Información sobre riesgo, prevención, detección, síntomas, diagnosis, tratamiento y apoyo para el cáncer.
Información sobre el tratamiento del cáncer incluyendo quirúrgica, quimioterapia, radioterapia, estudios clínicos, terapia con protón, medicina complementaria avanzadas.
OncoLink se complace en ofrecer una amplia lista de lista completa de los agentes quimioterapéuticos más comúnmente usados??. Esta guía de referencia incluye información sobre la forma en que cada fármaco se administra, cómo funcionan, y los pacientes los efectos secundarios comunes pueden experimentar.
Maneras que los pacientes de cáncer y las personas que le cuidan puedan enfrentar el cáncer, los efectos secundarios, nutrición, cuestiones en general sobre el apoyo para el cáncer, duelo/decisiones sobre el termino de vida, y experiencias compartidas por sobrevivientes.
Tipos de Cancer / Leucemia / Leucemia - Leucemia Linfocítica Aguda / Recursos de NCI
National Cancer Institute®
Ultima Vez Modificado: 1 de julio del 2002
1
UI - 11241057
AU - Halonen P; Salo MK; Makipernaa A
TI -
Fasting hypoglycemia is common during maintenance therapy for childhood
acute lymphoblastic leukemia.
SO - J Pediatr 2001 Mar;138(3):428-31
AD - Department of Pediatrics, Tampere University Hospital, Tampere, Finland.
Nineteen of 35 children (54%) with acute lymphoblastic leukemia
receiving maintenance therapy consisting of daily oral 6-mercaptopurine
and weekly oral methotrexate developed hypoglycemia (blood glucose level
<2.7 mmol/L [50 mg/dL] or <2.9 mmol/L [54 mg/dL] with symptoms) during
16 hours of overnight fasting. In 15 of 15 re-studied children, fasting
tolerance had improved, and in 67% (10/15), it had become normal a few
months after cessation of therapy.
2
UI - 11880704
AU - Gorin NC
TI -
Autologous stem cell transplantation for adult acute leukemia.
SO - Curr Opin Oncol 2002 Mar;14(2):152-9
AD - Department of Hematology, Hopital Saint-Antoine and Universite Paris VI,
Paris, France. norgert-claude.gorin@sat.ap-hop-paris.fr
Autologous stem cell transplantation using marrow or peripheral blood is
routinely used to consolidate patients with acute myelocytic leukemia in
complete remission. The situation is less clear for adult acute
lymphocytic leukemia in which results achieved with all strategies are
disappointing.In acute myelocytic leukemia, autografts should be done in
patients with good and standard risk factors. Patients with high-risk
acute myelocytic leukemia defined by poor cytogenetics or failure to
achieve remission with the first induction course, should proceed to
allogeneic stem cell transplantation with the best available human
leukocyte antigen-identical donor (family or unrelated), and the nature
of the conditioning regimen (myelo-ablative or non-myelo-ablative)
should be decided in relation to age, and the patient's clinical
condition. Results of autografting in acute myelocytic leukemia rely
strongly on the quality of the graft. Higher doses of infused stem cells
translate into lower relapse rates. Marrow purging with cyclophosphamide
derivatives also diminishes the relapse incidence. Autologous stem cell
transplantations using peripheral blood are presently preferred to
marrow as the source of stem cells, but an aggressive prior in vivo
purge (high-dose consolidation course(s) before cytaphereses) is then
mandatory. In good-risk acute myelocytic leukemia, autografting is
superior to high-dose ARA-C; in standard-risk acute myelocytic leukemia,
both are supposedly equivalent. There is no prospective randomized study
testing the two approaches in the good-standard-risk population. We
presently test the combination of marrow and blood both purged by
mafosfamide.In adult acute lymphocytic leukemia, good-risk patients get
the best benefit from autografting over conventional chemotherapy.
Maintenance chemotherapy after transplant is likely to bring
benefit.Research in progress aims at facilitating access of the largest
number of patients to autografting and at introducing posttransplant
immunomodulation maneuvers such as tumor vaccination.
3
UI - 11972512
AU - Chessells JM; Harrison CJ; Watson SL; Vora AJ; Richards SM; Medical
TI -
Research Council Working Party on Childhood Leukaemia
Treatment of infants with lymphoblastic leukaemia: results of the UK
Infant Protocols 1987-1999.
SO - Br J Haematol 2002 May;117(2):306-14
AD - Molecular Haematology Unit, Camelia Botnar Laboratories, Institute of
Child Health, 30 Guilford Street, London WC1N 1EH, UK.
j.chessels@ich.ucl.ac.uk
One hundred and twenty-six infants with acute lymphoblastic leukaemia
(ALL) were treated on two consecutive protocols, Infant 87 (n = 40) and
Infant 92 (n = 86), in an attempt to improve the poor prognosis of this
disease. Both included intensive induction and consolidation with
intrathecal and high-dose systemic therapy for central nervous system
(CNS) protection. Intensification therapy was modified and high-dose
chemotherapy with bone marrow transplantation in first remission was
permitted in Infant 92. Four-year event-free survival was superior in
Infant 92 (33%; 95% CI 23-44%) compared with Infant 87 (22.5%; 95% CI
12-37%) (P = 0.04) and survival at 4 years was also superior, 46% (95%
CI 35-57%) c.f. 32.5% (95% CI 20-48%) (P = 0.01), largely as a result of
a significant reduction in remission deaths. Twelve patients in Infant
92 underwent bone marrow transplantation (BMT) in first remission, but
their survival was no better than that of patients receiving
chemotherapy. Multivariate analysis of prognostic factors showed the
adverse influence of younger age, CNS involvement at diagnosis and a
high initial leucocyte count, but not of CD10 expression. Cytogenetic
analysis, available in 93% of patients in Infant 92, showed that 67% had
chromosomal rearrangements involving 11q23 of which 39% had the
translocation t(4;11) (q21;q23). There was no significant difference in
event-free survival between cytogenetic subgroups, although no children
under 6 months of age with 11q23 abnormalities, other than the t(4;11),
survived. In conclusion, infants with lymphoblastic leukaemia remain a
high-risk group, but it is unclear whether their adverse prognosis can
be attributed to unfavourable cytogenetics alone. The role of high-dose
therapy and BMT in first remission remains uncertain.
4
UI - 12010814
AU - Wuchter C; Ruppert V; Schrappe M; Dorken B; Ludwig WD; Karawajew L
TI -
In vitro susceptibility to dexamethasone- and doxorubicin-induced
apoptotic cell death in context of maturation stage, responsiveness to
interleukin 7, and early cytoreduction in vivo in childhood T-cell acute
lymphoblastic leukemia.
SO - Blood 2002 Jun 1;99(11):4109-15
AD - Department of Hematology, Oncology, and Tumor Immunology, Robert Rossle
Cancer Center, Charite, Humboldt-University of Berlin, Germany.
Within childhood T-cell acute lymphoblastic leukemia (T-ALL), patients
with a cortical (CD1a(+)) immunophenotype have been identified as a
subgroup with favorable outcome in the acute lymphoblastic
leukemia-Berlin-Frankfurt-Munster (ALL-BFM), Cooperative study group for
childhood acute lymphoblastic leukemia (COALL) and Pediatric Oncology
Group studies. We investigated in leukemic samples of children with
T-ALL (n = 81) whether the different in vivo therapy response could be
linked to differential in vitro susceptibility to apoptotic cell death.
The extent of dexamethasone- as well as doxorubicin-induced apoptosis,
detected by annexin V staining, positively correlated with the
expression levels of CD1a (Spearman correlation coefficient, r(s) = 0.3
and 0.4, respectively; P <.01). When compared to cortical T-ALL, mature
(CD1a(-), surface CD3(+)) T-ALL were significantly more resistant to
doxorubicin, and immature, pro-/pre-T-ALL were more resistant to both
drugs (P <.05). Apoptosis-related parameters (Bax, Bcl-2, CD95, and
CD95-induced apoptosis) did not account for differential susceptibility
to drug-induced apoptosis. By contrast, an interleukin 7-induced rescue
of leukemic cells from spontaneous apoptosis, recently proposed to
reflect distinct developmental stages and apoptotic programs in T-ALL,
was highly associated with susceptibility to dexamethasone- but not
doxorubicin-induced apoptosis (P <.001 versus P =.08). Analysis of
clinical data showed that in vitro susceptibility to dexamethasone (but
not to doxorubicin) closely correlated with early in vivo therapy
response characterized by percentages of blast cells in bone marrow on
day 15 (r(s) = -0.46, P =.001). Taken together, the in vitro assessment
of drug-induced apoptosis revealed maturation-dependent differences
within childhood T-ALL. The enhanced sensitivity to both drugs in
cortical T-ALL might account for the better in vivo treatment response
of this prognostically favorable T-ALL subgroup.
5
UI - 11505079
AU - Elhasid R; Lanir N; Sharon R; Weyl Ben Arush M; Levin C; Postovsky S;
TI -
Ben Barak A; Brenner B
Prophylactic therapy with enoxaparin during L-asparaginase treatment in
children with acute lymphoblastic leukemia.
SO - Blood Coagul Fibrinolysis 2001 Jul;12(5):367-70
AD - Department of Pediatric Hemato-Oncology, Rambam Medical Center and Bruce
Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Forty-one consecutive children with acute lymphoblastic leukemia (ALL)
received prophylaxis therapy with the low molecular weight heparin
(LMWH) enoxaparin during L-asparaginase treatment. Enoxaparin was given
every 24 h subcutaneously at a median dose of 0.84 mg/kg per day (range,
0.45-1.33 mg/kg per day) starting at the first dose of L-asparaginase
until 1 week after the last dose. Molecular analysis for thrombophilic
polymorphisms documented prothrombin G20210A mutation in 3/27 (11%),
homozygosity for MTHFR C677T mutation in 5/27 (18.5%, and heterozygosity
for factor V Leiden mutation in 5/27 (18.5%) children. There were no
thrombotic events during 76 courses of L-asparaginase in 41 patients who
had received enoxaparin. One patient suffered brain infarct 7 days after
enoxaparin was stopped. There were no bleeding episodes. In a historical
control group of 50 ALL children who had not received prophylactic
enoxaparin during L-asparaginase treatment, two had thromboembolisms
(one deep vein thrombosis and one pulmonary embolism). Enoxaparin is
safe and seems to be effective in prevention of thromboembolism in ALL
patients during L-asparaginase therapy. This study provides pilot data
for a future randomized trial of the use of LMWH during ALL therapy for
the prevention of asparaginase-associated thrombotic events.
6
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
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.
UI - 11895912
AU - Krajinovic M; Labuda D; Mathonnet G; Labuda M; Moghrabi A; Champagne J;
TI -
Sinnett D
Polymorphisms in genes encoding drugs and xenobiotic metabolizing
enzymes, DNA repair enzymes, and response to treatment of childhood
acute lymphoblastic leukemia.
SO - Clin Cancer Res 2002 Mar;8(3):802-10
AD - Service d'Hematologie-Oncologie, Centre de Recherche, Hopital
Sainte-Justine, Montreal, Quebec, H3T 1C5 Canada.
maja.krajinovic@umontreal.ca
PURPOSE: The most common childhood malignancy, acute lymphoblastic
leukemia (ALL), remains the leading cause of cancer-related death in
children because of resistant cases in which underlying predisposing
factors are poorly understood. The interindividual variation in the
activity of xenobiotic metabolizing enzymes that modify individual
somatic mutation burden in the context of environmental exposure was
shown to modify susceptibility to childhood ALL. Variable DNA repair
capacity may further modulate induced DNA lesions. Similarly,
differential capacity of ALL patients to process carcinogens and
chemotherapeutic drugs could both modify an individual's risk of
recurrent malignancy and response to therapy. EXPERIMENTAL DESIGN: We
investigated the relationship between the risk of relapse in ALL
patients and functional polymorphisms in genes encoding
carcinogen-metabolizing enzymes, including CYP1A1, CYP2D6, CYP2E1, MPO,
GSTM1, GSTT1, GSTP1, NAT1, NAT2, NQO1, as well as DNA-repair enzymes
hMLH1, hMSH3, XRCC1, XPF, and APE. Our study included 320 children with
ALL, of which 68 relapsed or died because of this disease within 5 years
of follow-up. RESULTS: Among children of the latter group, we found that
carriers of CYP1A1*2A and NQO1*2 variants had worse disease prognosis
according to Kaplan-Meier (P = 0.003) and Cox regression (P
UI - 11804271
AU - Brenner TL; Pui CH; Evan WE
TI -
Pharmacogenomics of childhood acute lymphoblastic leukemia.
SO - Curr Opin Mol Ther 2001 Dec;3(6):567-78
AD - Department of Pharmaceutical Sciences, St Jude Children's Research
Hospital, Memphis, TN 38105, USA.
Approximately 80% of children with acute lymphoblastic leukemia (ALL)
can be cured with modern therapy. Despite this success, the number of
cases of relapsed ALL remains greater than the number of new cases of
most childhood cancers. New strategies are needed to develop curative
therapy for the 20% of patients who are not being cured today, and to
develop less toxic and less onerous treatment for ALL patients.
Molecular genetics has already provided important insights to the
mechanisms of leukemogenesis and is now routinely used to define the
prognosis and guide treatment intensity for childhood ALL.
Pharmacogenomics is a burgeoning field that aims to elucidate inherited
differences in drug disposition and treatment response, toward
individualizing therapy to enhance efficacy and reduce toxicity. Herein,
we review recent progress in thesefields as they relate to childhood
ALL, and discuss the promise they hold to further enhance treatment of
the most common cancer in children.
UI - 12036866
AU - Willemse MJ; Seriu T; Hettinger K; d'Aniello E; Hop WC; Panzer-Grumayer
TI -
ER; Biondi A; Schrappe M; Kamps WA; Masera G; Gadner H; Riehm H; Bartram
CR; van Dongen JJ
Detection of minimal residual disease identifies differences in
treatment response between T-ALL and precursor B-ALL.
SO - Blood 2002 Jun 15;99(12):4386-93
AD - Department of Immunology, University Hospital Rotterdam/Erasmus
University Rotterdam, The Netherlands.
We performed sensitive polymerase chain reaction-based minimal residual
disease (MRD) analyses on bone marrow samples at 9 follow-up time points
in 71 children with T-lineage acute lymphoblastic leukemia (T-ALL) and
compared the results with the precursor B-lineage ALL (B-ALL) results (n
= 210) of our previous study. At the first 5 follow-up time points, the
frequency of MRD-positive patients and the MRD levels were higher in
T-ALL than in precursor-B-ALL, reflecting the more frequent occurrence
of resistant disease in T-ALL. Subsequently, patients were classified
according to their MRD level at time point 1 (TP1), taken at the end of
induction treatment (5 weeks), and at TP2 just before the start of
consolidation treatment (3 months). Patients were considered at low risk
if TP1 and TP2 were MRD negative and at high risk if MRD levels at TP1
and TP2 were 10(-3) or higher; remaining patients were considered at
intermediate risk. The relative distribution of patients with T-ALL (n =
43) over the MRD-based risk groups differed significantly from that of
precursor B-ALL (n = 109). Twenty-three percent of patients with T-ALL
and 46% of patients with precursor B-ALL were classified in the low-risk
group (P =.01) and had a 5-year relapse-free survival (RFS) rate of 98%
or greater. In contrast, 28% of patients with T-ALL were classified in
the MRD-based high-risk group compared to only 11% of patients with
precursor B-ALL (P =.02), and the RFS rates were 0% and 25%,
respectively (P =.03). Not only was the distribution of patients with
T-ALL different over the MRD-based risk groups, the prognostic value of
MRD levels at TP1 and TP2 was higher in T-ALL (larger RFS gradient), and
consistently higher RFS rates were found for MRD-negative T-ALL patients
at the first 5 follow-up time points.
UI - 12042585
AU - Nilsson A; De Milito A; Engstrom P; Nordin M; Narita M; Grillner L;
TI -
Chiodi F; Bjork O
Current chemotherapy protocols for childhood acute lymphoblastic
leukemia induce loss of humoral immunity to viral vaccination antigens.
SO - Pediatrics 2002 Jun;109(6):e91
AD - Pediatric Cancer Research Unit, Astrid Lindgren Children Hospital,
Stockholm, Sweden. anna.nilsson@mtc.ki.se
OBJECTIVE: To evaluate viral vaccination immunity and booster responses
in children treated successfully for acute lymphoblastic leukemia by
chemotherapy and to study the response to treatment of
antibody-producing plasma cells that are important for persistence of
humoral immunity. METHODS: Forty-three children who were in continuous
first remission for a median of 5 years (range: 2-12 years) were
studied. Before the leukemia was diagnosed, all children had been
immunized against measles, mumps, and rubella according to the Swedish
National immunization program. We analyzed levels of serum antibodies
against measles and rubella by enzyme immunoassays. Avidity tests for
measles antibodies were concomitantly performed by enzyme-linked
immunosorbent assay for measles virus immunoglobulin G detection. The
proportion of plasma cells in bone marrow was studied by flow cytometry
at different times during treatment and follow-up. Children who lacked
protective levels of antibodies to vaccination antigens were
reimmunized. Serum was collected 3 months after immunization to assess
vaccination responses. RESULTS: After completion of the treatment, only
26 of the 43 children (60%) were found to be immune against measles and
31 (72%) against rubella. The proportion of bone marrow plasma cells
decreased during treatment but returned to normal after 6 months.
Revaccination caused both primary and secondary immune responses. Six of
the 14 children without immunity failed to achieve protective levels of
specific antibodies against measles and 3 against rubella. CONCLUSIONS:
Our finding of loss of antibodies against measles and rubella in
children treated with intensive chemotherapy suggests that
reimmunization of these patients is necessary after completion of the
treatment. To determine reimmunization schedules for children treated
with chemotherapy, vaccination responses need to be studied further.
UI - 12053147
AU - Fogliatto L; Bittencourt H; Nunes AS; Salenave PR; Silva GS; Daudt LE;
TI -
Job FM; Bittencourt R; Onsten T; Silla LM
Outcome of treatment in adult acute lymphoblastic leukemia in southern
Brazil using a modified german multicenter acute lymphoblastic leukemia
protocol.
SO - Acta Haematol 2002;107(4):203-7
AD - Department of Hematology, Hospital de Clinicas, School of Medicine,
Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Reports on treatment outcomes in adults with acute lymphoblastic
leukemia (ALL) in Brazil are sparse. To evaluate the outcome of patients
with ALL managed by the public healthcare system, we studied 42 adults
treated from 1990 to 1997 in the Division of Hematology at Hospital de
Clinicas, Porto Alegre, Brazil. Of these patients, 14/42 were females
and their median age at diagnosis was 26 (17-64) years. The diagnosis of
ALL was based on cytological examination of marrow smears, and
immunophenotypic and cytogenetic studies, when available. Fifty percent
of the patients expressed CD10, 30% were CD10 negative and CD19 positive
and 20% expressed T markers. Philadelphia chromosome was found in 4
(7.14%). The chemotherapy protocol was adapted from the German
Multicenter ALL (GMALL) 02-84 protocol. The complete remission rate was
93% and the overall survival at 5 years was 41%. No particular risk
factor was identified in our series. These results are comparable to the
findings of other international studies. Copyright 2002 S. Karger AG,
Basel
UI - 12053149
AU - Fujiwara H; Arima N; Akasaki Y; Ohtsubo H; Ozaki A; Kukita T; Matsushita
TI -
K; Arimura K; Suruga Y; Wakamatsu S; Matsumoto T; Hidaka S; Eizuru Y;
Tei C
Interferon-alpha therapy following autologous peripheral blood stem cell
transplantation for adult T cell leukemia/lymphoma.
SO - Acta Haematol 2002;107(4):213-9
AD - First Department of Internal Medicine, Center for Chronic Viral Disease,
Faculty of Medicine, Kagoshima University, Kagoshima, Japan.
In the present report, we describe a case of adult T cell
leukemia/lymphoma (ATLL), a 58-year-old woman, successfully treated with
interferon (IFN)-alpha following autologous peripheral blood stem cell
transplantation (auto-PBSCT). The patient remains in remission with full
performance status for more than 12 months. Auto-PBSCT reduced the
abdominal lymphoma mass and IFN-alpha eliminated residual tumor cells,
possibly through the induction of specific T-cell subsets expressing
CD3, CD8 on their surfaces and either IFN-gamma or tumor necrosis factor
(TNF)-alpha in cytoplasm. We have treated a total of 4 ATLL patients
with auto-PBSCT, including the case presented herein. All other patients
treated with auto-PBSCT were not followed by adjuvant chemotherapy or
cytokine therapy and relapsed within 3 months after auto-PBSCT. This
evidence suggests that the therapeutic success of the present case was
attributable to the administration of IFN-alpha immunotherapy following
auto-PBSCT. Copyright 2002 S. Karger AG, Basel
UI - 12089225
AU - Leung W; Rose SR; Zhou Y; Hancock ML; Burstein S; Schriock EA; Lustig R;
TI -
Danish RK; Evans WE; Hudson MM; Pui CH
Outcomes of growth hormone replacement therapy in survivors of childhood
acute lymphoblastic leukemia.
SO - J Clin Oncol 2002 Jul 1;20(13):2959-64
AD - After Completion of Therapy Program and the Department of
Hematology-Oncology, St Jude Children's Research Hospital, Memphis, TN
38105-2794, USA. wing.leung@stjude.org
PURPOSE: Little is known about the long-term efficacy or adverse effects
of growth hormone (GH) replacement therapy in survivors of childhood
acute lymphoblastic leukemia (ALL) who have GH deficiency. We
investigated the adult height of patients who had received GH and
estimated their risk of leukemia relapse or development of a second
malignancy. PATIENTS AND METHODS: Of 910 patients treated for ALL at a
single institution, 47 had received GH replacement therapy. The linear
growth of these 47 patients was retrospectively evaluated. Their risk of
leukemia relapse or second malignancy was compared with that of
survivors who did not undergo GH therapy. RESULTS: The median height SD
score at the start of GH therapy had decreased by 1.0 since the time of
diagnosis of ALL. After a median duration of 4.5 years of GH therapy,
adult height SD scores improved and approached height SD scores at the
time of diagnosis of ALL. The median adult height for male patients was
173.2 cm (range, 157 to 191.9 cm), and for female patients, it was 158.1
cm (range, 141 to 168 cm). None of the patients developed adverse
effects requiring discontinuation of GH treatment. At the 7-year and
11-year landmarks in continuous hematologic remission, there was no
statistical evidence that GH therapy was associated with leukemia
relapse or development of a second malignancy. CONCLUSION: This study
suggests that GH replacement therapy is safe and efficacious for the
correction of GH deficiency in survivors of childhood ALL.
UI - 12057109
AU - Siegel RS; Gartenhaus RB; Kuzel TM
TI -
Human T-cell lymphotropic-I-associated leukemia/lymphoma.
SO - Curr Treat Options Oncol 2001 Aug;2(4):291-300
AD - Division of Hematology/Oncology, Department of Medicine, Northwestern
University Medical School, and the Robert H. Lurie Comprehensive Cancer
Center of Northwestern University, 676 N. St. Clair, Suite 850, Chicago,
IL 60611, USA.
Human T-cell lymphotropic virus-I (HTLV-I)-related adult T-cell
leukemia/lymphoma (ATL) is a model disease for proof of viral
oncogenesis. HTLV-I infection is endemic in southern Japan and the
Caribbean basin, and occurs sporadically in Africa, Central and South
America, the Middle East, and the southeastern United States. ATL occurs
in only 2% to 4% of HTLV-I-infected people [1-3]. When it does occur, it
is usually aggressive and difficult to treat; most people survive for
less than 1 year [1-3]. Combination chemotherapy with cytotoxic agents
has yielded complete response rates of 20% to 45%, but responses usually
last only a few months [3]. Recently, novel treatments, such as
monoclonal antibodies directed at the interleukin-2 receptor and the
combination of interferon alfa and zidovudine, have been shown to be
active in the treatment of patients with ATL. A small percentage of
patients achieve long-lasting remissions [2,3].
UI - 11866703
AU - Cremer L; Eilers J; Kinney-Wieland S; Nuss S; Engbrecht LM; Mattano LA
TI -
Jr; Mora-Pagkalinawan M
An adolescent with acute lymphoblastic leukemia.
SO - Cancer Pract 2002 Jan-Feb;10(1):6-10
AD - Rehabilitation Services, St. Jude Children's Research Hospital, Memphis,
Tennessee, USA.
UI - 12094249
AU - Takeuchi J; Kyo T; Naito K; Sao H; Takahashi M; Miyawaki S; Kuriyama K;
TI -
Ohtake S; Yagasaki F; Murakami H; Asou N; Ino T; Okamoto T; Usui N;
Nishimura M; Shinagawa K; Fukushima T; Taguchi H; Morii T; Mizuta S;
Akiyama H; Nakamura Y; Ohshima T; Ohno R
Induction therapy by frequent administration of doxorubicin with four
other drugs, followed by intensive consolidation and maintenance therapy
for adult acute lymphoblastic leukemia: the JALSG-ALL93 study.
SO - Leukemia 2002 Jul;16(7):1259-66
AD - First Department of Internal Medicine, Nihon University School of
Medicine, Japan.
In order to improve the disappointing prognosis of adult patients with
acute lymphoblastic leukemia (ALL), we applied similar induction therapy
as that used for acute myeloid leukemia (AML), ie frequent
administration of doxorubicin (DOX). DOX 30 mg/m(2) was administered
from days 1 to 3 and from days 8 to 10 together with vincristine,
prednisolone, cyclophosphamide and L-asparaginase, followed by three
courses of consolidation and four courses of intensification. From
novo ALL were entered. Of 263 evaluable patients (age 15 to 59; median
31), 205 (78%) obtained complete remission (CR). At a median follow-up
period of 63 months, the predicted 6-year overall survival (OS) rate of
all patients was 33%, and disease-free survival (DFS) rate of CR
patients was 30%, respectively. By multivariate analysis, favorable
prognostic factors for the achievement of CR were age <40 and WBC <50
000/microl; for longer OS were age <30 and WBC <30 000/microl; and for
longer DFS of CR patients were FAB L1 and ALT <50 IU/l. Among 229
patients who had adequate cytogenetic data, 51 (22%) had Philadelphia
(Ph) chromosome. Ph-negative chromosome was a common favorable
prognostic factor for CR, longer OS and DFS. DFS was not different
between early sequential intensification (n = 48) and intermittent
intensification (n = 43) during the maintenance phase. Among CR patients
under 40 years old, the 6-year survival was not different between the
allocated related allo-BMT group (34 patients) and the allocated
chemotherapy group (108 patients). However, among patients with
Ph-positive ALL, the survival of patients who actually received allo-BMT
was superior to that of patients who received chemotherapy (P = 0.046).
UI - 12094259
AU - Ito C; Tecchio C; Coustan-Smith E; Suzuki T; Behm FG; Raimondi SC; Pui
TI -
CH; Campana D
The antifungal antibiotic clotrimazole alters calcium homeostasis of
leukemic lymphoblasts and induces apoptosis.
SO - Leukemia 2002 Jul;16(7):1344-52
AD - Department of Hematology-Oncology, St Jude Children's Research Hospital,
Memphis, TN 38105-2794, USA.
Clotrimazole is an antimycotic imidazole derivative that interferes with
cellular Ca(2+) homeostasis. We investigated the effects of clotrimazole
on acute lymphoblastic leukemia (ALL) cells. Treatment with 10 microM
clotrimazole (a concentration achievable in vivo) reduced cell recovery
from cultures of all nine ALL cell lines studied (B-lineage: OP-1,
SUP-B15, RS4;11, NALM6, REH, and 380; T-lineage: MOLT4, CCRF-CEM, and
CEM-C7). After 4 days of culture, median cell recovery was 10% (range,
<1% to 37%) of cell recovery in parallel untreated cultures.
Clotrimazole also inhibited recovery of primary ALL cells cultured on
stromal feeder layers. After leukemic cells from 16 cases of ALL were
cultured for 7 days with 10 microM clotrimazole, median cell recovery
was <1% (range, <1% to 16%) of that in parallel untreated cultures.
Clotrimazole was active against leukemic cells with genetic
abnormalities associated with poor response to therapy and against
multidrug-resistant cell lines. In contrast, mature T lymphocytes and
bone marrow stromal cells were not affected. Clotrimazole induced
depletion of intracellular Ca(2+) stores in ALL cells, which was
followed by apoptosis, as shown by annexin V binding and DNA
fragmentation. Thus, clotrimazole is cytotoxic to ALL cells at
concentrations achievable in vivo.
UI - 12107017
AU - Boughton B
TI -
Childhood cranial radiotherapy reduces fertility in adulthood.
SO - Lancet Oncol 2002 Jun;3(6):330
UI - 12087062
AU - Holmuhamedov E; Lewis L; Bienengraeber M; Holmuhamedova M; Jahangir A;
TI -
Terzic A
Suppression of human tumor cell proliferation through mitochondrial
targeting.
SO - FASEB J 2002 Jul;16(9):1010-6
AD - Division of Cardiovascular Diseases, Department of Medicine, Mayo
Clinic, Mayo Foundation, Rochester, Minnesota, USA.
Intracellular calcium signaling plays a central role in cell
proliferation. In leukemic cells, the calcium release-activated calcium
channels provide a major pathway for calcium entry (I(CRAC))
perpetuating progression through the cell cycle. Although I(CRAC) is
under mitochondrial regulation, targeting mitochondrial function has not
been exploited to control malignant cell growth. The benzothiadiazine
diazoxide, which depolarized respiration-dependent mitochondrial
membrane potential, reduced the rate of proliferation and arrested human
acute leukemic T cells in the G0/G1 phase. Diazoxide did not alter
cellular energetics, but rather inhibited the mitochondria-controlled
I(CRAC) and reduced calcium influx into tumor cells. The
antiproliferative action of diazoxide was mimicked by removal of
extracellular calcium or by the tyrphostin A9, an I(CRAC) inhibitor.
Deletion of the mitochondrial genome, which encodes essential
respiratory chain enzyme subunits, attenuated the inhibitory effect of
diazoxide on I(CRAC)-mediated calcium influx and cell proliferation.
Thus, manipulation of mitochondrial function and associated calcium
signaling provides a basis for a novel anticancer strategy.
UI - 12057058
AU - Litzow MR
TI -
Acute lymphoblastic leukemia in adults.
SO - Curr Treat Options Oncol 2000 Apr;1(1):19-29
AD - Division of Hematology, Department of Internal Medicine, Mayo Clinic,
200 First Street, SW, Rochester, MN 55905, USA.
The therapy of acute lymphoblastic leukemia (ALL) in adults has built on
the remarkable success achieved in the treatment of this disease in
children. However, older age and other adverse risk factors seen more
commonly in adults than in children have lessened the success of the
treatment of ALL in comparison with what has been achieved in children.
The treatment of ALL depends on the use of intensive multi-agent
chemotherapy given over 6 to 9 months in combination with central
nervous system prophylactic therapy with cranial radiation and
intrathecal chemotherapy followed by maintenance chemotherapy for 2 to 3
years. This therapy has allowed younger patients with newly diagnosed
ALL to achieve complete remission in 80% to 90% of cases, but has still
resulted in subsequent relapse in most patients. For high-risk patients
with ALL, allogeneic blood and marrow transplant (BMT) from a related or
unrelated donor can improve the outcome compared with chemotherapy. The
role of autologous transplantation in ALL remains uncertain, as does the
role of allogeneic transplant in standard-risk patients. This issue
continues to be the subject of large, randomized trials. New agents and
improvements in supportive care bring the hope that more patients with
ALL will be cured in the future.
UI - 11982900
AU - Hongo T; Okada S; Ohzeki T; Ohta H; Nishimura S; Hamamoto K; Yagi K;
TI -
Misu H; Eguchi N; Suzuki N; Horibe K; Ueda K
Low plasma levels of hemostatic proteins during the induction phase in
children with acute lymphoblastic leukemia: A retrospective study by the
JACLS. Japan Association of Childhood Leukemia Study.
SO - Pediatr Int 2002 Jun;44(3):293-9
AD - Department of Pediatrics, Hamamatsu University School of Medicine,
Hamamatsu, Japan. hongot@hama-med.ac.jp
BACKGROUND: Thromboembolic and bleeding events are serious complications
associated with the administration of L-asparaginase (ASP) during the
induction phase in children with acute lymphoblastic leukemia (ALL).
Prophylactic supplementation of plasma-derived coagulation products
remains controversial. The purposes of this study were to examine the
plasma levels of hemostatic proteins during the induction phase and the
efficacy of prophylactic replacement of plasma-derived products.
METHODS: A multicenter retrospective survey on the incidence of
hemostatic complications and the frequency of prophylactic replacement
of plasma-derived products among children with ALL who under went ASP
therapy was conducted. All patients were treated according to the Japan
Association of Childhood Leukemia Study (JACLS) ALL-97 protocol.
RESULTS: Thirty-six (67%) of the 54 JACLS-treatment centers responded
and provided information on 127 patients. Clinically relevant hemostatic
complications occurred in two patients (1.6%;2/127); one patient
suffered intracranial bleeding 5 days after beginning the protocol, and
the second patient suffered an ischemic attack during an ASP treatment.
The administration of ASP(10 000 u/m2 x six doses) led to significant
reductions in the plasma fibrinogen (180 +/- 74 to 105 +/- 57
mg/dL),antithrombin III (AT III) (126 +/- 21 to 73 +/- 18%),and
plasminogen levels (97 +/- 17 to 52 +/- 18%).These laboratory parameters
returned to normal levels 2 weeks after completion of the ASP treatment.
Forty-eight patients (38%)received AT III concentrate (AT III-supplement
group). The AT III level of the AT III-supplement group was
significantly lower than that of the AT III non-supplement group, not
only during the ASP therapy, but also prior to the ASP therapy. A
greater percentage of patients in the AT III-supplement group received
fresh-frozen plasma and in greater amounts than those in the AT III
non-supplement group. CONCLUSIONS: Severe hemorrhage and thrombosis were
uncommon in the ALL patients who underwent ASP therapy in comparison
with the degree of coagulation changes. Prophylactic administration of
AT III concentrate or fresh-frozen plasma did not demonstrate clear
beneficial effects in the treatment of ALL in preventing thromboembolic
events.
UI - 12116061
AU - Stary J; Gajdos P; Hrstkova H; Blazek B; Slavik Z; Mihal V; Zahalka F;
TI -
Jabali Y; Vavra V; Kopecna L; Mydlil J; Trka J
Treatment of Czech children with acute lymphoblastic leukemia: a report
of the Czech Working Group for Pediatric Hematology.
SO - Med Pediatr Oncol 2002 Aug;39(2):125-7
AD - 2nd Department of Pediatrics, University Hospital Motol, Praha, Czech
Republic. jan.stary@lfmotol.cuni.cz
UI - 12116067
AU - Fioredda F; Micalizzi C; Lanciotti M; Dufour C; Lamba LD; Fiocchi I
TI -
Reversible vincristine-related flaccid paralysis in a child with acute
lymphoblastic leukemia.
SO - Med Pediatr Oncol 2002 Aug;39(2):141-2
Dr. Wein discusses prostate cancer, screening and treatment options. Read more.
Cancer Types
Bone Cancer
Brain Tumors
Breast Cancer
Carcinoid Tumors
Endocrine System Cancers
Gastrointestinal Cancers
Gynecologic Cancers
Head and Neck Cancers
Leukemia
Lung Cancers
Lymphomas
Myelomas
Pediatric Cancers
Penile Cancer
Prostate Cancer
Sarcomas
Skin Cancers
Testicular Cancer
Thyroid Cancer
Urinary Tract Cancers
OncoLink Vet
Cancer Treatment
Biologic Therapy
Bone Marrow Transplants
Chemotherapy
Clinical Trials
Complementary Medicine
Gene Therapy
General Treatment Concerns
Hormone Therapy
PDT Center
Proton Therapy
Radiation Oncology
Surgical Oncology
Targeted Therapies
Vaccine Therapies
Cancer Support
Caregivers
Hospice Care and Bereavement
Nutrition and Cancer
Sexuality & Fertility
Side Effects
Support
Survivorship
Exercise and Cancer
Cancer Resources
Cancer News
OncoLink University
Nurses' Notes
Conferences
Newly Diagnosed Patients
Causes and Prevention
Legal and Financial Information for Patients
LGBT Resources
NCI Resources
Global Resources
Cancer Resource List
Resources for Young Adults
OncoLink Media Library
OncoLink TV
Book, Music and Video Reviews
Ask the Experts
Brown Bag Chat
Tracy's Corner
About OncoLink
About OncoLink
Giving to OncoLink
Contact Information
Usage Policy
Editorial Board
How to Partner with OncoLink
Link to OncoLink
Mission Statement
Calcium Leucovorin, Citrovorum Factor, Folinic Acid
Cladribine (2-CDA, Leustatin®)
Cyclophosphamide (Cytoxan®, Neosar®, Endoxan®)
Cyclosporine (Neoral®, Sandimmune®, Restasis®, Gengraf®)
Cytarabine (Cytosar-U®, Ara-C)
Irinotecan (Camptosar®, CPT-11)
Leucovorin (Calcium Leucovorin, Citrovorum Factor, Folinic Acid)
Calcium Leucovorin, Citrovorum Factor, Folinic Acid
Leucovorin (Calcium Leucovorin, Citrovorum Factor, Folinic Acid)
Leuprolide Acetate (Lupron®, Lupron Depot®, Eligard®, Prostap®, Viadur®) - For Men
Leuprolide Acetate (Lupron®, Lupron Depot®, Eligard®, Prostap®, Viadur®) - For Women
Lupron®, Lupron Depot®, Eligard®, Prostap®, Viadur®
Lupron®, Lupron Depot®, Eligard®, Prostap®, Viadur®
Busulfan (Myleran®, Busulfex®)
Intravesicular Mitomycin (Mutamycin®, Mitomycin-C, given into the bladder)
Mechlorethamine (Mustargen®, Nitrogen Mustard)
mechlorethamine, mustine, Mustargen®
Megestrol (Megace®, Megace-ES®)
Mercaptopurine (Purinethol®, 6-MP)
Methotrexate (Mexate®, Folex®, Rheumatrex®, Amethopterin, MTX)
Mexate®, Folex®, Rheumatrex®, Amethopterin, MTX
Mitomycin (Mutamycin®, Mitomycin-C)
Morphine Sulfate (Given by IV)
Morphine Sulfate (MS Contin®, Avinza®, Kadian®, Oramorph SR®)
MS Contin®, Avinza®, Kadian®, Oramorph SR®
Mutamycin®, Mitomycin-C, given into the bladder
Nitrogen mustard (mechlorethamine, mustine, Mustargen®)
Bendamustine Hydrochloride (Treanda®)
Bexarotene (Targretin®), Oral Formulation
Bexarotene Gel (Targretin® Gel Formulation)
Etoposide (Toposar®, VePesid®, Etopophos®,VP-16)
Thioguanine (6-TG, Thioguanine Tabloid®)
Toposar®, VePesid®, Etopophos®,VP-16
Trelstar LA® and Trelstar Depot®
Tretinoin (Vesanoid®, All-Trans-Retinoic Acid, ATRA)
Triptorelin (Trelstar LA® and Trelstar Depot®)

