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NCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of AML - April 2002
National Cancer Institute®
Last Modified: April 1, 2002
Table of Contents
1
UI - 11834787
AU - Marx J
TI -
Cancer research. Leukemia protein spurs gene silencing.
SO - Science 2002 Feb 8;295(5557):943-5
2
UI - 11565797
AU - Wan J; Wang J; Cheng H; Yu Y; Xing G; Oiu Z; Qian X; He F
TI -
Proteomic analysis of apoptosis initiation induced by all-trans retinoic
acid in human acute promyelocytic leukemia cells.
SO - Electrophoresis 2001 Aug;22(14):3026-37
AD - Department of Genomics and Proteomics, Beijing Institute of Radiation
Medicine, Chinese National Human Genome Center at Beijing, PR China.
The irreversible destiny of apoptosis in its early stage might play a
critical role in the apoptosis of human acute promyelocytic leukemia
(APL) cell line induced by all-trans retinoic acid (ATRA). To
characterize protein alterations during the apoptosis-initiation phase
and to understand the metabolic status at that time, we investigated the
protein profiles in the apoptosis-initiation phase of APL cell line
HL-60 by proteomic analysis. ATRA-withdrawal was conducted to
demonstrate that there was committed initiation phase of apoptosis
triggered by 10(-6) M ATRA at day 3. Only after that time point,
ATRA-treated cells irreversibly went to apoptosis. Also at that time
point, the positive regulators of apoptosis such as STAT3 increased at
protein level, whereas negative regulators (Bcl-2 and p-STAT3)
decreased. In addition, caspase-3 also increased after that time.
Furthermore, comparative proteomic analysis was utilized to examine the
protein expression profiles during the initiation stage of apoptosis.
Our results showed 12 upregulated and 7 downregulated proteins
experiencing twofold alteration, including key regulators of signal
transduction such as G-proteins and nucleic receptors, proteins related
with metabolism, oxidation and reduction, proteins associated with the
nucleus and cytoskeleton-related proteins. Some of them could be
positive modulators to trigger apoptosis, whereas others could
contribute to intracellular defense against apoptosis induced by
exogenous triggers. The results above suggest that there is a subtle
balance between apoptosis and the intracellular defense against
apoptosis. Once the balance is disturbed, cells would irreversibly
initiate to undergo the execution of apoptosis.
3
UI - 11823047
AU - Re F; Arpinati M; Testoni N; Ricci P; Terragna C; Preda P; Ruggeri D;
TI -
Senese B; Chirumbolo G; Martelli V; Urbini B; Baccarani M; Tura S;
Rondelli D
Expression of CD86 in acute myelogenous leukemia is a marker of
dendritic/monocytic lineage.
SO - Exp Hematol 2002 Feb;30(2):126-34
AD - Institute of Hematology and Medical Oncology Seragnoli, University of
Bologna, Bologna, Italy.
OBJECTIVE: The aim of this study was to determine whether expression of
the CD86 costimulatory molecule in acute myeloid leukemia (AML) can
identify blast cells committed to the monocytic/dendritic lineage.
MATERIAL AND METHODS: One hundred ten consecutive AML patients observed
at diagnosis were studied by flow cytometry. In selected experiments, in
vitro cultures with CD34(+)CD86(+) or CD34(-)CD86(+) blasts were
performed in the presence of granulocyte-macrophage colony-stimulating
actor (GM-CSF) with or without tumor necrosis factor-alpha (TNF-alpha)
or GM-CSF + interleukin-4 (IL-4), respectively, to induce a dendritic
differentiation, documented by morphologic and immunophenotypic assays.
T-cell alloreactivity to CD86(+) AML cells and leukemic dendritic cells
(AML-DC) was tested in mixed leukocyte cultures and anti-leukemic
cytotoxic assays. RESULTS: CD86 was expressed in 54% AML, whereas CD80
and CD1a were only occasionally positive. CD86(+) AML samples included
M5 and M4, but also 47% M0-M1 FAB types, and were more frequently
CD14(+) (p < 0.00001) and CD34(-) (p = 0.00005) than CD86(-)AML. Six
different patterns of CD86(+) AML were identified, according to CD34 or
CD14 total or partial coexpression. Four samples enriched in
CD34(+)CD86(+) AML cells differentiated into AML-DC CD86(+), CD80(+),
CD40(+), CD11c(+), HLA-DR(++), CD14(+/-) that also were CD1a(+) or
CD83(+), after 6 days of in vitro culture with GM-CSF +/- TNF-alpha.
CD34(-)CD86(+) AML cells differentiated into AML-DC after 3 to 5 days (n
= 5 experiments), and trisomy 8 was found in two AML and AML-DC samples
by fluorescence in situ hybridization analysis. Finally, AML-DC induced
more potent allo-T-cell proliferation, cytokine release, and
anti-leukemic cytotoxicity than CD86(+) blasts. CONCLUSIONS: In AML,
CD86 is a marker of monocytic/dendritic lineage. Because CD86(+) blasts
may differentiate into DC rapidly, CD86(+)AML patients could be optimal
candidates for immunotherapy studies, both in autologous and allogeneic
settings.
4
UI - 11823051
AU - Datta NS; Long MW
TI -
Modulation of MDM2/p53 and cyclin-activating kinase during the
megakaryocyte differentiation of human erythroleukemia cells.
SO - Exp Hematol 2002 Feb;30(2):158-65
AD - Department of Pediatrics and the Comprehensive Cancer Center, University
of Michigan, Ann Arbor, MI, USA.
OBJECTIVE: This study was undertaken to address the involvement of CDK
activating kinase (CAK), p53, and MDM2 proteins in the mitotic arrest
associated with the acquisition of a polyploid DNA content during
megakaryocyte differentiation of human erythroleukemia (HEL) cells.
METHODS: To evaluate this mechanism we investigated HEL cells as a model
system in which there is a marked increase in DNA content during
megakaryocyte differentiation induced by phorbol-diesters. Specific
cell-cycle phases were separated by centrifugal elutriation and SDS PAGE
and Western analysis were performed to determine the relative abundance
of these proteins. Kinase assays were carried out following
immunoprecipitation of cellular lysates with the antibodies to the
proteins. RESULTS: Polyploid HEL cells show an increase in the abundance
of the CAK complex proteins, CDK7 and cyclin H, and a sixfold increase
in CAK-specific activity. Increased CAK activity in polyploid HEL cells
follows both the downregulation of p53 protein and its decreased
association with CAK complex. Consistent with the reduction of p53,
polyploid HEL cells undergo a dramatic increase in MDM2 protein
abundance that in turn facilitates increased interaction of this protein
with p53. CONCLUSION: These observations demonstrate that deregulated
expression of MDM2 and p53 during megakaryocyte differentiation allow a
relaxation of the control over genomic stability, allowing further
replicative rounds of DNA synthesis.
5
UI - 11921270
AU - Karrison T; Archer KJ; Espinosa R 3rd; Wen M; Huo D
TI -
Data management and statistical methods used in the analysis of balanced
chromosome abnormalities in therapy-related myelodysplastic syndromes
and therapy-related acute leukemia: report from an international
workshop.
SO - Genes Chromosomes Cancer 2002 Apr;33(4):346-61
AD - Department of Health Studies, University of Chicago, Chicago, Illinois
60637, USA. tkarrison@health.bsd.uchicago.edu
6
UI - 11921271
AU - Bloomfield CD; Archer KJ; Mrozek K; Lillington DM; Kaneko Y; Head DR;
TI -
Dal Cin P; Raimondi SC
11q23 balanced chromosome aberrations in treatment-related
myelodysplastic syndromes and acute leukemia: report from an
international workshop.
SO - Genes Chromosomes Cancer 2002 Apr;33(4):362-78
AD - Division of Hematology and Oncology and the Comprehensive Cancer Center,
The Ohio State University, Columbus, Ohio 43210, USA.
Among 511 patients with therapy-related myelodysplastic syndrome or
acute leukemia (t-MDS/t-AL) and balanced chromosome aberrations, 162
(32%) had translocations involving 11q23. The recurring translocation
partners were 9p22 (48%), 19p13.3 (11%), 19p13.1 (10%), 4q21 (9%), 6q27
(6%), 1p32 (2%), 16p13.1 (2%), 10p13 (1%), and 17q25 (1%); in 9%, the
translocations were seen only once. The remaining 349 patients were
divided into five subgroups based on the balanced aberration: 21q22,
inv(16), t(15;17), Rare, and Unique aberrations. Patients in the 11q23
subgroup had a sole cytogenetic abnormality more often than those in the
21q22, inv(16), Rare, and Unique subgroups, and a complex karyotype or
-5/del(5q) and/or -7/del(7q) less often than patients in the 21q22,
Rare, and Unique subgroups. Clinically, 11q23 patients had acute
lymphoblastic leukemia (ALL) more often as their primary disease and a
shorter latency from start of treatment for the primary disease to their
t-MDS/t-AL diagnosis, except when compared with the inv(16) subgroup.
The 11q23 subgroup demonstrated a younger age at t-MDS/t-AL diagnosis,
but this finding was not significant when patients with AL as their
primary diagnosis were excluded. Survival from the time of diagnosis of
t-MDS/t-AL was significantly shorter for the 11q23 subgroup compared
with that of the 21q22, inv(16), and t(15;17) subgroups (median 8 vs.
14, 28, and 29 months, respectively). Inferior survival occurred even
though 11q23 patients were younger and more often received blood or
marrow transplantation (BMT). Even among patients receiving BMT, 11q23
patients had a shorter median survival (9 vs. 12-31 months for the other
subgroups). However, among 11q23 patients, those receiving BMT survived
longer, with 1- and 5-year survivals of 43% and 18% compared with 23%
and 7% for patients not transplanted. With regard to prior therapy,
11q23 patients, compared with other patients, received radiotherapy less
often as their sole therapy and chemotherapy more often. They had
received VP16, methotrexate, 6MP/6TG, L-asparaginase, daunorubicin,
cytarabine, and VM26 more often, likely attributed to the high frequency
of AL as their primary disease. More patients in the 11q23 subgroup had
received doxorubicin, except in comparison with the 21q22 subgroup; more
vincristine, except in comparison with the Rare and Unique subgroups;
and more prednisone, except in comparison with the Unique subgroup.
Patients in the 11q23 subgroup more often received alkylating agents
(AAs) (86% vs. 59-82% for the other subgroups), and topoisomerase II
inhibitors (TIs) (84% vs. 49-75%), and they more often reported exposure
to AAs plus TIs without radiotherapy (33% vs. 12-21%), except in
comparison with the 21q22 subgroup (36%). We performed a multivariate
analysis to determine whether the adverse survival of 11q23 patients
compared to other Workshop patients was explained by factors other than
the presence of the 11q23 abnormality. Covariates in the final model
were the five cytogenetic subgroup indicators, where the 11q23 subgroup
was the referent (P < 0.0001); age at t-MDS/t-AL (P = 0.0036); previous
exposure to lomustine (P < 0.0001) and mitoxantrone (P = 0.0225); BMT
for t-MDS/t-AL (P = 0.0006); and karyotype complexity (P = 0.0114). The
risk of death for 11q23 patients relative to patients in the 21q22,
inv(16), t(15;17), and Unique subgroups was significant, even after
adjustment for other risk factors (relative risks 2.3, 3.6, 3.1, and
1.5, respectively; P < 0.0001 for the first three comparisons and P =
0.0125 for the last). When a multivariable model was constructed,
excluding patients with AL or MDS as their primary diagnosis, the
relative risk of death for 11q23 patients was significantly higher than
that of all five other cytogenetic subgroups. We conclude that among
t-MDS/t-AL patients with balanced aberrations, 11q23 translocations are
an independent adverse risk factor. Although BMT is the current therapy
of choice, new treatment is required.
7
UI - 11921273
AU - Andersen MK; Larson RA; Mauritzson N; Schnittger S; Jhanwar SC;
TI -
Pedersen-Bjergaard J
Balanced chromosome abnormalities inv(16) and t(15;17) in
therapy-related myelodysplastic syndromes and acute leukemia: report
from an international workshop.
SO - Genes Chromosomes Cancer 2002 Apr;33(4):395-400
AD - Cytogenetic Laboratory, Section of Hematology/Oncology, Department of
Clinical Genetics, Rigshospitalet, Copenhagen, Denmark. mka@rh.dk
The Workshop identified 48 unselected patients with therapy-related
myelodysplastic syndrome or acute myeloid leukemia (t-MDS/t-AML) and
inv(16), and 41 patients with t(15;17) after chemotherapy (CT) and/or
radiotherapy (RT) for a malignant or nonmalignant disease. The primary
diseases were: breast cancer, 33 patients; lymphomas, 24 patients;
various other solid tumors, 30 patients; and nonmalignant diseases, 2
patients. The general type of previous therapy was RT only in 10
patients with an inv(16) and in 12 patients with a t(15;17), alkylating
agents plus topoisomerase II inhibitors in 24 patients with an inv(16)
and in 18 patients with a t(15;17), topoisomerase II inhibitors only in
5 patients with an inv(16) and in 2 patients with a t(15;17), alkylating
agents only in 6 patients in each subgroup, and other types of
chemotherapy in 3 patients in each subgroup. Most CT-treated patients
(69%) also received RT. The latency period to development of t-MDS/t-AML
was short: a median of 22 months in patients with inv(16) and 29 months
in patients with t(15;17). Twenty-six patients (54%) with an inv(16) and
17 patients (41%) with a t(15;17) had additional cytogenetic
abnormalities, which were unrelated to age and survival in both
subgroups. Trisomy of chromosomes 8, 21, and 22 and del(7q) were the
most frequent additional abnormalities in the inv(16) subgroup, whereas
+8, -5, and del(16q) were most frequent in the t(15;17) subgroup. The
disease was overt t-AML in 38/48 patients (79%) with an inv(16) and in
38/41 patients (93%) with a t(15;17). Thirty-three of 39 intensively
treated patients (85%) with an inv(16) obtained a complete remission,
whereas 24 of 35 intensively treated patients (69%) with a t(15;17)
obtained a complete remission. The median overall survival of
intensively treated patients was 29 months in both cytogenetic
subgroups. In the inv(16) subgroup, patients younger than 55 years of
age had a longer survival when compared with older patients (P = 0.006).
The study supports the observation that t-MDS/t-AML with inv(16) and
t(15;17) is often associated with prior therapy with topoisomerase II
inhibitors; however, a notable finding was the high frequency of
treatment with only radiotherapy, 29% of t(15;17) and 21% of inv(16).
Response rates to intensive chemotherapy in this study were comparable
to those of de novo disease. Copyright 2002 Wiley-Liss, Inc.
8
UI - 11921274
AU - Block AW; Carroll AJ; Hagemeijer A; LM LM; van Lom K; Olney HJ; Baer MR
TI -
Rare recurring balanced chromosome abnormalities in therapy-related
myelodysplastic syndromes and acute leukemia: report from an
international workshop.
SO - Genes Chromosomes Cancer 2002 Apr;33(4):401-12
AD - Clinical Cytogenetics Laboratory, Roswell Park Cancer Institute,
Buffalo, New York 14263, USA. annemarie.block@roswellpark.org
Seventy-seven patients were identified with Rare recurring (excluding
11q23, 21q22, inv(16), and t(15;17)) chromosome abnormalities among 511
patients with treatment-related myelodysplastic syndromes and acute
leukemia accepted from centers in the United States, Europe, and Japan.
The abnormality subsets included 3q21q26 (17 patients), 11p15 (17
patients), t(9;22)(q34;q11) (10 patients), 12p13 (9 patients),
t(8;16)(p11;p13) (9 patients), and an "other" subset, which included
t(6;9)(p23;q34) (3 patients), t(10;11)(p13;q13 approximately q21) (3
patients), t(1;17)(p36;q21) (2 patients), t(8;14)(q24;q32) (2 patients),
t(11;19)(q13;q13) (2 patients), t(1;3)(p36;q21) (2 patients), and
t(3;5)(q21;q31) (1 patient). Increased karyotypic complexity with
additional balanced and unbalanced rearrangements was observed in 70% of
cases. Among 54 cases with secondary abnormalities, chromosome 5 and/or
7 abnormalities were observed in 59%. The most frequent primary diseases
were breast cancer (24 cases), Hodgkin disease (14 cases), non-Hodgkin
lymphoma (10 cases), and de novo ALL (5 cases). Thirty-seven patients
received alkylating agents plus topoisomerase II inhibitors with or
without radiation therapy. The presenting diagnosis was t-AML in 47
cases, t-MDS in 23 cases (10 progressed to t-AML), and t-ALL in seven
cases, five of whom had a t(9;22). The median latency time from
initiation of original therapy to therapy-related disease diagnosis was
quite long (69 months), and the overall median survival from the date of
therapy-related disease diagnosis was very short (7 months). The 1-year
survival rate was 34 +/- 7%, with no significant differences among
subsets. Comparison with previously reported cases showed increased
karyotypic complexity and adult presentation of pediatric-associated
chromosome abnormalities. Copyright 2002 Wiley-Liss, Inc.
9
UI - 11921275
AU - Olney HJ; Mitelman F; Johansson B; Mrozek K; Berger R; Rowley JD
TI -
Unique balanced chromosome abnormalities in treatment-related
myelodysplastic syndromes and acute myeloid leukemia: report from an
international workshop.
SO - Genes Chromosomes Cancer 2002 Apr;33(4):413-23
AD - Section of Hematology/Oncology, University of Chicago, Chicago,
Illinois, USA. hj.olney@umontreal.ca
A total of 123 balanced rearrangements, including 26 occurring as a sole
anomaly, not known to be recurrent in myelodysplastic syndromes (MDS) or
acute myeloid leukemia (AML) prior to the Workshop, were ascertained
retrospectively from 104 patients with treatment-related MDS/AML
(t-MDS/t-AML). Thirteen of the aberrations were reported previously in
single cases and hence may be classified as recurrent as a result of the
Workshop. Patients with Unique aberrations had complex karyotypes more
often (P < 0.001 for all pairwise comparisons) than did other Workshop
subgroups, with 72% having 3 or more aberrations. Among 85 cases with
secondary chromosomal abnormalities, -5, -7, del(5q), and del(7q) were
observed in 76%, which is significantly higher (P < or = 0.007 for all
pairwise comparisons) than the frequencies found in the Workshop
subgroups of patients with previously known recurring aberrations. The
chromosome bands most often involved in balanced aberrations were 1p36
and 3q26-27. Treatment exposure was significantly different (less
topoisomerase II inhibitor exposure, more radiotherapy-only exposure)
than for patients with 11q23 (P < 0.001 and P = 0.002, respectively) and
21q22 (P = 0.007 and P = 0.002, respectively) abnormalities. The median
time from the first toxic exposure to secondary disease, 59 months, was
significantly longer (P < or = 0.016 for all significant pairwise
comparisons) than the median latency of all other patients except those
in the Rare subgroup, and the median survival time, 7 months, was
significantly shorter than for patients in the 21q22, inv(16), and
t(15;17) subgroups (P < or = 0.002 for all pairwise comparisons), but
similar to patients in the 11q23 and Rare subgroups. In contrast to
known recurring abnormalities, significantly more patients (61%, all P <
0.001) presented with t-MDS, with over one-third of these patients
progressing to t-AML. Thus, this group of patients appears to be more
similar to the typical t-MDS/t-AML patients, with complex karyotypes as
well as chromosome 5 and 7 abnormalities, than to those with recurrent
balanced rearrangements. Copyright 2002 Wiley-Liss, Inc.
10
UI - 8213633
AU - Kawano S; Tatsumi E; Yoneda N; Yamaguchi N
TI -
Pattern of expression of CD45 RA/RO isoformic antigens in acute
myeloblastic leukemia cells.
SO - Am J Clin Pathol 1993 Oct;100(4):386-93
AD - Department of Laboratory Medicine, Kobe University School of Medicine,
Japan.
The authors used cell surface immunofluorescence to investigate the
expression of CD45 RA (4KB5)/RO (UCHL1) antigen by acute myeloblastic
leukemia (AML) cells from 78 patients. Four types--RA+/RO- (RO < 15%),
RA-/RO+ (RA < 15%), mixed (20% RA and 20% RO), and RA-/RO- (RA < 10% and
RO < 10%)--were observed. The number of cases with RA+/RO-, RA-/RO+,
mixed, and RA-/RO- types in each French-American-British subclass of AML
were as follows: M1 (n = 22): 18, 4, 0, 0; M2 (n = 21): 16, 0, 5, 0; M3
(n = 14): 11, 0, 0, 3; M4: 2, 2, 1, 0; and M5: 5, 5, 6, 0, respectively.
The M1 RA-/RO+ type, which was always CD7- CD34- HLA-DR-, constituted a
rare and distinct M1 subtype because there was no mixed type among the
M1 cases. All CD7+ AML cells were the RA+/RO- type and HLA-DR+ except
one. The expression of CD45 RO antigen, found in patients with M2, M4,
and M5 subtypes of AML, was thought to be associated with the maturity
of blasts as monocyte or granulocyte lineage cells. CD45 antigen has
tyrosine phosphatase activity in association with nonreceptor-type
tyrosine kinases. It was speculated that the functional status and stage
of differentiation of the granulocyte/monocyte lineage determine which
type of nonreceptor-type tyrosine kinases will operate, which then
select the pattern of expression of the CD45 isoform. Thus, the
determination of tyrosine kinases associated with CD45 isoforms seems to
be important in understanding the AML subsets defined by the pattern of
CD45 RA/RO expression.
11
UI - 8980370
AU - Arber DA; Glackin C; Lowe G; Medeiros LJ; Slovak ML
TI -
Presence of t(8;21)(q22;q22) in myeloperoxidase-positive, myeloid
surface antigen-negative acute myeloid leukemia.
SO - Am J Clin Pathol 1997 Jan;107(1):68-73
AD - Division of Pathology, City of Hope National Medical Center, Duarte,
California 91010, USA.
Although acute myeloid leukemias (AMLs) cytochemically negative for
myeloperoxidase are now well recognized, myeloid surface
antigen-negative AMLs are rare. The morphologic, cytochemical,
immunologic, and cytogenetic or molecular features of such cases are
described in four adults aged 19 to 60 years. All had AML with
maturation (FAB M2) and were myeloperoxidase positive. Immunologic
studies showed all to be HLA-DR positive but negative for the CD13,
CD14, and CD33 antigens. Two of four were CD34 antigen positive.
Cytogenetic studies were performed in three patients, and all
demonstrated t(8;21)(q22;q22). In studies using the reverse
transcriptase polymerase chain reaction in two patients, including the
patient in whom karytypic analysis was not performed, the AML1-ETO
fusion product of t(8;21) was identified. These findings suggest an
association between the lack of myeloid antigen expression in
myeloperoxidase-positive AML and the presence of t(8;21). In addition,
the results demonstrate the continued need for cytochemical studies in
the evaluation of acute leukemias.
12
UI - 11836165
AU - Domingo-Claros A; Larriba I; Rozman M; Irriguible D; Vallespi T; Aventin
TI -
A; Ayats R; Milla F; Sole F; Florensa L; Gallart M; Tuset E; Lopez C;
Woessner S
Acute erythroid neoplastic proliferations. A biological study based on
62 patients.
SO - Haematologica 2002 Feb;87(2):148-53
AD - Ciudad Sanitaria y Universitaria de Bellvitge, L'Hospitalet del
Llobregat 08907, Barcelona, Spain. alicia@domingo.com
BACKGROUND AND OBJECTIVES: The terms acute erythroleukemia and AML-M6
are defined in the FAB classification as proliferations of dysplastic
erythroid elements mixed with blasts of myeloid origin, but pure
erythroid leukemias are not included. The recent WHO classification has
a category of acute myeloid leukemia not otherwise categorized, which
includes acute erythroid leukemia (M6) of two subtypes:
M6a-erythroleukemia (erythroid/myeloid) and M6b-pure erythroid leukemia.
The aims of this co-operative study were to discover the incidences of
these different subtypes, and pay special attention to the morphology of
these entities. DESIGN AND METHODS: We reviewed a series of 62 patients
with erythroid neoplastic proliferations. Previous medical history, age,
sex, peripheral blood and bone marrow cell counts, cytochemical stains,
immunophenotype, and cytogenetics were evaluated at presentation. We
analyzed the incidence of erythrocyte, leukocyte and platelet
abnormalities in the peripheral blood. In bone marrow we analyzed
dysplastic features of erythroblasts, granulocytic elements and the
megakaryocytic lineage. RESULTS: Fifty-three patients met the criteria
of M6a subtype of the WHO classification, and 2 were classified as
having pure erythremia (M6b); 7 cases could not be classified according
to the WHO criteria. Fifty-five patients presented with de novo acute
leukemia, and seven patients had secondary acute leukemia. The most
frequent dysplastic features in blood smears were: schistocytes,
tear-drop and pincered cells in erythrocytes; hypogranulation and
hyposegmentation in leukocytes; gigantism and hypogranulation in
platelets. In bone marrow, megaloblastic changes, multinuclearity,
karyorrhexis and basophilic stippling in erythroblasts; hypogranulation
and gigantism in granulocytic series, and micromegakaryocytes and
unconnected nuclei in megakarocytes were the most dysplastic features. A
positive PAS reaction and increase of bone marrow iron with ring
sideroblasts were common features. Trilineage dysplasia was present in
54% of cases. Dysplastic features in granulocytic elements were absent
in 26% of patients and minimal erythroblastic dysplasia was observed in
seven patients. A complex karyotype was seen in 27% of patients;
chromosomes 5 and 7 were the most frequently involved. INTERPRETATION
AND CONCLUSIONS: De novo acute erythroid leukemia was more frequent than
secondary cases in our series. The most frequent type of acute erythroid
proliferation was the WHO M6a subtype and the least the pure erythroid
leukemia. We found a group of seven patients (11%) who could not be
classified according to the WHO criteria. Morphologic findings of
erythrocytes in peripheral blood, such as schistocytes, tear-drop and
pincered cells, were outstanding features. Morphologic aspects remain
one of the most important tools for diagnosing these entities.
13
UI - 11914187
AU - Reynolds P; Von Behren J; Elkin EP
TI -
Birth characteristics and leukemia in young children.
SO - Am J Epidemiol 2002 Apr 1;155(7):603-13
AD - California Department of Health Services, Environmental Health
Investigations Branch, Oakland, CA 94612, USA. preynold@dhs.ca.gov
The relation between birth characteristics and leukemia in young
children was investigated in a large population-based study in
California. Cases were obtained from the statewide cancer registry for
1988-1997. During this time, 1,957 leukemia cases were diagnosed among
children under age 5 years. Of these, 1,728 (88%) were matched to a
California birth certificate. Two control birth certificates, matched on
date of birth and sex, were randomly selected from the statewide birth
registry for each case. Analyses were performed separately for acute
lymphoid leukemia (ALL) and acute nonlymphoid leukemia (ANLL). Odds
ratios and 95% confidence intervals were estimated from conditional
logistic regression. The strongest finding was for greatly increased
risk of both types of leukemia in children with Down's syndrome (22
cases and no controls). African-American children had strikingly
decreased risk for ALL (odds ratio (OR) = 0.29, 95% confidence interval
(CI): 0.20, 0.42), and Asian/Pacific Islanders had increased risk for
ANLL (OR = 2.00, 95% CI: 1.19, 3.36). Older maternal age was associated
with slightly increased risk for ALL (maternal age > or =35 years, OR =
1.25, 95% CI: 1.04, 1.52), although this odds ratio was somewhat reduced
when adjusted for other factors. No strong relations were observed for
birth weight and ALL or ANLL.
14
UI - 11789265
AU - Tan H; Hao Y; Ying H
TI -
[Study on human leukemia cell apoptosis inducing effect of fraction C of
Naja naja Actra Venom]
SO - Zhongguo Zhong Xi Yi Jie He Za Zhi 2000 Apr;20(4):272-5
AD - Second Affiliated Hospital of Guangzhou Medical College, Guangzhou
(510260).
OBJECTIVE: To study the effect and mechanism of fraction C isolated from
Naja naja Actra Venom (FCNNAV) in inducing apoptosis of human leukemia
cells. METHODS: Light microscope, transmission electron microscope, DNA
electrophoresis, flow cytometry and RT-PCR assay were used to observe
the changes of human leukemia cells in morphology and biochemistry, and
Bcl-2/Bax expression after exposing to FCNNAV. RESULTS: FCNNAV could
induce HL60 cells apoptosis demonstrated by the typical morphological
and biochemical changes. Flow cytometry showed that J6-1, K562, HL60 and
fresh leukemia cells apoptosis could be induced by FCNNAV, and the
apoptosis rate was dose-dependent. RT-PCR detection showed the Bcl-2
gene expression of HL60 cells was down-regulated by FCNNAV, whereas the
Bax expression was unaffected. CONCLUSION: FCNNAV could induce apoptosis
of human leukemia cells and this effect is related to down-regulation of
Bcl-2 gene expression level.
15
UI - 11930663
AU - Li Y; Yang L; Chen S; Li R; Zhang Y; Lu Y; Luo G
TI -
Clonal expansion T cells identified in acute monoblastic leukemia by
CDR3 size analysis of TCR V beta repertoire using RT-PCR and genescan.
SO - Chin Med J (Engl) 2002 Jan;115(1):69-71
AD - Institute of Hematology, Medical College, Jinan University, Guangzhou
510632, China.
OBJECTIVE: To investigate the distribution and clonality of T cell
receptor (TCR) V beta repertoire in patients with acute monoblastic
leukemia (AML-M5). METHODS: Expression of the TCR V beta repertoire was
analyzed using reverse transcription-polymerase chain reaction (RT-PCR),
which amplified the complementarity determining region 3 of 24 TCR V
beta genes in peripheral blood from 9 cases with acute myclogenous
leukemia subtype 5 or acute monoblastic leukemia (AML-M5). PCR products
were further studied by genescan analysis to identify T cell clonality.
RESULTS: Expression of 1-10 V beta subfamilies was found in samples from
9 patients. Genescan analysis showed that some V beta subfamily products
from 8 of 9 cases contained an oligoclonal peak. Oligoclonal T cells of
the V beta 2 subfamily could be found in 6 patients with AML-M5.
CONCLUSIONS: T cell clonality expansion was found in AML-M5 cases and
were tendentious in the V beta 2 subfamily, suggesting a the specific
immune response for leukemia cell (M5) associated antigen and may
display antileukemia activity.
16
UI - 11925725
AU - Pigneux A; Marit G
TI -
[Acute myeloblastic leukemia]
SO - Rev Prat 2002 Feb 1;52(3):327-31
AD - Service des maladies du sang, centre hospitalier universitaire de
Bordeaux, hopital du Haut-Leveque, 33604 Pessac.
17
UI - 11939742
AU - Nagendra S; Meyerson H; Skallerud G; Rosenthal N
TI -
Leukemias resembling acute promyelocytic leukemia, microgranular
variant.
SO - Am J Clin Pathol 2002 Apr;117(4):651-7
AD - Department of Pathology, University of Iowa College of Medicine, Iowa
City, USA.
Acute promyelocytic leukemia (APL) should be distinguished from other
subtypes of acute myeloid leukemia (AML) because of the increased risk
of disseminated intravascular coagulation (DIC) and its response to
arsenic compounds and retinoids. Some cases of AML seem morphologically
similar to the microgranular variant of APL (French-American-British
[FAB] AML-M3v) but lack the t(15;17). We evaluated 8 cases of APL-like
leukemias for subtle morphologic, cytochemical, immunophenotypic, and
cytogenetic differences compared with 5 cases of promyelocytic
leukemia/retinoic receptor alpha (PML/RARalpha)-positive APL (FAB
AML-M3v). We also evaluated both groups for the presence of DIC. No
differences among the groups were noted in blast size, chromatin
pattern, nuclear morphologic features, intensity of myeloperoxidase
staining, or presence of Auer rods. Immunophenotypes were similar; both
types of cases lacked CD34 and HLA-DR and were CD13+ and CD33+. Two
cases of APL-like leukemias also were CD56+. DIC was present in 2
patients with M3v. Our study shows that there are no definitive
morphologic, cytochemical, or immunophenotypic findings that can
distinguish these cases from PML/RARalpha-positive APL.
18
UI - 7869766
AU - Belka C; Ahlers A; Sott C; Gaestel M; Herrmann F; Brach MA
TI -
Interleukin (IL)-6 signaling leads to phosphorylation of the small heat
shock protein (Hsp)27 through activation of the MAP kinase and MAPKAP
kinase 2 pathway in monocytes and monocytic leukemia cells.
SO - Leukemia 1995 Feb;9(2):288-94
AD - Max-Delbruck-Center for Molecular Medicine, Free University of Berlin,
Universitatsklinikum Rudolf Virchow, Germany.
Interleukin-6 is a multifunctional cytokine which regulates various
aspects of the host immune response. Here we show that signaling events
transferred by IL-6 in monocytes and the U937 human monocytic leukemia
cell line lead to the phosphorylation of the small heat shock protein
(Hsp)27. Phosphorylation of Hsp27 is both dose- and time-dependent. In
the absence of NaF, a serine/threonine phosphatase inhibitor, IL-6
failed to initiate Hsp27 phosphorylation in vitro. IL-6 also failed to
phosphorylate Hsp27 when cells had been deactivated with tyrosine kinase
inhibitors such as genistein. The capacity of cellular extracts to
phosphorylate Hsp27 could be, however, restored when either
immunoprecipitated activated MAP kinase or purified MAPKAP kinase 2 was
added to cell lysates. These findings suggest that IL-6-mediated
phosphorylation of Hsp27 results from activation of MAPKAP kinase 2, a
serine/threonine kinase which is activated by MAP kinase. Taking
together, our findings indicate that IL-6-induced activation of MAP
kinase by IL-6 entails the activation of MAPKAP kinase 2 and subsequent
phosphorylation of the Hsp27.
19
UI - 7780153
AU - Shurtleff SA; Meyers S; Hiebert SW; Raimondi SC; Head DR; Willman CL;
TI -
Wolman S; Slovak ML; Carroll AJ; Behm F; et al
Heterogeneity in CBF beta/MYH11 fusion messages encoded by the
inv(16)(p13q22) and the t(16;16)(p13;q22) in acute myelogenous leukemia.
SO - Blood 1995 Jun 15;85(12):3695-703
AD - Department of Pathology, St. Jude Children's Research Hospital, Memphis,
TN 38105, USA.
Inv(16)(p13q22) is one of the most frequent chromosomal rearrangements
found in acute myelogenous leukemia (AML), representing approximately
16% of documented karyotypic abnormalities. The inv(16) breakpoints have
been cloned and shown to involve the non-DNA binding component of the
AML-1 transcription factor complex termed core binding factor beta gene
(CBF beta) on 16q and the smooth muscle myosin heavy chain gene (MYH11)
on 16p. In this study, we analyzed 37 cases of inv(16)-containing AML
and 4 cases with t(16;16)(p13;q22) for expression of the CBF beta/MYH11
chimeric message by reverse transcription-polymerase chain reaction
(PCR) analysis. CBF beta/MYH11 chimeric messages were detected in 33 of
37 cases with the inv(16) and in the 4 t(16;16)-containing cases.
Sequence analysis of PCR products showed extensive breakpoint
heterogeneity in both CBF beta and MYH11. In addition to the previously
described breakpoint in CBF beta at nucleotide (nt) 495 (amino acid
165), we have identified a second novel fusion point at nt 399 (amino
acid 133) in 7% of the cases. Similarly, a unique breakpoint site was
identified in MYH11 at nt 1098, as well as at three previously
characterized sites at nts 994, 1201, and 1921. Of the 4 PCR-negative
cases, 2 of 3 tested lacked CBF beta rearrangements by Southern blot
analysis, suggesting the possible involvement of a different genomic
locus in some cases with cytogenetic evidence of inv(16). To assess
whether the portions of CBF-beta contained within the CBF beta/MYH11
chimeric products retain the ability to interact with their
heterodimeric DNA-binding partner AML-1, we performed in vitro
DNA-binding analysis. Recombinant CBF-beta polypeptides consisting of
the N-terminal 165 amino acids retained their ability to interact with
AML-1, whereas mutants containing only the N-terminal 133 amino acids
interacted with AML-1 less efficiently. These data suggest that
different CBF beta/MYH11 products may vary subtly in their biologic
activities.
20
UI - 7795233
AU - van der Reijden BA; Lombardo M; Dauwerse HG; Giles RH; Muhlematter D;
TI -
Bellomo MJ; Wessels HW; Beverstock GC; van Ommen GJ; Hagemeijer A; et al
RT-PCR diagnosis of patients with acute nonlymphocytic leukemia and
inv(16)(p13q22) and identification of new alternative splicing in
CBFB-MYH11 transcripts.
SO - Blood 1995 Jul 1;86(1):277-82
AD - Department of Human Genetics, Leiden University, Sylvius Laboratories,
The Netherlands.
As acute nonlymphocytic leukemia (ANLL) with inv(16) (p13q22) or
t(16;16)(p13;q22) has been shown to result from the fusion of
transcription factor subunit core binding factor (CBFB) to a myosin
heavy chain (MYH11), we sought to design methods to detect this
rearrangement using reverse transcriptase-polymerase chain reaction
(RT-PCR). In all of 27 inv(16)(p13q22) and four t(16;16)(p13;q22) cases
tested, a chimeric CBFB-MYH11 transcript coding for an in-frame fusion
protein was detected. In a more extensive RT-PCR analysis with different
primer pairs, we detected a second new chimeric CBFB-MYH11 transcript in
10 of 11 patients tested. The CBFB-MYH11 reading frame of the second
transcript was maintained in one patient but not in the others. We show
that the different CBFB-MYH11 transcripts in one patient arise from
alternative splicing. Translation of the transcript in which the
CBFB-MYH11 reading frame is not maintained leads to a slightly truncated
CBFB protein.
21
UI - 7670094
AU - Atkins KB; Troen BR
TI -
Comparative responsiveness of HL-60, HL-60R, and HL-60R+ (LRARSN) cells
to retinoic acid, calcitriol, 9 cis-retinoic acid, and sodium butyrate.
SO - Blood 1995 Oct 1;86(7):2475-80
AD - Department of Internal Medicine, Veterans Administration Medical Center,
Ann Arbor, MI, USA.
In HL-60 cells, retinoic acid (RA) and 9 cis-RA induce granulocytic
differentiation, and calcitriol and sodium butyrate induce monocytic
differentiation. To study the role of retinoid resistance on the
response to these agents, we investigated their effects in HL-60 cells,
retinoid-resistant HL-60R cells, and HL-60R+ cells in which retinoid
sensitivity has been restored. In HL-60 cells, cathepsin D (ctsd) mRNA
levels are increased by these agents and by cholera toxin after
pretreatment with each agent. Calcitriol, 9 cis-RA, and sodium butyrate
increase interleukin-8 (IL-8) mRNA expression, and pretreatment with
these agents or RA potentiates the stimulation of IL-8 by phorbol ester
(TPA). Pretreatment of HL-60 cells with all of the agents confers
inducibility of cathepsin L (ctsl) mRNA by TPA in previously
unresponsive cells. In HL-60R cells, none of the agents alone or in
combination significantly enhances the expression of the ctsd, IL-8, or
ctsl mRNAs. Retinoid stimulation (either alone or in combination with
the other agents) of the three mRNAs is partially restored in the
HL-60R+ cells. Calcitriol does not alter the expression of any of these
mRNAs, and only the stimulation of IL-8 mRNA by sodium butyrate is
recovered. Treatment with all of the agents inhibits proliferation and
stimulates differentiation of the HL-60 cells. RA and calcitriol are
unable to inhibit proliferation of the HL-60R cells, whereas only
calcitriol fails to inhibit proliferation of the HL-60R+ cells. None of
the agents induces differentiation in either the HL-60R or HL-60R+
cells. Therefore, the mutation of the RA receptor alpha is insufficient
to account for the altered responses of the HL-60R cells, and there are
likely defects in other signaling pathways in these cells. These cells
may prove useful in examining the mechanism of cross-resistance between
various differentiating agents.
22
UI - 9447846
AU - van der Reijden BA; Bloomfield CD; Touw IP; Jansen JH
TI -
Acute leukemias with structurally altered core binding factor subunits
Netherlands.
SO - Leukemia 1997 Dec;11(12):2217-9
AD - Institute of Hematology, Erasmus University Rotterdam, The Netherlands.
In the summer of 1997, the first meeting on 'Acute Leukemias with
Structurally Altered Core Binding Factor Subunits' was held. During the
meeting, which attracted more than 140 participants, many recognized
experts in the field of CBF and leukemia were present. In this short
report we summarize new data on CBF involvement in leukemia and other
diseases that were presented during the meeting.
23
UI - 11179492
AU - Ohyashiki JH; Hayashi S; Yahata N; Iwama H; Ando K; Tauchi T; Ohyashiki
TI -
K
Impaired telomere regulation mechanism by TRF1 (telomere-binding
protein), but not TRF2 expression, in acute leukemia cells.
SO - Int J Oncol 2001 Mar;18(3):593-8
AD - First Department of Internal Medicine, Tokyo Medical University,
Shinjuku-ku, Tokyo 160-0023, Japan.
Telomere regulation is suggested to be an important mechanism in
cellular proliferation and cellular senescence not only in normal
diploid cells but also in neoplastic cells, including human leukemia
cells. We studied the possible correlation among telomere length,
telomerase (a ribonuclear protein that synthesizes the telemeres de
novo) activity, hTERT (a catalytic subunit of telomerase) expression,
and TRF1 and TRF2 (telomere DNA binding proteins) expression in human
acute leukemia cells. The hTERT expression level was strongly associated
with telomerase activity (P=0.0001), indicating that the expression
level of the catalytic subunit (hTERT) regulates telomerase activity in
human acute leukemia cells. TRF1 expression, which is believed to
control telomere length, was significantly elevated in patients with
acute lymphoblastic leukemia (ALL) (P=0.0232) compared to those in acute
myeloid leukemia (AML); TRF1 expression tended to be higher in patients
without telomere shortening (P=0.077) and in those with hTERT expression
(P=0.055). This indicates that TRF1 may act to monitor telomere length
under the condition of up-regulated telomerase activity in some
neoplastic cells. In contrast, TRF2 expression in acute leukemia did not
show any correlation with telomere parameters in this study. Although
the precise regulation mechanism of telomere length is still uncertain,
these results may suggest that regulation of telomere length is
partially associated with TRF1 expression, whereas dysfunction of TRF1
expression may be speculated in a subset of acute leukemia.
24
UI - 11745387
AU - Zocchi MR; Pellegatta F; Pierri I; Gobbi M; Poggi A
TI -
Leukocyte-associated Ig-like receptor-1 prevents granulocyte-monocyte
colony stimulating factor-dependent proliferation and Akt1/PKB alpha
activation in primary acute myeloid leukemia cells.
SO - Eur J Immunol 2001 Dec;31(12):3667-75
AD - Laboratory of Tumor Immunology, Department of Internal Medicine,
Scientific Institute San Raffaele, Milan, Italy.
The leukocyte-associated Ig-like receptor-1 (LAIR-1), a surface
leukocyte receptor containing two immune receptor tyrosine-based
inhibitory motif (ITIM) is expressed on acute myeloid leukemia (AML)
blasts isolated from peripheral blood or bone marrow of 17 patients (2
M0, 3 M1, 5 M2, 2 M4 and 5 M5 according to French, American and British
classification). Further, we provide evidence thatLAIR-1 engagement
inhibits granulocyte-monocyte colony-stimulating factor (GM-CSF)-induced
proliferation of AML blasts. Indeed, leukemia cells stimulated with
GM-CSF were blocked in the G0/G1 phase of the cell cycle and underwent
apoptosis within 4 days after the engagement of LAIR-1. Remarkably,
LAIR-1 was functional also in AML blasts which do not express CD33,
mainly M4 and M5. Importantly, the LAIR-1 ligation led to a strong
inhibition of both GM-CSF receptor-mediated intracellular calcium
increases, phosphorylation and activation of Akt1/protein kinase B
alpha, a substrate of the phosphatidylinositol-3 kinase. This last
inhibitory effect was prevented by a synthetic peptide spanning the ITIM
portion of LAIR-1, suggesting the involvement of SHP-1 phosphatase in
LAIR-1-mediated inhibitory signal. Altogether, these findings indicate
that the engagement of LAIR-1 can down-regulate GM-CSF-mediated survival
and proliferation of AML blasts, suggesting an additional therapeutic
approach to the treatment of AML patients.
25
UI - 11911279
AU - Bruel A; Paschke S; Jainta S; Zhang Y; Vassy J; Rigaut J P; Beil M
TI -
Remodeling of vimentin cytoskeleton correlates with enhanced motility of
promyelocytic leukemia cells during differentiation induced by retinoic
acid.
SO - Anticancer Res 2001 Nov-Dec;21(6A):3973-80
AD - Institute of Hematology, Hospital St. Louis, Paris, France.
abruel@jupiter.chu-stlouis.fr
The intermediate filament (IFs) cytoskeleton is one of the major
determinants for the mechanical properties of cytoplasm. Vimentin is the
major IFs protein in peripheral blood neutrophils. We investigated its
expression and function during neutrophil differentiation using the
promyelocytic leukemia cell line NB4. The differentiation of NB4 cells
along the neutrophil lineage and the monocytic pathway was induced by
all-trans retinoic acid (ATRA) and phorbol esters (PMA), respectively.
We demonstrated a down-regulation of vimentin after ATRA treatment of
NB4 cells by immunoblotting and immunofluorescence. The architecture of
the vimentin cytoskeleton in differentiated NB4 cells resembled that
observed in mature neutrophils. In contrast, we showed a slight increase
of vimentin content in phorbol ester (PMA)-treated NB4 cells. The
structural features of the vimentin cytoskeleton obtained by image
analysis showed significant differences in network density and
directionality between ATRA-treated NB4 cells and controls. The
functional consequence of the cytoskeletal remodeling for the mechanical
properties of NB4 cells was assessed in migration assays. After ATRA
treatment, we found a 4-fold increased migration of NB4 cells across
transwell membranes with a 8 microm pore size without any cell size
modification. No significant differences between PMA-treated NB4 cells
and control cells could be observed using similar tests. These results
indicate that both vimentin expression and network architecture are
tightly controlled during neutrophil differentiation to regulate the
mechanical properties of these cells.
26
UI - 11921279
AU - Langabeer SE; Gale RE; Rollinson SJ; Morgan GJ; Linch DC
TI -
Mutations of the AML1 gene in acute myeloid leukemia of FAB types M0 and
M7.
SO - Genes Chromosomes Cancer 2002 May;34(1):24-32
AD - Department of Haematology, University College London, London, United
Kingdom. stephenl@icr.ac.uk
The AML1 gene encodes a transcription factor that, together with its
heterodimeric partner CBFB, regulates a number of target genes that are
essential for normal hemopoiesis. In acute myeloid leukemia (AML), AML1
is disrupted not only by chromosomal translocations but also by
mutations in the runt domain, which binds both DNA and CBFB. Acquired
mutations have been described predominantly in the AML FAB type M0. To
date, most patients appear to have biallelic disease, suggesting a
complete lack of normal AML1 function. Inherited loss of function
mutations thought to lead to haploinsufficiency also have been described
in patients who have a familial disorder with predisposition to AML
(FPD/AML), indicating the role of AML1 in megakaryopoiesis. Using
single-strand conformation polymorphism analysis, we studied the AML1
runt domain in 41 patients with M0 AML and identified potentially
pathologic mutations in five (12%). Biallelic disease could be confirmed
in only one patient, using loss of heterozygosity studies. At least
three of the
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