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NCI CANCERLIT® Search: Therapy of Acute Myeloid Leukemia - February 2002
National Cancer Institute®
Last Modified: February 1, 2002
Table of Contents
1
UI - 11593299
AU - Dorlhiac-Llacer PE; Marquezini MV; Toffoletto O; Carneiro RC; Maranhao
TI -
RC; Chamone DA
In vitro cytotoxicity of the LDE: daunorubicin complex in acute
myelogenous leukemia blast cells.
SO - Braz J Med Biol Res 2001 Oct;34(10):1257-63
AD - Departamento de Hematologia e Hemoterapia, Faculdade de Medicina,
Universidade de Sao Paulo, Sao Paulo, SP, Brasil. llacer.ops@zaz.com.br
Acute myelogenous leukemia (AML) blast cells show high-affinity
degradation of low-density lipoprotein (LDL), suggesting an increased
expression of cellular LDL receptors. LDE is a lipid microemulsion
easily synthesized in vitro which is known to mimic the metabolic
pathway of LDL. We used LDE as a carrier for daunorubicin and assayed
the cytotoxicity of the complex using AML blast cells since RT-PCR
analysis showed that AML cells express LDL receptor mRNA. The
LDE:daunorubicin complex killed 46.7% of blast cells and 20.2% of normal
bone marrow cells (P<0.001; Student t-test). Moreover, this complex
destroyed AML blast cells as efficiently as free daunorubicin. Thus, LDE
might be a suitable carrier of chemotherapeutic agents targeting these
drugs to neoplastic cells and protecting normal tissues.
2
UI - 11804070
AU - Wollina U; Sayer HG; Wollina K; Graefe T
TI -
Very late appearance of acute graft-versus-host disease after tapering
immunosuppression.
SO - J Dermatol 2001 Dec;28(12):734-6
AD - Department of Dermatology and Allergology, School of Medicine,
Friedrich-Schiller-University of Jena, Germany.
Graft-versus-host disease (GVHD) is a major complication of stem cell
transplantation. Here we report a 40-year-old woman who developed an
acute GVHD 30 months after transplantation. Late and very late
appearance of acute GVHD has only been described in rare cases.
3
UI - 11501968
AU - Ozpolat B; Lopez-Berestein G; Mehta K
TI -
ATRA(ouble) in the treatment of acute promyelocytic leukemia.
SO - J Biol Regul Homeost Agents 2001 Apr-Jun;15(2):107-22
AD - Department of Bioimmunotherapy, The University of Texas, MD Anderson
Cancer Center, Houston 77030, USA.
Acute promyelocytic leukemia (APL) is a unique disease that responds to
differentiation-inducing effects of all-trans-retinoic acid (ATRA). ATRA
induces complete clinical remissions (CRs) in most patients and now
constitutes a standard therapy in patients with APL. However, CRs
induced by ATRA are usually brief, and resistance to the therapy rapidly
develops, leading to relapses in almost every patient; thus limiting the
use of ATRA as a single agent. On the basis of clinical and in vitro
studies, the following mechanisms have been proposed to explain ATRA
resistance: 1) induction of accelerated metabolism of ATRA, 2) increased
expression of cellular retinoic acid-binding proteins (CRABPs), 3)
constitutive degradation of PML-RAR alpha, 4) point mutations in the
ligand-binding domain of RAR alpha of PML-RAR alpha, 5) P-glycoprotein
expression, 6) transcriptional repression by histone deacetylase
activity, 7) isoforms of PML-RAR alpha, 8) persistent telomerase
activity, and 9) expression of type II transglutaminase. In this review,
we discuss the evidence provided in support of each mechanism, the
mechanism's possible impact on the outcome of APL, and the newer
approaches that are being employed to overcome ATRA resistance.
4
UI - 11737750
AU - Sakamoto O; Yoshinari M; Rikiishi T; Fujiwara I; Imaizumi M; Tsuchiya S;
TI -
Iinuma K
Hypercalcemia due to all-trans retinoic acid therapy for acute
promyelocytic leukemia: a case report of effective treatment with
bisphosphonate.
SO - Pediatr Int 2001 Dec;43(6):688-90
AD - Department of Pediatrics, Tohoku University School of Medicine, 1-1
Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan.
osakamoto@ped.med.tohoku.ac.jp
5
UI - 11743652
AU - Suwanai H; Matsushita H; Kobayashi H; Ikeda Y; Kizaki M
TI -
A novel therapeutic technology of specific RNA inhibition for acute
promyelocytic leukemia: improved design of maxizymes against
PML/RARalpha mRNA.
SO - Int J Oncol 2002 Jan;20(1):127-30
AD - Division of Hematology, Keio University School of Medicine, Tokyo
160-8582, Japan.
Targeting of PML/RARalpha using a loss of function strategy in acute
promyelocytic leukemia (APL) is a direct therapeutic approach for
patients and may be the basis of future gene therapy for this leukemia.
To achieve this, we designed specific maxizymes, novel allosterically
controllable ribozymes, against both short and long PML/RARalpha
isoforms. The maxizyme has sensor arms that can only recognize target
sequences, and it can form a cavity that captures catalytically
indispensable Mg2+. We deleted 1 base nucleotide in the Mg2+-binding
pocket designed MzPRT50 and MzPRK55. The distance from the PML/RARalpha
junction site to the center of effectors is only 2 bases, and there are
8 and 9 complementary bases in their inactive forms, respectively. Both
maxizymes specifically cleaved PML/RARalpha mRNA but not wild-type
RARalpha mRNA in a cell-free system. Modification of the sequence of the
Mg2+-binding pocket will be important in designing the sequence-specific
maxizymes against oncogenic genes.
6
UI - 11779431
AU - Guo W; Wang H; Zhao W; Zhu J; Ju B; Wang X
TI -
Effect of all-trans retinoic acid and arsenic trioxide on tissue factor
expression in acute promyelocytic leukemia cells.
SO - Chin Med J (Engl) 2001 Jan;114(1):30-4
AD - Shanghai Institute of Hematology, Ruijin Hospital Affiliated Shanghai
Second Medical University, Shanghai 200025, China.
OBJECTIVE: To study the effect of all-trans retinoic acid (ATRA) and
arsenic troxide (As2O3) on tissue factor (TF) expression and
procoagulant activity (PCA) of acute promyelocytic leukemia (APL) cells
in vivo and in vitro. METHODS: PCA from freshly isolated APL blasts from
APL patients treated with ATRA or As2O3 was detected using a one-stage
clotting assay. TF antigen was detected by ELISA and TF mRNA by RT-PCR.
The maturation sensitive (NB4) or resistant subclones (NB4-R1) of the
promyelocytic NB4 cell line, as well as U937 cells infected with
pMSCV-PML-RARa treated with or without ATRA or As2O3, were also
examined. RESULTS: Both ATRA and As2O3 can down-regulate the TF antigen,
its mRNA transcription and membrane PCA of APL cells in vivo and in
vitro, in a time-dependent manner. The TF antigen level in PML-RARa +
U937 cells was significantly higher than that in U937 cells infected
with retrovirus vector. Both ATRA and As2O3 can also down-regulate the
TF antigen in U937 cells transfected with or without PML-RARa.
CONCLUSION: Tissue factor expression and PCA in APL cells may be
down-regulated by ATRA and As2O3. By down-regulating TF expression,
As2O3 might also be used to improve the DIC-related hemorrhage in APL.
Our data indicate that elevated TF antigen in PML-RARa + U937 may be
related to the fusion protein PML-RARa. The down-regulating effect of
ATRA and As2O3 on TF expression in U937 cells might not involve this
fusion protein.
7
UI - 11697629
AU - Ritchie DS; Wirth A; Grigg AP
TI -
Successful transplant outcome in a morbidly obese patient with acute
myeloblastic leukemia.
SO - Leuk Lymphoma 2001 Sep-Oct;42(5):1111-4
AD - Department of Clinical Haematology and Medical Oncology, Royal Melbourne
Hospital, Australia.
We report a case of matched unrelated bone marrow transplant (BMT) in a
morbidly obese patient with acute myeloblastic leukaemia. The challenges
presented in the management of this case included the calculation of
chemotherapy and radiotherapy doses and the acute presentation of
obstructive sleep apnea. Despite these difficulties, an ultimately
successful outcome was obtained, indicating that although associated
with increased risk of peri-transplant morbidity, obesity need not
represent a contraindication to BMT.
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 - 11734299
AU - Kishino K; Muroi K; Kawano C; Obata T; Sugano N; Nakagi Y; Nagashima T;
TI -
Watari K; Iwamoto S; Ozawa K
Evaluation of engraftment by ABO genotypic analysis of erythroid
burst-forming units after bone marrow transplantation.
SO - Leuk Res 2002 Jan;26(1):13-7
AD - Division of Cell Transplantation and Transfusion, Jichi Medical School,
Minamikawachi, 329-0498, Tochigi, Japan.
Six patients received an allogeneic bone marrow transplant from
HLA-identical ABO-mismatched donors. ABO genotype of erythroid
burst-forming units (BFU-E) from peripheral blood was analyzed using
polymerase chain reaction with sequence specific primers (PCR-SSP).
After bone marrow transplantation (BMT), engraftment of donor cells by
ABO genotypic analysis of BFU-E was compared with ABO phenotypic
analysis of red blood cells (RBCs). During the early stage after BMT,
ABO genotype of BFU-E in the recipients converted to that of the donors.
In contrast, mixed ABO phenotype of RBCs persisted for about 3 months.
In one patient, autologous hemopoietic cell recovery was detected by the
ABO genotypic analysis before clinical manifestation. ABO genotypic
analysis of BFU-E is relevant for enagraftment after ABO-mismatched BMT.
10
UI - 11587228
AU - Fadilah SA; Hatta AZ; Keng CS; Jamil MA; Singh S
TI -
Successful treatment of acute promyelocytic leukemia in pregnancy with
all-trans retinoic acid.
SO - Leukemia 2001 Oct;15(10):1665-6
11
UI - 11086179
AU - Thomas X; Cambier N; Taksin AL; Reman O; Vekhoff A; Pautas C; Leblond V;
TI -
Soler-Michel P; Ecstein-Fraisse E; Archimbaud E
Dose-escalation study of single dose mitoxantrone in combination with
timed sequential chemotherapy in patients with refractory or relapsing
acute myelogenous leukemia.
SO - Leuk Res 2000 Nov;24(11):957-63
AD - Service d'Hematologie, Hopital Edouard Herriot, Lyon, France.
xavier.thomas@chu-lyon.fr
A dose-escalation study was realized in order to assess the maximally
tolerated dose (MTD) of high-dose mitoxantrone in a single injection
combined with cytarabine and etoposide (EMA regimen) in refractory or
1998, 24 patients with relapsed or refractory AML entered the study. All
but one patient had normal left ventricular ejection fraction (LVEF) at
baseline. Performance status according to World Health Organization
(WHO) criteria was less than two in all cases. All patients have been
previously treated by mitoxantrone or anthracyclines. Four cohort of ten
patients were scheduled with the following doses: (1) mitoxantrone 36
mg/m2 on day 1; (2) mitoxantrone 45 mg/m2 on day 1; (3) mitoxantrone 60
mg/m2 on day 1; (4) mitoxantrone 75 mg/m2 on day 1 in combination with
cytarabine 500 mg/m2 per day (days 1-3, and days 8-10), and etoposide
200 mg/m2 per day (days 8-10). All patients received the full doses of
the three drugs. The limiting toxicity was defined as WHO grade 4
nonhematologic toxicity and for impairment of cardiac function by
Alexander's criteria (moderate or severe toxicity). The occurrence of
limiting toxicity in at least three patients from the same dose level
determined the MDT. No limiting toxicity was observed in mitoxantrone
dose level 1. Two limiting toxicities were observed in mitoxantrone dose
level 2 (one mucositis, one moderate cardiac toxicity), and three
limiting toxicities in mitoxantrone dose level 3 (1 high transaminase
levels, two moderate cardiac toxicities) ending the assay. Overall, 16
patients (67%) achieved complete remission (CR). One drug-addict patient
died from cerebral hemorrhage due to severe aspergillosis and was not
considered as a limiting toxicity. After EMA chemotherapy, 13 patients
received subsequent chemotherapy courses involving anthracyclines or
their derivatives. Six patients underwent allogeneic bone marrow
transplantation. No late toxicity occurred. The median survival of the
entire cohort was 41.4 weeks. We conclude that (i) EMA chemotherapy
using a single injection of mitoxantrone is effective in the treatment
of refractory or relapsing AML; (ii) the recommended phase II dose of
mitoxantrone is 45 mg/m2 administered over 30 min as a single dose in
combination with cytarabine and etoposide.
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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