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NCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of AML - February 2002
National Cancer Institute®
Last Modified: February 1, 2002
Table of Contents
1
UI - 11340522
AU - Viscoli C; Paesmans M; Sanz M; Castagnola E; Klastersky J; Martino P;
TI -
Glauser M; International Antimicrobial Therapy Cooperative Group of the
European Organization for Research and Treatment of Cancer
Association between antifungal prophylaxis and rate of documented
bacteremia in febrile neutropenic cancer patients.
SO - Clin Infect Dis 2001 Jun 1;32(11):1532-7
AD - University of Genova and National Institute for Cancer Research, Genova,
Italy. viscolic@unige.it
Published data have suggested a correlation between antifungal
prophylaxis and bacteremia in febrile neutropenia. This correlation was
investigated among 3002 febrile neutropenic patients enrolled in 4
trials during 1986-1994. Globally, 1322 patients (44%) did not receive
antifungal prophylaxis; 835 (28%) received poorly absorbable antifungal
agents and 845 (28%) received absorbable antifungal agents. The rates of
bacteremia for these groups were 20%, 26%, and 27%, respectively
(P=.0001). In a multivariate model without including antifungal
prophylaxis, factors associated with bacteremia were: age, duration of
hospitalization, duration of neutropenia before enrollment, underlying
disease, presence of an intravenous catheter, shock, antibacterial
prophylaxis, temperature, and granulocyte count at onset of fever. When
antifungal prophylaxis was included, the adjustment quality of the model
improved slightly (P=.05), with an odds ratio of 1.19 (95% confidence
interval [CI], 0.92-1.55) for patients receiving nonabsorbable and 1.42
(95% CI, 1.07-1.88) for those who were receiving absorbable antifungal
agents. Antifungal prophylaxis with absorbable agents might have an
impact on the rate of documented bacteremia in febrile neutropenia. This
effect should be confirmed prospectively.
2
UI - 11778550
AU - Chen Y; Miao J; Fang Z
TI -
[Effects of PML and PML-RAR alpha antisense oligonucleotides on
promyelocytic leukemia cell line NB4]
SO - Zhonghua Zhong Liu Za Zhi 2000 Jul;22(4):283-6
AD - Shanghai Institute of Hematology, Renji Hospital, Laboratory of Leukemia
Research, Shanghai Second Medical University, Shanghai 200001, China.
OBJECTIVE: To investigate the different effects of anti-PML
(promyelocytic leukemia) and anti-PML/RAR alpha (promyelocytic
leukemia/retionic acid receptor alpha) antisense oligonucleotides on
cell growth, expression of PML-RAR alpha mRNA and PML-RAR alpha/PML
protein location of NB4 cell line. METHODS: RT-PCR was used for PML-RAR
alpha mRNA expression, trypan blue exclusion for cell count,
methylcellulose assay for leukemic colony forming unit,
immuno-fluorescence for PML-RAR alpha/PML protein localization. RESULTS:
Both anti-PML start codon region antisense (STAS) and anti-PML-RAR alpha
fusion region antisense (FUAS) could inhibit cell growth and formation
AML-CFU. Cells became partially differentiated on day 5, being more
marked in FUAS-treated cells than in STAS-treated ones. Down regulated
PML-RAR alpha mRNA expression occurred at 24 h was in STAS and
FUAS-treated cells and maintained for up to 72 h. Immuno-fluorescence
analysis with anti-PML monoclonal antibody showed a remarkable decrease
to almost complete disappearance of microgranules. The residual granules
became enlarged to become discrete dots (< 10 per cell), similar to
normal POD structure in some STAS-treated cells at 24 h. AT 72 h, nearly
all the granules disappeared. Similar changes were observed in
FUAS-treated cells. CONCLUSION: Both PML and PML-RAR alpha antisense
oligonucleotides can specifically block the expression of PML-RAR alpha
at mRNA and protein levels. PML protein is implicated in the regulation
of cell differentiation.
3
UI - 9354674
AU - Falini B; Flenghi L; Fagioli M; Lo Coco F; Cordone I; Diverio D;
TI -
Pasqualucci L; Biondi A; Riganelli D; Orleth A; Liso A; Martelli MF;
Pelicci PG; Pileri S
Immunocytochemical diagnosis of acute promyelocytic leukemia (M3) with
the monoclonal antibody PG-M3 (anti-PML).
SO - Blood 1997 Nov 15;90(10):4046-53
AD - Institutes of Hematology and Internal Medicine, University of Perugia,
Perugia, Italy.
Acute promyelocytic leukemia (APL) is characterized by a reciprocal 15;
17 chromosomal translocation, which fuses the promyelocytic leukemia
(PML) and retinoic acid receptor alpha (RARalpha) genes, leading to the
expression of the PML/RARalpha fusion oncoprotein. Immunocytochemical
labeling of the wild-type PML protein with the PG-M3 monoclonal antibody
(MoAb) directed against the amino terminal portion of the human PML gene
product, produces a characteristic nuclear speckled pattern that is due
to localization of the protein into discrete dots (5 to 20 per nucleus),
named PML nuclear bodies. The architecture of PML nuclear bodies appears
to be disrupted in APL cells that bear the t(15; 17), thus resulting in
a change of the nuclear staining pattern from speckled (wild-type PML
protein) to microgranular (PML-RARalpha fusion protein). To assess
whether the PG-M3 MoAb could assist in the diagnosis of APL (M3), bone
marrow and/or peripheral blood samples from 100 cases of acute
nonlymphoid leukemias of different subtypes were blindly immunostained
with the PG-M3 MoAb, using the immunoalkaline phosphatase (APAAP) or
immunofluorescence technique as detection system. Notably, the abnormal
(micropunctate) pattern of the PML/RARalpha fusion protein (usually
>/=50 small granules/per nucleus) was observed in APL (M3) samples, but
not in other types of acute nonlymphoid leukemias. Immunocytochemical
labeling with PG-M3 was particularly useful in the diagnosis of
microgranular variant of APL (M3V) (three cases misdiagnosed as M4 and
M5), and also to exclude a morphologic misdiagnosis of APL (six of 78
cases). In all cases investigated, immunocytochemical results were in
agreement with those of reverse transcription-polymerase chain reaction
(RT-PCR) for PML/RARalpha. Because the epitope identified by PG-M3 is
located in the aminoterminal portion of PML (AA 37 to 51), the antibody
was suitable for recognizing APL cases characterized by breakpoint
occurring at different sites of PML (bcr 1, bcr 2 and bcr 3). In
conclusion, immunocytochemical labeling with PG-M3 represents a rapid,
sensitive, and highly-specific test for the diagnosis of APL that bears
the t(15; 17). This should allow an easy and correct diagnosis of this
subtype of acute leukemia to any laboratory provided with a minimal
equipment for immunocytochemistry work.
4
UI - 9680345
AU - Diverio D; Rossi V; Avvisati G; De Santis S; Pistilli A; Pane F; Saglio
TI -
G; Martinelli G; Petti MC; Santoro A; Pelicci PG; Mandelli F; Biondi A;
Lo Coco F
Early detection of relapse by prospective reverse
transcriptase-polymerase chain reaction analysis of the PML/RARalpha
fusion gene in patients with acute promyelocytic leukemia enrolled in
the GIMEMA-AIEOP multicenter "AIDA" trial. GIMEMA-AIEOP Multicenter
"AIDA" Trial.
SO - Blood 1998 Aug 1;92(3):784-9
AD - Dipartimento di Biotecnologie Cellulari ed Ematologia, Universita "La
Sapienza", Rome, Italy.
Although the majority of patients with acute promyelocytic leukemia
(APL) are potentially cured by treatments combining all-trans retinoic
acid (ATRA) and chemotherapy (CHT), a sizable proportion (around 30%)
will relapse during follow-up. Retrospective molecular monitoring
studies using reverse transcriptase-polymerase chain reaction (RT-PCR)
for the specific PML/RARalpha fusion gene, have shown that a positive
test usually precedes the occurrence of hematologic relapse. Prospective
RT-PCR analyses were performed since 1993 at diagnosis and at
preestablished time intervals during follow-up in bone marrow (BM)
samples of 163 patients with PML/RARalpha+ APL enrolled in the
multicenter Gruppo Italiano Malattie Ematologiche Maligne dell' Adulto
(GIMEMA) trial AIDA (All-trans retinoic acid plus Idarubicin). Treatment
consisted of ATRA and idarubicin for induction followed by three
polychemotherapy courses as consolidation. The sensitivity level of the
RT-PCR assay for PML/RARalpha, as assessed by serial dilution
experiments, was 10(-4). All patients were in hematologic remission and
tested PCR- at the end of consolidation. Of 21 who converted to
PCR-positive thereafter, 20 underwent hematologic relapse at a median
time of 3 months (range, 1 to 14) from the first PCR+ result. Seventeen
of these 21 (81%) PCR+ conversions were recorded within the first 6
months postconsolidation. Of 142 who tested persistently PCR- in >/=2
tests after consolidation, 8 had hematologic relapse and 134 remained in
complete remission (CR) after a median follow-up of 18 months (range, 6
to 38) postconsolidation. Using a time-dependent Cox model, the relative
risk of hematologic relapse of patients who converted to PCR+ was 31.8
(confidence limits 95%, 12.9 to 78.3). Our results indicate that
conversion to PCR positivity for PML/RARalpha during remission is highly
predictive of subsequent hematologic relapse and highlight the
prognostic value of stringent molecular monitoring during the early
postconsolidation phase in APL. As a result of the present study,
salvage treatment in patients enrolled in the GIMEMA trial AIDA is now
anticipated at the time of molecular relapse, defined as the conversion
to PCR positivity in two successive BM samplings during follow-up.
Copyright 1998 by The American Society of Hematology.
5
UI - 10720132
AU - Bolognesi E; Cimino G; Diverio D; Rapanotti MC; D'Alfonso S;
TI -
Fleischhauer K; Migliaretti G; Momigliano-Richiardi P
HLA class I in acute promyelocytic leukemia (APL): possible correlation
with clinical outcome.
SO - Leukemia 2000 Mar;14(3):393-8
AD - Dipartimento di Scienze Mediche, Universita del Piemonte Orientale A
Avogadro, Novara, Italy.
The majority of patients with acute promyelocytic leukemia (APL) possess
either a bcr1 or a bcr3 type fusion between PML and RARalpha genes. The
junction sequences may possibly be a target for immune response and
influence susceptibility to the disease. In this case, HLA class I
allele frequencies would be different between bcr1 and bcr3 patients. To
test this hypothesis, we typed 102 APL patients for HLA-A, -B and -Cw
alleles. The A*1, A*30, B*51, B*41, Cw*0602, and Cw*1701 alleles showed
a different distribution between bcr1 and bcr3 patients, but in no case
was this statistically significant after correction for the number of
comparisons or was confirmed in an independent panel. Moreover, no
difference was detected between bcr1 and bcr3 when HLA alleles were
grouped according to their peptide binding specificities. Comparing HLA
frequencies, clinical features at diagnosis and clinical outcome of the
64 patients homogeneously treated with all-trans retinoic acid and
idarubicin (AIDA protocol) we observed a statistically significant
association between HLA-B*13 and risk of relapse by univariate and
multivariate regression analysis. Should this finding be confirmed in
larger future studies, this observation would be of outmost importance
in identifying patients at high risk of relapse in which more aggressive
consolidation therapies should be used.
6
UI - 11698395
AU - Kwon SH; Ahn SH; Kim YK; Bae GU; Yoon JW; Hong S; Lee HY; Lee YW; Lee
TI -
HW; Han JW
Apicidin, a histone deacetylase inhibitor, induces apoptosis and Fas/Fas
ligand expression in human acute promyelocytic leukemia cells.
SO - J Biol Chem 2002 Jan 18;277(3):2073-80
AD - Department of Biochemistry and Molecular Biology, College of Pharmacy
and Department of Genetic Engineering, College of Life Science and
Natural Resources, Sungkyunkwan University, Suwon 440-746, Korea.
We previously reported that apicidin arrested human cancer cell growth
through selective induction of p21(WAF1/Cip1). In this study, the
apoptotic potential of apicidin and its mechanism in HL60 cells was
investigated. Treatment of HL60 cells with apicidin caused a decrease in
viable cell number in a dose-dependent manner and an increase in DNA
fragmentation, nuclear morphological change, and apoptotic body
formation, concomitant with progressive accumulation of hyperacetylated
histone H4. In addition, apicidin converted the procaspase-3 form to
catalytically active effector protease, resulting in subsequent
cleavages of poly(ADP-ribose) polymerase and p21(WAF1/Cip1). Incubation
of HL60 cells with z-DEVD-fmk, a caspase-3 inhibitor, almost completely
abrogated apicidin-induced activation of caspase-3, DNA fragmentation,
and cleavages of poly(ADP-ribose) polymerase and p21(WAF1/Cip1).
Moreover, these effects were preceded by an increase in translocation of
Bax into the mitochondria, resulting in the release of cytochrome c and
cleavage of procaspase-9. The addition of cycloheximide greatly
inhibited activation of caspase-3 by apicidin by interfering with
cleavage of procaspase-3 and DNA fragmentation, suggesting that
apicidin-induced apoptosis was dependent on de novo protein synthesis.
Consistent with these results, apicidin transiently increased the
expressions of both Fas and Fas ligand. Preincubation with NOK-1
monoclonal antibody, which prevents the Fas-Fas ligand interaction and
is inhibitory to Fas signaling, interfered with apicidin-induced
translocation of Bax, cytochrome c release, cleavage of procaspase-3,
and DNA fragmentation. Taken together, the results suggest that apicidin
might induce apoptosis through selective induction of Fas/Fas ligand,
resulting in the release of cytochrome c from the mitochondria to the
cytosol and subsequent activation of caspase-9 and caspase-3.
7
UI - 11775836
AU - Hu J; Yu T; Zhao W; Gu B; Shen Z; Li X; Sun G; Chen S; Wang Z
TI -
Impact of RT-PCR monitoring on the long-term survival in acute
promyelocytic leukemia.
SO - Chin Med J (Engl) 2000 Oct;113(10):899-902
AD - Shanghai Institute of Hematology, Ruijin Hospital, Shanghai Second
Medical University, Ruijin Hospital-Samuel Waxman Cancer Research
Foundation, Joint Center for Cancer Differentiation Therapy, Shanghai
200025, China.
OBJECTIVE: To evaluate the impact of kinetics of molecular remission via
retro-transcriptase polymerase chain reaction (RT-PCR) assay on the
long-term survival in patients with acute promyelocytic leukemia (APL).
METHODS: Seventy patients with newly-diagnosed APL in remission were
involved in this study. Monitoring of minimal residual disease (MRD) was
performed regularly by RT-PCR assay for PML-RAR alpha during
consolidation. RESULTS: A 5-year relapse-free survival (RFS) and
overall-survival (OS) were estimated as 46.8% +/- 8.4% and 69.9% +/-
9.4% for the whole group. Fifty-two (74.3%) patients got negative RT-PCR
result at least once. Serial monitoring of RT-PCR was available in 38
cases and 24 (63.2%) patients presented with persistent negative PCR
results. The achievement and continuous negative RT-PCR result was
significantly related to the RFS. CONCLUSIONS: Achievement of negative
RT-PCR in remission is associated with favorable RFS and OS. Continuous
negative RT-PCR results are associated with long-term relapse-free
survival and may be considered as potentially curative. RT-PCR assay for
detection of MRD should be performed regularly during post-remission
period as an important prognostic factor.
8
UI - 11697646
AU - Stein RS; Wolff SN; Greer JP; Flexner JM; Goodman S; Jagasia M; Brandt
TI -
SJ; Morgan DS; Arrowsmith E; McCurley TL
Age and cytogenetics as predictors of event free survival in patients
with acute non-lymphocytic leukemia receiving high dose cytosine
arabinoside and daunorubicin as consolidation chemotherapy.
SO - Leuk Lymphoma 2001 Sep-Oct;42(5):913-22
AD - Department of Medicine, Vanderbilt University School of Medicine, and VA
Medical Center, Nashville, TN, USA. ssmd46@hotmail.com
Between 1991 and 1999, 67 patients with acute non-lymphocytic leukemia
(ANLL) in complete remission received high dose cytarabine (HiDAC) 3
gm/m2 q12h x 12 doses followed by daunorubicin 45 mg/m2/day x 3 days as
consolidation therapy. Five year actuarial event free survival (EFS) was
34% +/- 6%. Age was significantly associated with EFS. EFS was 60% +/-
15% in patients age 20 to 29, 48% +/- 16% in patients age 30 to 39, 23%
+/- 10% in patients age 40 to 49, 31% +/- 11% in patients age 50 to 59,
and 0% in patients age > or = 60. Contrary to other reports which have
used different HiDAC regimens, we found no relationship between
cytogenetics and EFS. Cytogenetics were defined as favorable risk:
t(8;21), inv (16), and del (16); neutral risk: normal or t(15;17); and
unfavorable risk: any abnormality not included in favorable risk or
neutral risk. EFS was 29% +/- 17% in patients with favorable
cytogenetics, 37% +/- 14% in patients with neutral cytogenetics, and 31%
+/- 12% in patients with unfavorable cytogenetics. These differences
were not statistically significant. Because of the successful use of
allogeneic transplantation at relapse in patients with matched related
donors, five year actuarial survival (S) in this series was 40% +/- 6%.
Five year actuarial survival was 57% +/- 9% for patients age < or = 44
and 25% +/- 8% for patients age > or = 45. This difference is
statistically significant, p < .025. Clinicians should be cautious about
making clinical decisions regarding consolidation therapy of ANLL on the
basis of the presence or absence of cytogenetic abnormalities as the
importance of cytogenetics may depend on the specific therapy which is
employed.
9
UI - 11835353
AU - Ito K; Kinjo K; Nakazato T; Ikeda Y; Kizaki M
TI -
Expression and sequence analyses of p33(ING1) gene in myeloid leukemia.
SO - Am J Hematol 2002 Feb;69(2):141-3
AD - Division of Hematology, Keio University School of Medicine, Tokyo,
Japan.
p33(ING1) is a novel candidate tumor suppressor gene which is involved
in the regulation of apoptosis. p33(ING1) interacts with p53 signaling
pathway and regulates cellular growth. It has reported that the
expression of p33(ING1) mRNA was decreased in lymphoid malignancies. We
thus investigated the potential involvement of p33(ING1) abnormalities
in myeloid leukemias. However, the levels of p33(ING1) transcript were
almost equal in 3 AML cell lines and 10 fresh AML samples. In addition,
neither point mutations nor deletions in p33(ING1) gene were found in
myeloid leukemias. These results suggest that p33(ING1) may not be a
major candidate tumor suppressor gene in myeloid leukemias. Copyright
2002 Wiley-Liss, Inc.
10
UI - 11587217
AU - Preisler HD; Li B; Chen H; Fisher L; Nayini J; Raza A; Creech S;
TI -
Venugopal P
P15INK4B gene methylation and expression in normal, myelodysplastic, and
acute myelogenous leukemia cells and in the marrow cells of cured
lymphoma patients.
SO - Leukemia 2001 Oct;15(10):1589-95
AD - Rush Cancer Institute, Chicago, Illinois 60612, USA.
P15INK4B methylation and expression was studied in bone marrow cells
obtained from normal individuals, from patients who had been cured of
lymphoma, and from patients with either MDS or AML. The level of p15
methylation was very low in normal BM cells and in CD34+ and CD34-
subpopulations (0-6.5%; med, = 2.5%). P15INK4B transcripts were present
in each of these cell populations. In contrast, methylation was the
usual situation in MDS and AML marrows. The presence of methylation of
the p15INK4B gene did not always indicate an absence of expression nor
was expression always present if methylation was absent. P15INK4B
methylation was studied in the marrows of nine patients (one studied
twice) who had been cured of lymphoma and in whom hemopoiesis was
believed to be normal. Increased methylaton was present in all 10
marrows. These data indicate that p15INK4B methylation is likely to be a
very early event in the development of the secondary hematologic
disorders.
11
UI - 11587231
AU - Takagi K; Yoshida A; Yamauchi T; Yamashita T; Iwasaki H; Tsutani H;
TI -
Maezawa Y; Baba H; Ueda T
Successful treatment of Aspergillus spondylodiscitis with high-dose
itraconazole in a patient with acute myelogenous leukemia.
SO - Leukemia 2001 Oct;15(10):1670-1
12
UI - 11801314
AU - Salido M; Sole F; Espinet B; Fernandez C; Zamora L; Woessner S; Florensa
TI -
L
Pentasomy 21 with two isochromosomes 21 in a case of acute myeloid
leukemia without maturation.
SO - Cancer Genet Cytogenet 2002 Jan 1;132(1):71-3
AD - Laboratori de Citologia Hematologica, Escola de Citologia Hematologica
S. Woessner-IMAS, Hospital del Mar, IMAS, IMIM, Barcelona, Spain.
e0037@imas.imim.es
Here, we report a 72-year-old male patient with acute myeloid leukemia
(AML) without maturation. Cytogenetic study of a bone marrow culture
revealed the following karyotype: 47,XX,+21,+i(21)(q10)x2. Fluorescence
in situ hybridization study with a locus specific probe for 21q22
verified a pentasomy of 21q as a sole clonal cytogenetic abnormality. To
our knowledge, this is the first report of pentasomy 21q in AML without
Down syndrome.
13
UI - 11721412
AU - Chen W; Zhang W; Zhu J
TI -
[Homozygous deletion and methylation of p16 and p15 gene in acute
leukemia]
SO - Zhonghua Xue Ye Xue Za Zhi 1999 Sep;20(9):474-6
AD - Beijing Red-cross Chaoyang Hospital, Capital University of Medical
Sciences, Beijing 100020.
OBJECTIVE: To investigate the frequency of p16 and p15 gene inactivation
in acute leukemia and to evaluate its clinical significance. METHODS:
Fifty-six patients with newly diagnosed acute leukemia was studied. PCR
technique was used to detect homozygous deletion of p16 and p15 gene,
restriction enzyme-PCR technique was used to detect gene methylation,
and TdT-mediated dUTP-digoxygenin end-labeling (TUNEL) technique was
used to detect cell apoptosis. RESULTS: p16 and/or p15 gene inactivation
was detected in 33 of the 56 patients, including 23/38 (60.5%) of the
ALL patients (T-ALL 12/16, B-ALL 11/22) and 10/18 (55.5%) of the ANLL
patients. For All patients, methylation was the major pathway of p16 and
p15 gene inactivation. Patients with p16 and/or p15 gene inactivation
had a delayed apoptosis, a poor response to chemotherapy, a lower
remission rate and a shortened remission duration. CONCLUSION: The
inactivation of p16 and p15 gene plays a key role in the pathogenesis of
acute leukemia.
14
UI - 11845985
AU - Tothova E; Elbertova A; Fricova M; Kafkova A; Hlebaskova M; Svorcova E;
TI -
Stecova N; Guman T; Raffac S
P-glycoprotein expression in adult acute myeloid leukemia: correlation
with induction treatment outcome.
SO - Neoplasma 2001;48(5):393-7
AD - Department of Hematology, Medical Faculty Hospital and UPJS, Kosice,
Slovak Republic. etothova@post.sk
Drug resistance has become a major cause of the treatment failure in
patients with acute leukemia. P-glycoprotein (P-gp), which is associated
with multidrug resistance (MDR) phenotype, has been reported to be an
important predictor of the treatment outcome. The aim of this study was
to analyze the value of P-gp expression in bone marrow cells as a
predictor of the response to remission induction chemotherapy, as well
as duration of remission in adult patients with newly diagnosed acute
myeloid leukemia (AML). We examined the expression of P-gp in 31
patients using the monoclonal antibody UIC2. Direct immunofluorescent
labeling was performed and samples were analyzed by flow cytomery.
Kolmogorov-Smirnov test (D-value) was used to estimate UIC2 staining. A
D > or = 0.3 for labeling of gated leukaemic blasts as compared to that
of the isotypic control was defined positive (+) and compared to
clinical data. P-gp expression was found in 14/31 (45.6%) patients,
17/31 (54.8%) of the samples were found P-gp negative(-). No correlation
was found regarding age, sex and FAB subtype, altough 6/14 (43%) cases
with more than 50% of cells having P-gp expression, were CD34+/CD7+.
Complete remission rates were significantly lower in UIC2+ patients than
in UIC2- cases (70% vs 35%, p < 0.01). Complete remission duration was
also shorter in UIC2+ patients (6 vs 12.4 months). Our data indicate,
that P-gp expression is a reliable marker of resistance to induction
treatment in patients with de novo AML and can help to identify patients
who may require alternative regimens designed to overcome therapy
resistance.
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