tyrosine Kinases / genetics. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Ribosomal Protein S6 Kinases, 70-kDa / biosynthesis. Signal Transduction. Sirolimus / analogs & derivatives. Sirolimus / pharmacology. TOR Serine-Threonine Kinases
Hazardous Substances Data Bank.
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(PMID = 17041096.001).
[ISSN]
1535-7163
[Journal-full-title]
Molecular cancer therapeutics
[ISO-abbreviation]
Mol. Cancer Ther.
[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 / Antineoplastic Agents; 0 / EIF4EBP1 protein, human; 0 / Indoles; 0 / Phosphoproteins; 0 / Pyrroles; 0 / sunitinib; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
39.
Park AH, Muntz HR, Smith ME, Afify Z, Pysher T, Pavia A:
Pediatric invasive fungal rhinosinusitis in immunocompromised children with cancer.
Otolaryngol Head Neck Surg
; 2005 Sep;133(3):411-6
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RESULTS: Seventeen consecutive pediatric immunocompromised patients with hematologic
and lymphoid
neoplasms underwent nasal endoscopy and biopsy for possible FS.
Eight patients had
acute
myelogenous
leukemia
(AML); 6 patients had
acute
lymphoblastic
leukemia
(ALL); 1 patient had Burkitt's lymphoma, 1 patient had undifferentiated
leukemia
; and 1 patient had
biphenotypic acute leukemia
.
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.
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.
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.
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(PMID = 16143192.001).
[ISSN]
0194-5998
[Journal-full-title]
Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
[ISO-abbreviation]
Otolaryngol Head Neck Surg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
40.
Márkász L, Hajas G, Kiss A, Lontay B, Rajnavölgyi E, Erdodi F, Oláh E:
Granulocyte colony stimulating factor increases drug resistance of leukaemic blast cells to daunorubicin.
Pathol Oncol Res
; 2008 Sep;14(3):285-92
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Acute
leukaemia
is known as the most common cancer in childhood.
The clinical use of Granulocyte Colony Stimulating Factor (G-CSF) has become widespread to minimize chemotherapy-induced myelosuppression and febrile neutropenia in childhood solid tumors,
acute
lymphoid leukaemia
(ALL) and in several trials with AML.
In case of ALL this seems to be reasonable because, due to the absence of G-CSF receptor (G-CSFR) on the surface of normal
lymphoid
cells, G-CSF does not have any influence on the pathways of proliferation and differentiation of
lymphoid lineage
cells.
It has been suggested, however, that ALL blasts with B or
T cell
surface antigens as well as
biphenotypic
leukaemia
cells express G-CSFR, and they are able to respond to exogenously added G-CSF with proliferation.
In this study we investigated how G-CSF might influence the sensitivity of leukemic cells to daunorubicin induced
cell
death using MTT assay, flow cytometry and Western blot analysis.
[MeSH-major]
Antibiotics, Antineoplastic / therapeutic use. Daunorubicin / therapeutic use. Drug Resistance, Neoplasm / drug effects. Granulocyte Colony-Stimulating Factor / pharmacology.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Myeloid
Cells / drug effects
[MeSH-minor]
Cell
Line, Tumor. Chemotherapy, Adjuvant. Dose-Response Relationship, Drug. Humans. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / pathology. Receptors, Granulocyte Colony-Stimulating Factor / drug effects
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DAUNORUBICIN
.
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(PMID = 18493867.001).
[ISSN]
1219-4956
[Journal-full-title]
Pathology oncology research : POR
[ISO-abbreviation]
Pathol. Oncol. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antibiotics, Antineoplastic; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; ZS7284E0ZP / Daunorubicin
41.
Marques-Salles Tde J, Barros JE, Soares-Ventura EM, Cartaxo Muniz MT, Santos N, Ferreira da Silva E, Silva ML, Liehr T, Mkrtchyan H:
Unusual childhood biphenotypic acute leukemia with a yet unreported t(3;13)(p25.1;q13).
Leuk Res
; 2010 Aug;34(8):e206-7
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[Title]
Unusual childhood
biphenotypic acute leukemia
with a yet unreported t(3;13)(p25.1;q13).
[MeSH-major]
Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 3 / genetics. Killer Cells, Natural / pathology.
Leukemia
,
Myeloid
,
Acute
/ pathology. Precursor T-
Cell Lymphoblastic
Leukemia
-Lymphoma / pathology. Translocation, Genetic / genetics
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(PMID = 20338638.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
42.
Wang L, Lin D, Zhang X, Chen S, Wang M, Wang J:
Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese acute leukemia patients.
Leuk Res
; 2005 Dec;29(12):1393-8
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[Title]
Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese
acute leukemia
patients.
Genomic aberrations of Fms-like tyrosine kinase 3 (FLT3), including internal tandem duplication (ITD) and point mutations, have been demonstrated in 25-30% of adults
acute
myeloid
leukemia
(AML) and are markers of poor prognosis.
FLT3/ITD and D835 mutations were analyzed in 194 Chinese patients with
acute leukemia
and myelodysplastic syndromes (MDS) by polymerase chain reaction (PCR).
However, neither aberrations was found in 25 patients with
acute
lymphoblastic
leukemia
(ALL), 2
acute
hybrid
leukemia
, 17 MDS and 7 chronic
myeloid
leukemia
in blast crisis (CML-BC).
[MeSH-major]
Leukemia
/ genetics. Mutation, Missense. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / genetics
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Amino Acid Sequence. Asian Continental Ancestry Group / genetics. DNA Mutational Analysis. Female. Humans. Leukocytosis. Male. Middle Aged. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Prognosis. Remission Induction
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(PMID = 15996732.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
43.
Choi EK, Byun JH, Lee SJ, Jung SE, Park MS, Park SH, Lee MG:
Imaging findings of leukemic involvement of the pancreaticobiliary system in adults.
AJR Am J Roentgenol
; 2007 Jun;188(6):1589-95
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CONCLUSION: Pancreatic
myeloid and lymphoid
leukemia
show single or multiple mass lesions of homogeneous low attenuation and poor contrast enhancement on CT that is radiographically indistinguishable from that of pancreatic lymphoma.
[MeSH-major]
Biliary Tract Neoplasms / radiography.
Leukemia
/ radiography. Pancreatic Neoplasms / radiography. Radiographic Image Enhancement / methods
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(PMID = 17515381.001).
[ISSN]
1546-3141
[Journal-full-title]
AJR. American journal of roentgenology
[ISO-abbreviation]
AJR Am J Roentgenol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Contrast Media
44.
Ono R, Nakajima H, Ozaki K, Kumagai H, Kawashima T, Taki T, Kitamura T, Hayashi Y, Nosaka T:
Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis.
J Clin Invest
; 2005 Apr;115(4):919-29
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[Title]
Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-
lineage
leukemogenesis.
The mechanisms by which
mixed
-
lineage
leukemia
(MLL) fusion products resulting from in utero translocations in 11q23 contribute to leukemogenesis and infant
acute leukemia
remain elusive.
It is still controversial whether the MLL fusion protein is sufficient to induce
acute leukemia
without additional genetic alterations, although carcinogenesis in general is known to result from more than 1 genetic
disorder
accumulating during a lifetime.
MLL-SEPT6 induced myeloproliferative
disease
with long latency in mice, but not
acute leukemia
, implying that secondary genotoxic events are required to develop
leukemia
.
We developed in vitro and in vivo model systems of leukemogenesis by MLL fusion proteins, where activated FMS-like receptor tyrosine kinase 3 (FLT3) together with MLL-SEPT6 not only transformed hematopoietic progenitors in vitro but also induced
acute biphenotypic
or
myeloid
leukemia
with short latency in vivo.
[MeSH-major]
Cell
Transformation, Neoplastic. DNA-Binding Proteins. GTP-Binding Proteins.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Oncogene Proteins, Fusion. Proto-Oncogene Proteins / metabolism. Proto-Oncogenes. Receptor Protein-Tyrosine Kinases / metabolism. Recombinant Fusion Proteins. Transcription Factors
[MeSH-minor]
Animals.
Cell
Transplantation. Cells, Cultured. Cytoskeletal Proteins. DNA Damage. Dimerization. Enzyme Activation. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Histone-Lysine N-Methyltransferase. Humans. Infant. Liver / pathology. Liver / physiology. Mice. Mice, Inbred C57BL.
Myeloid
-
Lymphoid
Leukemia
Protein. Protein Structure, Tertiary. Septins. Spleen / pathology. Spleen / physiology. fms-Like Tyrosine Kinase 3
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[Cites]
Proc Natl Acad Sci U S A. 1998 May 26;95(11):6413-8
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(PMID = 15761502.001).
[ISSN]
0021-9738
[Journal-full-title]
The Journal of clinical investigation
[ISO-abbreviation]
J. Clin. Invest.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.1.- / GTP-Binding Proteins; EC 3.6.1.- / SEPT6 protein, human; EC 3.6.1.- / Septins
[Other-IDs]
NLM/ PMC1062890
45.
Johny A, Song KW, Nantel SH, Lavoie JC, Toze CL, Hogge DE, Forrest DL, Sutherland HJ, Le A, Nitta JY, Barnett MJ, Smith CA, Shepherd JD, Nevill TJ:
Early stem cell transplantation for refractory acute leukemia after salvage therapy with high-dose etoposide and cyclophosphamide.
Biol Blood Marrow Transplant
; 2006 Apr;12(4):480-9
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[Title]
Early stem
cell
transplantation for refractory
acute leukemia
after salvage therapy with high-dose etoposide and cyclophosphamide.
Primary refractory
acute leukemia
(AL) has a poor prognosis, although some patients can be salvaged with allogeneic stem
cell
transplantation (SCT).
Forty-two patients had
acute
myelogenous
leukemia
(AML), 13 patients had
acute
lymphoblastic
leukemia
(ALL), and 4 patients had
acute biphenotypic leukemia
.
CR1 rates were similar in AML (54%) and ALL/
acute biphenotypic leukemia
(67%; P = .52), and analysis of baseline characteristics did not reveal any predictors of response to VP/Cy.
[MeSH-major]
Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Cyclophosphamide / administration & dosage. Etoposide / administration & dosage.
Leukemia
/ mortality. Salvage Therapy / mortality. Stem
Cell
Transplantation
[MeSH-minor]
Adolescent. Adult.
Disease
-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Remission Induction. Retrospective Studies. Survival Rate
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.
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consumer health - Childhood Leukemia
.
MedlinePlus Health Information.
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.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
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(PMID = 16545732.001).
[ISSN]
1083-8791
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide
46.
Hager JL, Mir MR, Hsu S:
Candida krusei fungemia in an immunocompromised patient.
Dermatol Online J
; 2010;16(4):5
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We present a case of a patient with
acute
lymphoblastic
leukemia
who, despite being treated prophylactically with fluconazole, developed disseminated C. krusei.
[MeSH-major]
Candidiasis, Cutaneous /
diagnosis
. Candidiasis, Cutaneous / immunology. Fungemia /
diagnosis
. Fungemia / immunology. Immunocompromised Host.
Leukemia
,
Biphenotypic
,
Acute
/ complications
Hazardous Substances Data Bank.
FLUCONAZOLE
.
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(PMID = 20409412.001).
[ISSN]
1087-2108
[Journal-full-title]
Dermatology online journal
[ISO-abbreviation]
Dermatol. Online J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antifungal Agents; 8VZV102JFY / Fluconazole
47.
Kobayashi K, Ogasawara M, Kiyama Y, Miyazono T, Kagawa K, Imai K, Hirano T, Kobayashi N, Tanimoto M, Kasai M:
Successful voriconazole treatment of invasive pulmonary aspergillosis in a patient with acute biphenotypic leukemia.
Acta Med Okayama
; 2009 Aug;63(4):213-6
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[Title]
Successful voriconazole treatment of invasive pulmonary aspergillosis in a patient with
acute biphenotypic leukemia
.
A 23-year old woman with
acute biphenotypic leukemia
(ABL) complained of chest pain with cough, high fever and hemoptysis during induction chemotherapy, although she had been treated with anti-biotics and micafungin.
We made a clinical
diagnosis
of invasive pulmonary aspergillosis (IPA) based on a consolidation in the right upper lung field on a chest radiograph as well as a high level of serum beta-D-glucan (with no evidence of tuberculosis and candidiasis).
Later, we discovered an air-crescent sign by CT scan that supported the
diagnosis
of IPA.
Serological tests and CT findings can aid in early
diagnosis
of IPA, which, along with treatment for IPA, will improve clinical outcomes.
[MeSH-major]
Antifungal Agents / therapeutic use. Invasive Pulmonary Aspergillosis / drug therapy.
Leukemia
,
Biphenotypic
,
Acute
/ complications. Pyrimidines / therapeutic use. Triazoles / therapeutic use
Genetic Alliance.
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.
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(PMID = 19727206.001).
[ISSN]
0386-300X
[Journal-full-title]
Acta medica Okayama
[ISO-abbreviation]
Acta Med. Okayama
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
48.
Sárová I, Brezinová J, Zemanová Z, Izáková S, Lizcová L, Malinová E, Berková A, Cermák J, Maaloufová J, Nováková L, Michalová K:
Cytogenetic manifestation of chromosome 11 duplication/amplification in acute myeloid leukemia.
Cancer Genet Cytogenet
; 2010 Jun;199(2):121-7
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[Title]
Cytogenetic manifestation of chromosome 11 duplication/amplification in
acute
myeloid
leukemia
.
Gene amplification is a frequent genetic
abnormality
in solid tumors, and many oncogenes are activated in this way.
In
acute
myeloid
leukemia
(AML), a frequent target of gene amplification is chromosome 11, particularly chromosome region 11q23, including the MLL (
myeloid
/
lymphoid
leukemia
) gene.
[MeSH-major]
Chromosomes, Human, Pair 11 / genetics. Gene Amplification. Gene Duplication.
Leukemia
,
Myeloid
,
Acute
/ genetics. Trisomy
Genetic Alliance.
consumer health - Chromosome 11
.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
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author profiles
.
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[Copyright]
Copyright 2010 Elsevier Inc. All rights reserved.
(PMID = 20471515.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
49.
Wu X, Hua X:
Menin, histone h3 methyltransferases, and regulation of cell proliferation: current knowledge and perspective.
Curr Mol Med
; 2008 Dec;8(8):805-15
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[Title]
Menin, histone h3 methyltransferases, and regulation of
cell
proliferation: current knowledge and perspective.
However, until recently little has been known as to how menin regulates
cell
proliferation.
Rapid research progress in the past several years suggests that menin represses proliferation of endocrine cells yet promotes proliferation in certain types of
leukemia
cells via interacting with various transcriptional regulators.
Menin interacts with histone H3 methyltransferases such as MLL (
mixed lineage
leukemia
) protein.
Increasing evidence has linked the biological function of menin to epigenetic histone modifications, control of the pattern of gene expression, and regulation of
cell
proliferation in
a cell
type-specific manner.
In light of these recent findings, an emerging model suggests that menin is a crucial regulator of histone modifiers by acting as a scaffold protein to coordinate gene transcription
and cell
proliferation in
a cell
context-dependent manner.
This recent progress unravels the coordinating role of menin in epigenetics and regulation of
cell
cycle, providing novel insights into understanding regulation of beta
cell
functions and diabetes, as well as the development and therapy of endocrine tumors and
leukemia
.
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[
10879731.001
]
[Cites]
Mol Cell Biol. 2000 Aug;20(16):6147-58
[
10913196.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Jan 30;98(3):1118-23
[
11158604.001
]
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Gene. 2001 Jan 24;263(1-2):31-8
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]
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[
11343896.001
]
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Oncogene. 2001 Sep 10;20(40):5695-707
[
11607819.001
]
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Leukemia. 2001 Nov;15(11):1743-9
[
11681416.001
]
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Proc Natl Acad Sci U S A. 2001 Nov 6;98(23):12902-7
[
11687631.001
]
(PMID = 19075677.001).
[ISSN]
1566-5240
[Journal-full-title]
Current molecular medicine
[ISO-abbreviation]
Curr. Mol. Med.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA113962-02; United States / NCI NIH HHS / CA / CA113962-03; United States / NCI NIH HHS / CA / CA100912-04; United States / NCI NIH HHS / CA / R01 CA113962; United States / NCI NIH HHS / CA / R01 CA113962-03; United States / NCI NIH HHS / CA / R01 CA100912; United States / NCI NIH HHS / CA / R01 CA100912-04; United States / NCI NIH HHS / CA / CA100912-03; United States / NCI NIH HHS / CA / R01 CA100912-03; United States / NCI NIH HHS / CA / CA113962-02
[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 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.- / Protein Methyltransferases; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
[Number-of-references]
92
[Other-IDs]
NLM/ NIHMS183824; NLM/ PMC2858577
50.
Hur M, Park JY, Cho HC, Lee KM, Shin HY, Cho HI:
Methylenetetrahydrofolate reductase A1298C genotypes are associated with the risks of acute lymphoblastic leukaemia and chronic myelogenous leukaemia in the Korean population.
Clin Lab Haematol
; 2006 Jun;28(3):154-9
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[Title]
Methylenetetrahydrofolate reductase A1298C genotypes are associated with the risks of
acute
lymphoblastic leukaemia
and chronic myelogenous
leukaemia
in the Korean population.
We investigated the association between MTHFR polymorphisms and the risks of
acute
and chronic
leukaemias
.
They were
acute
lymphoblastic leukaemia
(ALL, n = 89),
acute
myeloid leukaemia
(AML, n = 55),
biphenotypic acute
leukaemia
(n = 12), chronic myelogenous
leukaemia
(CML, n = 40), and normal controls (n = 200).
C677T genotypes were not associated with the risk of each
disease
.
[MeSH-major]
Folic Acid / metabolism.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Genetic / genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics
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.
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.
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.
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FOLIC ACID
.
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(PMID = 16706930.001).
[ISSN]
0141-9854
[Journal-full-title]
Clinical and laboratory haematology
[ISO-abbreviation]
Clin Lab Haematol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
935E97BOY8 / Folic Acid; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
51.
Vanura K, Vrsalovic MM, Le T, Marculescu R, Kusec R, Jäger U, Nadel B:
V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.
Genes Chromosomes Cancer
; 2009 Aug;48(8):725-36
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[Title]
V(D)J targeting mistakes occur at low frequency in
acute
lymphoblastic
leukemia
.
Translocations of proto-oncogenes to the B-
cell
or T-
cell
antigen receptor loci in
acute
T- or B-
cell
leukemia
and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.
[MeSH-major]
Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism
[MeSH-minor]
Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-
Cell
Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-
Cell
/ genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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(PMID = 19455608.001).
[ISSN]
1098-2264
[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 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases
52.
Rudinskiy N, Grishchuk Y, Vaslin A, Puyal J, Delacourte A, Hirling H, Clarke PG, Luthi-Carter R:
Calpain hydrolysis of alpha- and beta2-adaptins decreases clathrin-dependent endocytosis and may promote neurodegeneration.
J Biol Chem
; 2009 May 1;284(18):12447-58
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Proteolysis of alpha- and beta2-adaptins, as well as the accessory clathrin adaptors epsin 1, adaptor protein 180, and the clathrin assembly
lymphoid myeloid
leukemia
protein, was detected in brain tissues after experimentally induced ischemia and in cases of human Alzheimer
disease
.
[MeSH-major]
Adaptor Protein Complex alpha Subunits / metabolism. Adaptor Protein Complex beta Subunits / metabolism. Alzheimer
Disease
/ metabolism. Brain / metabolism. Calpain / metabolism. Clathrin / metabolism. Endocytosis. Neurons / metabolism
[MeSH-minor]
Adaptor Proteins, Vesicular Transport. Animals. Brain Ischemia / genetics. Brain Ischemia / metabolism. Brain Ischemia / pathology. Calcium / metabolism.
Cell
Line.
Cell
Membrane / genetics.
Cell
Membrane / metabolism.
Cell
Membrane / pathology. Female. Glutamic Acid / metabolism. Humans. Hydrolysis. Male. Membrane Lipids / genetics. Membrane Lipids / metabolism. Monomeric Clathrin Assembly Proteins / genetics. Monomeric Clathrin Assembly Proteins / metabolism. Rats. Rats, Sprague-Dawley. Rats, Wistar
MedlinePlus Health Information.
consumer health - Alzheimer's Disease
.
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GLUTAMIC ACID HYDROCHLORIDE
.
Hazardous Substances Data Bank.
CALCIUM, ELEMENTAL
.
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(PMID = 19240038.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Adaptor Protein Complex alpha Subunits; 0 / Adaptor Protein Complex beta Subunits; 0 / Adaptor Proteins, Vesicular Transport; 0 / Clathrin; 0 / Membrane Lipids; 0 / Monomeric Clathrin Assembly Proteins; 0 / PICALM protein, human; 0 / Picalm protein, rat; 0 / epsin; 3KX376GY7L / Glutamic Acid; EC 3.4.22.- / Calpain; SY7Q814VUP / Calcium
[Other-IDs]
NLM/ PMC2673311
53.
Aribi A, Bueso-Ramos C, Estey E, Estrov Z, O'Brien S, Giles F, Faderl S, Thomas D, Kebriaei P, Garcia-Manero G, Pierce S, Cortes J, Kantarjian H, Ravandi F:
Biphenotypic acute leukaemia: a case series.
Br J Haematol
; 2007 Jul;138(2):213-6
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[Title]
Biphenotypic acute
leukaemia
: a case series.
Biphenotypic acute
leukaemia
(BAL) is a rare type of
leukaemia
.
Whether patients with BAL should be treated with regimens designed for
acute
myeloid leukaemia
(AML),
acute
lymphocytic leukaemia
(ALL) or both remain unclear.
Most patients co-expressed B-
lymphoid and myeloid
markers.
No specific chromosomal
abnormality
was identified.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
/ drug therapy
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Cytarabine / therapeutic use. Dexamethasone / therapeutic use. Doxorubicin / therapeutic use. Female. Humans. Immunophenotyping.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Male. Methotrexate / therapeutic use. Middle Aged. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Treatment Outcome. Vincristine / therapeutic use
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CYTARABINE
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
Hazardous Substances Data Bank.
METHOTREXATE
.
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(PMID = 17593028.001).
[ISSN]
0007-1048
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; YL5FZ2Y5U1 / Methotrexate; HCVAD protocol
54.
Schimmer AD:
Induction of apoptosis in lymphoid and myeloid leukemia.
Curr Oncol Rep
; 2006 Nov;8(6):430-6
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[Title]
Induction of apoptosis in
lymphoid and myeloid
leukemia
.
Defects in the core machinery of the apoptosis pathway contribute to chemoresistance and poor outcomes in patients with
acute leukemia
.
This review highlights compounds that target the mitochondrial, death receptor, and convergence pathways of caspase activation that are being developed for the treatment of
acute leukemia
.
[MeSH-major]
Apoptosis / physiology.
Leukemia
,
Lymphoid
/ therapy.
Leukemia
,
Myeloid
/ therapy
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.
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9915859.001
]
[Cites]
Cancer Res. 2005 Mar 15;65(6):2378-86
[
15781653.001
]
[Cites]
Genes Dev. 1998 Jun 1;12(11):1551-70
[
9620844.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7124-9
[
10860979.001
]
[Cites]
Cell Death Differ. 2006 Feb;13(2):179-88
[
16322751.001
]
[Cites]
Mol Biol Cell. 2003 Jan;14(1):78-92
[
12529428.001
]
[Cites]
Br J Haematol. 2000 Jul;110(1):154-60
[
10930993.001
]
(PMID = 17040621.001).
[ISSN]
1523-3790
[Journal-full-title]
Current oncology reports
[ISO-abbreviation]
Curr Oncol Rep
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / Receptors, Death Domain; EC 3.4.22.- / Caspases
[Number-of-references]
68
55.
Park JA, Ghim TT, Bae Kw, Im HJ, Jang SS, Park CJ, Chi HS, Seo JJ:
Stem cell transplant in the treatment of childhood biphenotypic acute leukemia.
Pediatr Blood Cancer
; 2009 Sep;53(3):444-52
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[Title]
Stem
cell
transplant in the treatment of childhood
biphenotypic acute leukemia
.
BACKGROUND: Many studies have found that
biphenotypic acute leukemia
(BAL) is associated with a poor outcome.
RESULTS: BAL constituted 4.4% of all
acute
childhood
leukemia
cases.
In terms of immunophenotype, 14 patients had
leukemia
with
myeloid
plus B-
lymphoid
(M + B) marker, 7 with
myeloid
plus T-
lymphoid
(M + T) marker, and 4 with
myeloid
plus B-
lymphoid and
T-
lymphoid
(M + B + T) markers.
Hematopoietic stem
cell
transplantation (HSCT) did not improve either overall survival or event-free survival compared to chemotherapy alone (hazard ratio 0.98, 95% CI 0.35-2.76, P = 0.966; hazard ratio 1.07, 95% CI 0.41-2.78, P = 0.88).
[MeSH-major]
Hematopoietic Stem
Cell
Transplantation.
Leukemia
,
Biphenotypic
,
Acute
/ therapy
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(PMID = 19489056.001).
[ISSN]
1545-5017
[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
56.
Nishioka C, Ikezoe T, Yang J, Takeuchi S, Koeffler HP, Yokoyama A:
MS-275, a novel histone deacetylase inhibitor with selectivity against HDAC1, induces degradation of FLT3 via inhibition of chaperone function of heat shock protein 90 in AML cells.
Leuk Res
; 2008 Sep;32(9):1382-92
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This study explored the effect of MS-275, a novel histone deacetylase inhibitor (HDACI), against a variety of human
leukemia
cells with defined genetic alterations.
MS-275 profoundly induced growth arrest of
acute
myelogenous
leukemia
(AML) MOLM13 and
biphenotypic leukemia
MV4-11 cells, which possess internal tandem duplication mutation in the fms-like tyrosine kinase 3 (FLT3) gene (FLT3-ITD), with IC50s less than 1 microM, as measured by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay on day two of culture.
Moreover, we found that further inhibition of MEK/ERK signaling potentiated the action of MS-275 in
leukemia
cells.
Taken together, MS-275 may be useful for treatment of individuals with
leukemia
possessing activating mutation of FLT3 gene.
[MeSH-major]
Benzamides / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Histone Deacetylase Inhibitors.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Pyridines / pharmacology. Signal Transduction / drug effects. fms-Like Tyrosine Kinase 3 / metabolism
[MeSH-minor]
Acetylation. Blotting, Western.
Cell
Cycle / drug effects.
Cell
Proliferation / drug effects. Enzyme Inhibitors / pharmacology. Female. Flow Cytometry. Genotype. Histone Deacetylase 1. Histone Deacetylases / metabolism. Humans. Immunoprecipitation. MAP Kinase Kinase 1 / metabolism. Male. Middle Aged. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. STAT5 Transcription Factor / metabolism. Tumor Cells, Cultured
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(PMID = 18394702.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Benzamides; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyridines; 0 / STAT5 Transcription Factor; 1ZNY4FKK9H / entinostat; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylases
57.
Mohan AV, Ramnath VR, Patalas E, Attar EC:
Non-specific interstitial pneumonia as the initial presentation of biphenotypic acute leukemia: a case report.
Cases J
; 2009;2:8217
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[Title]
Non-specific interstitial pneumonia as the initial presentation of
biphenotypic acute leukemia
: a case report.
We present a 46-year-old woman with recent-onset rheumatologic illness who developed pulmonary symptoms as the presenting feature of
biphenotypic acute
leukaemia
.
Corticosteroid therapy resulted in resolution of both her pulmonary and rheumatologic symptoms, and her pulmonary symptoms did not recur following treatment of her
leukemia
.
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[Cites]
Leuk Lymphoma. 2002 Nov;43(11):2083-92
[
12533032.001
]
[Cites]
J Am Acad Dermatol. 2001 Mar;44(3):530-1
[
11209130.001
]
[Cites]
Am J Respir Crit Care Med. 2008 Jun 15;177(12):1338-47
[
18388353.001
]
[Cites]
Crit Rev Oncol Hematol. 2007 Aug;63(2):100-10
[
17391977.001
]
[Cites]
Intern Med. 2004 Aug;43(8):721-6
[
15468974.001
]
[Cites]
Semin Respir Crit Care Med. 2006 Dec;27(6):652-8
[
17195141.001
]
[Cites]
Respiration. 2005 Jan-Feb;72(1):39-45
[
15753633.001
]
[Cites]
Haematologica. 1997 Jan-Feb;82(1):64-6
[
9107085.001
]
[Cites]
Br J Haematol. 2007 Jul;138(2):213-6
[
17593028.001
]
(PMID = 19918465.001).
[ISSN]
1757-1626
[Journal-full-title]
Cases journal
[ISO-abbreviation]
Cases J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2769415
58.
Kern W, Haferlach T:
[Quantification of minimal residual disease by multiparameter flow cytometry in acute myeloid leukemia. From diagnosis to prognosis].
Med Klin (Munich)
; 2005 Jan 15;100(1):54-9
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[Title]
[Quantification of minimal residual
disease
by multiparameter flow cytometry in
acute
myeloid
leukemia
. From
diagnosis
to prognosis].
Today, multiparameter flow cytometry allows the simultaneous assessment of up to five surface and cytoplasmic antigens in different
cell
populations from peripheral blood and bone marrow samples.
In the setting of diagnosing
acute
myeloid leukemias
(AML) this method is used not only to subclassify AML and separate it from
acute
lymphoblastic and
biphenotypic
leukemias
but also for the identification of
leukemia
-associated aberrant immunophenotypes (LAIPs).
Since these LAIPs are defined individually for each patient, leukemic bone marrow cells can be detected during the course of treatment using the LAIP allowing the quantification of minimal residual
disease
(MRD) which is not detectable by cytomorphology.
Due to its close correlation with the course of the
disease and
with the risk of relapse the MRD represents an important prognostic parameter which is increasingly used for stratification of therapy in clinical trials.
[MeSH-major]
Flow Cytometry / methods.
Leukemia
,
Myeloid
,
Acute
/
diagnosis
. Neoplasm, Residual /
diagnosis
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(PMID = 15654545.001).
[ISSN]
0723-5003
[Journal-full-title]
Medizinische Klinik (Munich, Germany : 1983)
[ISO-abbreviation]
Med. Klin. (Munich)
[Language]
ger
[Publication-type]
Comparative Study; English Abstract; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Epitopes; EC 3.1.3.48 / Antigens, CD45
59.
Kozlov I, Beason K, Yu C, Hughson M:
CD79a expression in acute myeloid leukemia t(8;21) and the importance of cytogenetics in the diagnosis of leukemias with immunophenotypic ambiguity.
Cancer Genet Cytogenet
; 2005 Nov;163(1):62-7
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[Title]
CD79a expression in
acute
myeloid
leukemia
t(8;21) and the importance of cytogenetics in the
diagnosis
of
leukemias
with immunophenotypic ambiguity.
Acute
leukemias
that express antigens associated with more than one
lineage
have been classified as
acute
lymphocytic
leukemia
with
myeloid
markers,
acute
myeloid
leukemia
with
lymphoid
markers, or
biphenotypic acute leukemia
(BAL).
CD79a functions in and has a high degree of specificity for B-
cell
differentiation.
It has only recently begun to be reported in
biphenotypic acute
leukemias
.
Cases of
acute leukemia
submitted to the flow cytometry laboratory were retrospectively reviewed beginning from the time analysis for cytoplasmic CD79a was added to
leukemia
and lymphoma panels.
The immunophenotyping met proposed scoring criteria for
a diagnosis
of BAL.
Nevertheless, the cytogenetic and FISH findings indicate that CD79a, despite its specificity for B-
cell
differentiation, represented the aberrant presence of
a B
-
cell
antigen in
leukemias
of distinct
myeloid
linage.
It is doubtful that, in this setting, CD79a expression should be considered a manifestation of
lineage
ambiguity.
[MeSH-major]
Antigens, CD79 / genetics. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8.
Leukemia
,
Myeloid
/ genetics. Translocation, Genetic
[MeSH-minor]
Acute
Disease
. Adult. Antigens, CD / genetics. Antigens, CD / immunology. B-Lymphocytes / immunology. Blast Crisis. Bone Marrow Cells / pathology. Cytarabine / therapeutic use. Flow Cytometry. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. T-Lymphocytes / immunology
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.
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.
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[CommentIn]
Cancer Genet Cytogenet. 2007 Apr 1;174(1):76-7
[
17350472.001
]
(PMID = 16271957.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD79; 04079A1RDZ / Cytarabine
60.
Manola KN, Georgakakos VN, Marinakis T, Stavropoulou C, Paterakis G, Anagnostopoulos NI, Pantelias GE, Sambani C:
Translocation (X;12)(p11;p13) as a sole abnormality in biphenotypic acute leukemia.
Cancer Genet Cytogenet
; 2007 Mar;173(2):159-63
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[Title]
Translocation (X;12)(p11;p13) as a sole
abnormality
in
biphenotypic acute leukemia
.
A reciprocal t(X;12)(p11;p13) was found as the sole clonal
abnormality
in
biphenotypic leukemia
with
myeloid and
B-
lymphoid
differentiation.
To our knowledge, this cytogenetic aberration has not been reported previously as a sole
abnormality
in hematological malignancies.
Its presence may suggest an important role in the pathogenesis of
biphenotypic leukemia
.
[MeSH-major]
Chromosomes, Human, Pair 12. Chromosomes, Human, X.
Leukemia
/ genetics. Translocation, Genetic
[MeSH-minor]
Acute
Disease
. Chromosome Banding. Chromosome Painting. Female. Humans. Karyotyping. Lymphocytes / metabolism. Lymphocytes / pathology. Middle Aged.
Myeloid
Cells / metabolism.
Myeloid
Cells / pathology
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(PMID = 17321333.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
61.
Fujiwara S, Yamashita Y, Choi YL, Watanabe H, Kurashina K, Soda M, Enomoto M, Hatanaka H, Takada S, Ozawa K, Mano H:
Transforming activity of purinergic receptor P2Y, G protein coupled, 8 revealed by retroviral expression screening.
Leuk Lymphoma
; 2007 May;48(5):978-86
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Biphenotypic acute leukemia
(BAL) is a relatively rare subtype of
acute leukemia
characterized by the presence of both
myeloid and lymphoid cell
surface antigens.
A variety of luciferase-based reporter assays revealed that P2RY8 increased both the trans-activation activities of CREB and Elk-1 as well as the transcriptional activities of the serum response element and enhancer-promoter fragments of the c-Fos
and c
-Myc genes.
Quantitation of P2RY8 mRNA in CD34(+) cells of bone marrow showed that P2RY8 expression is frequently increased in
leukemia
patients, especially in those with refractory
disease
.
Our data thus reveal an abundant expression of P2RY8 in leukemic cells and its unexpected role in the pathogenesis of
acute leukemia
.
[MeSH-major]
Gene Expression Regulation, Leukemic.
Leukemia
/ genetics.
Leukemia
/ metabolism. Receptors, Purinergic / physiology. Receptors, Purinergic P2 / metabolism. Receptors, Purinergic P2Y / metabolism. Receptors, Purinergic P2Y / physiology. Retroviridae / metabolism
[MeSH-minor]
3T3 Cells. Animals. Antigens, CD34 / biosynthesis. Bone Marrow Cells / metabolism.
Cell
Line, Tumor. DNA, Complementary / genetics. Gene Library. Humans. Mice. Mice, Nude. Transcription, Genetic
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(PMID = 17487742.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD34; 0 / DNA, Complementary; 0 / P2RY8 protein, human; 0 / P2RY9 receptor, human; 0 / P2RY9 receptor, mouse; 0 / Receptors, Purinergic; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2Y
62.
Kim HR, Hong JH, Yoon CH, Lee SH, Park SH, Kim HY:
Arthritis preceding acute biphenotypic leukemia.
Clin Rheumatol
; 2006 May;25(3):380-1
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[Title]
Arthritis preceding
acute biphenotypic leukemia
.
[MeSH-major]
Arthritis / etiology.
Leukemia
/ complications
[MeSH-minor]
Acute
Disease
. Adult. Ankle / pathology. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antineoplastic Agents / therapeutic use. Female. Humans. Magnetic Resonance Imaging. Pain / drug therapy. Phenotype
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[Cites]
Acta Haematol. 1999 Mar;101(1):1-6
[
10085431.001
]
[Cites]
Wiad Lek. 1998;51 Suppl 4:296-9
[
10731987.001
]
[Cites]
Semin Arthritis Rheum. 1994 Aug;24(1):48-56
[
7985037.001
]
(PMID = 16220224.001).
[ISSN]
0770-3198
[Journal-full-title]
Clinical rheumatology
[ISO-abbreviation]
Clin. Rheumatol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents
63.
Hegedus CM, Gunn L, Skibola CF, Zhang L, Shiao R, Fu S, Dalmasso EA, Metayer C, Dahl GV, Buffler PA, Smith MT:
Proteomic analysis of childhood leukemia.
Leukemia
; 2005 Oct;19(10):1713-8
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[Title]
Proteomic analysis of childhood
leukemia
.
Childhood
acute
lymphoblastic and myeloid leukemias
are stratified into molecular and cytogenetic subgroups important for prognosis and therapy.
Studies have shown that gene expression profiles can discriminate between
leukemia
subtypes.
Thus, proteome analysis similarly holds the potential for characterizing different subtypes of childhood
leukemia
.
We used surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to analyze
cell
lysates from childhood
leukemia
cell
lines as well as pretreatment leukemic bone marrow derived from childhood
leukemia
cases.
Comparison of the
acute
myeloid
leukemia
(AML)
cell
line, Kasumi, and the
biphenotypic
myelomonocytic
cell
line, MV4;11, with the
acute
lymphoblastic
leukemia
(ALL)
cell
lines, 697 and REH, revealed many differentially expressed proteins.
In particular, one 8.3 kDa protein has been identified as
a C
-terminal truncated ubiquitin.
Analysis of childhood
leukemia
bone marrow showed differentially expressed proteins between AML and ALL, including a similar peak at 8.3 kDa, as well as several proteins that differentiate between the ALL t(12;21) and hyperdiploid subtypes.
These results demonstrate the potential for proteome analysis to distinguish between various forms of childhood
leukemia
.
[MeSH-major]
Biomarkers, Tumor / metabolism.
Leukemia
,
Myeloid
/ metabolism. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / metabolism. Proteomics
[MeSH-minor]
Acute
Disease
. Adolescent. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Child. Humans. Peptide Mapping. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
ClinicalTrials.gov.
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(PMID = 16136170.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Grant]
United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P30 ES01896; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / R01 ES09137
[Publication-type]
Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor
64.
Ning BT, Tang YM, Chen YH, Shen HQ, Qian BQ:
Comparison between CD19 and CD20 expression patterns on acute leukemic cells.
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2005 Dec;13(6):943-7
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[Title]
Comparison between CD19 and CD20 expression patterns on
acute
leukemic cells.
In order to provide the evidences for CD19 as a better antibody targeting molecule for
B lineage
acute
leukemias
than CD20 through the multi-parameter flow-cytometry analysis of
leukemia
cells, the samples from 321 patients with
acute leukemia
(AL) were immunophenotyped by multi-color flow cytometry and CD45/SSC gating strategy followed by the analysis of CD19 and CD20 expression.
The results showed that the positive rate of CD19 (115/116, 99.1%) in 116 cases with
B lineage
acute
lymphoblastic
leukemia
(
B lineage
ALL) was significantly higher than that of CD20 (33/116, 28.4%) (P < 0.01); in 17 patients with
B lineage
/
Myeloid
(B/My)
acute
mixed lineage
leukemia
(AMLL), the former positive rate (17/17, 100%) was also higher than the latter (5/17, 29.4%) (P < 0.01).
Both of the two antigens were negative in 29 patients with
acute
T lymphoblastic
leukemia
and 7 patients with T/My AMLL.
The positive rates of CD19 and CD20 in 152 patients with
acute
myeloid
leukemia
(AML) were 7.2% and 2.0%, respectively.
The difference of the fluorescence intensity between the two antigens on the cells from each patient with
B lineage
ALL or B/My AMLL was statistically significant (t = 20.68, P < 0.001).
The specificity of CD19 and CD20 in
B lymphocytic lineage
was 92.3% (132/143) and 92.7% (38/41), respectively, while the sensitivity was 99.2% (132/133) and 28.6% (38/133), respectively, the former sensitivity was significantly higher than the latter (chi(2) = 144.018, P = 0.001).
It is concluded that CD19 continuously and steadily express on almost all subtypes of
B lineage
leukemic cells with homogeneous pattern while only a small number of
leukemias
express CD20.
These indicate that CD19 may be a better antibody targeting molecule than CD20 for patients with B-
lineage
acute leukemia
.
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(PMID = 16403255.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
ENG
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD19; 0 / Antigens, CD20
65.
Lotem J, Netanely D, Domany E, Sachs L:
Human cancers overexpress genes that are specific to a variety of normal human tissues.
Proc Natl Acad Sci U S A
; 2005 Dec 20;102(51):18556-61
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We have analyzed gene expression data from three different kinds of samples: normal human tissues, human cancer
cell
lines, and leukemic cells from
lymphoid and myeloid
leukemia
pediatric patients.
Analysis of the expression levels of these two groups of genes in the human cancer
cell
lines
and leukemias
identified genes that were highly expressed in cancer cells but not in their normal counterparts and, thus, were overexpressed in the cancers.
The different cancer
cell
lines
and leukemias
varied in the number and identity of these overexpressed genes.
[MeSH-minor]
Adenocarcinoma / genetics.
Cell
Line.
Cell
Line, Tumor. Health. Humans.
Leukemia
/ classification.
Leukemia
/ genetics. Multigene Family / genetics
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[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ PMC1317977
66.
Xia ZB, Popovic R, Chen J, Theisler C, Stuart T, Santillan DA, Erfurth F, Diaz MO, Zeleznik-Le NJ:
The MLL fusion gene, MLL-AF4, regulates cyclin-dependent kinase inhibitor CDKN1B (p27kip1) expression.
Proc Natl Acad Sci U S A
; 2005 Sep 27;102(39):14028-33
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MLL, involved in many chromosomal translocations associated with
acute
myeloid and lymphoid
leukemia
, has >50 known partner genes with which it is able to form in-frame fusions.
Characterizing important downstream target genes of MLL and of MLL fusion proteins may provide rational therapeutic strategies for the treatment of MLL-associated
leukemia
.
To this end, we developed inducible MLL-AF4 fusion
cell
lines in different backgrounds.
Overexpression of MLL-AF4 does not lead to increased proliferation in either
cell
line, but rather,
cell
growth was slowed compared with similar
cell
lines inducibly expressing truncated MLL.
We found that in the MLL-AF4-induced
cell
lines, the expression of the cyclin-dependent kinase inhibitor gene CDKN1B was dramatically changed at both the RNA and protein (p27kip1) levels.
Further, we confirmed CDKN1B promoter binding by ChIP in MLL-AF4 as well as in MLL-AF9
leukemia
cell
lines.
Our results suggest that CDKN1B is a downstream target of MLL and of MLL-AF4, and that, depending on the background
cell
type, MLL-AF4 inhibits or activates CDKN1B expression.
This
finding
may have implications in terms of
leukemia
stem
cell
resistance to chemotherapy in MLL-AF4
leukemias
.
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[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA104300; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA78438; United States / NCI NIH HHS / CA / R01 CA104300; United States / NCI NIH HHS / CA / CA81269
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
[Other-IDs]
NLM/ PMC1236570
67.
Amakawa R, Hiramoto N, Kawano S, Hyo A, Nakamichi N, Tajima K, Ito T, Mori S, Kishimoto Y, Fukuhara S:
Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia.
J Clin Exp Hematop
; 2010;50(1):51-8
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[Title]
Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with
de
novo
mixed
-
lineage
leukemia
.
We report a case of
acute
mixed
-
lineage
leukemia
, as seen in a 65 year-old female with MLL gene amplification and biallelic loss of wild type p53 gene.
The
diagnosis
was based on the findings that her bone marrow (BM) blasts expressed cytoplasmic CD3 (cyCD3), B-
lineage
antigens
and myeloid
antigens accompanied by clonal rearrangements of IgH gene.
Add (11q23)
abnormality
was found in sideline karyotypes as well as the stemline
abnormality
of dic(17;20) (p11;q11).
[MeSH-major]
Gene Amplification.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Translocation, Genetic
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(PMID = 20505276.001).
[ISSN]
1880-9952
[Journal-full-title]
Journal of clinical and experimental hematopathology : JCEH
[ISO-abbreviation]
J Clin Exp Hematop
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
68.
Costantini AS, Benvenuti A, Vineis P, Kriebel D, Tumino R, Ramazzotti V, Rodella S, Stagnaro E, Crosignani P, Amadori D, Mirabelli D, Sommani L, Belletti I, Troschel L, Romeo L, Miceli G, Tozzi GA, Mendico I, Maltoni SA, Miligi L:
Risk of leukemia and multiple myeloma associated with exposure to benzene and other organic solvents: evidence from the Italian Multicenter Case-control study.
Am J Ind Med
; 2008 Nov;51(11):803-11
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[Title]
Risk of
leukemia
and multiple myeloma associated with exposure to benzene and other organic solvents: evidence from the Italian Multicenter Case-control study.
BACKGROUND: While there is a general consensus about the ability of benzene to induce
acute
myeloid
leukemia
(AML), its effects on chronic
lymphoid
leukemia
and multiple myeloma (MM) are still under debate.
We conducted a population-based case-control study to evaluate the association between exposure to organic solvents and risk of
myeloid and lymphoid
leukemia
and MM.
METHODS: Five hundred eighty-six cases of
leukemia
(and 1,278 population controls), 263 cases of MM (and 1,100 population controls) were collected.
There were elevated point estimates for the associations between medium/high benzene exposure and chronic lymphatic
leukemia
(OR = 1.8, 95% CI = 0.9-3.9) and MM (OR = 1.9, 95% CI = 0.9-3.9).
Risks of chronic lymphatic
leukemia
were somewhat elevated, albeit with wide confidence intervals, from medium/high exposure to xylene and toluene as well.
Our results support the association between benzene, xylene, and toluene and chronic lymphatic
leukemia
and between benzene and MM with longer latencies than have been observed for AML in other studies.
[MeSH-major]
Benzene / adverse effects.
Leukemia
,
Lymphoid
/ chemically induced. Multiple Myeloma / chemically induced. Occupational Exposure / adverse effects. Solvents / adverse effects
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commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
Hazardous Substances Data Bank.
TOLUENE
.
Hazardous Substances Data Bank.
BENZENE
.
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[Copyright]
Copyright 2008 Wiley-Liss, Inc.
(PMID = 18651579.001).
[ISSN]
1097-0274
[Journal-full-title]
American journal of industrial medicine
[ISO-abbreviation]
Am. J. Ind. Med.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA51086
[Publication-type]
Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Solvents; 0 / Xylenes; 3FPU23BG52 / Toluene; J64922108F / Benzene
69.
Rénard C, Girard S, Pracros JP, Dijoud F, André JM, Mialou V, Bertrand Y:
[Granulocytic sarcoma, a diagnostic challenge: 3 pediatric cases].
Arch Pediatr
; 2010 Feb;17(2):149-53
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[Transliterated title]
Le sarcome granulocytaire, un diagnostic à connaître : à propos
de
3 observations pédiatriques.
Granulocytic sarcoma (GS) is a rare extramedullary tumor frequently associated with
acute
myeloblastic
leukemia
(AML).
In all 3 cases, the
diagnosis
was delayed or initially missed.
Pathology and immunohistochemistry data identified the
disease
.
[MeSH-major]
Facial Neoplasms /
diagnosis
. Intestinal Neoplasms /
diagnosis
. Intestine, Small.
Leukemia
,
Myeloid
,
Acute
/
diagnosis
. Neoplasms, Multiple Primary /
diagnosis
. Orbital Neoplasms /
diagnosis
. Sarcoma,
Myeloid
/
diagnosis
. Skin Neoplasms /
diagnosis
[MeSH-minor]
Antineoplastic Combined Chemotherapy Protocols. Biopsy. Bone Marrow / pathology. Bone Marrow Transplantation. Child, Preschool. Combined Modality Therapy. Diagnostic Errors. Female. Follow-Up Studies. Humans. Infant.
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
.
Leukemia
,
Biphenotypic
,
Acute
/ drug therapy.
Leukemia
,
Biphenotypic
,
Acute
/ pathology. Male. Tomography, X-Ray Computed
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[Copyright]
Copyright 2009 Elsevier Masson SAS. All rights reserved.
(PMID = 19945260.001).
[ISSN]
1769-664X
[Journal-full-title]
Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
[ISO-abbreviation]
Arch Pediatr
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
70.
Zhao XF, Gojo I, York T, Ning Y, Baer MR:
Diagnosis of biphenotypic acute leukemia: a paradigmatic approach.
Int J Clin Exp Pathol
; 2009;3(1):75-86
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[Title]
Diagnosis
of
biphenotypic acute leukemia
: a paradigmatic approach.
Biphenotypic acute leukemia
(BAL), or
acute leukemia
with a single population of blasts coexpressing markers of two different lineages, is a rare clinical entity.
To define BAL, a scoring system was proposed by the European Group of Immunological Markers for
Leukemias
(EGIL) in 1995.
However, increasing evidence suggests that this system has limitations, as acknowledged by the 2008 World Health Organization (WHO) Classification of Tumors of Hematopoietic
and Lymphoid
Tissues.
We propose a new paradigmatic approach to defining BAL based on recent clinical studies of BAL and advances in immunologic marker definition and cytogenetics, and applied our new approach to 8 cases of "BAL" among a cohort of 742 new
acute
leukemias
in our Cancer Center.
By our new criteria, 6 cases were reclassified as
acute
lymphoblastic
leukemia
(ALL), while only 2 were still classified as BAL.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
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Am J Clin Pathol. 2001 Jul;116(1):25-33
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]
(PMID = 19918331.001).
[ISSN]
1936-2625
[Journal-full-title]
International journal of clinical and experimental pathology
[ISO-abbreviation]
Int J Clin Exp Pathol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
[Other-IDs]
NLM/ PMC2776262
[Keywords]
NOTNLM ; ALL / AML / Biphenotypic acute leukemia / EGIL / classification
71.
Harel A, Wu F, Mattson MP, Morris CM, Yao PJ:
Evidence for CALM in directing VAMP2 trafficking.
Traffic
; 2008 Mar;9(3):417-29
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Clathrin assembly
lymphoid myeloid
leukemia
protein (CALM) is a clathrin assembly protein with a domain structure similar to the neuron-specific assembly protein AP180.
Overexpression of CALM leads to the reduction of
cell
surface VAMP2, whereas knockdown of CALM by RNA interference results in the accumulation of surface VAMP2.
[MeSH-minor]
Animals.
Cell
Line.
Cell
Membrane / metabolism. Endocytosis. Humans. Mutagenesis, Site-Directed. PC12 Cells. Protein Structure, Tertiary. Protein Transport. RNA Interference. RNA, Small Interfering / genetics. Rats. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transfection. Transferrin / metabolism
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Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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(PMID = 18182011.001).
[ISSN]
1398-9219
[Journal-full-title]
Traffic (Copenhagen, Denmark)
[ISO-abbreviation]
Traffic
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Monomeric Clathrin Assembly Proteins; 0 / PICALM protein, human; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / Transferrin; 0 / VAMP2 protein, human; 0 / Vesicle-Associated Membrane Protein 2
72.
Faber J, Armstrong SA:
Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies.
Klin Padiatr
; 2007 Nov-Dec;219(6):306-11
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[Title]
Defining
leukemia
stem cells in MLL-translocated
leukemias
: implications for novel therapeutic strategies.
An important question in the development of novel, less toxic antileukemic strategies specifically targeting
leukemia
stem cells is how closely
leukemia
stem cells are related to normal hematopoietic stem cells.
It has been recently demonstrated that
leukemia
stem cells can be derived from different stages in normal hematopoiesis and have unique phenotypic and genetic features.
Introduction of
Mixed
-
lineage
leukemia
( MLL)-fusion oncoproteins, frequently found in infant
leukemias and
therapy-related
leukemias
, into differentiated hematopoietic progenitor cells results in the generation of
leukemias
with a high frequency of
leukemia
stem cells.
The progenitor-derived
leukemia
stem cells ectopically express a limited stem
cell
program while maintaining the global identity of differentiated
myeloid
cells.
Development of therapeutic strategies that specifically target the
leukemia
stem
cell
program while sparing normal hematopoietic stem cells may represent a novel therapeutic approach in human
leukemias
with high efficacy yet less side effects.
[MeSH-major]
Leukemia
/ therapy.
Leukemia
,
Biphenotypic
,
Acute
.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Neoplastic Stem Cells
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(PMID = 18050039.001).
[ISSN]
0300-8630
[Journal-full-title]
Klinische Pädiatrie
[ISO-abbreviation]
Klin Padiatr
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
[Number-of-references]
62
73.
Michaud J, Simpson KM, Escher R, Buchet-Poyau K, Beissbarth T, Carmichael C, Ritchie ME, Schütz F, Cannon P, Liu M, Shen X, Ito Y, Raskind WH, Horwitz MS, Osato M, Turner DR, Speed TP, Kavallaris M, Smyth GK, Scott HS:
Integrative analysis of RUNX1 downstream pathways and target genes.
BMC Genomics
; 2008 Jul 31;9:363
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BACKGROUND: The RUNX1 transcription factor gene is frequently mutated in sporadic
myeloid and lymphoid
leukemia
through translocation, point mutation or amplification.
It is also responsible for a familial platelet
disorder
with predisposition to
acute
myeloid
leukemia
(FPD-AML).
The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of
leukemia
.
We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to
leukemia
.
1)
cell
lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFbeta, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays.
A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair
cell
proliferation, microtubule dynamics and possibly genetic stability.
CONCLUSION: This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and
leukemia
.
The biological pathways and target genes controlled by RUNX1 will have considerable importance in
disease
progression in both familial and sporadic
leukemia
as well as therapeutic implications.
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(PMID = 18671852.001).
[ISSN]
1471-2164
[Journal-full-title]
BMC genomics
[ISO-abbreviation]
BMC Genomics
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK058161; United States / NHLBI NIH HHS / HL / R01 HL079507; United States / NIDDK NIH HHS / DK / DK58161; United States / NHLBI NIH HHS / HL / HL079507
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / CBFB protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / RUNX1 protein, human; 0 / Runx1 protein, mouse
[Other-IDs]
NLM/ PMC2529319
74.
Pagano L, Caira M, Nosari A, Rossi G, Locatelli F, Viale P, Aversa F, Hema E-Chart Group Italy:
Hema e-Chart: Italian Registry for prospective analysis of epidemiology, management and outcome of febrile events in patients with hematological malignancies.
J Chemother
; 2010 Feb;22(1):20-4
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A systematic approach that starts from the registration of new
diagnosis and
complete follow-up can be of help for the study of treatment and evolution of these complications.
Its aim is to improve the speed, quality and integration of information related to subjects with febrile event, ultimately resulting in improving patients' care.Patients included adults and children with
acute
and chronic
myeloid
or
lymphoid
leukemia
, Hodgkin's and non-Hodgkin's lymphoma, myelodysplastic syndrome, or multiple myeloma.
The registry also included data regarding event onset in hematopoietic stem
cell
transplants (HSCTs).
[MeSH-minor]
Hematopoietic Stem
Cell
Transplantation. Humans. Incidence. Italy. Prospective Studies
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(PMID = 20227988.001).
[ISSN]
1973-9478
[Journal-full-title]
Journal of chemotherapy (Florence, Italy)
[ISO-abbreviation]
J Chemother
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Investigator]
Levis A; Leoni P; Liso V; Baccarani M; Cortellazzo S; Rossi G; Russo D; La Nasa G; Storti S; Giustolisi R; Morabito F; Cuneo A; Bosi A; Capalbo SF; Cascavilla N; Ghio R; Carella A; Brugiatelli M; Ciceri F; Martinelli G; Morra E; Pogliani E; Mettivier V; Carli M; Abbadessa V; Musso M; Aricò M; Lazzarino M; Visani G; Fioritoni G; Di Bartolomeo P; Vallisa D; Petrini M; Favre C; Olivieri A; Gugliotta L; Leone G; Amadori S; De Rossi G; De Fabritiis P; Majolino I; D'Arco A; Lauria F; Mazza P; Fagioli F; Gherlinzoni F; Chesesi T; Rodeghiero F
75.
Chatterjee T, Panigrahi I, Agrawal N, Naithani R, Mahapatra M, Pati HP, Wadhwa S, Saxena R:
Cytochemical, immunophenotypic and ultrastructural characterization of acute leukemias: a prospective study of fifty cases: haematological malignancy.
Hematology
; 2006 Jun;11(3):147-51
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[Title]
Cytochemical, immunophenotypic and ultrastructural characterization of
acute
leukemias
: a prospective study of fifty cases: haematological malignancy.
Cytochemistry and immunophenotyping are established methods in the
diagnosis
of most
leukemias
but the role of electron microscopy in
diagnosis
, apart from understanding the cellular morphology is less studied.
We present here 50 cases of
acute
leukemias
that were studied for morphology, conventional cytochemistry, immunophenotyping and transmission electron microscopy (TEM), including ultrastructural cytochemistry using myeloperoxidase (MPO) and platelet peroxidase activity.
TEM morphology using ultrastructural cytochemistry helped in definitive typing in one
mixed lineage
leukemia
case, one AML-M5b, one AML-M6b and one microgranular variant of APML.
Thus, ultrastructural studies may be useful in accurate
diagnosis
of
biphenotypic leukemia
and further classification of
acute
leukemias
.
Also, in cases with hypercellular marrow and with associated myelofibrosis, where the marrow aspirate gives low
cell
count, ultrastructural studies are a valuable aid to arriving at an accurate
diagnosis
.
[MeSH-major]
Leukemia
/ pathology
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Antigens, CD / analysis. Antigens, Neoplasm / analysis. Child. Child, Preschool. Female. Humans. Immunophenotyping. Male. Microscopy, Electron. Middle Aged. Neoplasm Proteins / analysis. Neoplastic Stem Cells / chemistry. Neoplastic Stem Cells / ultrastructure. Peroxidase / analysis. Prospective Studies
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.
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consumer health - Leukemia
.
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(PMID = 17325954.001).
[ISSN]
1607-8454
[Journal-full-title]
Hematology (Amsterdam, Netherlands)
[ISO-abbreviation]
Hematology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Neoplasm Proteins; EC 1.11.1.7 / Peroxidase
76.
Li XL, Li R, Chen Y:
[Clinical characteristics and immunophenotypes of mixed-lineage acute leukemia].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2007 Jun;15(3):636-9
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[Title]
[Clinical characteristics and immunophenotypes of
mixed
-
lineage
acute leukemia
].
The aim of study was to analyze the clinical, biological features, treatment outcome and prognosis of
mixed
-
lineage
acute leukemia
(MAL).
48 MAL patients diagnosed according to European Group of International
Leukemia
(EGIL) scoring system were retrospectively analyzed and the analysis results were compared with that from 68 cases of AML and 61 cases of ALL.
The results showed that the incidence of MAL in
acute leukemia
was 9.6%.
The median of white blood
cell
count in MAL was significantly higher than that of non-
mixed
-
lineage
cases (AML and ALL) observed during the same period (P < 0.05).
Coexpression of
myeloid and B lymphoid
antigens in MAL patients was predominant, its rate was 70.9%.
The coexpression rate of
T lymphoid and myeloid
antigens was 20.8%, coexpression of B,
T lymphoid and myeloid
antigens was 8.3%.
In MAL Ph chromosome
abnormality
incidence was 25% and was significantly higher than that in AML group (0%) (P < 0.01), but was not statistical defference with that in ALL group (16.7%) (P > 0.05).
It is concluded that MAL is supposed to be originated from stem cells, coexpression of
lymphoid
/
myeloid
antigens is the major feature of MAL which accompanies many poor prognosis factors and lower CR rate.
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(PMID = 17605883.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
CHI
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD34
77.
Weir EG, Ali Ansari-Lari M, Batista DA, Griffin CA, Fuller S, Smith BD, Borowitz MJ:
Acute bilineal leukemia: a rare disease with poor outcome.
Leukemia
; 2007 Nov;21(11):2264-70
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[Title]
Acute
bilineal
leukemia
: a rare
disease
with poor outcome.
Most cases of
acute leukemia
can be assigned to the
myeloid
, B or
T lineage
.
In a few cases, definitive assignment cannot be achieved because blasts express antigens of more than one
lineage
.
A subset of these, referred to as
acute
bilineal
leukemias
(aBLLs), is characterized by the presence of more than one population of blasts, each comprising a single
lineage
.
We identified 19 cases of aBLL, including 10
mixed T and myeloid
(T-My) and nine
mixed B and myeloid
(B-My); no
mixed B and T
cases were identified.
Three of seven patients with B-My had
a t
(9;22)(q34q11.2), two had 11q23 translocations and one had del(9).
Of 16 patients with outcome data, only six achieved complete remission and only two remain free of
disease
2.5 and 4.5 years after chemotherapy or stem
cell
transplantation. aBLL is a rare
disease
that combines B or
T and myeloid
blasts.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
.
Leukemia
,
Biphenotypic
,
Acute
/ therapy
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(PMID = 17611554.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
78.
Wang LH, Wang M, Zhou CL, Chen S, Zhang XW, Xing HY, Wang JX:
[Detection of point mutation at second tyrosine kinase domain of FLT3 gene in acute myeloid leukemia].
Zhonghua Xue Ye Xue Za Zhi
; 2005 Jun;26(6):335-8
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[Title]
[Detection of point mutation at second tyrosine kinase domain of FLT3 gene in
acute
myeloid
leukemia
].
OBJECTIVE: To evaluate the prevalence of a novel FLT3 activating mutation in tyrosine kinase domain (TDK) in
acute leukemia
patients and its clinical implication.
METHODS: Genomic DNA from bone marrow mononuclear cells of 143 cases of
acute
myeloid
leukemia
(AML), 25
acute
lymphocytic
leukemia
(ALL), 2
acute
hybrid
leukemia
(AHL), 17 myelodysplastic syndromes (MDS) and 7 chronic myelogenous
leukemia
in blast crisis (CML-BC) was screened by polymerase chain reaction (PCR) and gel electrophoresis for FLT3-TKD point mutations.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics. fms-Like Tyrosine Kinase 3 / genetics
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(PMID = 16185475.001).
[ISSN]
0253-2727
[Journal-full-title]
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
[ISO-abbreviation]
Zhonghua Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
79.
Goldstein BD:
Benzene as a cause of lymphoproliferative disorders.
Chem Biol Interact
; 2010 Mar 19;184(1-2):147-50
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There is a long standing issue concerning the strength of evidence relating benzene to
lymphocytic
neoplasms.
Because benzene is a known cause of human
acute
myelogenous
leukemia
there has been little reason for organizations such as the International Agency for Research on Cancer (IARC) or the US National Toxicology Program (NTP) to perform standard hazard identification reviews of benzene as a possible cause of other cancers such as lymphomas.
There is also increasing evidence of a close relationship between
lymphoid
tumors and the types of
myeloid
tumors known to be caused by benzene.
This includes the not infrequent
finding
of
biphenotypic
lineage
as well as the formation of
lymphoid
as well as
myeloid leukemias
following chemotherapy.
Studies of the mechanism of benzene toxicity are consistent with a relatively non-specific mechanism capable of producing multiple chromosomal changes, and there is evidence that the early hematopoietic stem
cell
, which is believed to be targeted by benzene in causing
myeloid
cancers, is also the progenitor of
lymphocytic cell
types.
Furthermore, the classification of lymphomas has evolved so that non-Hodgkin lymphoma now includes such formerly distinct disorders as chronic
lymphocytic
leukemia
and multiple myeloma, and there is less of a distinction between
leukemia
and non-
leukemia
forms of lymphoma.
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BENZENE
.
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[Copyright]
Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
(PMID = 20035727.001).
[ISSN]
1872-7786
[Journal-full-title]
Chemico-biological interactions
[ISO-abbreviation]
Chem. Biol. Interact.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Ireland
[Chemical-registry-number]
J64922108F / Benzene
[Number-of-references]
54
80.
Al-Seraihy AS, Owaidah TM, Ayas M, El-Solh H, Al-Mahr M, Al-Ahmari A, Belgaumi AF:
Clinical characteristics and outcome of children with biphenotypic acute leukemia.
Haematologica
; 2009 Dec;94(12):1682-90
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[Title]
Clinical characteristics and outcome of children with
biphenotypic acute leukemia
.
BACKGROUND: Knowledge concerning the clinical and biological presentation, as well as the outcome of treatment, of
biphenotypic acute leukemia
in children is limited.
DESIGN AND METHODS: This retrospective review analyzes the clinical features and outcome of children with
biphenotypic acute leukemia
diagnosed and treated over an 8-year period.
According to the EGIL scoring system 24 (3.7%) of 633 patients with
acute leukemia
were classified as having
biphenotypic acute leukemia
.
The diagnostic work-up and results were reviewed specifically for this study in the light of the newly published WHO criteria for the
diagnosis
of
leukemia
of ambiguous
lineage
.
Based on these criteria, 11 (1.7%) patients were categorized according to the new nomenclature as having
mixed
phenotype
acute leukemia
.
The majority of the patients (58.3%) had
a B
-
lymphoid
/
myeloid
phenotype, followed by the T-
lymphoid
/
myeloid
phenotype.
The most frequent chromosomal
abnormality
involved the 14q32 locus.
Patients received therapy based on a treatment regimen for
acute
lymphocytic
leukemia
regimen, which included
myeloid
-effective agents.
The survival of those patients who underwent hematopoietic stem
cell
transplantation in first complete remission was not different from that of the patients who were treated with chemotherapy alone (overall survival: 70.1% versus 81.1%, respectively, p=0.39; event-free survival: 70.1% versus 76.2%, respectively, p=0.75).
The outcome of the 11 patients who were retrospectively classified as having
mixed
phenotype
acute leukemia
according to the new WHO criteria was excellent, with no relapses or deaths occurring among these patients.
CONCLUSIONS: An
acute
lymphocytic
leukemia
type of induction therapy, using agents that are active against
lymphoid and myeloid leukemias
, appears to be more effective in achieving and maintaining complete remissions regardless of whether the patients are classified according to EGIL criteria or the new WHO criteria.
Hematopoietic stem
cell
transplantation may not be necessary for all patients in first complete remission.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
.
Leukemia
,
Biphenotypic
,
Acute
/ therapy
[MeSH-minor]
Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Flow Cytometry. Follow-Up Studies. Hematopoietic Stem
Cell
Transplantation. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Outcome Assessment (Health Care) / methods. Remission Induction. Retrospective Studies
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[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antigens, CD
[Other-IDs]
NLM/ PMC2791935
81.
Miyazawa Y, Irisawa H, Matsushima T, Mitsui T, Uchiumi H, Saitohi T, Handa H, Karasawa M, Murakami H, Tsukamoto N, Nojima Y:
[Reversible posterior leukoencephalopathy syndrome probably caused by L-asparaginase].
Rinsho Ketsueki
; 2006 Jun;47(6):531-5
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A 46-year-old male with refractory
biphenotypic acute leukemia
was treated with doxorubicin (days 1-3, 15-17), vincristine (days 1, 8, 15, 22), prednisolone (days 1-28), and L-asparaginase (L-ASP: days 15-28) as reinduction therapy.
[MeSH-major]
Asparaginase / adverse effects. Brain / pathology. Brain Diseases / chemically induced. Brain Diseases /
diagnosis
[MeSH-minor]
Acute
Disease
. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Doxorubicin / administration & dosage. Humans. Hypertension / chemically induced.
Leukemia
/ drug therapy. Male. Middle Aged. Prednisolone / administration & dosage. Seizures / chemically induced. Vincristine / administration & dosage
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.
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.
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.
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(PMID = 16862982.001).
[ISSN]
0485-1439
[Journal-full-title]
[Rinshō ketsueki] The Japanese journal of clinical hematology
[ISO-abbreviation]
Rinsho Ketsueki
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase
82.
Pratz KW, Cho E, Levis MJ, Karp JE, Gore SD, McDevitt M, Stine A, Zhao M, Baker SD, Carducci MA, Wright JJ, Rudek MA, Smith BD:
A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias.
Leukemia
; 2010 Aug;24(8):1437-44
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[Title]
A pharmacodynamic study of sorafenib in patients with relapsed and refractory
acute
leukemias
.
We report the results of a phase I dose escalation trial of the multikinase inhibitor sorafenib in relapsed and refractory
acute leukemia
patients using an intermittent dosing regimen.
Fifteen patients with advanced
leukemia
(12 with
acute
myeloid
leukemia
, 2 with
acute
lymphoblastic
leukemia
, 1 with
biphenotypic
)
and a
median age of 63 (range 37-85) years were enrolled and treated on a dose escalation trial.
Out of 15 patients, 11 experienced stable
disease
as best response.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use
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.
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.
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.
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(PMID = 20535150.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA128864; United States / NCI NIH HHS / CA / P30 CA006973-48; United States / NCRR NIH HHS / RR / UL1 RR025005; United States / NCI NIH HHS / CA / P30CA006973; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCRR NIH HHS / RR / UL1 RR025005-04; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / P50 CA100632-06; United States / NCI NIH HHS / CA / R01 CA128864-04; United States / NCI NIH HHS / CA / U01 CA070095-17; United States / NCI NIH HHS / CA / U01CA70095
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
[Other-IDs]
NLM/ NIHMS201571; NLM/ PMC2921005
83.
Verheyden S, Demanet C:
Susceptibility to myeloid and lymphoid leukemia is mediated by distinct inhibitory KIR-HLA ligand interactions.
Leukemia
; 2006 Aug;20(8):1437-8
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[Title]
Susceptibility to
myeloid and lymphoid
leukemia
is mediated by distinct inhibitory KIR-HLA ligand interactions.
[MeSH-major]
HLA-B Antigens / physiology. HLA-C Antigens / physiology. Killer Cells, Natural / immunology.
Leukemia
,
Lymphoid
/ immunology.
Leukemia
,
Myeloid
/ immunology. Receptors, Immunologic / physiology. Tumor Escape
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.
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.
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.
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(PMID = 16761016.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Letter; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / HLA-B Antigens; 0 / HLA-C Antigens; 0 / Receptors, Immunologic; 0 / Receptors, KIR
84.
Chen X, Zhang Y, Li Y, Lei P, Zhai Y, Liu L:
Biphenotypic hematologic malignancy: a case report of the 8p11 myeloproliferative syndrome in a child.
J Pediatr Hematol Oncol
; 2010 Aug;32(6):501-3
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[Title]
Biphenotypic
hematologic malignancy: a case report of the 8p11 myeloproliferative syndrome in a child.
SUMMARY: The 8p11 myeloproliferative syndrome, also known as stem
cell
leukemia
/lymphoma, is a rare, atypical, myeloproliferative
disorder and lymphoid
malignancy associated with chromosomal abnormalities involving the 8p11 chromosomal band.
Disease
phenotypes associated with this translocation include poor prognosis and transformation to
acute leukemia
and non-Hodgkin lymphoma.
In common with
a T
-
cell
phenotype, obtaining and maintaining remission is difficult by conventional chemotherapy.
This study describes an illustrative case of 8p11 myeloproliferative syndrome/stem
cell
leukemia
/lymphoma outlining its chief features and historical developments.
[MeSH-minor]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Cyclophosphamide / therapeutic use. Dexamethasone / therapeutic use. Doxorubicin / therapeutic use. Etoposide / therapeutic use. Humans. Male. Phenotype. Precursor B-
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Precursor B-
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor B-
Cell Lymphoblastic
Leukemia
-Lymphoma / physiopathology. Precursor T-
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Precursor T-
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor T-
Cell Lymphoblastic
Leukemia
-Lymphoma / physiopathology. Prednisone / therapeutic use. Syndrome. Translocation, Genetic. Vincristine / therapeutic use
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.
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.
Hazardous Substances Data Bank.
ETOPOSIDE
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
PREDNISONE
.
Hazardous Substances Data Bank.
VINCRISTINE
.
NCI CPTAC Assay Portal.
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(PMID = 20562652.001).
[ISSN]
1536-3678
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CVAD protocol; EPOCH protocol
85.
Steiner M, Attarbaschi A, Dworzak M, Strobl H, Pickl W, Kornmüller R, Haas O, Gadner H, Mann G, Austrian Berlin-Frankfurt-Münster Study Group:
Cytochemically myeloperoxidase positive childhood acute leukemia with lymphoblastic morphology treated as lymphoblastic leukemia.
J Pediatr Hematol Oncol
; 2010 Jan;32(1):e4-7
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[Title]
Cytochemically myeloperoxidase positive childhood
acute leukemia
with
lymphoblastic
morphology treated as
lymphoblastic
leukemia
.
SUMMARY: Cytochemical myeloperoxidase (MPO) positivity represents the gold standard for discrimination between lymphatic
and myeloid
blasts.
Rarely, cytochemical MPO reaction may be positive in >or=3% of blasts with clear
lymphoblastic
morphology.
We present 5 patients with cytochemically MPO-positive
acute leukemia
classified as
lymphoblastic
by cytomorphology
and lymphoblastic
(n=3) or
biphenotypic
(n=2) by immunophenotyping, who entered first-line treatment for
lymphoblastic
leukemia
.
The former 3 are in first remission and both with
biphenotypic leukemia
relapsed with
acute
myeloid
leukemia
.
The study primarily shows that cytochemical MPO expression in childhood
acute leukemia
revealing typical
lymphoblastic
morphology and phenotype does rarely exist.
Although a small number of patients studied, cytochemical MPO expression in
acute leukemia
does not seem to require
myeloid
leukemia
treatment in case of otherwise
lymphoblastic
cytomorphology and phenotype.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ etiology. Peroxidase / analysis. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / pathology
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(PMID = 19935430.001).
[ISSN]
1536-3678
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 1.11.1.7 / Peroxidase
86.
Georgy M, Yonescu R, Griffin CA, Batista DA:
Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults.
Cancer Genet Cytogenet
; 2008 Aug;185(1):28-31
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[Title]
Acute
mixed lineage
leukemia
and a
t(6;14)(q25;q32) in two adults.
Acute
mixed lineage
leukemia
(AMLL) is a rare form of
leukemia
in which both
myeloid and lymphoid
markers are present.
Few chromosome abnormalities have been identified associated with this form of
leukemia
.
A translocation involving the long arms of chromosomes 6 and 14 was previously described in four young individuals with
acute leukemia
and in three of these cases the
diagnosis
was
mixed lineage
.
[MeSH-major]
Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 6.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Translocation, Genetic
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(PMID = 18656690.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
87.
El-Sissy A, El-Mashari M, Bassuni W, El-Swaayed A:
Molecular detection of BCR/ABL fusion gene in Saudi acute lymphoblastic leukemia patients.
J Egypt Natl Canc Inst
; 2006 Jun;18(2):109-16
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[Title]
Molecular detection of BCR/ABL fusion gene in Saudi
acute
lymphoblastic
leukemia
patients.
A fraction of
acute
lymphoblastic
leukemia
(ALL) cases carry the translocation t(9;22) (q34;q11.2) which juxtaposes the ABL proto-oncogene to the BCR gene generating a chimeric gene, BCR/ABL.
PATIENTS AND METHODS: Twenty newly diagnosed ALL patients, 16 adult and 4 paediatric cases, were included in the study, 11 cases (55%) were of precursor B phenotype, 8 cases (40%) belonged to
T lineage
, while one case was
biphenotypic
expressing mainly precursor
B cell
markers tether with CD13, CD33, CD117, Detection of BCR/ABL fusion gene was done using interphase FISH technique and was confirmed molecularly using the RT-PCR technique.
RESULTS: BCR/ABL fusion gene was negative in all the examined cases, yet
abnormality
involving 9q34, ABL gene, either by addition or deletion was detected in three cases (15%).
CONCLUSION: This may reflect the frequency of association of ABL gene and BCR gene
abnormality
in our cases, and that absence of fusion gene BCR/ABL does not exclude their role in the leukomogenic process, yet a larger study is required to confirm and detect the prevalence of these gene disturbances in ALL and their association.
[MeSH-major]
Fusion Proteins, bcr-abl / genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma /
diagnosis
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(PMID = 17496935.001).
[ISSN]
1110-0362
[Journal-full-title]
Journal of the Egyptian National Cancer Institute
[ISO-abbreviation]
J Egypt Natl Canc Inst
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Egypt
[Chemical-registry-number]
0 / Antigens, Differentiation, B-Lymphocyte; 0 / RNA, Messenger; EC 2.7.10.2 / Fusion Proteins, bcr-abl
88.
Jacobsohn DA, Hewlett B, Morgan E, Tse W, Duerst RE, Kletzel M:
Favorable outcome for infant acute lymphoblastic leukemia after hematopoietic stem cell transplantation.
Biol Blood Marrow Transplant
; 2005 Dec;11(12):999-1005
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[Title]
Favorable outcome for infant
acute
lymphoblastic
leukemia
after hematopoietic stem
cell
transplantation.
Infants with
acute
lymphoblastic
leukemia
(ALL) have a poor prognosis when treated with standard chemotherapy.
A subset of these infants, particularly those with
mixed
-
lineage
leukemia
(MLL) rearrangements, has a high likelihood of relapse.
Hematopoietic stem
cell
transplantation (HSCT) performed early in first remission may improve outcome.
Six patients were < or =6 months of age at
diagnosis
, 11 had an initial white blood
cell
count of >50000/microL, and all patients with determinable cytogenetics had a high-risk karyotype [t(4:11)
abnormality
or other MLL rearrangement].
Two patients, 1 of whom had minimal residual
disease
at HSCT, died after relapse following HSCT.
Acute
and chronic graft-versus-host
disease
were minimal in these patients.
[MeSH-major]
Hematopoietic Stem
Cell
Transplantation.
Leukemia
,
Biphenotypic
,
Acute
/ therapy. Transplantation Conditioning
[MeSH-minor]
Adolescent. Child. Child, Preschool.
Disease
-Free Survival. Female. Humans. Male. Recurrence. Remission Induction. Retrospective Studies. Risk Factors. Time Factors. Translocation, Genetic / genetics
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(PMID = 16338622.001).
[ISSN]
1083-8791
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
89.
Bae SY, Yoon SY, Huh JH, Sung HJ, Choi IK:
Hypereosinophilia in biphenotypic (B-cell/T-cell) acute lymphoblastic leukemia.
Leuk Lymphoma
; 2007 Jul;48(7):1417-9
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[Title]
Hypereosinophilia in
biphenotypic
(B-
cell
/T-
cell
)
acute
lymphoblastic
leukemia
.
[MeSH-major]
Hypereosinophilic Syndrome / etiology. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / complications
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(PMID = 17613773.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
90.
Kiyomizu K, Yagi T, Yoshida H, Minami R, Tanimura A, Karasuno T, Hiraoka A:
Fulminant septicemia of Bacillus cereus resistant to carbapenem in a patient with biphenotypic acute leukemia.
J Infect Chemother
; 2008 Oct;14(5):361-7
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[Title]
Fulminant septicemia of Bacillus cereus resistant to carbapenem in a patient with
biphenotypic acute leukemia
.
A 33-year-old man was suffering from febrile neutropenia (FN) on day 15 after the start of remission-induction therapy for
biphenotypic acute leukemia
under gut decontamination with polymyxin
B and
nystatin.
If B. cereus resistant to carbapem increases, our method of gut decontamination with polymyxin
B and
nystatin may have to be changed to one containing a new quinolone for the prevention of septicemia.
[MeSH-major]
Bacillus cereus / drug effects. Bacteremia / microbiology. Carbapenems / therapeutic use.
Leukemia
,
Biphenotypic
,
Acute
/ complications
[MeSH-minor]
Adult. Anti-Bacterial Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Stem / microbiology. Brain Stem / pathology. Fever / drug therapy. Gram-Positive Bacterial Infections / complications. Gram-Positive Bacterial Infections /
diagnosis
. Gram-Positive Bacterial Infections / drug therapy. Gram-Positive Bacterial Infections / pathology. Humans. Liver / microbiology. Liver / ultrastructure. Lung / microbiology. Lung / ultrastructure. Male. Microbial Sensitivity Tests. Neutropenia / drug therapy. Remission Induction. beta-Lactam Resistance
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(PMID = 18936889.001).
[ISSN]
1341-321X
[Journal-full-title]
Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy
[ISO-abbreviation]
J. Infect. Chemother.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Anti-Bacterial Agents; 0 / Carbapenems
91.
Faber J, Armstrong SA:
Mixed lineage leukemia translocations and a leukemia stem cell program.
Cancer Res
; 2007 Sep 15;67(18):8425-8
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[Title]
Mixed lineage
leukemia
translocations
and a
leukemia
stem
cell
program.
One possibility is that CSC arise from the stem
cell
counterparts in normal tissues.
In support of this idea, we showed recently that
mixed lineage
leukemia
fusion oncoproteins can convert committed hematopoietic progenitors into
leukemias
, which include
leukemia
stem cells expressing a self-renewal associated program in the context of a differentiated
myeloid cell
.
[MeSH-major]
Hematopoietic Stem Cells / pathology.
Leukemia
,
Biphenotypic
,
Acute
/ pathology. Neoplastic Stem Cells / pathology
[MeSH-minor]
Animals.
Cell
Transformation, Neoplastic / genetics.
Cell
Transformation, Neoplastic / metabolism.
Cell
Transformation, Neoplastic / pathology. Humans. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
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(PMID = 17875678.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Oncogene Proteins, Fusion
[Number-of-references]
24
92.
Naunheim MR, Nahed BV, Walcott BP, Kahle KT, Soupir CP, Cahill DP, Borges LF:
Diagnosis of acute lymphoblastic leukemia from intracerebral hemorrhage and blast crisis. A case report and review of the literature.
Clin Neurol Neurosurg
; 2010 Sep;112(7):575-7
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[Title]
Diagnosis
of
acute
lymphoblastic
leukemia
from intracerebral hemorrhage and blast crisis. A case report and review of the literature.
Intracerebral hemorrhage (ICH) contributes significantly to the morbidity and mortality of patients suffering from
acute leukemia
.
While ICH is often identified in autopsy studies of leukemic patients, it is rare for ICH to be the presenting sign that ultimately leads to the
diagnosis
of
leukemia
.
We report a patient with previously undiagnosed
acute
precursor B-
cell lymphoblastic
leukemia
(ALL) who presented with diffuse encephalopathy due to ICH in the setting of an
acute
blast crisis.
The
diagnosis
of ALL was initially suspected, because of the hyperleukocytosis observed on presentation, then confirmed with a bone marrow biopsy and flow cytometry study of the peripheral blood.
This case demonstrates that the presence of hyperleukocytosis in a patient with intracerebral hemorrhage should raise clinical suspicion for
acute leukemia
as the cause of the ICH.
[MeSH-major]
Blast Crisis /
diagnosis
. Intracranial Hemorrhages /
diagnosis
.
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
[MeSH-minor]
Benzamides. Blood
Cell
Count.
Diagnosis
, Differential. Flow Cytometry. Humans. Imatinib Mesylate. In Situ Hybridization. Leukocyte Count. Male. Middle Aged. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Tomography, X-Ray Computed
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(PMID = 20493628.001).
[ISSN]
1872-6968
[Journal-full-title]
Clinical neurology and neurosurgery
[ISO-abbreviation]
Clin Neurol Neurosurg
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
93.
Aplan PD:
Chromosomal translocations involving the MLL gene: molecular mechanisms.
DNA Repair (Amst)
; 2006 Sep 8;5(9-10):1265-72
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Leukemias
with MLL translocations have been the topic of intense interest because of the unusual,
biphenotypic
immunophenotype of these
leukemias
, because of the unique clinical presentation of some MLL translocations (infant
leukemia
and therapy-related
leukemia
), and because of the large number of different chromosomal loci that partner with MLL in these translocations.
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[ISSN]
1568-7864
[Journal-full-title]
DNA repair
[ISO-abbreviation]
DNA Repair (Amst.)
[Language]
ENG
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Chromatin; 0 / MLL protein, human; 0 / Topoisomerase II Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
[Number-of-references]
71
[Other-IDs]
NLM/ NIHMS13506; NLM/ PMC1635494
94.
Lou Z, Zhang CC, Tirado CA, Slone T, Zheng J, Zaremba CM, Oliver D, Chen W:
Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10.
Leuk Res
; 2010 Aug;34(8):1107-9
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[Title]
Infantile
mixed
phenotype
acute leukemia
(bilineal and
biphenotypic
) with t(10;11)(p12;q23);MLL-MLLT10.
We report a case of a 6-month-old boy with
a mixed
phenotype
acute leukemia
(MPAL), bilineal and
biphenotypic
immunophenotype (B-
lymphoid lineage
and combined B-
lymphoid and
monocytic
lineage
) with t(10;11)(p12;q23);MLL-MLLT10.
He was treated with
acute
myeloid
leukemia
protocol and in complete remission at 7-month follow-up.
From a clinical practice standpoint, this case illustrates the importance of detection of MLL rearrangement due to its prognostic implication and the effectiveness of flow cytometry immunophenotyping in diagnosing MPAL and monitoring minimal residual
disease
.
[MeSH-major]
Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 11 / genetics.
Leukemia
,
Biphenotypic
,
Acute
/ genetics.
Leukemia
, Monocytic,
Acute
/ genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Translocation, Genetic / genetics
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[Copyright]
Copyright (c) 2010 Elsevier Ltd. All rights reserved.
(PMID = 20299091.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
95.
Yao PJ, Petralia RS, Bushlin I, Wang Y, Furukawa K:
Synaptic distribution of the endocytic accessory proteins AP180 and CALM.
J Comp Neurol
; 2005 Jan 3;481(1):58-69
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AP180 and clathrin assembly
lymphoid myeloid
leukemia
protein (CALM) are clathrin accessory proteins that promote the formation of clathrin-coated vesicles.
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.
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
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.
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(PMID = 15558718.001).
[ISSN]
0021-9967
[Journal-full-title]
The Journal of comparative neurology
[ISO-abbreviation]
J. Comp. Neurol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Monomeric Clathrin Assembly Proteins; 0 / Picalm protein, rat; 0 / clathrin assembly protein AP180
96.
Gupta A, Modi CJ, Gujral S:
Hemophagocytosis by leukemic cells in biphenotypic acute leukaemia: a rare case.
Indian J Pathol Microbiol
; 2010 Apr-Jun;53(2):370-1
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[Title]
Hemophagocytosis by leukemic cells in
biphenotypic acute
leukaemia
: a rare case.
[MeSH-major]
Lymphocytes / pathology. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma /
diagnosis
. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / pathology
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(PMID = 20551563.001).
[ISSN]
0974-5130
[Journal-full-title]
Indian journal of pathology & microbiology
[ISO-abbreviation]
Indian J Pathol Microbiol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
India
97.
Gobbi G, Mirandola P, Malinverno C, Sponzilli I, Carubbi C, Ricci F, Binazzi R, Basso G, Giuliani-Piccari G, Ramazzotti G, Pasquantonio G, Cocco L, Vitale M:
Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin.
Int J Oncol
; 2008 Aug;33(2):371-4
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[Title]
Aberrant expression of B203.13 antigen in
acute
lymphoid
leukemia
of B-
cell
origin.
The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte
biphenotypic
cell
line B1b.
We tested this antibody as a marker of childhood B-
acute
lymphoblastic
leukemia
(B-ALL).
The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common
acute
lymphoblastic
leukemia
(c-ALL) did not express B203.13.
We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-
acute
lymphoblastic
leukemia
.
[MeSH-major]
Antigens, Neoplasm / biosynthesis. Precursor B-
Cell Lymphoblastic
Leukemia
-Lymphoma / metabolism
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(PMID = 18636158.001).
[ISSN]
1019-6439
[Journal-full-title]
International journal of oncology
[ISO-abbreviation]
Int. J. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
98.
Jun KR, Jang S, Chi HS, Lee KH, Lee JH, Choi SJ, Seo JJ, Moon HN, Im HJ, Park CJ:
Relationship between in vitro chemosensitivity assessed with MTT assay and clinical outcomes in 103 patients with acute leukemia.
Korean J Lab Med
; 2007 Apr;27(2):89-95
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[Title]
Relationship between in vitro chemosensitivity assessed with MTT assay and clinical outcomes in 103 patients with
acute leukemia
.
METHODS: For MTT assay, we obtained bone marrow aspirates from 103 patients with
acute leukemia
at the time of initial
diagnosis
or relapse.
CONCLUSIONS: Although it does not provide the insight into the mechanisms that cause drug resistance, the MTT assay may be a useful tool in individually optimizing the chemotherapy of patients with
acute leukemia
.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
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CYTARABINE
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(PMID = 18094557.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Antibiotics, Antineoplastic; 0 / Coloring Agents; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 298-93-1 / thiazolyl blue; ZS7284E0ZP / Daunorubicin
99.
Thavaraj V, Seth R:
Prophylaxis of central nervous system leukemia: a case of chronic myeloid leukemia with lymphoid blast crisis treated with imatinib mesylate.
World J Pediatr
; 2008 May;4(2):145-7
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[Title]
Prophylaxis of central nervous system
leukemia
: a case of chronic
myeloid
leukemia
with
lymphoid
blast crisis treated with imatinib mesylate.
BACKGROUND: Chronic
myeloid
leukemia
(CML) in blast crisis has a dismal prognosis.
METHODS: A child with CML in
lymphoid
blast crisis was diagnosed by complete hematological and bone marrow examination.
There was no central nervous system (CNS)
leukemia
at presentation.
Results of cerebrospinal fluid taken for cytopathology showed CNS
leukemia
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Central Nervous System Neoplasms / prevention & control. Piperazines / administration & dosage. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy. Pyrimidines / administration & dosage
[MeSH-minor]
Anti-Inflammatory Agents / administration & dosage. Benzamides. Blood
Cell
Count. Chemoprevention / methods. Child. Clinical Protocols. Cytarabine / administration & dosage. Drug Therapy, Combination. Female. Humans. Hydrocortisone / administration & dosage. Imatinib Mesylate. Injections, Spinal. Methotrexate / therapeutic use. Remission Induction
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.
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.
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CYTARABINE
.
Hazardous Substances Data Bank.
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.
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HYDROCORTISONE
.
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METHOTREXATE
.
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1708-8569
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World journal of pediatrics : WJP
[ISO-abbreviation]
World J Pediatr
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Anti-Inflammatory Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate
100.
Cerveira N, Meyer C, Santos J, Torres L, Lisboa S, Pinheiro M, Bizarro S, Correia C, Norton L, Marschalek R, Teixeira MR:
A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia.
BMC Cancer
; 2010;10:518
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[Title]
A novel spliced fusion of MLL with CT45A2 in a pediatric
biphenotypic acute leukemia
.
BACKGROUND: Abnormalities of 11q23 involving the MLL gene are found in approximately 10% of human
leukemias
.
In this work we present the identification of a novel MLL fusion partner in a pediatric patient with
de
novo
biphenotypic acute leukemia
.
METHODS: Cytogenetics, fluorescence in situ hybridization (FISH), molecular studies (RT-PCR and LDI-PCR), and bioinformatic sequence analysis were used to characterize the CT45A2 gene as novel MLL fusion partner in pediatric
acute leukemia
.
CONCLUSION: We have identified CT45A2 as a novel spliced MLL fusion partner in a pediatric patient with
de
novo
biphenotypic acute leukemia
, as a result of a cryptic insertion of 11q23 in Xq26.3.
Since CT45A2 is the first Cancer/Testis antigen family gene found fused with MLL in
acute leukemia
, future studies addressing its biologic relevance for leukemogenesis are warranted.
[MeSH-major]
Antigens, Neoplasm / genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Oncogene Proteins, Fusion / genetics
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
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[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / CT45A1 protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
[Other-IDs]
NLM/ PMC2956734
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