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Abramson Cancer Center
NCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of AML - October 2001
National Cancer Institute®
Last Modified: November 21, 2001
Table of Contents
1
UI - 21402012
AU - Cabrera ME; Campbell M; Quintana J; Undurraga MS; Ford AA; Greaves MF
TI -
[Clinical significance and frequency of the 11q23/MLL genetic molecular
alteration in Chilean infants with acute leukemia]
SO - Rev Med Chil 2001 Jun;129(6):634-42
AD - Departamento de Medicina, Campus Oriente, Facultad de Medicina
Universidad de Chile. mcabrera@mi-mail.cl
BACKGROUND: Acute leukemia (AL) in infants generally shows distinctive
biologic features and has a poor prognosis. AIM: To study the frequency
of the cytogenetic alteration of 11q23 chromosome or the recombination
of MLL gene in infants less than 18 months old, with acute leukemia.
PATIENTS AND METHODS: We analyzed 37 cases of AL in infants less than 18
months of age diagnosed in Chile from 1989 to 1999. The clinical
features and cytogenetic/molecular defects of 11q23MLL gene
rearrangement and their influence in prognosis were determined. RESULTS:
There were 18 cases of acute Lymphoblastic leukemia (ALL) characterized
by female sex (67%) high presenting leukocyte count (median 99 x 109/L),
blast cells with a CD10 negative phenotype (50%) and 11q23/MLL
rearrangement (39%). Molecular abnormalities of 11q23 were significantly
associated with adverse prognosis, with an event free survival (EFS) of
only 14 +/- 12%. Interestingly, infants with germ line 11q23 had a very
good outcome with an EFS of 73 +/- 11% (p < 0.025). There were 19 cases
of acute myeloblastic leukemia (AML) characterized by male sex (63%)
high leukocyte count (median 93 x 109/L), FAB-MS morphology (53%) and
11q23/MLL rearrangement (53%). EFS was very poor, 20 +/- 9% and 33 +/-
4% for rearranged and germinal group respectively (p = NS), due to a
high mortality rate during the first month of diagnosis. CONCLUSIONS:
These findings demonstrate that Chilean ALL infants with 11q23
abnormalities have a very poor prognosis. However those with germinal
state can enjoy a prolonged disease free survival with the current
treatment protocols.
2
UI - 21450469
AU - Smith A; Robson L; Heaps LS; Sharma P; Dunlop L; Bhave A; Bradstock K
TI -
Routine fluorescence in situ hybridization with the MLL probe does not
reliably detect two separate signals on one chromosome 11 in patients
with trisomy 11.
SO - Cancer Genet Cytogenet 2001 Sep;129(2):173-6
AD - Department of Cytogenetics, Royal Alexandra Hospital for Children,
Locked Bag 4001, NSW 2145, Westmead, Australia. ellies@nch.edu.au
Trisomy 11 is considered to be a rare cytogenetic abnormality in
myelodysplastic syndromes (MDS) and acute myelogenous leukemia (AML).
Duplication of the MLL gene (localized to 11q23) has been found on one
chromosome 11 in patients with trisomy 11, detected by DNA techniques.
We investigated copy number of MLL in seven patients with trisomy 11 to
see if duplication could be assessed by the detection of two separate
signals on fluorescence in situ hybridization (FISH). If so, FISH could
provide a quick easy screen of MLL status in routine referrals. The
diagnostic bone marrow aspirate showed trisomy 11 in five adult patients
with MDS/AML as part of a complex karyotype and in two children with
acute lymphoblastic leukemia (ALL) as part of a hyperdiploid karyotype.
Fluorescence in situ hybridization utilized the suspensions remaining
after the cytogenetic harvest. Two FISH probes were used on the adult
patients (MLL - Oncor and Vysis), and one (Vysis) for the two children
with ALL. Analysis showed that the proximity of the two putative
hybridization signals made it very difficult to unambiguously see two
separate signals. The hybridisations (Oncor probe) were convincing of
MLL duplication (namely two distinct signals) in only one patient, but
this was not borne out with the other MLL probe (Vysis). We conclude
that conventional FISH with MLL probe is not suited to act as a screen
for MLL duplication in patients with trisomy 11.
3
UI - 21390867
AU - Chen H; Sun G; Han R
TI -
[In vitro study on the effects of the novel retinoids combined with
IFN-gamma on the proliferation and differentiation of fresh acute
monocytic leukemic cells]
SO - Zhonghua Xue Ye Xue Za Zhi 1999 Jan;20(1):10-3
AD - Ruijin Hospital, Shanghai Second Medical University, Shanghai 200025.
OBJECTIVE: To investigate the prospect for clinical use of novel
retinoids YS 904012 and R 9158 in combination with IFN-gamma in inducing
differentiation of acute monocytic leukemia. METHODS: The effects of
novel retinoids with IFN-gamma on the differentiation and clonal
proliferation of fresh leukemia cell from 6 monocytic leukemia patients
were studied in vitro. Cell morphological examination, nitro tetrazolium
blue reduction test and DCE, expression of CD14 and CD68 and CFU-L were
used in the study. RESULTS: The primary leukemia cell, cultured with the
combination of YS 904012 and IFN-gamma, became more mature in
morphology. The NBT reduction rate and DCE were increased from 23.4% and
25.0% to 61.5% and 52.0%, respectively. The expression of CD14 and CD68
was increased. The growth of the leukemic colony in semi-solid culture
was markedly inhibited. The activity of YS 904012 combined with
IFN-gamma in inhibiting proliferation and inducing differentiation of
monoblast was greater than that of R9158 or all-trans retinoic acid in
combination with IFN-gamma (P < 0.01). CONCLUSION: The YS 904012
combined with IFN-gamma is worthy of further study for clinical
differentiation therapy of acute monocytic leukemia.
4
UI - 21390870
AU - Hua D; Li J; Xia X
TI -
[The clinical and biological significance of megakaryocytic antigen
expression in acute myeloid leukemia]
SO - Zhonghua Xue Ye Xue Za Zhi 1999 Jan;20(1):21-3
AD - First Affiliated Hospital of Suzhou Medical College, Suzhou 215006.
OBJECTIVE: To explore megakaryocytic (MK) antigen expression in
previously untreated adult acute myeloid leukemia (AML) and its relation
to the clinical and biological characteristics. METHODS: Two hundred and
eleven cases of AML were detected with flow cytometric
immunofluorescence assay. RESULTS: Twenty-seven cases (12.8%) were MK
antigen positive with the higher positive rates in hybrid acute leukemia
(45.5%) and acute monoblastic leukemia (24.1%). MK antigen expression
was significantly correlated with CD34 antigen expression, high white
cell count, high P-glycoprotein positivity and had no correlation with
chromosome aberration. 33.3% of MK positive AML patients achieved
complete remission which was significantly lower than that (71.9%) in MK
negative cases. CONCLUSION: MK antigen positive AML might derived from
malignant transformation of hemotopoietic stem cell at earlier stage and
the detection of MK expression was of values in predicting treatment
effect and prognosis for adult AML.
5
UI - 21329582
AU - Benoit GR; Flexor M; Besancon F; Altucci L; Rossin A; Hillion J;
TI -
Balajthy Z; Legres L; Segal-Bendirdjian E; Gronemeyer H; Lanotte M
Autonomous rexinoid death signaling is suppressed by converging
signaling pathways in immature leukemia cells.
SO - Mol Endocrinol 2001 Jul;15(7):1154-69
AD - INSERM U-496, Centre G. Hayem Hopital Saint-Louis 75010 Paris, France.
On their own, retinoid X receptor (RXR)-selective ligands (rexinoids)
are silent in retinoic acid receptor (RAR)-RXR heterodimers, and no
selective rexinoid program has been described as yet in cellular
systems. We report here on the rexinoid signaling capacity that triggers
apoptosis of immature promyelocytic NB4 cells as a default pathway in
the absence of survival factors. Rexinoid-induced apoptosis displays all
features of bona fide programmed cell death and is inhibited by RXR, but
not RAR antagonists. Several types of survival signals block
rexinoid-induced apoptosis. RARalpha agonists switch the cellular
response toward differentiation and induce the expression of
antiapoptosis factors. Activation of the protein kinase A pathway in the
presence of rexinoid agonists induces maturation and blocks immature
cell apoptosis. Addition of nonretinoid serum factors also blocks cell
death but does not induce cell differentiation. Rexinoid-induced
apoptosis is linked to neither the presence nor stability of the
promyelocytic leukemia-RARalpha fusion protein and operates also in
non-acute promyelocytic leukemia cells. Together our results support a
model according to which rexinoids activate in certain leukemia cells a
default death pathway onto which several other signaling paradigms
converge. This pathway is entirely distinct from that triggered by RAR
agonists, which control cell maturation and postmaturation apoptosis.
6
UI - 21341701
AU - Goto Y; Yue L; Yokoi A; Nishimura R; Uehara T; Koizumi S; Saikawa Y
TI -
A novel single-nucleotide polymorphism in the 3'-untranslated region of
the human dihydrofolate reductase gene with enhanced expression.
SO - Clin Cancer Res 2001 Jul;7(7):1952-6
AD - Department of Pediatrics, Kanazawa University School of Medicine,
Kanazawa, Ishikawa 920-8641, Japan.
A novel single-nucleotide polymorphism (SNP), 829C-->T in the
3'-untranslated region of the human dihydrofolate reductase (DHFR) gene
transcript, was identified in the study population of 37 patients with
childhood leukemias/lymphomas and 83 healthy Japanese children.
Frequencies of the DHFR 829C/C, 829C/T, and 829T/T genotypes were 83.8,
10.8, and 5.4%, respectively, in the cases and 74.7, 19.3, and 6.0% in
the controls, showing no significant difference in genotype frequencies
between the cases and controls. When determined by real-time
quantitative reverse transcription-PCR analysis, the highest expression
of the DHFR transcript was demonstrated in the samples with a DHFR
829T/T polymorphism (P < 0.001). Direct association of the presence of
the SNP with methotrexate-related adverse events in each patient was not
demonstrated in this limited analysis. These data suggest that the novel
DHFR 829 polymorphism is associated with a positive role in gene
expression and provide evidence of a functional SNP in the 3' regulatory
region of the gene.
7
UI - 21371226
AU - Tan H; Ying H; Chu J
TI -
[Augmented effect of Composite Radix Salviae Miltiorrhizae Injection on
radiosensitivity of leukemia cells]
SO - Zhongguo Zhong Xi Yi Jie He Za Zhi 1998 May;18(5):279-81
AD - Second Affiliated Hospital, Guangzhou Medical College, Guangzhou 510260.
OBJECTIVE: To explore the effect of Composite Radix Salviae
Miltiorrhizae Injection (CSMI) on radiosensitivity of leukemia cells.
METHODS: Semisolid agar culture and flow cytometry assay were performed
for studying the change in radiosensitivity of HL60 cell line and fresh
human leukemia cells after exposing to CSMI. RESULTS: The D0(the inverse
of the slope of the survival curve) and SF2(survival fraction at 2 Gy)
of HL60 cell line were decreased from 1.53, 0.34 to 0.93, 0.12,
respectively and apoptosis rates after radiation were raised
significantly by CSMI. Furthermore, the concentration of CSMI and the
time of mixed culture with CSMI before irradiation had positive relation
to the effects mentioned above. Compared with control group, CSMI could
increase the radiation-induced apoptosis of fresh leukemia cells (5.89
+/- 2.91% vs 12.05 +/- 3.06%). CONCLUSION: CSMI could obviously enhance
the radiosensitivity of leukemia cells.
8
UI - 21424592
AU - Kilian PH; Skrzypek S; Becker N; Havemann K
TI -
Exposure to armament wastes and leukemia: a case-control study within a
cluster of AML and CML in Germany.
SO - Leuk Res 2001 Oct;25(10):839-45
AD - Department of Haematology, Marburg University Medical Center,
Baldingerstrasse, 35033, Marburg, Germany.
An unusually high incidence of acute myeloid leukemia (AML) and chronic
myeloid leukemia (CML) concentrated in a specific locality of a region
in Germany motivated a descriptive incidence study in that region which
showed a near 10-fold increased risk of CML among males but not among
females (Kolb G, Becker N, Scheller S, Zugmaier G, Pralle H, Wahrendorf
J, Havemann K. Increased risk of acute myelogenous leukemia (AML) and
chronic myelogenous leukemia (CML) in a County of Hesse, Germany, Soc
Prev Med 1993;38:190-195). Since a serious environmental contamination
of areas in this locality with armament wastes containing
toluene-derivatives has been known for a long time, the hypothesis arose
that TNT production and the related severe contamination of soil and
water might be responsible for the observed higher risk. We carried out
a case-control study within the cluster to test this hypothesis.
Overall, the results do not confirm the hypothesis. There is an
indication of a relationship of an increased odds ratio with the
exposure for a small group of persons who lived at a particular site in
one of the two communities involved during the peak phase of TNT
production during the 1940s. However, this finding is spurious and
cannot explain the large majority of cases which occurred in that area
in the 1980s. At the moment, no other explanation can be given for the
increased risk of leukemias in that area.
9
UI - 21424603
AU - Dodge JE; Munson C; List AF
TI -
KG-1 and KG-1a model the p15 CpG island methylation observed in acute
myeloid leukemia patients.
SO - Leuk Res 2001 Oct;25(10):917-25
AD - Department of Pharmacology and Toxicology, University of Arizona,
Arizona Cancer Center, Tucson, AZ 85724-5024, USA.
dodge@cvrc.mgh.harvard.edu
p15 and p16 are tumor suppressor genes that have 5' CpG islands and both
are subject to hypermethylation associated with their transcriptional
inactivation in hematological malignancies. In this study, we used
sodium bisulfite sequencing to obtain a complete map of the
5-methylcytosine status of 80 CpGs covering approximately 900 bp in the
5' p15 CpG island, and 53 CpGs covering approximately 700 bp in the 5'
p16 CpG island in the hematopoietic cell lines HL60, KG-1, and KG-1a,
two normal human bone marrow samples (NBM), and eight cytosine
arabinoside (ara-C)-resistant adult acute myeloid leukemia (AML)
patients. We found methylation of the p15 CpG island in 75% of the AML
cases studied spread throughout the 5' region analyzed but only minimal
methylation of p15 in NBM. Further, the p16 CpG island was not
aberrantly methylated in NBM or the eight AML patients studied. Two
distinct modes of p15 methylation in AML were identified, variegated and
complete. Interestingly, KG-1 and KG-1a model the methylation of p15
observed in AML, where KG-1 methylation is variegated and KG-1a
methylation is complete. Both KG-1 and KG-1a had no detectable p15 mRNA
or protein. These results demonstrate that rather than continuous
increases in p15 methylation, surprisingly two punctuated modes of
aberrant p15 methylation, variegated and complete, were observed in
vitro and in vivo. Thus aberrant methylation of tumor suppressor genes
is not a binary switch but in the case of p15 occurs in two independent
and stable states.
10
UI - 21329982
AU - Watanabe M; Kohri M; Takaishi M; Horie R; Higashihara M
TI -
Molecular cloning and sequencing of myosin light chains in human
megakaryoblastic leukemia cells.
SO - J Smooth Muscle Res 2001 Feb;37(1):25-38
AD - Fourth Department of Internal Medicine, School of Medicine, Kitasato
University, Sagamihara-shi, Kanagawa, Japan.
Myosin light chain genes of hematopoietic cells have yet to be
characterized. We cloned the full-length cDNAs of 20 kDa regulatory
myosin light chain (MLC-2) and 17 kDa essential myosin light chain
(MLC-3) from Meg-01, a human megakaryoblastic leukemia cell line. Both
MLC-2 and MLC-3 gene are transcribed ubiquitously in various
hematopoietic cells. The MLC-2 open reading frame of 516 nucleotides
encoding a protein of 172 residues was detected in cloned cDNA of 967
nucleotides. The Ca2+-binding domain and five phosphorylation sites were
highly conserved. The deduced amino acid sequence has a 99.4% and 100%
homology with that of human fetus brain and human lymphocyte,
respectively. The MLC-3 open reading frame of 453 nucleotides encoding a
protein of 151 residues was detected in cloned cDNA of 742 nucleotide.
The MLC-3 protein is 99.3% identical to that of human fibroblasts. These
results suggest that hematopoietic myosin light chain proteins are
similar to those of other nonmuscle cells and smooth muscle, thus
differing from skeletal and cardiac muscles.
11
UI - 21519129
AU - Alcalay M; Orleth A; Sebastiani C; Meani N; Chiaradonna F; Casciari C;
TI -
Sciurpi MT; Gelmetti V; Riganelli D; Minucci S; Fagioli M; Pelicci PG
Common themes in the pathogenesis of acute myeloid leukemia.
SO - Oncogene 2001 Sep 10;20(40):5680-94
AD - Department of Experimental Oncology, European Institute of Oncology,
20141 Milan, Italy. malcalay@ieo.it
The pathogenesis of acute myeloid leukemia is associated with the
appearance of oncogenic fusion proteins generated as a consequence of
specific chromosome translocations. Of the two components of each fusion
protein, one is generally a transcription factor, whereas the other
partner is more variable in function, but often involved in the control
of cell survival and apoptosis. As a consequence, AML-associated fusion
proteins function as aberrant transcriptional regulators that interfere
with the process of myeloid differentiation, determine a stage-specific
arrest of maturation and enhance cell survival in a cell-type specific
manner. The abnormal regulation of transcriptional networks occurs
through common mechanisms that include recruitment of aberrant
co-repressor complexes, alterations in chromatin remodeling, and
disruption of specific subnuclear compartments. The identification and
analysis of common and specific target genes regulated by AML fusion
proteins will be of fundamental importance for the full understanding of
acute myeloid leukemogenesis and for the implementation of
disease-specific drug design.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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