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1
acute mixed lineage leukemia 2005:2010[pubdate] *count=100
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acute mixed lineage leukemia
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Concept C0023464: acute biphenotypic leukemia disorder;
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Items 1 to 100 of about 311
1.
Kong CT, Sham MH, So CW, Cheah KS, Chen SJ, Chan LC:
The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice.
Leukemia
; 2006 Oct;20(10):1829-39
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[Title]
The Mll-Een knockin fusion gene enhances proliferation of
myeloid
progenitors derived from mouse embryonic stem cells and causes
myeloid leukaemia
in chimeric mice.
Rearrangement of the
mixed lineage
leukaemia
(MLL) gene with extra eleven nineteen (EEN) was previously identified in an infant with
acute
myeloid leukaemia
.
Using homologous recombination, we have created a mouse equivalent of the human MLL-EEN allele and showed that when Mll(Een/+) embryonic stem (ES) cells were induced to differentiate in vitro into haemopoietic cells, there was increased proliferation of
myeloid
progenitors with self-renewal property.
We also generated Mll(Een/+) chimeric mice, which developed
leukaemia
displaying enlarged livers, spleens, thymuses and lymph nodes owing to infiltration of Mll(Een/+)-expressing leukemic cells.
Immunophenotyping of cells from enlarged organs and bone marrow (BM) of the Mll(Een/+) chimeras revealed an accumulation of Mac-1+/Gr-1- immature
myeloid
cells
and a
reduction in normal B-
and T
-
cell
populations.
We observed differential regulation of Hox genes between
myeloid
cells derived from Mll(Een/+) ES cells and mouse BM leukemic cells which suggested different waves of Hox expression may be activated by MLL fusion proteins for initiation (in ES cells) and maintenance (in leukemic cells) of the
disease
.
We believe studies of MLL fusion proteins in ES cells combined with in vivo animal models offer new approaches to the dissection of molecular events in multistep pathogenesis of
leukaemia
.
[MeSH-major]
Hematopoietic Stem Cells / pathology. Intracellular Signaling Peptides and Proteins / genetics.
Leukemia
,
Myeloid
/ genetics.
Leukemia
,
Myeloid
/ pathology.
Myeloid
Cells / pathology.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics
[MeSH-minor]
Amino Acid Sequence. Animals. Base Sequence.
Cell
Division / physiology. Chimera.
Disease
Models, Animal. Female. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Genes, Homeobox / physiology. Humans. Infant. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Molecular Sequence Data. Translocation, Genetic
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author profiles
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gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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(PMID = 16888613.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Intracellular Signaling Peptides and Proteins; 0 / SH3GL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
2.
Strick R, Zhang Y, Emmanuel N, Strissel PL:
Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.
Hum Genet
; 2006 Jun;119(5):479-95
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[Title]
Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and
acute
leukemias
.
The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of
acute
lymphocytic
leukemia
.
Chromosome 11q23 translocations in
acute
myeloid and lymphoid
leukemia
cells demonstrate
myeloid lymphoid
leukemia
(MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively.
Therapy-related
leukemia
is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors.
In this report, using
cell
lines and primary cells, chromatin structural elements were analyzed in BCR, ABL and AF4 and, for comparison, in MLL2, which is a homolog to MLL, but not associated with chromosome translocations.
Although MLL2 was expressed in all
cell
lines tested, except for the presence of one DNAse I site in the promoter, no other structural elements were found in MLL2.
A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with
leukemia
.
[MeSH-major]
Chromatin / chemistry. Chromosome Breakage. Chromosomes, Human / genetics.
Leukemia
/ genetics.
Leukemia
/ metabolism. Translocation, Genetic
[MeSH-minor]
Acute
Disease
.
Cell
Line, Tumor. Cells, Cultured. Chronic
Disease
. Humans. K562 Cells. Proto-Oncogene Proteins c-bcr / chemistry. Proto-Oncogene Proteins c-bcr / genetics. Recombination, Genetic
MedlinePlus Health Information.
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.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
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NCI CPTAC Assay Portal.
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(PMID = 16572268.001).
[ISSN]
0340-6717
[Journal-full-title]
Human genetics
[ISO-abbreviation]
Hum. Genet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
[Publication-country]
Germany
[Chemical-registry-number]
0 / Chromatin; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
3.
Takasaki H, Tachibana T, Tanaka M, Maruta A, Ishigatsubo Y, Kanamoari H:
[Successful selection of chemotherapy based on cell surface antigens in a patient with mixed phenotype acute leukemia].
Rinsho Ketsueki
; 2010 May;51(5):339-44
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[Title]
[Successful selection of chemotherapy based on
cell
surface antigens in a patient with
mixed
phenotype
acute leukemia
].
The patient was diagnosed as having
mixed
phenotype
acute leukemia
, T/
myeloid
, NOS, according to the WHO classification.
After initial treatment, residual leukemic cells with CD13, CD33 and MPO were detected by FCM; therefore, he received
re
-induction chemotherapy for AML, and achieved CR.
Acute leukemia
of ambiguous
lineage
is a relatively rare subtype in
acute leukemia
and standard chemotherapy has not been established.
[MeSH-major]
Antigens, Surface. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
/ drug therapy.
Leukemia
/ immunology
[MeSH-minor]
Acute
Disease
. Cyclophosphamide. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Humans. Male. Middle Aged. Prednisolone / administration & dosage. Treatment Outcome. Vincristine / administration & dosage
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(PMID = 20534955.001).
[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]
0 / Antigens, Surface; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; ZS7284E0ZP / Daunorubicin
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4.
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
[MeSH-minor]
Adolescent. Adult. Aged, 80 and over. Antigens, Neoplasm / analysis. Biomarkers, Tumor / genetics. Biomarkers, Tumor / immunology. Child. Female. Humans. Immunophenotyping. Male. Middle Aged.
Phenotype
. Retrospective Studies. World Health Organization. Young Adult
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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
5.
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.
To the best of our knowledge, this is the first reported MLL-MLLT10 rearranged case presenting as
MPAL
in an infant.
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
[MeSH-minor]
Flow Cytometry. Gene Rearrangement. Humans. Immunophenotyping. Infant. Karyotyping. Male. Neoplasm, Residual / genetics. Neoplasm, Residual / pathology. Neoplasm, Residual / therapy.
Phenotype
. Prognosis. Remission Induction
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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
6.
Dixon N, Kishnani PS, Zimmerman S:
Clinical manifestations of hematologic and oncologic disorders in patients with Down syndrome.
Am J Med Genet C Semin Med Genet
; 2006 Aug 15;142C(3):149-57
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Increased erythrocyte mean corpuscular volume (MCV) is frequently found among DS infants and remains elevated throughout life in two-thirds of patients, making interpretation of red
cell
indices for
diagnosis
of nutritional anemias or bone marrow failure disorders more challenging.
Transient myeloproliferative
disorder
(TMD) associated with pancytopenia, hepatosplenomegaly, and circulating immature WBCs, is found almost exclusively in DS infants with an incidence of approximately 10%.
Despite the high rate of spontaneous regression, TMD can be a preleukemic
disorder
in 20-30% of children with DS.
There is an increased risk of
leukemia
with an equal incidence of
lymphoid and myeloid
leukemia
.
Acute
megakaryocytic
leukemia
(AMKL) subtype is the most common form of
acute
myeloid
leukemia
(AML) in this setting, and is uncommon in children without DS.
Children with DS and
leukemia
are more sensitive to some chemotherapeutic agents such as methotrexate than other children which requires careful monitoring for toxicity.
Although the risk for
leukemia
is higher in individuals with DS, these patients have a lower risk of developing solid tumors, with the exception of germ
cell
tumors, and perhaps retinoblastoma and lymphoma.
[MeSH-major]
Down Syndrome / complications. Hematologic Diseases /
diagnosis
. Hematologic Diseases / etiology. Neoplasms /
diagnosis
. Neoplasms / etiology
[MeSH-minor]
Child. Female. Humans. Infant.
Leukemia
/
diagnosis
.
Leukemia
/ etiology. Male. Myeloproliferative Disorders /
diagnosis
. Myeloproliferative Disorders / etiology
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(PMID = 17048354.001).
[ISSN]
1552-4868
[Journal-full-title]
American journal of medical genetics. Part C, Seminars in medical genetics
[ISO-abbreviation]
Am J Med Genet C Semin Med Genet
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 2T32 CA 09307
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
72
7.
Aljurf M, Nassar A, Saleh AJ, Almhareb F, Alzahrani H, Walter C, Bakr M, Ahmed SO, Chaudhri N:
Maternal acute lymphoctic leukemia with rearrangement of the mixed lineage leukemia gene occurring during pregnancy.
Hematol Oncol Stem Cell Ther
; 2009;2(3):399-402
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[Title]
Maternal
acute
lymphoctic
leukemia
with rearrangement of the
mixed lineage leukemia
gene occurring during pregnancy.
Acute
lymphoblastic
leukemia
(ALL) is a relatively rare
disease
during pregnancy, accounting for about 15% of all cases of pregnancy-associated
leukemia
.
Although
mixed lineage leukemia
gene (MLL) rearrangement is the dominant genetic aberration in infantile
acute leukemia
, the occurrence of MLL gene rearrangement in maternal ALL occurring during pregnancy has not been reported.
Out of 31 cases of maternal
leukemia
diagnosed during pregnancy at our institution, 5 were ALL cases.
We believe that the association of MLL gene rearrangement with maternal
leukemia
is biologically plausible and this observation needs to be validated in a larger cohort of pregnancy-associated maternal
leukemia
cases.
[MeSH-major]
Gene Rearrangement.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Pregnancy Complications, Neoplastic
[MeSH-minor]
Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Cell
Lineage
. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Combined Modality Therapy. Female. Gestational Age. Histone-Lysine N-Methyltransferase. Humans. Pregnancy. Prognosis. Stem
Cell
Transplantation. Translocation, Genetic. Young Adult
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(PMID = 20139053.001).
[ISSN]
1658-3876
[Journal-full-title]
Hematology/oncology and stem cell therapy
[ISO-abbreviation]
Hematol Oncol Stem Cell Ther
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Saudi Arabia
[Chemical-registry-number]
0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
8.
Bhojwani D, Howard SC, Pui CH:
High-risk childhood acute lymphoblastic leukemia.
Clin Lymphoma Myeloma
; 2009;9 Suppl 3:S222-30
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[Title]
High-risk childhood
acute
lymphoblastic
leukemia
.
Although most children with
acute
lymphoblastic
leukemia
(ALL) are cured, certain subsets have a high risk of relapse.
Though early treatment response can be assessed by the peripheral blast
cell
count after 1 week of single-agent glucocorticoid treatment or percent of bone marrow blasts by morphology after 1 or 2 weeks of multiagent induction treatment, determination of minimal residual
disease
by polymerase chain reaction (PCR) or flow cytometry after 2 to 6 weeks of induction is the most precise and useful measure.
Infants with
mixed
-
lineage leukemia
(MLL)-rearranged ALL comprise a very poor-risk group wherein further intensification of chemotherapy causes significant toxicity.
Hybrid
protocols incorporating drugs effective for
acute
myeloid
leukemia
could improve survival, a strategy being tested in international trials.
New agents and methods to overcome resistance are under investigation, and allogeneic stem
cell
transplantation is recommended for certain subsets of patients, for example those with Ph+
and T
-
cell
ALL with poor early response.
Genome-wide interrogation of leukemic
cell
genetic abnormalities and germline genetic variations promise to identify new molecular targets for therapy.
[MeSH-major]
Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma /
diagnosis
. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / pathology
[MeSH-minor]
Adolescent. Antineoplastic Agents / therapeutic use. Child. Child, Preschool.
Disease
-Free Survival. Glucocorticoids / therapeutic use. Humans. Infant. Neoplasm, Residual / drug therapy. Polymerase Chain Reaction. Recurrence. Remission Induction. Treatment Outcome
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(PMID = 19778845.001).
[ISSN]
1938-0712
[Journal-full-title]
Clinical lymphoma & myeloma
[ISO-abbreviation]
Clin Lymphoma Myeloma
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-31; United States / NCI NIH HHS / CA / CA21765
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Glucocorticoids
[Number-of-references]
92
[Other-IDs]
NLM/ NIHMS163517; NLM/ PMC2814411
9.
Hatoum HA, Mahfouz RA, Otrock ZK, Hudaib AR, Taher AT, Shamseddine AI:
Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report.
Am J Hematol
; 2007 Jan;82(1):69-72
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[Title]
Acute
myeloid
leukemia
with T-
cell
receptor gamma gene rearrangement occurring in a patient with chronic
lymphocytic
leukemia
: a case report.
The association of chronic
lymphocytic
leukemia
(CLL) and
acute leukemia
, either
lymphoid
or
myeloid
is a rare event.
Our review of the medical literature revealed only 6 cases of CLL transformation to
acute
myeloid
leukemia
(AML) (M0, M1 and M2) with no other associated malignancy.
We report a similar case but with occurrence of AML-M4 associated with normal cytogenetic analysis and molecular testing but with positive T-
cell
receptor gamma gene rearrangement rather than the usual Vbeta rearrangement.
[MeSH-major]
Gene Rearrangement, gamma-Chain T-
Cell
Antigen Receptor.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics. Neoplasms, Second Primary / genetics
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(PMID = 16947317.001).
[ISSN]
0361-8609
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
[Number-of-references]
22
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.
Mori T, Nishimura N, Hasegawa D, Kawasaki K, Kosaka Y, Uchide K, Yanai T, Hayakawa A, Takeshima Y, Nishio H, Matsuo M:
Persistent detection of a novel MLL-SACM1L rearrangement in the absence of leukemia.
Leuk Res
; 2010 Oct;34(10):1398-401
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[Title]
Persistent detection of a novel MLL-SACM1L rearrangement in the absence of
leukemia
.
Most chromosomal rearrangements including the
mixed lineage leukemia
(MLL) gene are manifested as
leukemia
and predict a poor prognosis.
Here we report a case of a 3-year old boy bearing a novel MLL-rearrangement with the suppressor of actin mutations 1-like (SACM1L) gene in the absence of
leukemia
.
Bone marrow cells harboring the MLL-SACM1L rearrangement appeared during chemotherapy for
acute
lymphoblastic
leukemia
with hyperdiploidy and were continuously detected over 7 years without clonal expansion.
[MeSH-major]
Gene Rearrangement. Membrane Proteins / genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Precursor B-
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics
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[Copyright]
Copyright (c) 2010 Elsevier Ltd. All rights reserved.
(PMID = 20553989.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / MLL protein, human; 0 / Membrane Proteins; 0 / SACM1L protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
12.
Cheng F, Liu J, Zhou SH, Wang XN, Chew JF, Deng LW:
RNA interference against mixed lineage leukemia 5 resulted in cell cycle arrest.
Int J Biochem Cell Biol
; 2008;40(11):2472-81
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[Title]
RNA interference against
mixed lineage leukemia
5 resulted in
cell
cycle arrest.
Mixed lineage leukemia
5 (MLL5) encodes a mammalian trithorax group (TrxG) protein located within chromosome band 7q22, which is a frequently deleted region found in
acute
myeloid
malignancies.
Recently, the emerging roles of TrxG and PcG group proteins in
cell
cycle regulation have begun to be elucidated.
In this study, we demonstrated that the mammalian trxG protein MLL5 is involved in multiple
cell
cycle regulation.
Knockdown of MLL5 by small interfering RNA resulted in the retarded
cell
growth and attenuated intake of BrdU in multiple tumor and normal diploid cells.
The
cell
cycle arrest induced by knockdown of MLL5 took place at both the G1 and G2/M phases.
This growth-inhibitory effect and dual-phase arrest were also found in p53-knockout
cell
lines, suggesting that the transactivation activity of p53 was dispensable for the MLL5-knockdown-mediated
cell
cycle arrest.
In addition, up-regulation of cyclin-dependent kinase inhibitor p21
and de
-phosphorylation of retinoblastoma protein were observed in all
cell
lines tested regardless of their p53 status.
These findings provide evidence that MLL5 might be an important
cell
cycle regulator, participating in
cell
cycle regulatory network machinery at multiple
cell
cycle stages.
[MeSH-major]
Cell
Cycle / physiology. DNA-Binding Proteins
[MeSH-minor]
Animals.
Cell
Line. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Humans. RNA Interference. Retinoblastoma Protein / genetics. Retinoblastoma Protein / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism
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(PMID = 18573682.001).
[ISSN]
1357-2725
[Journal-full-title]
The international journal of biochemistry & cell biology
[ISO-abbreviation]
Int. J. Biochem. Cell Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / MLL5 protein, human; 0 / Retinoblastoma Protein; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
13.
Yin B, Delwel R, Valk PJ, Wallace MR, Loh ML, Shannon KM, Largaespada DA:
A retroviral mutagenesis screen reveals strong cooperation between Bcl11a overexpression and loss of the Nf1 tumor suppressor gene.
Blood
; 2009 Jan 29;113(5):1075-85
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NF1 inactivation occurs in specific human cancers, including juvenile myelomonocytic
leukemia
, an aggressive myeloproliferative
disorder
of childhood.
However, evidence suggests that Nf1 loss alone does not cause
leukemia
.
We therefore hypothesized that inactivation of the Nf1 tumor suppressor gene requires cooperating mutations to cause
acute leukemia
.
One of these genes, Bcl11a, confers a growth advantage in cultured Nf1 mutant hematopoietic cells and causes early onset of
leukemia
of either
myeloid
or
lymphoid
lineage
in mice when expressed in Nf1-deficient bone marrow.
Importantly, Bcl11a is expressed in human chronic myelomonocytic
leukemia
and juvenile myelomonocytic
leukemia
samples.
These findings suggest that deregulated Bcl11a cooperates with Nf1 in leukemogenesis,
and a
therapeutic strategy targeting the BCL11A pathway may prove beneficial in the treatment of
leukemia
.
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[
17277161.001
]
[Cites]
Blood. 2007 Feb 15;109(4):1687-91
[
17090653.001
]
[Cites]
Biochem Biophys Res Commun. 2007 Apr 6;355(2):538-42
[
17306224.001
]
[Cites]
Nat Genet. 2007 Apr;39(4):476-85
[
17369827.001
]
[Cites]
Br J Haematol. 2007 May;137(3):252-61
[
17408467.001
]
(PMID = 18948576.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221
[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 / BCL11A protein, human; 0 / Bcl11a protein, mouse; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Neurofibromin 1; 0 / Nuclear Proteins
[Other-IDs]
NLM/ PMC2635073
14.
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
15.
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
16.
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
17.
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
18.
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
Genetic Alliance.
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.
Genetic Alliance.
consumer health - Leukemia, Myeloid
.
Hazardous Substances Data Bank.
CYTARABINE
.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
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HYDROCORTISONE
.
Hazardous Substances Data Bank.
METHOTREXATE
.
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.
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[Cites]
Clin Cancer Res. 2003 Oct 15;9(13):4674-81
[
14581336.001
]
[Cites]
Blood. 1983 Jan;61(1):85-91
[
6571717.001
]
[Cites]
Ann Hematol. 2004 Jun;83(6):401-2
[
14673623.001
]
[Cites]
Am J Med. 1993 Jan;94(1):69-74
[
8420302.001
]
[Cites]
N Engl J Med. 2001 Apr 5;344(14):1038-42
[
11287973.001
]
[Cites]
Leuk Lymphoma. 2004 Apr;45(4):695-8
[
15160941.001
]
[Cites]
Blood. 2004 Nov 1;104(9):2655-60
[
15231574.001
]
[Cites]
FDA Consum. 2001 Jul-Aug;35(4):6
[
11692893.001
]
[Cites]
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[
11870241.001
]
[Cites]
N Engl J Med. 1983 Oct 6;309(14):826-31
[
6412140.001
]
(PMID = 18661773.001).
[ISSN]
1708-8569
[Journal-full-title]
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
19.
Shen Q, Chen Z, Liu XP, Xing HY, Wang M, Wang JX:
[Expression of PTEN mRNA in acute leukemia and its clinical significance].
Zhonghua Xue Ye Xue Za Zhi
; 2005 Aug;26(8):493-6
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[Title]
[Expression of PTEN mRNA in
acute leukemia
and its clinical significance].
OBJECTIVE: To explore PTEN gene expression and its clinical significance in
acute leukemia
.
METHODS: The expression levels of PTEN mRNA in 5
leukemia
cell
lines, 87 patients with
acute
leukemias
(AL), including 59
acute
myeloid
leukemia
(AML), 26
acute
lymphoblastic
leukemia
(ALL), and 2
acute
hybrid
leukemia
, 21 AL in complete remission (AL-CR), 31 chronic myelogenous
leukemia
(CML) and 14 normal controls were assayed by RT-PCR.
RESULTS: PTEN mRNA was detected in K562
cell
line, but not in Kasumi-1, HL-60, U937, Nalm-6
cell
lines.
The decreased level of PTEN mRNA had a positive correlation with poor-prognostic factors (high white blood
cell
count of > or = 20 x 10(9)/L and chromosome
abnormality
).
[MeSH-major]
Leukemia
/ metabolism. PTEN Phosphohydrolase / metabolism
[MeSH-minor]
Cell
Line, Tumor. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction
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.
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.
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(PMID = 16383243.001).
[ISSN]
0253-2727
[Journal-full-title]
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
[ISO-abbreviation]
Zhonghua Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / RNA, Messenger; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
20.
Unal S, Cetin M, Tuncer AM, Gümrük F, Yetgin S:
The prognostic impact of myeloid antigen expression in pediatric acute lymphoblastic leukemia patients.
Turk J Pediatr
; 2008 Nov-Dec;50(6):533-6
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[Title]
The prognostic impact of
myeloid
antigen expression in pediatric
acute
lymphoblastic
leukemia
patients.
The incidence of
mixed
-
lineage
leukemias
in the pediatric age group was previously reported as 13.8% for
myeloid
antigen-positive ALL and 11.1% for
lymphoid
antigen-positive
acute
myeloid
leukemia
(AML).
Recent studies showed that extensive chemotherapy protocols overcome the risk of
myeloid
lineage
.
Our study also supports most of the previous data and we postulate that
myeloid
antigen expression in pediatric ALL cases has insignificant effect on clinical presentation, relapse rates and survival.
Importantly, 54% of
myeloid
antigen-expressing ALL patients received high-risk treatment protocols for some other reasons and this may also have contributed to similar outcome in these patients to that observed in
myeloid
antigen-negative ALL patients.
[MeSH-major]
Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antigens, Neoplasm / immunology. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / immunology
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.
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consumer health - Leukemia, Myeloid
.
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(PMID = 19227415.001).
[ISSN]
0041-4301
[Journal-full-title]
The Turkish journal of pediatrics
[ISO-abbreviation]
Turk. J. Pediatr.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Turkey
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Neoplasm
21.
Ara AI, Xia M, Ramani K, Mato JM, Lu SC:
S-adenosylmethionine inhibits lipopolysaccharide-induced gene expression via modulation of histone methylation.
Hepatology
; 2008 May;47(5):1655-66
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We previously showed that S-adenosylmethionine (SAMe) and its metabolite methylthioadenosine (MTA) blocked lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNFalpha) expression in RAW (murine macrophage
cell
line) and Kupffer cells at the transcriptional level without affecting nuclear factor kappa B nuclear binding.
LPS increased the binding of histone methyltransferases Set1
and myeloid
/
lymphoid
leukemia
to these promoters, which was unaffected by SAMe or MTA.
Exogenous SAMe is unstable and converts spontaneously to MTA, which is stable
and cell
-permeant.
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(PMID = 18393372.001).
[ISSN]
1527-3350
[Journal-full-title]
Hepatology (Baltimore, Md.)
[ISO-abbreviation]
Hepatology
[Language]
ENG
[Grant]
United States / NIAAA NIH HHS / AA / T32 AA007578; None / None / / R01 AT001576-05; United States / NCCIH NIH HHS / AT / R01 AT001576-05; United States / NIAAA NIH HHS / AA / AA007578-07; United States / NIAAA NIH HHS / AA / AA12677; United States / NIDDK NIH HHS / DK / R01 DK051719-11; United States / NCCIH NIH HHS / AT / R01 AT001576; United States / NIDDK NIH HHS / DK / DK048522-139003; United States / NIDDK NIH HHS / DK / R01 DK051719; United States / NIAAA NIH HHS / AA / T32 AA07578; United States / NCCIH NIH HHS / AT / AT1576; United States / NIAAA NIH HHS / AA / T32 AA007578-07; United States / NIDDK NIH HHS / DK / DK48522; United States / NIAAA NIH HHS / AA / R01 AA013847; United States / NIAAA NIH HHS / AA / R01 AA012677; United States / NIDDK NIH HHS / DK / DK051719-11; United States / NIAAA NIH HHS / AA / R01 AA012677-05; United States / NIDDK NIH HHS / DK / DK51719; United States / NIAAA NIH HHS / AA / R01 AA013847-05; United States / NIDDK NIH HHS / DK / P30 DK048522; United States / NIAAA NIH HHS / AA / AA13847; United States / NIDDK NIH HHS / DK / P30 DK048522-139003; United States / NIAAA NIH HHS / AA / AA012677-05; United States / NIAAA NIH HHS / AA / AA013847-05
[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 / Chromatin; 0 / DNA Primers; 0 / Histones; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA; 7LP2MPO46S / S-Adenosylmethionine
[Other-IDs]
NLM/ NIHMS49821; NLM/ PMC2408693
22.
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]
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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
23.
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)
24.
Daser A, Rabbitts TH:
The versatile mixed lineage leukaemia gene MLL and its many associations in leukaemogenesis.
Semin Cancer Biol
; 2005 Jun;15(3):175-88
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[Title]
The versatile
mixed lineage
leukaemia
gene MLL and its many associations in leukaemogenesis.
The marked association of abnormalities of chromosome 11 long arm, band q23, with human
leukaemia
led to the identification of the 11q23 gene called MLL (or HTRX, HRX, TRX1, ALL-1).
MLL can become fused with one of a remarkable panoply of genes from other chromosome locations in individual
leukaemias
, leading to either
acute
myeloid
or
lymphoid
tumours (hence the name MLL for
mixed lineage
leukaemia
).
The unusual
finding
that a single protein could be involved in both
myeloid and lymphoid
malignancies and that the truncated protein could do so as a fusion with very disparate partners has prompted studies to define the molecular role of MLL-fusions in leukaemogenesis and to the development of MLL-controlled mouse models of leukaemogenesis.
[MeSH-major]
Cell
Transformation, Neoplastic / metabolism.
Cell
Transformation, Neoplastic / pathology.
Leukemia
/ metabolism.
Leukemia
/ pathology.
Myeloid
-
Lymphoid
Leukemia
Protein / metabolism
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(PMID = 15826832.001).
[ISSN]
1044-579X
[Journal-full-title]
Seminars in cancer biology
[ISO-abbreviation]
Semin. Cancer Biol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
149025-06-9 / Myeloid-Lymphoid Leukemia Protein
[Number-of-references]
123
25.
Gujral S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Jain H, Pais A, Amre Kadam PS, Banavali SD, Arora B, Kumar P, Hari Menon VG, Kurkure PA, Parikh PM, Mahadik S, Chogule AB, Shinde SC, Nair CN:
Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India.
Cytometry B Clin Cytom
; 2009 May;76(3):199-205
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[Title]
Immunophenotypic profile of
acute leukemia
: critical analysis and insights gained at a tertiary care center in India.
BACKGROUND: To analyze the spectrum of various types and subtypes of
acute leukemia
.
METHODS: Two thousand five hundred and eleven consecutive new referral cases of
acute leukemia
(AL) were evaluated based on WHO classification.
RESULTS: It included 1,471 cases (58%) of
acute
lymphoblastic
leukemia
(ALL), 964 cases (38%) of
acute
myeloid
leukemia
(AML), 45 cases (1.8%) of chronic myelogenous
leukemia
in blast crisis (CMLBC), 37 cases (1.5%) of
biphenotypic
acute leukemia
(BAL), 1 case of Triphenotypic AL, and 2 cases of
acute
undifferentiated
leukemia
(AUL).
Common subtypes of ALL were B-
cell
ALL (76%), which comprised of intermediate stage/CALLA positive (73%), early precursor/proBALL (3%).
T-
cell
ALL constituted 24% (351 cases) of ALL.
CMLBC was commonly of
myeloid
blast crisis subtype (40 cases).
CONCLUSION: B-
cell
ALL was the commonest subtype in children and AML in adults.
CD13 was most sensitive and CD117 most specific for determining
myeloid
lineage
.
A minimal primary panel of nine antibodies consisting of three
myeloid
markers (CD13, CD33, and CD117), B-
cell lymphoid
marker (CD19), T-
cell
marker (CD7), with CD45, CD10, CD34, and HLADR could assign
lineage
to 92% of AL.
Cytogenetics findings lead to a change in the diagnostic subtype of
myeloid
malignancy in 38 (1.5%) cases.
[MeSH-major]
Immunophenotyping.
Leukemia
/ immunology.
Leukemia
/ pathology
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Histocytochemistry. Humans. In Situ Hybridization. India. Infant. Infant, Newborn. Male. Middle Aged. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Young Adult
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[Copyright]
(c) 2008 Clinical Cytometry Society.
(PMID = 18803279.001).
[ISSN]
1552-4957
[Journal-full-title]
Cytometry. Part B, Clinical cytometry
[ISO-abbreviation]
Cytometry B Clin Cytom
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
26.
Liu HX, Cao XY, Tong CR, Wu T, Wang T, Fan QZ, Wu P, Zhang X, Cai P, Zhu P:
[Major molecular response to imatinib in a patient with acute mixed lineage leukemia expressing a novel BCR/ABL transcript].
Zhonghua Yi Xue Za Zhi
; 2009 Feb 3;89(4):220-3
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[Title]
[Major molecular response to imatinib in a patient with
acute mixed lineage leukemia
expressing a novel BCR/ABL transcript].
OBJECTIVE: To identify the novel BCR/ABL transcript in a patient with
acute mixed lineage leukemia
(AMLL), and to evaluate the imatinib treatment response by quantitatively monitoring the aberrant BCR/ABL.
Morphological analysis of the bone marrow showed the
myeloid
blast cells accounted for 66%, and immunophenotyping analysis showed 2 groups of aberrant blast cells:
myeloid and
B
lineage
.
Chemical therapy and bone marrow transplantation failed to control the
disease
,
and a
novel BCR/ABL transcript (GenBank: EF423615) was found by using several detection protocols.
[MeSH-major]
Fusion Proteins, bcr-abl / genetics.
Leukemia
,
Biphenotypic
,
Acute
/ drug therapy.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use
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(PMID = 19552835.001).
[ISSN]
0376-2491
[Journal-full-title]
Zhonghua yi xue za zhi
[ISO-abbreviation]
Zhonghua Yi Xue Za Zhi
[Language]
chi
[Publication-type]
Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
27.
Tan S, Wang G, Peng M, Zhang X, Shen G, Jiang J, Chen F:
Detection of myeloperoxidase activity in primary leukemic cells by an enhanced chemiluminescent assay for differentiation between acute lymphoblastic and non-lymphoblastic leukemia.
Clin Chim Acta
; 2009 May;403(1-2):216-8
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[Title]
Detection of myeloperoxidase activity in primary leukemic cells by an enhanced chemiluminescent assay for differentiation between
acute
lymphoblastic and
non-
lymphoblastic
leukemia
.
BACKGROUND: Myeloperoxidase (MPO) plays a crucial role in the differentiation of
acute
lymphoblastic
leukemia
(ALL) and
acute
non-
lymphoblastic
leukemia
(ANLL).
In this report, we proposed the application of the enhanced chemiluminescent (ECL) technique to the determination of MPO activity in blasts of
acute leukemia
(AL).
METHODS: Bone-marrow samples were obtained from 23 patients with AL (ALL, 5 cases; ANLL, 13 cases; AUL, 1 cases;
mixed
-
lineage
AL, 4 cases).
In addition, this technique was able to demonstrate MPO activity in 4
mixed
-
lineage
AL cases which did not stain for MPO in cytochemistry preparations.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ enzymology.
Leukemia
,
Myeloid
,
Acute
/ pathology. Luminescent Measurements / methods. Peroxidase / metabolism. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / enzymology. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / pathology
[MeSH-minor]
Adolescent. Adult. Aged. Child.
Diagnosis
, Differential. Female. HL-60 Cells. Humans. Infant. Male. Middle Aged
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(PMID = 19298796.001).
[ISSN]
1873-3492
[Journal-full-title]
Clinica chimica acta; international journal of clinical chemistry
[ISO-abbreviation]
Clin. Chim. Acta
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
[Chemical-registry-number]
EC 1.11.1.7 / Peroxidase
28.
Milne TA, Dou Y, Martin ME, Brock HW, Roeder RG, Hess JL:
MLL associates specifically with a subset of transcriptionally active target genes.
Proc Natl Acad Sci U S A
; 2005 Oct 11;102(41):14765-70
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MLL (
mixed
-
lineage leukemia
) is a histone H3 Lys-4 specific methyltransferase that is a positive regulator of Hox expression.
MLL rearrangements and amplification are common in
acute
lymphoid and myeloid leukemias
and myelodysplastic disorders and are associated with abnormal up-regulation of Hox gene expression.
[MeSH-major]
Gene Expression Regulation. Genes, Homeobox / genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / metabolism. RNA Polymerase II / metabolism. Transcription, Genetic / genetics
[MeSH-minor]
Animals.
Cell
Line. Chromatin Immunoprecipitation. Glutathione Transferase. Mice. Mice, Inbred C57BL. Polymerase Chain Reaction
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Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14481-2
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]
(PMID = 16199523.001).
[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.5.1.18 / Glutathione Transferase; EC 2.7.7.- / RNA Polymerase II
[Other-IDs]
NLM/ PMC1253553
29.
Burmeister T, Marschalek R, Schneider B, Meyer C, Gökbuget N, Schwartz S, Hoelzer D, Thiel E:
Monitoring minimal residual disease by quantification of genomic chromosomal breakpoint sequences in acute leukemias with MLL aberrations.
Leukemia
; 2006 Mar;20(3):451-7
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[Title]
Monitoring minimal residual
disease
by quantification of genomic chromosomal breakpoint sequences in
acute
leukemias
with MLL aberrations.
An estimated 10% of
acute
leukemias
carry
mixed
-
lineage leukemia
(MLL) fusion genes.
These
leukemias
are commonly regarded as high-risk cases and are treated accordingly with intensified therapy regimens, including hematopoietic stem
cell
transplantation.
Monitoring minimal residual
disease
(MRD) is undoubtedly of great value in clinical decision making, also in the pre- and post-transplant setting.
Here, we describe a novel method for detecting MRD in
leukemias
with MLL aberrations.
[MeSH-major]
Chromosome Fragile Sites.
Leukemia
/ genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Neoplasm, Residual / genetics
[MeSH-minor]
Acute
Disease
. Base Sequence. DNA Primers. DNA Probes. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping
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(PMID = 16424875.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA Primers; 0 / DNA Probes; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
30.
Shand JC, Jansson J, Hsu YC, Campbell A, Mullen CA:
Differential gene expression in acute lymphoblastic leukemia cells surviving allogeneic transplant.
Cancer Immunol Immunother
; 2010 Nov;59(11):1633-44
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[Title]
Differential gene expression in
acute
lymphoblastic
leukemia
cells surviving allogeneic transplant.
The effectiveness of allogeneic graft-versus-
leukemia
(GVL) activity in control of
acute
lymphoblastic
leukemia
is generally regarded as poor.
One possible factor is dynamic adaptation of the
leukemia
cell
to the allogeneic environment.
This work tested the hypothesis that the pattern of gene expression in
acute
lymphoblastic
leukemia
cells in an allogeneic environment would differ from that in a non-allogeneic environment.
Expression microarray studies were performed in murine B
lineage acute
lymphoblastic
leukemia
cells recovered from mice that had undergone allogeneic MHC-matched but minor histocompatibility antigen mismatched transplants.
Several genes with known immune activities potentially relevant to
leukemia
survival (Ly6a/Sca-1, TRAIL and H2-T23) were examined in independent validation experiments.
Increased expression in vivo in allogeneic hosts was observed, and could be mimicked in vitro with soluble supernatants of
mixed
lymphocyte reactions or interferon-gamma.
The changes in gene expression were reversible when the
leukemia
cells were removed from the allogeneic environment.
These findings suggest that
acute
lymphoblastic
leukemia
cells respond to cytokines present after allogeneic transplantation and that these changes may reduce the effectiveness of GVL activity.
[MeSH-major]
Biomarkers, Tumor / genetics. Bone Marrow Transplantation. Graft Survival / physiology. Graft vs
Leukemia
Effect / genetics. Precursor B-
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics
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(PMID = 20602231.001).
[ISSN]
1432-0851
[Journal-full-title]
Cancer immunology, immunotherapy : CII
[ISO-abbreviation]
Cancer Immunol. Immunother.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 1R01CA10628
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Minor Histocompatibility Antigens; 0 / RNA, Messenger; 82115-62-6 / Interferon-gamma
31.
Zhang J, Mi YC, Wang Y, Lin D, Li W, Sun XM, Zhou K, Bian SG, Wang JX:
[Study on the clinical characteristics of adult biphenotypic acute leukaemia].
Zhonghua Xue Ye Xue Za Zhi
; 2009 Jan;30(1):18-21
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[Title]
[Study on the clinical characteristics of adult
biphenotypic
acute
leukaemia
].
OBJECTIVE: To analyze the clinical and biological characteristics and prognosis of adult
biphenotypic
acute
leukaemia
(BAL).
The chemotherapy regimens were accordingly for
acute
lymphoblastic leukaemia
(ALL),
acute
myeloid leukaemia
(AML) or for both ALL and AML.
(1) The incidence of BAL in
acute
leukaemias
was 6.7%, with a male predominance and 52.3% of BAL patients had WBC > or = 30 x 10(9)/L and 16.9% WBC > or = 100 x 10(9)/L. (2) Percentages of coexpression of
myeloid and B lymphoid
antigens were 81.5%, of
myeloid and T lymphoid
antigens 10.8%, of
myeloid
, B-
and T lymphoid
antigens 4.6%, and of
B and T lymphoid
antigens 3.1%. (3) Normal and abnormal karyotypes accounted for 41.5% and 58.5%, respectively in 53 BAL patients with karyotype analysis.
(1) High white blood
cell
count and coexpression of
myeloid
/
B lymphoid
antigens are common in BAL. (2) Abnormal karyotypes and Ph (+) or bcr-abl( +) often happen. (3) The treatment outcome of BAL is poor.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
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(PMID = 19563029.001).
[ISSN]
0253-2727
[Journal-full-title]
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
[ISO-abbreviation]
Zhonghua Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
32.
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
[MeSH-minor]
Child. Hematopoietic Stem Cells. Histone-Lysine N-Methyltransferase. Humans. Infant. Oncogene Proteins, Fusion.
Phenotype
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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
33.
Kakihana K, Ohashi K, Sakai F, Kamata N, Hosomi Y, Nishiwaki M, Yokoyama R, Kobayashi T, Yamashita T, Akiyama H, Sakamaki H:
Leukemic infiltration of the lung following allogeneic hematopoietic stem cell transplantation.
Int J Hematol
; 2009 Jan;89(1):118-22
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[Title]
Leukemic infiltration of the lung following allogeneic hematopoietic stem
cell
transplantation.
Pulmonary leukemic infiltration (PLI) is more common than generally recognized, but accurate antemortem
diagnosis
with pathological proof is rarely achieved.
We describe herein the clinical courses of two patients with PLI following hematopoietic stem
cell
transplantation (HSCT).
One case is a male patient with
acute
biphenotypic
leukemia
, and the other is a female patient with myelodysplastic syndrome.
Moreover, the former case presented PLI as the initial manifestation of relapsed
leukemia
and the latter was accompanied with the fungal pneumonia.
High-resolution computed tomography (HRCT) of the chest at onset of PLI showed diffuse small nodular lesions along peribronchovascular bundle,
and diagnosis
of leukemic infiltration was made based on pathological findings obtained from transbronchial lung biopsy.
Thus, radiological and pathological corroborating assessment was important to reach the correct
diagnosis
.
[MeSH-major]
Hematopoietic Stem
Cell
Transplantation / adverse effects. Leukemic Infiltration /
diagnosis
. Lung Neoplasms / etiology
[MeSH-minor]
Adult. Female. Humans.
Leukemia
/ pathology. Lung / pathology. Male. Middle Aged. Myelodysplastic Syndromes /
diagnosis
. Myelodysplastic Syndromes / etiology. Opportunistic Infections. Transplantation, Homologous
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International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
34.
Xu XQ, Wang JM, Lü SQ, Chen L, Yang JM, Zhang WP, Song XM, Hou J, Ni X, Qiu HY:
Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population.
Haematologica
; 2009 Jul;94(7):919-27
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[Title]
Clinical and biological characteristics of adult
biphenotypic
acute leukemia
in comparison with that of
acute
myeloid
leukemia
and
acute
lymphoblastic
leukemia
: a case series of a Chinese population.
BACKGROUND:
Biphenotypic
acute leukemia
is a rare
disorder
that is difficult to diagnose.
It displays features of both
myeloid and lymphoid
lineage
.
There is still a lack of studies in
biphenotypic
acute leukemia
in a Chinese population.
We present here a comprehensive investigation of the clinical and biological characteristics, and outcome of
biphenotypic
acute leukemia
in our hospital in over a seven year period.
DESIGN AND METHODS: We retrospectively analyzed 452 adult
acute leukemia
patients diagnosed according to French-American-British (FAB) classification
and biphenotypic
acute leukemia
diagnosed according to European Group for the Immunological Characterization of
Leukemias
(EGIL) classification, respectively.
Biological characteristics, response to treatment, and outcome were examined in
biphenotypic
acute leukemia
patients and compared with that in
acute
myeloid
leukemia
and
acute
lymphoblastic
leukemia
patients with complete follow-up profiles diagnosed in the same period.
RESULTS: Of 452
acute leukemia
patients, 21 cases (4.6%) were diagnosed as
biphenotypic
acute leukemia
.
Among them, 14 (66.7%) were
B lymphoid and myeloid
, 5 (23.8%) were
T lymphoid and myeloid
, one (4.8%) was T/
B lymphoid
and one (4.8%) was trilineage differentiation.
When compared with
acute
myeloid
leukemia
and
acute
lymphoblastic
leukemia
, patients with
biphenotypic
acute leukemia
showed significantly higher incidence of CD34 antigen expression, unfavorable karyotypes, and extramedullary infiltration (p<0.05).
In this cohort of patients with
biphenotypic
acute leukemia
, t(9;22) was the most common
abnormality
in chromosome structure.
The median
disease
-free survival and overall survival in
biphenotypic
acute leukemia
patients was five months and ten months, respectively, significantly shorter than those in
acute
myeloid
leukemia
and
acute
lymphoblastic
leukemia
patients (p<0.05).
CONCLUSIONS: The prognosis of
biphenotypic
acute leukemia
patients is poor when compared with
de
novo
acute
myeloid
leukemia
or
acute
lymphoblastic
leukemia
.
Biphenotypic
acute leukemia
patients showed a much higher incidence of CD34 antigen expression, complex abnormal karyotype, extramedullary infiltration, relapse, and resistance to therapy after relapse.
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/
diagnosis
.
Leukemia
,
Myeloid
,
Acute
/
diagnosis
. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma /
diagnosis
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.
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.
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.
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.
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[Cites]
Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7521-6
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10861016.001
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Zhonghua Xue Ye Xue Za Zhi. 2000 Jul;21(7):352-4
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Nature. 2008 Apr 10;452(7188):768-72
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18401412.001
]
[Cites]
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Blood. 2002 Sep 15;100(6):1965-71
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[CommentIn]
Haematologica. 2009 Jul;94(7):891-3
[
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]
(PMID = 19454497.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antigens, CD34
[Other-IDs]
NLM/ PMC2704302
35.
Carretta A, Ciriaco P, Melloni G, Bandiera A, Libretti L, Puglisi A, Giovanardi M, Zannini P:
Surgical treatment of multiple primary adenocarcinomas of the lung.
Thorac Cardiovasc Surg
; 2009 Feb;57(1):30-4
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The aim of this study was to assess the results of surgical treatment of multiple primary adenocarcinomas of the lung (
MPAL
) analyzing the radiological and histological features.
METHODS: From 1988 to 2005, 26 patients underwent surgical treatment for
MPAL
at our department, for a total of 52 tumors.
RESULTS: Thirty-seven tumors were classified as solid, two as ground-glass opacities (GGO) and 13 as
mixed
solid/GGO tumors on the basis of CT scan evaluation.
CONCLUSIONS: Surgical treatment of
MPAL
is associated with favorable results.
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(PMID = 19169994.001).
[ISSN]
0171-6425
[Journal-full-title]
The Thoracic and cardiovascular surgeon
[ISO-abbreviation]
Thorac Cardiovasc Surg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
36.
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
37.
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
).
MPAL
with t(9;22) and MLL rearrangement have been separated.
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
38.
Liu Z, Liu XL, Du QF, Xu N, Zhong M, Song LL, Yi ZS, Liu QF, Meng FY, Zhou SY:
[Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL].
Nan Fang Yi Ke Da Xue Xue Bao
; 2009 Mar;29(3):512-5
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[Title]
[Clinical characteristics and outcomes of 59 patients with
acute
lymphoblastic
leukemia
positive for BCR/ABL].
OBJECTIVE: To study the clinical characteristics and outcomes of BCR/ABL-positive
acute
lymphoblastic
leukemia
(BCR/ABL360888725-ALL) and screen the prognostic factors for BCR/ABL360888725-ALL.
METHODS: From January 2001 to May 2008, 59 patients (median age of 32 years ranging from 3 to 69 years) with the
diagnosis
of BCR/ABL360888725-ALL by fluorescence in situ hybridization received induction chemotherapy with VDLP-/+Ara-C regimen.
The patients who failed to respond to the chemotherapy received subsequent consolidation chemotherapy with imatinib (400-800 mg/day) (17 cases) or allogeneic hematopoietic stem
cell
transplantation (allo-HSCT) (16 cases).
In patients with peripheral white blood
cell
(WBC) count <30=10(9)/L, 30-99.9(9)/L and > or =100(9)/L, the CR rates were 75.0% (18/24), 56.3% (9/15) and 26.3% (5/19) (P=0.006), and the overall survival probability of 2 years ( OSs of 2-yrs) was 24.7%, 22.5% and 21.1%, respectively (P=0.180).
According to the FAB classification, 56 cases were divided into L1, L2
and biphenotypic
acute leukemia
(BAL) subgroups, and their CR rates were 66.7% (6/9), 63.2% (24/38) and 22.2% (2/9) (P=0.029), with OSs of 2-yrs of 22.2%, 27.0% and 22.0%, respectively (P=0.623).
In terms of immunophenotype grouping by EGIL, the patients with ALL,
myeloid
antigen-positive ALL and BAL had CR rates of 61.1% (11/18), 60.6% (20/33) and 12.5% (1/8) (P=0.039), and the OSs of 2-yrs of 22.7%, 21.0% and 18.8%, respectively (P=0.643).
In 55 patients with known karyotype, the CR rates were 71.4%(5/7), 70.8% (17/24) and 37.5% (9/24) in normal, sole t(9;22)
abnormality
, t(9;22) with additional abnormalities groups (P=0.046), with the OSs of 2-yrs of 42.9%, 34.0% and 7.3%, respectively (P=0.000).
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Genes, abl / genetics. Hematopoietic Stem
Cell
Transplantation. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / therapy
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.
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(PMID = 19304540.001).
[ISSN]
1673-4254
[Journal-full-title]
Nan fang yi ke da xue xue bao = Journal of Southern Medical University
[ISO-abbreviation]
Nan Fang Yi Ke Da Xue Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
39.
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
[MeSH-minor]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Banding. Fatal Outcome. Humans. Karyotyping. Male. Middle Aged.
Phenotype
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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
40.
Xu B, Li L, Tang JH, Zhou SY:
Detection of FLT3 gene and FLT3/ITD mutation by polymerase chain reaction-single-strand conformation polymorphism in patients with acute lymphoblastic leukemia.
Di Yi Jun Yi Da Xue Xue Bao
; 2005 Oct;25(10):1207-10
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[Title]
Detection of FLT3 gene and FLT3/ITD mutation by polymerase chain reaction-single-strand conformation polymorphism in patients with
acute
lymphoblastic
leukemia
.
OBJECTIVE: To analyze Fms-like tyrosine kinase 3 (FLT3) gene and FLT3 internal tandem duplication (ITD) mutation in
acute
lymphoblastic
leukemia
(ALL) patients of different immunological subtypes.
The positivity rate of FLT3 gene in pre-pre B-
lineage
ALL, pre-B-ALL, B-
lineage
ALL
and T
-
lineage
ALL cases were 93.3% (14/15), 77.8% (14/18), 41.7% (5/12) and 28.6% (4/14), respectively.
Two cases (3.2%) were found to have FLT3/ITD mutation, which were also positive for
myeloid
antigen expression and diagnosed as
acute mixed
-
lineage leukemia
, showing leukocytosis and high percentage of bone marrow blast cells with poor prognosis.
CONCLUSIONS: FLT3 gene can be detected in both B-
and T
-
lineage
ALL patients, but more frequently in the former.
In B-
lineage
ALL patients, FLT3 gene is more frequent in cases with undifferentiated than those with differentiated blast cells.
FLT3/ITD is rarely detected in ALL patients and FLT3/ITD mutation detection might be helpful to identify the genotypes and evaluate the prognosis of
acute leukemia
.
[MeSH-major]
Mutation. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Receptor Protein-Tyrosine Kinases / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
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(PMID = 16234090.001).
[ISSN]
1000-2588
[Journal-full-title]
Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA
[ISO-abbreviation]
Di Yi Jun Yi Da Xue Xue Bao
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
41.
Schwartz CM, Cheng A, Mughal MR, Mattson MP, Yao PJ:
Clathrin assembly proteins AP180 and CALM in the embryonic rat brain.
J Comp Neurol
; 2010 Sep 15;518(18):3803-18
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In this study, we focus on two closely related clathrin assembly proteins, AP180 and CALM (clathrin assembly
lymphoid myeloid
leukemia
protein), in the developing embryonic rat brain.
[MeSH-minor]
Animals.
Cell
Line. Clathrin / metabolism. Clathrin-Coated Vesicles / metabolism. Female. Neurons / cytology. Neurons / metabolism. Pregnancy. Rats. Stem Cells / cytology. Stem Cells / metabolism
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(PMID = 20653035.001).
[ISSN]
1096-9861
[Journal-full-title]
The Journal of comparative neurology
[ISO-abbreviation]
J. Comp. Neurol.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z99 AG999999
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Clathrin; 0 / Monomeric Clathrin Assembly Proteins; 0 / Picalm protein, rat; 0 / clathrin assembly protein AP180
[Other-IDs]
NLM/ NIHMS215726; NLM/ PMC2909614
42.
Kaltenbach S, Soler G, Barin C, Gervais C, Bernard OA, Penard-Lacronique V, Romana SP:
NUP98-MLL fusion in human acute myeloblastic leukemia.
Blood
; 2010 Sep 30;116(13):2332-5
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[Title]
NUP98-MLL fusion in human
acute
myeloblastic
leukemia
.
H3K4 (histone H3 lysine 4) methylation by the SET domain of the trithorax-group protein MLL (
mixed
-
lineage leukemia
) is important for the control of homeobox (HOX) gene expression during development.
MLL fusion proteins associated with human
leukemia
contain the menin interaction peptide and frequently recruit H3K79 (histone H3 lysine 79) methylation activity.
We have characterized a novel recurrent chromosomal aberration, inv(11)(p15q23), as an isolated chromosomal
abnormality
in 2 patients with
acute
myeloid
leukemia
.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics
[MeSH-minor]
Adult. Aged. Base Sequence.
Cell
Transformation, Neoplastic / genetics. Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DNA Primers / genetics. DNA, Neoplasm / genetics. Female. Gene Expression. Genes, Homeobox. Histone-Lysine N-Methyltransferase. Histones / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Oncogene Fusion. Proto-Oncogene Proteins / metabolism
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(PMID = 20558618.001).
[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 / DNA Primers; 0 / DNA, Neoplasm; 0 / Histones; 0 / Homeodomain Proteins; 0 / MEN1 protein, human; 0 / MLL protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 157907-48-7 / HoxA protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
43.
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
44.
Cóser VM, Meyer C, Basegio R, Menezes J, Marschalek R, Pombo-de-Oliveira MS:
Nebulette is the second member of the nebulin family fused to the MLL gene in infant leukemia.
Cancer Genet Cytogenet
; 2010 Apr 15;198(2):151-4
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[Title]
Nebulette is the second member of the nebulin family fused to the MLL gene in infant
leukemia
.
Genetic aberrations involving the
mixed lineage leukemia
(MLL) gene are frequently diagnosed in infant
acute
lymphoblastic and
acute
myeloid
leukemia
.
More than 60 fusion partner genes have been described at the molecular level, 31 of which have been characterized solely in infant
leukemia
cases.
Here we describe a new MLL fusion partner gene, NEBL, which was identified in a case of
acute
myeloid
leukemia
in an infant.
[MeSH-major]
Carrier Proteins / genetics. Cytoskeletal Proteins / genetics.
Leukemia
/ genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Oncogene Proteins, Fusion / genetics
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[Copyright]
Copyright 2010 Elsevier Inc. All rights reserved.
(PMID = 20362230.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Carrier Proteins; 0 / Cytoskeletal Proteins; 0 / LIM Domain Proteins; 0 / MLL protein, human; 0 / Muscle Proteins; 0 / NEBL protein, human; 0 / Oncogene Proteins, Fusion; 0 / nebulin; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
45.
Skiljević D, Colović M, Bogatić D, Popadić S, Medenica L:
Granulomatous rosacea-like leukemid in a patient with acute myeloid leukemia.
Vojnosanit Pregl
; 2008 Jul;65(7):565-8
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[Title]
Granulomatous rosacea-like leukemid in a patient with
acute
myeloid
leukemia
.
INTRODUCTION: Skin findings in
leukemias
may be divided into specific lesions (
leukemia
cutis) and non-specific lesions (leukemids) which may be found in up to 80% of all patients with
leukemias
.
The leukemids vary clinically and they are usually a manifestation of bone marrow or immunologic impairment, but also Sweet syndrome, pyoderma gangrenosum, erythroderma, maculopapular exanthema, prurigo-like papules, generalized pigmentation, follicular mucinosis, generalized pruritus may be found during the course of
leukemia
.
Histopathologic findings of involved skin showed diffuse
mixed
inflammatory
cell
infiltrate with perifollicular accentuation and focal granulomatous inflammation in the papillary and upper reticular dermis.
Extensive checkup revealed the presence of
acute
myeloid
leukemia
French-American-British (FAB) classification subtype M2, with signs of three-
lineage
dysplasia.
The patient was treated by L6 protocol which led to complete remission, both in bone marrow and skin, but after seven months he had relapse of
leukemia
with the fatal outcome.
[MeSH-major]
Leukemia
,
Myeloid
,
Acute
/ complications. Rosacea / complications
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(PMID = 18700468.001).
[ISSN]
0042-8450
[Journal-full-title]
Vojnosanitetski pregled
[ISO-abbreviation]
Vojnosanit Pregl
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Serbia
46.
Shimada A, Taki T, Tabuchi K, Taketani T, Hanada R, Tawa A, Tsuchida M, Horibe K, Tsukimoto I, Hayashi Y:
Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric acute myeloid leukemia: a study of the Japanese childhood AML Cooperative Study Group.
Pediatr Blood Cancer
; 2008 Feb;50(2):264-9
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[Title]
Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric
acute
myeloid
leukemia
: a study of the Japanese childhood AML Cooperative Study Group.
BACKGROUND:
Mixed
-
lineage leukemia
(MLL)-partial tandem duplication (PTD) is associated with poor prognosis in adult
acute
myeloid
leukemia
(AML), but its relationship to pediatric AML is unknown.
The differences between patients with and without MLL-PTD were significant for 3-year overall survival (OS) (56.3% vs. 83.2%, P = 0.018),
disease
-free survival (DFS) (41.7% vs. 69.6%, P = 0.010), and relapse rate (RR) (54.3% vs. 27.6%, P = 0.0085) of 135 AML patients excluding the FAB-M3 and DS patients.
[MeSH-major]
Gene Duplication.
Leukemia
,
Myeloid
/ genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. fms-Like Tyrosine Kinase 3 / genetics
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
(PMID = 17763464.001).
[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
[Chemical-registry-number]
0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
47.
Nakada S, Katsuki Y, Imoto I, Yokoyama T, Nagasawa M, Inazawa J, Mizutani S:
Early G2/M checkpoint failure as a molecular mechanism underlying etoposide-induced chromosomal aberrations.
J Clin Invest
; 2006 Jan;116(1):80-9
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Topoisomerase II (Topo II) inhibitors are
cell
cycle-specific DNA-damaging agents and often correlate with secondary
leukemia
with chromosomal translocations involving the
mixed
-
lineage leukemia
/
myeloid lymphoid
leukemia
(MLL) gene on chromosome 11 band q23 (11q23).
[MeSH-major]
Cell
Cycle / physiology. Chromosome Aberrations / chemically induced. Etoposide / pharmacology.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Translocation, Genetic
[MeSH-minor]
Bone Neoplasms.
Cell
Division.
Cell
Line.
Cell
Line, Tumor. Chromosome Banding. Chromosomes, Human, Pair 11. Cloning, Molecular. G2 Phase. Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Histone-Lysine N-Methyltransferase. Humans. Osteosarcoma
Coriell Cell Repositories.
culture/stock collections - Coriell Cell Repositories
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
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[ErratumIn]
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(PMID = 16357944.001).
[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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
[Other-IDs]
NLM/ PMC1312016
48.
Wei J, Wunderlich M, Fox C, Alvarez S, Cigudosa JC, Wilhelm JS, Zheng Y, Cancelas JA, Gu Y, Jansen M, Dimartino JF, Mulloy JC:
Microenvironment determines lineage fate in a human model of MLL-AF9 leukemia.
Cancer Cell
; 2008 Jun;13(6):483-95
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[Title]
Microenvironment determines
lineage
fate in a human model of MLL-AF9
leukemia
.
Faithful modeling of
mixed
-
lineage leukemia
in murine cells has been difficult to achieve.
We show that expression of MLL-AF9 in human CD34+ cells induces
acute
myeloid
,
lymphoid
, or
mixed
-
lineage leukemia
in immunodeficient mice.
Some
leukemia
stem cells (LSC) were multipotent and could be
lineage
directed by altering either the growth factors or the recipient strain of mouse, highlighting the importance of microenvironmental cues.
Other LSC were strictly
lineage
committed, demonstrating the heterogeneity of the stem
cell
compartment in MLL
disease
.
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.
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Cancer Cell. 2008 Jun;13(6):465-7
[
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]
(PMID = 18538732.001).
[ISSN]
1878-3686
[Journal-full-title]
Cancer cell
[ISO-abbreviation]
Cancer Cell
[Language]
ENG
[Databank-accession-numbers]
GEO/ GSE7011
[Grant]
United States / NCI NIH HHS / CA / CA090370-06; 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 / R01 CA118319-01; United States / NCI NIH HHS / CA / CA118319-01; United States / NCI NIH HHS / CA / K01 CA090370-06; 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 / Antigens, CD34; 0 / Intercellular Signaling Peptides and Proteins; 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/ NIHMS54902; NLM/ PMC2486365
49.
Kim KE, Kim SH, Han JY:
[Acute Monocytic Leukemia with t(11;17)(q23;q21) Involving a Rearrangement of Mixed Lineage Leukemia Gene.].
Korean J Lab Med
; 2006 Oct;26(5):329-33
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[Title]
[
Acute
Monocytic
Leukemia
with t(11;17)(q23;q21) Involving a Rearrangement of
Mixed Lineage Leukemia
Gene.].
A case of
acute
monocytic
leukemia
(AMoL) by French-American-British (FAB) classification in a 63-year-old male showed the abnormal karyotype 46,XY,t(11;17)(q23;q21), previously reported as a variant translocation in
acute
promyelocytic
leukemia
(APL).
Fluorescence in situ hybridization (FISH) analysis identified a
mixed lineage leukemia
(MLL) gene rearrangement, but not visible disruptions of promyelocytic
leukemia
(PML) or retinoic acid receptor alpha (RARA) genes.
Now, a few cases of AMoL with a similar translocation have been reported in the literature, and these cases emphasize the importance of cytogenetic and FISH studies in addition to morphology, cytochemistry, and immunophenotype in classifying
acute
myeloid
leukemia
(AML).
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(PMID = 18156746.001).
[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)
50.
Rosenbluth MJ, Lam WA, Fletcher DA:
Force microscopy of nonadherent cells: a comparison of leukemia cell deformability.
Biophys J
; 2006 Apr 15;90(8):2994-3003
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[Title]
Force microscopy of nonadherent cells: a comparison of
leukemia
cell
deformability.
We apply this technique to compare the deformability of human
myeloid and lymphoid
leukemia
cells and neutrophils at low deformation rates, and we find that the cells are well described by an elastic model based on Hertzian mechanics.
Myeloid
(HL60) cells were measured to be a factor of 18 times stiffer than
lymphoid
(Jurkat) cells and six times stiffer than human neutrophils on average (E(infinity) = 855 +/- 670 Pa for HL60 cells, E(infinity) = 48 +/- 35 Pa for Jurkat cells, E(infinity) = 156 +/- 87 for neutrophils, mean +/- SD).
This work demonstrates a simple method for extending AFM mechanical property measurements to nonadherent cells and characterizes properties of human
leukemia
cells that may contribute to leukostasis, a complication associated with
acute leukemia
.
[MeSH-major]
Leukemia
,
Myeloid
/ pathology. Neutrophils / pathology. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / pathology
[MeSH-minor]
Acute
Disease
.
Cell
Adhesion.
Cell
Line, Tumor. Cells, Cultured. Elasticity. Humans. Micromanipulation. Microscopy, Atomic Force. Models, Biological. Viscosity
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[ISSN]
0006-3495
[Journal-full-title]
Biophysical journal
[ISO-abbreviation]
Biophys. J.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Other-IDs]
NLM/ PMC1414579
51.
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
[MeSH-minor]
Adolescent. Humans. Male.
Phenotype
. Prognosis
Genetic Alliance.
consumer health - Acute Biphenotypic Leukemia
.
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
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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
52.
Hu XX, Gong SL, Song XM, Chen L, Qiu HY, Gao L, Wang JM:
[Report of a case of hybrid acute leukemia with t (12; 22) and literature review].
Zhonghua Xue Ye Xue Za Zhi
; 2006 May;27(5):331-4
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[Title]
[Report of a case of
hybrid
acute leukemia
with t (12; 22) and literature review].
OBJECTIVE: To report
a hybrid
acute leukemia
(HAL) patient with t (12;.
Leukemia
surface markers were detected by anti-biotin-biotin complex and monoclonal antibodies.
RESULTS: The clinical and hematological findings were compatible with the
diagnosis
of HAL.
Lymphoid and myeloid
markers were positive on the
leukemia
cells.
22) translocation is a rare chromosome
abnormality
in
leukemia
.
This translocation as a cytogenetic marker for poor-prognosis in
leukemia
needs to be further studied.
[MeSH-major]
Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 22 / genetics.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Translocation, Genetic
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(PMID = 16875585.001).
[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]
Case Reports; English Abstract; Journal Article; Review
[Publication-country]
China
[Number-of-references]
20
53.
Jeha S, Kantarjian H:
Clofarabine for the treatment of acute lymphoblastic leukemia.
Expert Rev Anticancer Ther
; 2007 Feb;7(2):113-8
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[Title]
Clofarabine for the treatment of
acute
lymphoblastic
leukemia
.
A marked improvement in the outcome of patients with
acute
lymphoblastic
leukemia
has been achieved with chemotherapeutic agents developed between the 1950s and 1970s.
As the limits of optimizing the use of old drugs are reached, most adults with
acute
lymphoblastic
leukemia
still succumb to their
disease and
leukemia
remains the leading cause of nonaccidental death in children.
Clofarabine, a next-generation deoxyadenosine analog, has demonstrated significant activity in children and adults with refractory
lymphoid and myeloid
leukemia
in early clinical trials and was granted approval for use in children with
acute
lymphoblastic
leukemia
in second or higher relapse.
[MeSH-major]
Adenine Nucleotides / therapeutic use. Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy
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(PMID = 17288522.001).
[ISSN]
1744-8328
[Journal-full-title]
Expert review of anticancer therapy
[ISO-abbreviation]
Expert Rev Anticancer Ther
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
[Number-of-references]
36
54.
Kinjo K, Sandoval S, Sakamoto KM, Shankar DB:
The role of CREB as a proto-oncogene in hematopoiesis.
Cell Cycle
; 2005 Sep;4(9):1134-5
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Cyclic-AMP response element binding protein (CREB) is a transcription factor that functions in glucose homeostasis, growth-factor- dependent
cell
survival, proliferation and memory.
Data from our laboratory shows that a majority of patients with
acute
lymphoid and myeloid
leukemia
overexpress CREB in the bone marrow.
CREB overexpression is associated with poor initial outcome of clinical
disease
in AML patients.
To study its role in hematopoiesis, we overexpressed CREB in
leukemia
cell
lines and in mice.
CREB overexpression resulted in increased survival and proliferation of
myeloid
cells and blast-transformation of bone marrow progenitor cells from transgenic mice expressing CREB in the
myeloid
lineage
.
CREB transgenic mice also develop myeloproliferative
disease
after one year.
Thus, CREB acts as a proto-oncogene to regulate hematopoiesis and contributes to the
leukemia
phenotype
.
Our results suggest that CREB-dependent pathways may serve as targets for directed therapies in
leukemia
in the future.
[MeSH-minor]
Animals. Bone Marrow Cells / metabolism.
Cell
Line, Tumor.
Cell
Proliferation.
Cell
Survival.
Cell
Transformation, Neoplastic. Gene Expression Regulation, Neoplastic. Glucose / metabolism. Granulocyte-Macrophage Colony-Stimulating Factor / metabolism. Humans.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Mice. Mice, Transgenic. Neoplasms / metabolism.
Phenotype
. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / metabolism. Proto-Oncogene Proteins / chemistry. Signal Transduction. Up-Regulation
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(PMID = 16096372.001).
[ISSN]
1551-4005
[Journal-full-title]
Cell cycle (Georgetown, Tex.)
[ISO-abbreviation]
Cell Cycle
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Cyclic AMP Response Element-Binding Protein; 0 / Proto-Oncogene Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; IY9XDZ35W2 / Glucose
[Number-of-references]
18
55.
Sung PA, Libura J, Richardson C:
Etoposide and illegitimate DNA double-strand break repair in the generation of MLL translocations: new insights and new questions.
DNA Repair (Amst)
; 2006 Sep 8;5(9-10):1109-18
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Faithful repair of chromosomal double-strand breaks (DSBs) is central to genome integrity and the suppression of genome rearrangements including translocations that are a hallmark of
leukemia
, lymphoma, and soft-tissue sarcomas [B.
Elliott, M. Jasin, Double-strand breaks and translocations in cancer,
Cell
. Mol. Life Sci.
Chemotherapy agents that target the essential cellular enzyme topoisomerase II (topo II) are known promoters of DSBs and are associated with therapy-related
leukemias
.
There is a clear clinical association between previous exposure to etoposide and therapy-related
acute
myeloid
leukemia
(t-AML) characterized by chromosomal rearrangements involving the
mixed lineage leukemia
(MLL) gene on chromosome band 11q23 [C.A.
Felix,
Leukemias
related to treatment with DNA topoisomerase II inhibitors, Med. Pediatr. Oncol.
[MeSH-major]
Antineoplastic Agents, Phytogenic / adverse effects. Chromosome Breakage. DNA Damage. DNA Repair. Etoposide / adverse effects.
Leukemia
,
Myeloid
,
Acute
/ chemically induced. Topoisomerase II Inhibitors
[MeSH-minor]
Chromosomes, Human, Pair 11. DNA Topoisomerases, Type II / genetics. Histone-Lysine N-Methyltransferase. Humans. Models, Genetic.
Myeloid
-
Lymphoid
Leukemia
Protein. Sensitivity and Specificity
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(PMID = 16809075.001).
[ISSN]
1568-7864
[Journal-full-title]
DNA repair
[ISO-abbreviation]
DNA Repair (Amst.)
[Language]
eng
[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 / Antineoplastic Agents, Phytogenic; 0 / MLL protein, human; 0 / Topoisomerase II Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 5.99.1.3 / DNA Topoisomerases, Type II
[Number-of-references]
94
56.
Zhang LJ, Lu XL, He J, Li Y:
[Rearrangements of the mixed lineage leukemia gene in acute myeloid leukemia].
Zhonghua Yi Xue Za Zhi
; 2006 Aug 29;86(32):2256-60
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[Title]
[Rearrangements of the
mixed lineage leukemia
gene in
acute
myeloid
leukemia
].
OBJECTIVE: To study the frequency of
mixed lineage leukemia
(MLL) gene rearrangements in patients with
acute
myeloid
leukemia
(AML) and to determine the significance thereof.
METHODS: Conventional cytogenetics (CC) and karyotype analysis were conducted on the bone marrow cells from 58 patients with
acute
myelocytic
leukemia
(AML), 47 adults (aged 15 approximately 67) and 11 children (aged 1 approximately 14).
[MeSH-major]
Gene Rearrangement.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics
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(PMID = 17064570.001).
[ISSN]
0376-2491
[Journal-full-title]
Zhonghua yi xue za zhi
[ISO-abbreviation]
Zhonghua Yi Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
149025-06-9 / Myeloid-Lymphoid Leukemia Protein
57.
Ohe M, Hashino S:
[Successful treatment with clarithromycin for Mixed phenotype acute leukemia, T/myeloid, NOS].
Rinsho Ketsueki
; 2010 Apr;51(4):297-9
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[Title]
[Successful treatment with clarithromycin for
Mixed
phenotype
acute leukemia
, T/
myeloid
, NOS].
The
diagnosis
was
Mixed
phenotype
acute leukemia
, T/
myeloid
, NOS.
This clinical course suggests CAM is effective for this
leukemia
.
[MeSH-major]
Anti-Bacterial Agents / administration & dosage. Clarithromycin / administration & dosage.
Leukemia
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Precursor T-
Cell Lymphoblastic
Leukemia
-Lymphoma / drug therapy
[MeSH-minor]
Acute
Disease
. Aged. Drug Synergism. Drug Therapy, Combination. Female. Humans. Pneumonia, Bacterial / complications. Pneumonia, Bacterial / drug therapy. Prednisolone / administration & dosage
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PREDNISOLONE
.
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Clarithromycin
.
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(PMID = 20467229.001).
[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]
0 / Anti-Bacterial Agents; 9PHQ9Y1OLM / Prednisolone; H1250JIK0A / Clarithromycin
58.
Pullarkat V, Veliz L, Chang K, Mohrbacher A, Teotico AL, Forman SJ, Slovak ML:
Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus.
J Clin Pathol
; 2007 May;60(5):562-4
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[Title]
Therapy-related,
mixed
-
lineage
leukaemia
translocation-positive, monoblastic
myeloid
sarcoma of the uterus.
Myeloid
sarcomas are tumour masses of
myeloid
leukaemic cells at extramedullary sites.
These tumours can, on occasion, occur without concurrent or antecedent
leukaemia
.
Myeloid
sarcomas have been described at unusual locations including the female genital tract.
An unusual case of therapy-related
acute
myeloid leukaemia
(t-AML) presenting as isolated monoblastic
myeloid
sarcoma of the uterus in a patient who had received adjuvant chemotherapy for breast cancer is presented.
Fluorescence in situ hybridisation analysis performed on paraffin-wax-embedded tumour tissue revealed a
mixed
-
lineage
leukaemia
(MLL) gene rearrangement, supporting the association of this malignancy with prior chemotherapy.
This case illustrates that t-AML can rarely present as isolated extramedullary tumours, and the detection of specific chromosomal abnormalities in these
myeloid
sarcomas can be useful for risk assessment and guiding definitive therapy.
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[Cites]
Am J Clin Pathol. 2000 Nov;114(5):807-11
[
11068557.001
]
[Cites]
Leuk Lymphoma. 2001 Apr;41(3-4):255-76
[
11378539.001
]
[Cites]
Am J Pathol. 2002 Jun;160(6):1967-72
[
12057901.001
]
[Cites]
Leuk Lymphoma. 2002 Nov;43(11):2151-3
[
12533040.001
]
[Cites]
Int J Surg Pathol. 2003 Oct;11(4):271-82
[
14615822.001
]
[Cites]
Leukemia. 2005 Feb;19(2):183-90
[
15618964.001
]
[Cites]
Urology. 1986 Mar;27(3):268-70
[
3082059.001
]
[Cites]
Gynecol Oncol. 1992 Jul;46(1):128-37
[
1634133.001
]
[Cites]
Blood. 1993 Dec 15;82(12):3705-11
[
8260707.001
]
[Cites]
Am J Clin Pathol. 1995 Oct;104(4):431-43
[
7572794.001
]
[Cites]
Am J Surg Pathol. 1997 Oct;21(10):1156-65
[
9331287.001
]
[Cites]
Leuk Res. 2004 Nov;28(11):1165-9
[
15380340.001
]
(PMID = 17513515.001).
[ISSN]
0021-9746
[Journal-full-title]
Journal of clinical pathology
[ISO-abbreviation]
J. Clin. Pathol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01 CA030206; United States / NCI NIH HHS / CA / 2 P01 CA030206-24A1; United States / NCI NIH HHS / CA / 5P30 CA33572
[Publication-type]
Case Reports; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Other-IDs]
NLM/ PMC1994540
59.
Shi M, Cui F, Li B, Li SY, Ma HJ:
Mixed phenotype acute leukaemia with giant inclusions.
Br J Haematol
; 2010 Apr;149(1):2
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[Title]
Mixed
phenotype
acute
leukaemia
with giant inclusions.
[MeSH-major]
Inclusion Bodies / ultrastructure.
Leukemia
,
Biphenotypic
,
Acute
/ pathology
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(PMID = 20015299.001).
[ISSN]
1365-2141
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
60.
Tenney K, Shilatifard A:
A COMPASS in the voyage of defining the role of trithorax/MLL-containing complexes: linking leukemogensis to covalent modifications of chromatin.
J Cell Biochem
; 2005 Jun 1;95(3):429-36
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The trithorax-related
mixed lineage leukemia
(Mll) gene located on chromosome 11 is rearranged in a variety of aggressive human
B and T lymphoid
tumors as well as
acute
myeloid
leukemia
(AML) in both children and adults.
[MeSH-major]
Chromatin / metabolism. DNA-Binding Proteins / metabolism.
Leukemia
/ metabolism. Multiprotein Complexes / metabolism. Transcription Factors / metabolism
[MeSH-minor]
Adult. Animals. Child. Histone-Lysine N-Methyltransferase. Humans. Methylation.
Myeloid
-
Lymphoid
Leukemia
Protein. Proto-Oncogenes / genetics. Transcription, Genetic
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[Copyright]
(c) 2005 Wiley-Liss, Inc.
(PMID = 15786493.001).
[ISSN]
0730-2312
[Journal-full-title]
Journal of cellular biochemistry
[ISO-abbreviation]
J. Cell. Biochem.
[Language]
eng
[Grant]
United States / NIGMS NIH HHS / GM / 1R01GM069905; United States / NCI NIH HHS / CA / 2R01CA089455
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Chromatin; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Multiprotein Complexes; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
[Number-of-references]
49
61.
Pajuelo-Gámez JC, Cervera J, García-Casado Z, Mena-Durán AV, Valencia A, Barragán E, Such E, Bolufer P, Sanz MA:
MLL amplification in acute myeloid leukemia.
Cancer Genet Cytogenet
; 2007 Apr 15;174(2):127-31
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[Title]
MLL amplification in
acute
myeloid
leukemia
.
The chromosomal alterations at 11q23 that involve the
mixed
-
lineage leukemia
gene (MLL, HTRX1, HRX, ALL1) are one of the most common cytogenetic abnormalities in
acute leukemia
and have been associated with a poor prognosis.
[MeSH-major]
Gene Amplification.
Leukemia
,
Myeloid
/ genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics
[MeSH-minor]
Acute
Disease
. Aged. Aneuploidy. Base Sequence. Chromosome Banding. Chromosome Deletion. Female. Genome, Human. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Molecular Sequence Data. Nucleic Acid Hybridization / methods. Sequence Analysis, DNA
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(PMID = 17452254.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
62.
Vega F, Medeiros LJ, Davuluri R, Cromwell CC, Alkan S, Abruzzo LV:
t(8;13)-positive bilineal lymphomas: report of 6 cases.
Am J Surg Pathol
; 2008 Jan;32(1):14-20
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The 8p11 myeloproliferative syndrome (EMS) is a rare hematologic malignancy characterized by
myeloid
hyperplasia, eosinophilia, and precursor
lymphoblastic
lymphoma, associated with balanced translocations involving chromosome 8p11, most commonly t(8;13)(p11;q12).
Approximately 75% of EMS patients present with or develop precursor T-
cell lymphoblastic
lymphoma, and most subsequently develop
acute
myeloid
leukemia
.
Here we describe the
morphologic and
immunophenotypic features of 6 cases of t(8;13)-positive bilineal lymphoma of
mixed
T-
cell and myeloid
lineage
, 5 in lymph nodes and 1 in breast.
Histologically, each tumor was composed of 2 distinct cellular components: small to medium-sized T cells with scant cytoplasm that resembled lymphoblasts, and larger immature-appearing cells with more abundant eosinophilic cytoplasm that resembled myeloblasts, a subset of which expressed
myeloid
antigens.
In all cases, the latter component tended to surround residual
lymphoid
follicles and/or blood vessels.
We believe that these bilineal neoplasms of
mixed
T-
cell and myeloid
lineages, which present as lymphoma, are analogous to bilineal
leukemias
.
They likely arise from an early hematopoietic
cell
with potential to differentiate along T-
cell and myeloid
pathways.
[MeSH-minor]
Adolescent. Adult. Antigens, CD / metabolism.
Cell
Lineage
. Child. Female. Granulocyte Precursor Cells / metabolism. Granulocyte Precursor Cells / pathology. Humans. Immunohistochemistry. Immunophenotyping. Lymphocytes / metabolism. Lymphocytes / pathology. Male. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic
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(PMID = 18162765.001).
[ISSN]
0147-5185
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD
63.
Bitoun E, Oliver PL, Davies KE:
The mixed-lineage leukemia fusion partner AF4 stimulates RNA polymerase II transcriptional elongation and mediates coordinated chromatin remodeling.
Hum Mol Genet
; 2007 Jan 01;16(1):92-106
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[Title]
The
mixed
-
lineage leukemia
fusion partner AF4 stimulates RNA polymerase II transcriptional elongation and mediates coordinated chromatin remodeling.
AF4 gene, frequently translocated with
mixed
-
lineage leukemia
(MLL) in childhood
acute leukemia
, encodes a putative transcriptional activator of the AF4/LAF4/FMR2 (ALF) protein family previously implicated in lymphopoiesis and Purkinje
cell
function in the cerebellum.
[MeSH-major]
Chromatin Assembly and Disassembly.
Leukemia
/ genetics. Nuclear Proteins / genetics. RNA Polymerase II / genetics. Transcription, Genetic
[MeSH-minor]
Animals.
Cell
Line. DNA Polymerase II / metabolism. Down-Regulation. HeLa Cells. Humans. Methylation. Methyltransferases / metabolism. Mice. Models, Biological. Multiprotein Complexes / metabolism. Phosphorylation. Phosphotransferases / metabolism. Positive Transcriptional Elongation Factor B / metabolism. Proteasome Endopeptidase Complex / metabolism. Signal Transduction. Transcription Factors / metabolism. Transcriptional Activation. Transfection
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(PMID = 17135274.001).
[ISSN]
0964-6906
[Journal-full-title]
Human molecular genetics
[ISO-abbreviation]
Hum. Mol. Genet.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / MC/ U137761449
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Aff2 protein, mouse; 0 / Mllt10 protein, mouse; 0 / Mllt3 protein, mouse; 0 / Multiprotein Complexes; 0 / Nuclear Proteins; 0 / Transcription Factors; EC 2.1.1.- / Dot1l protein, mouse; EC 2.1.1.- / Methyltransferases; EC 2.7.- / Phosphotransferases; EC 2.7.11.- / Positive Transcriptional Elongation Factor B; EC 2.7.7.- / DNA Polymerase II; EC 2.7.7.- / RNA Polymerase II; EC 3.4.25.1 / Proteasome Endopeptidase Complex
64.
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)
65.
Popovic R, Zeleznik-Le NJ:
MLL: how complex does it get?
J Cell Biochem
; 2005 May 15;95(2):234-42
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The
mixed lineage leukemia
(MLL) gene encodes a very large nuclear protein homologous to Drosophila trithorax (trx).
MLL was identified as a common target of chromosomal translocations associated with human
acute
leukemias
.
MLL gene rearrangements are found in
leukemias
with both
lymphoid and myeloid
phenotypes and are often associated with infant and secondary
leukemias
.
The immature
phenotype
of the leukemic blasts suggests an important role for MLL in the early stages of hematopoietic development.
[MeSH-minor]
Animals. Gene Expression Regulation, Developmental / physiology. Genes, Homeobox. Histone-Lysine N-Methyltransferase. Humans.
Leukemia
,
Lymphoid
/ genetics.
Leukemia
,
Myeloid
/ genetics. Mice.
Myeloid
-
Lymphoid
Leukemia
Protein.
Phenotype
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(PMID = 15779005.001).
[ISSN]
0730-2312
[Journal-full-title]
Journal of cellular biochemistry
[ISO-abbreviation]
J. Cell. Biochem.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA40046
[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.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse
[Number-of-references]
49
66.
Dou Y, Hess JL:
Mechanisms of transcriptional regulation by MLL and its disruption in acute leukemia.
Int J Hematol
; 2008 Jan;87(1):10-8
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[Title]
Mechanisms of transcriptional regulation by MLL and its disruption in
acute leukemia
.
Fusion of the
mixed lineage leukemia
protein (MLL) to one of over 50 different translocation partners converts it into a potent leukemogenic oncoprotein.
Considerable progress has been made in delineating the differences between normal Hox gene regulation by MLL and deregulated transcription in MLL-induced
leukemias
.
[MeSH-major]
Leukemia
/ genetics. Leukopoiesis / genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Transcription, Genetic / genetics
[MeSH-minor]
Animals. DNA Methylation.
Disease
Models, Animal. Histone-Lysine N-Methyltransferase. Homeodomain Proteins / genetics. Homeodomain Proteins / physiology. Humans. Mice. Mice, Knockout. Neoplasm Proteins / genetics. Neoplasm Proteins / physiology
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(PMID = 18224408.001).
[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
Japan
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / Hoxa7 protein, mouse; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / myeloid ecotropic viral integration site 1 protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
67.
Yamamoto K, Sada A, Kawano Y, Katayama Y, Shimoyama M, Matsui T:
Therapy-related, mixed phenotype acute leukemia with t(1;21)(p36;q22) and RUNX1 rearrangement.
Cancer Genet Cytogenet
; 2010 Sep;201(2):122-7
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[Title]
Therapy-related,
mixed
phenotype
acute leukemia
with t(1;21)(p36;q22) and RUNX1 rearrangement.
We describe here a new case of therapy-related
acute leukemia
with t(1;21)(p36;q22).
Immunophenotypic analyses revealed that blasts were positive for CD19, CD79a, and cytCD22, as well as MPO, CD13, and CD33, fulfilling the diagnostic criteria of
mixed
phenotype
acute leukemia
, B/
myeloid
.
The patient died of
disease
progression after 10 months.
Thus,
acute leukemia
with t(1;21) and RUNX1 rearrangement could be associated with B/
myeloid
mixed
phenotype
as well as previous topoisomerase II inhibitor therapy and poor prognoses.
[MeSH-major]
Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Gene Rearrangement.
Leukemia
,
Myeloid
,
Acute
/ genetics. Neoplasms, Second Primary / genetics
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[Copyright]
2010 Elsevier Inc. All rights reserved.
(PMID = 20682397.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
68.
Serefhanoglu S, Buyukasik Y, Goker H, Sayinalp N, Ozcebe OI:
Biphenotypic acute leukemia treated with acute myeloid leukemia regimens: a case series.
J Natl Med Assoc
; 2009 Mar;101(3):270-2
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[Title]
Biphenotypic
acute leukemia
treated with
acute
myeloid
leukemia
regimens: a case series.
This study retrospectively analyzed 8 cases of
biphenotypic
acute leukemia
(BAL) in respect of morphology, immune
phenotype
, karyotype, and clinical manifestations.
Six patients had
myeloid
plus
T lymphoid
, and 2 cases had
myeloid
plus B-
lymphoid
immune phenotypic markers.
Because selection of an antileukemic chemotherapy regimen for
acute leukemia
is largely based on whether a case is classified as
myeloid
or
lymphoid
, the presence of markers for both lineages may have important implications for treatment.
All of our patients were treated with regimens designed for
acute
myeloid
leukemia
(AML).
[MeSH-major]
Leukemia
,
Biphenotypic
,
Acute
/ drug therapy
[MeSH-minor]
Adult. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents / therapeutic use. Biomarkers. Case-Control Studies. Cytarabine / therapeutic use. Female. Humans. Idarubicin / therapeutic use. Immunophenotyping.
Leukemia
,
Myeloid
,
Acute
/ drug therapy.
Leukemia
,
Myeloid
,
Acute
/ physiopathology. Male. Middle Aged. Mitoxantrone / therapeutic use. Retrospective Studies
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(PMID = 19331261.001).
[ISSN]
1943-4693
[Journal-full-title]
Journal of the National Medical Association
[ISO-abbreviation]
J Natl Med Assoc
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Biomarkers; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin
69.
Balgobind BV, Zwaan CM, Reinhardt D, Arentsen-Peters TJ, Hollink IH, de Haas V, Kaspers GJ, de Bont ES, Baruchel A, Stary J, Meyer C, Marschalek R, Creutzig U, den Boer ML, Pieters R, van den Heuvel-Eibrink MM:
High BRE expression in pediatric MLL-rearranged AML is associated with favorable outcome.
Leukemia
; 2010 Dec;24(12):2048-55
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Translocations involving the
mixed lineage leukemia
(MLL) gene, localized at 11q23, frequently occur in pediatric
acute
myeloid
leukemia
(AML).
Forced expression of BRE did not result in altered
cell
proliferation, apoptosis or drug sensitivity, which could explain the favorable outcome.
[MeSH-major]
Gene Rearrangement.
Leukemia
,
Myeloid
,
Acute
/ genetics.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Nerve Tissue Proteins / genetics
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(PMID = 20861917.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / BRE protein, human; 0 / MLL protein, human; 0 / Nerve Tissue Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
70.
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
71.
Di Croce L:
Chromatin modifying activity of leukaemia associated fusion proteins.
Hum Mol Genet
; 2005 Apr 15;14 Spec No 1:R77-84
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[Title]
Chromatin modifying activity of
leukaemia
associated fusion proteins.
The
leukaemias
, which are divided into chronic and
acute
forms, are malignant diseases of haematopoietic cells in which the proper balance between proliferation, differentiation and apoptosis is no longer operative.
Genes, such as those of
mixed
-
lineage
leukaemia
, AML1 and retinoic acid receptor alpha, have been found to be aberrantly fused to different partners, which often encode transcription factors or other chromatin modifying enzymes, in numerous types of
acute
lymphoid and myeloid leukaemias
.
These chimeric fusion oncoproteins, generated by reciprocal chromosomal translocations, are responsible for chromatin alterations on target genes whose expression is critical to stem
cell
development or
lineage
specification in haematopoiesis.
[MeSH-major]
Chromatin / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Neoplastic.
Leukemia
/ metabolism. Proto-Oncogene Proteins / metabolism. Receptors, Retinoic Acid / metabolism. Transcription Factors / metabolism
[MeSH-minor]
Amino Acid Sequence. Animals.
Cell
Differentiation. Core Binding Factor Alpha 2 Subunit. DNA Methylation. Epigenesis, Genetic. Gene Silencing. Hematopoiesis. Humans. Models, Biological. Molecular Sequence Data. Oncogene Proteins, Fusion / chemistry
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(PMID = 15809276.001).
[ISSN]
0964-6906
[Journal-full-title]
Human molecular genetics
[ISO-abbreviation]
Hum. Mol. Genet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Chromatin; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / retinoic acid receptor alpha
[Number-of-references]
64
72.
Fais F, Tenca C, Cimino G, Coletti V, Zanardi S, Bagnara D, Saverino D, Zarcone D, De Rossi G, Ciccone E, Grossi CE:
CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis.
Leukemia
; 2005 Apr;19(4):551-6
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[Title]
CD1d expression on B-precursor
acute
lymphoblastic
leukemia
subsets with poor prognosis.
Acute
lymphoblastic
leukemia
(ALL) is the most frequent malignancy of childhood.
We investigated CD1d expression in 80 pediatric B-
cell
precursor (BCP) ALL cases defined according to immunophenotype, cytogenetic features and age at onset.
CD1d+ ALLs were significantly associated with infant
leukemia
, pro-
B phenotype
and
mixed
-
lineage leukemia
(MLL)/AF4 gene rearrangement.
[MeSH-major]
Antigens, CD1 / metabolism. Hematopoietic Stem Cells / metabolism. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / metabolism. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / pathology
[MeSH-minor]
Antigens, CD1d. B-Lymphocytes / cytology. Biomarkers, Tumor / metabolism.
Cell
Communication.
Cell
Line. Child. Galactosylceramides / metabolism. Humans. Infant. Killer Cells, Natural / cytology. Killer Cells, Natural / metabolism. Predictive Value of Tests. Prognosis. Survival Rate
Genetic Alliance.
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.
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consumer health - Stem Cells
.
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(PMID = 15744356.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD1; 0 / Antigens, CD1d; 0 / Biomarkers, Tumor; 0 / CD1D protein, human; 0 / Galactosylceramides; 0 / alpha-galactosylceramide
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.
Kim MK, Mun YC, Seong CM, Chung WS, Huh J:
[Variant Philadelphia chromosome identified by interphase fluorescence in situ hybridization (FISH) without evidence on G-banded karyotyping and metaphase FISH].
Korean J Lab Med
; 2010 Dec;30(6):711-7
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A 52-year-old man was diagnosed with
acute leukemia
of
mixed
phenotype
.
[MeSH-minor]
Adult. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Humans. Interphase. Karyotyping.
Leukemia
/
diagnosis
.
Leukemia
/ genetics.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive /
diagnosis
.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / genetics. Male. Metaphase. Middle Aged.
Phenotype
. Translocation, Genetic
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(PMID = 21157160.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
kor
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Korea (South)
75.
Liu H, Yu H, Jia HY, Zhang W, Guo CJ:
[Detection of FLT3 gene mutation in hematologic malignancies and its clinical significance].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2007 Aug;15(4):709-13
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To study the FLT3 gene expression and its internal tandem duplication in hematologic malignancies and its clinical significance, polymerase chain reaction (PCR) and DNA sequencing were used to detect the FLT3/ITD mutation in blast cells of bone marrow from 86 patients with hematologic malignancies, including 32 cases of
acute
myeoloid
leukemia
(AML), 18 cases of
acute
lymphoblastic
leukemia
(ALL), 2 cases of
acute
hybrid
leukemia
(AHL), 12 cases of myelodysplastic syndromes (MDS), 10 cases of chronic myelogenous
leukemia
(CML), 3 cases of non-Hodgkin's lymphoma (NHL) and 9 cases of multiple myeloma (MM).
FLT3/ITD was associated with a higher peripheral blood white
cell
count (p < 0.01), higher percentage of bone marrow blast cells (p < 0.01) and lower complete mission rate.
FLT3/ITD mutation is associated with higher peripheral blood white
cell
count, higher percentage of bone marrow blast cells and lower complete remission rate, FIT3/IID gene mutation may be used to predict prognosis of patients with AML.
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(PMID = 17708788.001).
[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]
EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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.
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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7938000.001
]
(PMID = 16169901.001).
[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[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
78.
Papenhausen PR, Griffin S, Tepperberg J:
Oncogene amplification in transforming myelodysplasia.
Exp Mol Pathol
; 2005 Oct;79(2):168-75
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The MLL gene, located within band 11q23, has been shown to be involved in translocations with a large variety of reciprocal sites in both
lymphoid and myeloid
leukemia
and has also been shown to undergo submicroscopic self-fusion/partial duplication.
The frequency and clinical correlations of MLL gene amplification in
leukemia
will need careful follow-up, since the frequently cryptic amplification described in these cases may not generally provoke confirmatory FISH studies.
A common cytogenetic profile of 5 q-, -17/17 p-, -18/18 q-,
and a
missing or abnormal chromosome 11, may help direct appropriate follow-up studies.
Both genes also show a high degree of diversity of pathogenic mechanisms of
leukemia
evolution, including numerous reciprocal fusion genes in transformation to either AML or ALL and gain of function amplification.
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged.
Myeloid
-
Lymphoid
Leukemia
Protein. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Proto-Oncogene Proteins / genetics
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(PMID = 16026782.001).
[ISSN]
0014-4800
[Journal-full-title]
Experimental and molecular pathology
[ISO-abbreviation]
Exp. Mol. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
79.
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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(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
80.
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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.
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.
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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
81.
Lee JC, Yang S, Zou Y, Joseph L:
Erythroid/B-cell biphenotypic acute leukemia first case report.
Leukemia
; 2009 Oct;23(10):1920-3
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[Title]
Erythroid/B-
cell biphenotypic
acute leukemia
first case report.
[MeSH-major]
B-Lymphocytes / pathology. Erythroid Cells / pathology.
Leukemia
,
Biphenotypic
,
Acute
/ pathology
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(PMID = 19458630.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD
82.
Mejstrikova E, Volejnikova J, Fronkova E, Zdrahalova K, Kalina T, Sterba J, Jabali Y, Mihal V, Blazek B, Cerna Z, Prochazkova D, Hak J, Zemanova Z, Jarosova M, Oltova A, Sedlacek P, Schwarz J, Zuna J, Trka J, Stary J, Hrusak O:
Prognosis of children with mixed phenotype acute leukemia treated on the basis of consistent immunophenotypic criteria.
Haematologica
; 2010 Jun;95(6):928-35
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[Title]
Prognosis of children with
mixed
phenotype
acute leukemia
treated on the basis of consistent immunophenotypic criteria.
BACKGROUND:
Mixed
phenotype
acute leukemia
(
MPAL
) represents a diagnostic and therapeutic dilemma.
The European Group for the Immunological Classification of
Leukemias
(EGIL) scoring system unambiguously defines
MPAL
expressing aberrant
lineage
markers.
DESIGN AND METHODS: Simple immunophenotypic criteria were used to classify all cases of childhood
acute leukemia
in order to provide therapy directed against
acute
lymphoblastic
leukemia
or
acute
myeloid
leukemia
.
Prognosis, genotype and immunoglobulin/T-
cell
receptor gene rearrangement status were analyzed.
RESULTS: The incidences of
MPAL
were 28/582 and 4/107 for children treated with
acute
lymphoblastic
leukemia
and
acute
myeloid
leukemia
regimens, respectively.
In immunophenotypic principal component analysis,
MPAL
treated as T-
cell
acute
lymphoblastic
leukemia
clustered between cases of non-
mixed
T-
cell
acute
lymphoblastic
leukemia
and
acute
myeloid
leukemia
, while other
MPAL
cases were included in the respective non-
mixed
B-
cell
progenitor
acute
lymphoblastic
leukemia
or
acute
myeloid
leukemia
clusters.
Analogously, immunoglobulin/T-
cell
receptor gene rearrangements followed the expected pattern in patients treated as having
acute
myeloid
leukemia
(non-rearranged, 4/4) or as having B-
cell
progenitor
acute
lymphoblastic
leukemia
(rearranged, 20/20), but were missing in 3/5 analyzed cases of
MPAL
treated as having T-
cell
acute
lymphobastic
leukemia
.
In patients who received
acute
lymphoblastic
leukemia
treatment, the 5-year event-free survival of the
MPAL
cases was worse than that of the non-
mixed
cases (53+/-10% and 76+/-2% at 5 years, respectively, P=0.0075), with a more pronounced difference among B
lineage
cases.
The small numbers of
MPAL
cases treated as T-
cell
acute
lymphoblastic
leukemia
or as
acute
myeloid
leukemia
hampered separate statistics.
CONCLUSIONS: Simple immunophenotypic criteria are useful for therapy decisions in
MPAL
.
In B
lineage leukemia
,
MPAL
confers poorer prognosis.
However, our data do not justify a preferential use of current
acute
myeloid
leukemia
-based therapy in
MPAL
.
[MeSH-major]
Immunophenotyping.
Leukemia
/
diagnosis
.
Leukemia
/ therapy.
Phenotype
[MeSH-minor]
Adolescent. Child. Child, Preschool.
Diagnosis
, Differential. Follow-Up Studies. Humans. Infant. Infant, Newborn.
Leukemia
,
Myeloid
,
Acute
/
diagnosis
.
Leukemia
,
Myeloid
,
Acute
/ immunology.
Leukemia
,
Myeloid
,
Acute
/ therapy. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma /
diagnosis
. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / immunology. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / therapy. Prognosis. Receptors, Antigen, T-
Cell
/ immunology
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.
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consumer health - Leukemia
.
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[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Receptors, Antigen, T-Cell
[Other-IDs]
NLM/ PMC2878790
83.
Bardini M, Spinelli R, Bungaro S, Mangano E, Corral L, Cifola I, Fazio G, Giordan M, Basso G, De Rossi G, Biondi A, Battaglia C, Cazzaniga G:
DNA copy-number abnormalities do not occur in infant ALL with t(4;11)/MLL-AF4.
Leukemia
; 2010 Jan;24(1):169-76
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The pathogenesis of infant
acute
lymphoblastic
leukemia
(ALL) is still not well defined.
Short latency to
leukemia
and very high concordance rate for ALL in
Mixed
-
Lineage Leukemia
(MLL)-positive infant twins suggest that the MLL rearrangement itself could be sufficient for overt
leukemia
.
Attempts to generate a suitable mouse model for MLL-AF4-positive ALL did not thoroughly resolve the issue of whether cooperating mutations are required to reduce latency and to generate overt
leukemia
in vivo.
In contrast to pediatric, adolescent and adult ALL cases, the MLL rearrangement in infant ALL is associated with an exceptionally low frequency of copy-number abnormalities, thus confirming the unique nature of this
disease
.
By contrast, additional genetic aberrations are acquired at
disease
relapse.
It can be argued that the MLL rearrangement as a first hit, rather than inducing the acquisition of additional genetic lesions, has a major role to drive and hasten the onset of
leukemia
.
[MeSH-major]
Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. Gene Dosage.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Translocation, Genetic
SciCrunch.
ArrayExpress: Data: Microarray
.
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(PMID = 19907438.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
84.
Rice KL, Licht JD:
HOX deregulation in acute myeloid leukemia.
J Clin Invest
; 2007 Apr;117(4):865-8
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[Title]
HOX deregulation in
acute
myeloid
leukemia
.
The deregulation of homeobox (HOX) genes in
acute
myeloid
leukemia
(AML) and the potential for these master regulators to perturb normal hematopoiesis is well established.
To date, overexpression of HOX genes in AML has been attributed to specific chromosomal aberrations and abnormalities involving
mixed
-
lineage leukemia
(MLL), an upstream regulator of HOX genes.
The
finding
reported in this issue of the JCI by Scholl
et
al. that caudal-type homeobox transcription factor 2 (CDX2), which is capable of affecting HOX gene expression during embryogenesis, is overexpressed in 90% of patients with AML and induces a transplantable AML in murine models provides an alternative mechanism for HOX-induced leukemogenesis and yields important insights into the hierarchy of HOX gene regulation in AML (see the related article beginning on page 1037).
[MeSH-major]
Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics.
Leukemia
,
Myeloid
/ genetics.
Leukemia
,
Myeloid
,
Acute
/ genetics
[MeSH-minor]
Animals.
Disease
Models, Animal. Genes, Homeobox. Humans. Mice. Transcription Factors / genetics
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[CommentOn]
J Clin Invest. 2007 Apr;117(4):1037-48
[
17347684.001
]
(PMID = 17404613.001).
[ISSN]
0021-9738
[Journal-full-title]
The Journal of clinical investigation
[ISO-abbreviation]
J. Clin. Invest.
[Language]
eng
[Publication-type]
Comment; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / CDX2 protein, human; 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors
[Other-IDs]
NLM/ PMC1838955
85.
Van Etten RA:
Aberrant cytokine signaling in leukemia.
Oncogene
; 2007 Oct 15;26(47):6738-49
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[Title]
Aberrant cytokine signaling in
leukemia
.
Abnormalities of cytokine and growth factor signaling pathways are characteristic of all forms of
leukemia
:
lymphoid and myeloid
,
acute
and chronic.
In this review, our current knowledge of leukemic
cell
cytokine signaling will be summarized, and some speculations on the significance and implications of these insights will be advanced.
A better understanding of aberrant cytokine signaling in
leukemia
should provide additional targets for the rational therapy of these diseases.
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(PMID = 17934482.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA090576; United States / NCI NIH HHS / CA / R01 CA105043; United States / NCI NIH HHS / CA / CA090576; United States / NCI NIH HHS / CA / CA105043
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Cytokines
[Number-of-references]
139
[Other-IDs]
NLM/ NIHMS579951; NLM/ PMC4344827
86.
Milne TA, Martin ME, Brock HW, Slany RK, Hess JL:
Leukemogenic MLL fusion proteins bind across a broad region of the Hox a9 locus, promoting transcription and multiple histone modifications.
Cancer Res
; 2005 Dec 15;65(24):11367-74
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Chromosome translocations involving the
mixed lineage leukemia
gene MLL are associated with aggressive
acute
leukemias
in both children and adults.
[MeSH-major]
Homeodomain Proteins / metabolism.
Myeloid
-
Lymphoid
Leukemia
Protein / metabolism. Oncogene Proteins, Fusion / metabolism. Transcription, Genetic
Hazardous Substances Data Bank.
L-Lysine
.
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(PMID = 16357144.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA78815; United States / NCI NIH HHS / CA / CA92251
[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 / Histones; 0 / Homeodomain Proteins; 0 / MLL-ENL oncoprotein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine
87.
Fender AB, Gust A, Wang N, Scott GA, Mercurio MG:
Congenital leukemia cutis.
Pediatr Dermatol
; 2008 Jan-Feb;25(1):34-7
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[Title]
Congenital
leukemia
cutis.
We describe a premature neonate who was born with pancytopenia
and a
single subcutaneous nodule on her right lower extremity.
Immunohistochemical stains and bone marrow examination confirmed
a diagnosis
of
acute
myelogenous
leukemia
.
A split in the
mixed lineage leukemia
gene was identified by fluorescence in situ hybridization.
As
leukemia
cutis more typically presents as multiple infiltrative papules, nodules, or plaques, we stress the importance of including
leukemia
in the differential
diagnosis
of a solitary nodule in a neonate.
[MeSH-major]
Infant, Premature.
Leukemia
,
Myeloid
,
Acute
/ congenital.
Leukemia
,
Myeloid
,
Acute
/ pathology. Neoplasm Invasiveness / pathology. Skin Neoplasms / congenital. Skin Neoplasms / pathology
[MeSH-minor]
Biopsy, Needle. Bone Marrow / pathology. Chromosome Aberrations. Chromosomes, Human, X. Cytogenetics / methods.
Disease
Progression. Fatal Outcome. Female. Humans. Immunohistochemistry. Infant, Newborn. Karyotyping. Risk Assessment
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(PMID = 18304150.001).
[ISSN]
1525-1470
[Journal-full-title]
Pediatric dermatology
[ISO-abbreviation]
Pediatr Dermatol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
88.
Stasik C, Ganguly S, Cunningham MT, Hagemeister S, Persons DL:
Infant acute lymphoblastic leukemia with t(11;16)(q23;p13.3) and lineage switch into acute monoblastic leukemia.
Cancer Genet Cytogenet
; 2006 Jul 15;168(2):146-9
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[Title]
Infant
acute
lymphoblastic
leukemia
with t(11;16)(q23;p13.3) and
lineage
switch into
acute
monoblastic
leukemia
.
Rearrangements of the
mixed
-
lineage leukemia
(MLL) gene have been associated with a poor prognosis in infant
acute
lymphoblastic
leukemia
(ALL).
Previously, MLL translocations involving the CREP-binding protein (CREBBP) gene at chromosome band 16p13.3 have primarily been reported in treatment-related
acute
myeloid
leukemia
, after chemotherapy for other primary malignancies using topoisomerase II inhibitors.
We report a case of
de
novo infant ALL with t(11;16)(q23;p13.3).
After chemotherapy, this patient developed an
acute
monoblastic
leukemia
(M5b) with retention of the t(11;16)(q23;p13.3), indicating that this is a
lineage
switch of the original leukemic clone.
[MeSH-major]
Cell
Lineage
. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 16 / genetics.
Leukemia
, Monocytic,
Acute
/ genetics. Precursor
Cell Lymphoblastic
Leukemia
-Lymphoma / genetics. Translocation, Genetic / genetics
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(PMID = 16843104.001).
[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
89.
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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[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
90.
Takeda S, Chen DY, Westergard TD, Fisher JK, Rubens JA, Sasagawa S, Kan JT, Korsmeyer SJ, Cheng EH, Hsieh JJ:
Proteolysis of MLL family proteins is essential for taspase1-orchestrated cell cycle progression.
Genes Dev
; 2006 Sep 1;20(17):2397-409
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[Title]
Proteolysis of MLL family proteins is essential for taspase1-orchestrated
cell
cycle progression.
Taspase1 was identified as the threonine endopeptidase that cleaves
mixed
-
lineage leukemia
(MLL) for proper Hox gene expression in vitro.
Remarkably, our in vivo studies uncover an unexpected role of Taspase1 in the
cell
cycle.
Taspase1(-/-) mouse embryonic fibroblasts (MEFs) exhibit impaired proliferation, and
acute
deletion of Taspase1 leads to a marked reduction of thymocytes.
Lastly, Taspase1(-/-) cells are resistant to oncogenic transformation, and Taspase1 is overexpressed in many cancer
cell
lines.
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