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Abramson Cancer Center
NCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of AML - May 2002
National Cancer Institute®
Last Modified: May 1, 2002
Table of Contents
1
UI - 11960354
AU - Salonen MJ; Siimes MA; Salonen EM; Vaheri A; Koskiniemi M
TI -
Antibody status to HHV-6 in children with leukaemia.
SO - Leukemia 2002 Apr;16(4):716-9
AD - Haartman Institute, Department of Virology, University of Helsinki,
Helsinki, Finland.
Forty children with acute lymphoblastic (33) or myeloid leukaemia
(seven) were studied for IgG and IgM antibodies and IgG avidity against
human herpesvirus 6 (HHV-6) at the time of diagnosis, and compared with
age-, sex- and season-matched children with various neurological
diseases of suspected viral origin. Of the children with leukaemia,
97.5% had IgG antibodies and 40% IgM antibodies to HHV-6 compared with
92.3% and 7.7% of reference subjects (P = 0.005). A seronegative child
with leukaemia seroconverted 3 weeks after the diagnosis. The avidity of
IgG antibodies (based on the resistance to urea treatment) was high in
all children with leukaemia. One reference child had HHV-6-specific IgG
antibodies with low avidity, which together with his positive IgM
indicated an acute infection. The presence of specific IgM antibodies in
40% of children with leukaemia and the high avidity of IgG suggest a
reactivation or an inaproppriate primary response to HHV-6 infection.
The results support the conclusion of the role of the HHV-6 infection at
the onset of childhood leukaemia.
2
UI - 11960357
AU - Cooper MA; Caligiuri MA
TI -
Immunologic manipulation in AML: from bench to bedside.
SO - Leukemia 2002 Apr;16(4):736-7
AD - Department of Internal Medicine and the Comprehensive Cancer Center, The
College of Medicine and Public Health, The Ohio State University,
Columbus, OH 43210, USA.
3
UI - 11960359
AU - Deguchi K; Gilliland DG
TI -
Cooperativity between mutations in tyrosine kinases and in hematopoietic
transcription factors in AML.
SO - Leukemia 2002 Apr;16(4):740-4
AD - Howard Hughes Medical Institute, Brigham and Women's Hospital,
Dana-Farber Cancer Institute, Boston, MA, USA.
4
UI - 11782470
AU - Furukawa K; Yokoyama K; Sato T; Wiels J; Hirayama Y; Ohta M; Furukawa K
TI -
Expression of the Gb3/CD77 synthase gene in megakaryoblastic leukemia
cells: implication in the sensitivity to verotoxins.
SO - J Biol Chem 2002 Mar 29;277(13):11247-54
AD - Department of Biochemistry II, Nagoya University School of Medicine, 65
Tsurumai, Nagoya 466-0065, Japan.
Expression levels of Gb3/CD77 synthase together with Gb3/CD77 antigen
were analyzed using human hematopoietic tumor cell lines and normal
cells. Among about 40 kinds of cells, Burkitt lymphoma cells showed the
highest gene expression concomitant with the expression levels of
Gb3/CD77. Unexpectedly, megakaryoblastic leukemia lines also expressed
fairly high levels of mRNA of Gb3/CD77 synthase and its product. A
megakaryoblastic leukemia line, MEG-01 was sensitive to verotoxins from
Escherichia coli O157 and apoptosis was induced via the caspase pathway.
We also demonstrated that the cell surface Gb3/CD77 expression was
reduced on differentiated MEG-01 although the mRNA level of the
alpha1,4Gal-T gene increased. In this case, the localization of Gb3/CD77
was changed from the cell surface to the cytoplasm as stained with a
granular pattern, co-localizing with platelet GPIIb-IIIa, indicating
that some of them were platelet precursors. Small particles outside of
cells also showed similar staining patterns. These results agreed with
the previous report that platelets produced in mature megakaryoblasts
abundantly contained Gb3/CD77 antigen. Here, we propose the possibility
that verotoxins bind immature megakaryoblasts and induce their
apoptosis, leading to the arrest of platelet generation in the bone
marrow. This may be one of the causes of thrombocytopenia in patients
with hemolytic uremic syndrome.
5
UI - 11996793
AU - Dubourg C; Toutain B; Helias C; Henry C; Lessard M; Le Gall JY; Le Treut
TI -
A; Guenet L
Evaluation of ETF1/eRF1, mapping to 5q31, as a candidate myeloid tumor
suppressor gene.
SO - Cancer Genet Cytogenet 2002 Apr 1;134(1):33-7
AD - Departement de Biochimie et Biologie Moleculaire, UMR 6061, Faculte de
Medecine CS 34317, 35043 Rennes Cedex, France.
Interstitial deletion of the long arm of chromosome 5 is a recurrent
abnormality, mainly associated with myelodysplastic syndromes (MDS) and
acute myeloid leukemia (AML), and it has been proposed therefore that
the deleted region may contain a myeloid tumor suppressor gene. We have
recently mapped a human translation termination factor gene, ETF1, to
band 5q31 at D5S500, and thus to the smallest commonly deleted segment.
We have evaluated ETF1 as a candidate myeloid tumor suppressor gene by
analysis of the human acute myeloid leukemia cell line HL60, and of
patients suffering from malignant myeloid diseases with
cytogenetically-defined abnormalities of chromosome 5. Fluorescence in
situ hybridization analysis revealed hemizygous loss of the ETF1 locus
in HL60 cells and in four of five leukemic samples, but no inactivating
mutations were identified by sequencing of the remaining ETF1 allele.
6
UI - 11846198
AU - Myoken Y; Sugata T; Kyo T; Fujihara M; Mikami Y
TI -
Itraconazole prophylaxis for invasive gingival aspergillosis in
neutropenic patients with acute leukemia.
SO - J Periodontol 2002 Jan;73(1):33-8
AD - Department of Oral Surgery, Hiroshima Red Cross and Atomic Bomb
Survivors Hospital, Japan. myoken@do5.enjoy.ne.jp
BACKGROUND: Due to an increasing number of leukemic patients with
invasive gingival aspergillosis during neutropenia (neutrophils <500
cells/microl for >10 days), we evaluated the efficacy of oral
itraconazole prophylaxis for preventing this invasive infection at our
hospital. METHODS: This was a retrospective, non-randomized study to
analyze the onset of identified invasive gingival aspergillosis among
536 patients with acute leukemia at risk due to the presence of
neutropenia from 1991 to 1998. Patients received itraconazole capsules
levels at day 10 were measured in some patients. RESULTS: In the 39
invasive gingival aspergillosis were detected in 192 high risk patients
with 469 episodes of neutropenia (7.8% of the high risk patients).
100 mg/day, there was a dramatic decrease in the infections resulting in
3 of 198 high risk patients with 511 episodes of neutropenia (1.5% of
1998, using itraconazole prophylaxis at 200 mg/day, no cases of the
infection were observed in the 146 high risk patients with 380 episodes
of neutropenia. The incidence of invasive gingival aspergillosis was
significantly lower among patients administered itraconazole than among
those without itraconazole (100 mg/day; P = 0.006 and 200 mg/day; P =
0.001). The mean itraconazole serum level in 20 patients receiving 100
mg/day was 71.78 ng/mL and in 16 patients receiving 200 mg/day was
202.67 ng/ml. CONCLUSIONS: These findings suggest that oral itraconazole
could be effective for preventing invasive gingival aspergillosis in
neutropenic patients with acute leukemia and warrants further randomized
investigation.
7
UI - 11869936
AU - Di Bona E; Sartori R; Zambello R; Guercini N; Madeo D; Rodeghiero F
TI -
Prognostic significance of CD56 antigen expression in acute myeloid
leukemia.
SO - Haematologica 2002 Mar;87(3):250-6
AD - Department of Cellular Therapy and Hematology, Division of Hematology,
San Bartolo Hospital, Vicenza, Italy. dibona@hemato.ven.it
BACKGROUND AND OBJECTIVES. CD56 antigen expression has been reported in
several hematologic malignancies. In acute myeloid leukemia (AML)M2 with
t(8;21) and acute promyelocytic leukemia (APL) it has been found to be
consistently associated with an unfavorable prognosis, whereas in other
AML subtypes its role remains uncertain. We investigated CD56 expression
in a cohort of AML patients in order to assess its frequency and
prognostic relevance. DESIGN AND METHODS. Immunophenotypic analysis
including that of CD56 antigen was available for 171 consecutive AML
cells taken at diagnosis was recorded as positive when at least 20% of
the cells double-stained with specific monoclonal antibodies against
CD56 and CD33 antigens. RESULTS. CD56 positivity was demonstrated in 37
cases (21.6%). Its frequency was lower in M4 (6%) and higher in M5
(37%). The median percentage for CD56+ blasts was 56% (range 21-99%).
CD56 positivity did not correlate with age, sex, blast count, favorable
or unfavorable cytogenetics at diagnosis, nor did it influence the
outcome in terms of complete remission (CR) duration (606 vs. 417 days,
p=n.s.) or overall survival (OS) (210 vs. 277 days, p= n.s.). In the APL
subgroup a significant difference in relapse rate was found at 3 years
(71.4% in the CD56 positive group vs. 12% in the CD56 negative group,
p=0.005). INTERPRETATION AND CONCLUSIONS. Our data confirm that CD56
positivity in APL patients at diagnosis is associated with a worse
prognosis, suggesting that close molecular monitoring is necessary in
CD56 positive APL patients. In contrast, the prognostic role of CD56
remains uncertain in the other AML subtypes.
8
UI - 11263441
AU - Hromas R; Shopnick R; Jumean HG; Bowers C; Varella-Garcia M; Richkind K
TI -
Radiation-induced leukemia.
SO - Blood 2001 Mar 15;97(6):1897-8
9
UI - 11263442
AU - Strauchen JA
TI -
Criteria for diagnosis of acute megakaryocytic leukemia.
SO - Blood 2001 Mar 15;97(6):1898
10
UI - 11918536
AU - Salih HR; Starling GC; Brandl SF; Pelka-Fleischer R; Haferlach T;
TI -
Hiddemann W; Kiener PA; Nuessler V
Differentiation of promyelocytic leukaemia: alterations in Fas
(CD95/Apo-1) and Fas ligand (CD178) expression.
SO - Br J Haematol 2002 Apr;117(1):76-85
AD - Department of Immunology, Inflammation and Pulmonary Diseases,
Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, USA.
Helmut.Salih@md.uni-tuebingen.de
The survival of leukaemic blasts contributes to the pathological
mechanism of acute promyelocytic leukaemia (APL). While treatment of APL
using retinoic acid (RA) is a model of differentiation therapy, little
is known about possible effects of this treatment on the Fas/FasL
system. Investigation of APL cells from patients undergoing
differentiation therapy with RA and of promyelocytic HL-60 and
monoblastic U-937 cells cultured with RA revealed a reduction of surface
expression of both Fas and its ligand. Accordingly, the sensitivity of
the cells to anti-Fas-induced apoptosis decreased proportionally and the
reduced expression of FasL resulted in a decreased ability of the
leukaemic cells to induce apoptosis in T cells. Our findings demonstrate
that there are significant changes in Fas and FasL expression during RA
treatment of APL, which probably have consequences for the interaction
between host immune and leukaemia cells, and thus may be involved in the
beneficial effects of differentiation therapy.
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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