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NCI CANCERLIT® Search: Therapy of Acute Myeloid Leukemia - July 2002
National Cancer Institute®
Last Modified: July 1, 2002
- Impact of addition of maintenance therapy to intensive induction and consolidation chemotherapy for childhood acute myeloblastic leukemia:
- Arsenic trioxide newly joins treatment strategies for acute promyelocytic leukemia.
- Autologous stem cell transplantation for advanced acute myeloid leukemia.
- Tretinoin for the treatment of acute promyelocytic leukemia.
- Prolonged complete remission in two cases of acute promyelocytic leukaemia treated with atra alone.
- New developments in the treatment of acute myeloid leukemia.
- New agents for induction and postremission therapy of acute myeloid leukemia.
- Targeting of the CD33-calicheamicin immunoconjugate Mylotarg (CMA-676) in acute myeloid leukemia: in vivo and in vitro saturation and
- Approval summary: gemtuzumab ozogamicin in relapsed acute myeloid leukemia.
- Current use and future development of gemtuzumab ozogamicin.
- Gemtuzumab ozogamicin.
- Mylotarg: antibody-targeted chemotherapy comes of age.
- Prolonged molecular remission in advanced acute promyelocytic leukaemia after treatment with gemtuzumab ozogamicin (Mylotarg CMA-676).
- Development of hepatic veno-occlusive disease after Mylotarg infusion for relapsed acute myeloid leukemia.
- Mylotarg approved for patients with CD33+ acute myeloid leukemia.
- Targeting leukemia cells with gemtuzumab ozogamicin.
- Tumor lysis syndrome secondary to Gemtuzumab Ozogamicin in a patient with acute myelogenous leukemia.
- Experience with gemtuzumab ozogamycin ("mylotarg") and all-trans retinoic acid in untreated acute promyelocytic leukemia.
- A minor's refusal of treatment.
- Acute myelogenous leukemia: advances and limitations of treatment.
- Early lymphocyte recovery is a predictive factor for prolonged survival after autologous hematopoietic stem cell transplantation for acute
- Arsenic trioxide.
- Acute promyelocytic leukemia.
- Mononucleosis syndrome and acute monocytic leukemia.
- [Fatal side-effects of all-trans retinoic acid in the treatment of acute promyelocytic leukemia]
- Acquired pulmonary alveolar proteinosis after umbilical cord blood transplantation for acute myeloid leukemia.
- Advances in the understanding and management of acute promyelocytic leukemia.
- Encouraging results from phase I trial of GVAX.
Table of Contents
1
UI - 12065553
AU - Perel Y; Auvrignon A; Leblanc T; Vannier JP; Michel G; Nelken B;
TI -
Gandemer V; Schmitt C; Lamagnere JP; De Lumley L; Bader-Meunier B;
Couillaud G; Schaison G; Landman-Parker J; Thuret I; Dalle JH; Baruchel
A; Leverger G; Group LAME of the French Society of Pediatric Hematology
and Immunology
Impact of addition of maintenance therapy to intensive induction and
consolidation chemotherapy for childhood acute myeloblastic leukemia:
results of a prospective randomized trial, LAME 89/91. Leucamie Aique
Myeloide Enfant.
SO - J Clin Oncol 2002 Jun 15;20(12):2774-82
AD - Unite d'Onco-Hematologie, Departement de Pediatrie, Hopital des Enfants,
Groupe Hospitalier Pellegrin, Centres Hospitalo-Universitaires de
Bordeaux, France. yves.perel@chu-bordeaux.fr
PURPOSE: To determine whether the use of maintenance therapy (MT)
delivered after intensive induction and consolidation therapy confers
any advantage in childhood acute myeloid leukemia (AML). PATIENTS AND
METHODS: A total of 268 children with AML were registered in the
Leucamie Aique Myeloide Enfant (LAME) 89/91 protocol. This regimen
included an intensive induction phase (mitoxantrone plus cytarabine)
and, for patients without allograft, two consolidation courses, one
containing timed-sequential high-dose cytarabine, asparaginase, and
amsacrine. In the LAME 89 pilot study, patients were given an additional
MT consisting of mercaptopurine and cytarabine for 18 months. In the
LAME 91 trial, patients were randomized to receive or not receive MT.
RESULTS: A total of 241 (90%) of 268 patients achieved a complete
remission. The overall survival and event-free survival at 6 years were
60% +/- 6% and 48% +/- 6%, respectively. For the complete responders
after consolidation therapy, the 5-year disease-free survival was not
significantly different in MT-negative and in MT-positive randomized
patients (respectively, 60% +/- 19% v 50% +/- 15%; P =.25), whereas the
5-year overall survival was significantly better in MT-negative
randomized patients (81% +/- 13% v 58% +/- 15%; P =.04) due to a higher
salvage rate after relapse. CONCLUSION: More than 50% of patients can be
cured of AML in childhood. Either drug intensity or each of the
induction and postremission phases may have contributed to the
outstanding improvement in outcome. Low-dose MT is not recommended.
Exposure to this low-dose MT may contribute to clinical drug resistance
and treatment failure in patients who experience relapse.
2
UI - 11813833
AU - Kuriyama K
TI -
Arsenic trioxide newly joins treatment strategies for acute
promyelocytic leukemia.
SO - Intern Med 2001 Dec;40(12):1165
3
UI - 11896426
AU - Linker CA; Damon LE; Ries CA; Navarro WA; Case D; Wolf JL
TI -
Autologous stem cell transplantation for advanced acute myeloid
leukemia.
SO - Bone Marrow Transplant 2002 Feb;29(4):297-301
AD - University of California, San Francisco, CA, USA.
We studied the efficacy of a two-step approach to autologous stem cell
transplantation for patients with advanced acute myeloid leukemia. Step
1 consisted of consolidation chemotherapy using cytarabine 2000 mg/m(2)
twice daily for 4 days plus etoposide 40 mg/kg by continuous infusion
over the same 4 days. Peripheral blood stem cells were collected under
granulocyte colony-stimulating factor (G-CSF) stimulation during
recovery from this chemotherapy. Step 2, autologous stem cell
transplantation, utilized the preparative regimen of oral busulfan 16
mg/kg followed by etoposide 60 mg/kg i.v. During step 1, there were no
treatment-related deaths among 28 patients, but two patients did not
proceed to transplantation because of failure of mobilization. A median
CD34+ dose (x10(6)/kg) of 13.6 was collected. Of 26 patients undergoing
autologous transplant, there was one treatment-related death and 12
relapses. With a median follow-up of 5.4 years, 5 year event-free
survival (EFS) of all patients entered is 54%. The most important
prognostic factor was cytogenetic changes. All seven patients with
t(15,17) remained in long-term remission whereas EFS for other patients
was 38%. We conclude that this two-step approach to autologous
transplantation produces excellent stem cell yields, allows a high
percentage of patients to receive the intended therapy, and provides
effective treatment.
4
UI - 11903277
AU - Wu H
TI -
Tretinoin for the treatment of acute promyelocytic leukemia.
SO - Cancer Pract 2002 Mar-Apr;10(2):109-11
AD - University of California Medical Center, Department of Clinical
Pharmacy, San Francisco, California, USA.
5
UI - 12028058
AU - Shehata N; Walker IR; Carter RC; Neame PB; Leber B
TI -
Prolonged complete remission in two cases of acute promyelocytic
leukaemia treated with atra alone.
SO - Br J Haematol 2002 Jun;117(3):768
6
UI - 11195406
AU - Radich J; Sievers E
TI -
New developments in the treatment of acute myeloid leukemia.
SO - Oncology (Huntingt) 2000 Nov;14(11A):125-31
AD - Clinical Research Division, Program in Genetics and Genomics, Fred
Hutchinson Cancer Research Center, Seattle, Washington, USA.
jradich@fhcrc.org
Curative therapy for acute myeloid leukemia (AML) remains
unsatisfactory. However, three recent advances may play an important
role in determining how AML is treated in the near future. First, the
development of targeted antibody therapy using the
anti-CD33-calicheamicin conjugate (gemtuzumab ozogamicin, Mylotarg)
represents a novel targeted approach to the killing of leukemia cells.
Second, modern molecular methods have improved our ability to identify
minimal residual disease (MRD) in patients who appear to be in
remission. These methods will allow physicians to tailor therapy,
offering, for example, more intensive therapy to patients who harbor
MRD. Lastly, the development of microarray gene expression technology
allows for the simultaneous study of thousands of genes. With this
technology, we may determine the genes responsible for the biological
properties of treatment response and relapse in leukemia patients.
7
UI - 11368378
AU - Larson RA
TI -
New agents for induction and postremission therapy of acute myeloid
leukemia.
SO - Leukemia 2001 Apr;15(4):675-6
AD - University of Chicago, IL 60637, USA.
8
UI - 11342449
AU - van Der Velden VH; te Marvelde JG; Hoogeveen PG; Bernstein ID;
TI -
Houtsmuller AB; Berger MS; van Dongen JJ
Targeting of the CD33-calicheamicin immunoconjugate Mylotarg (CMA-676)
in acute myeloid leukemia: in vivo and in vitro saturation and
internalization by leukemic and normal myeloid cells.
SO - Blood 2001 May 15;97(10):3197-204
AD - Department of Immunology, Erasmus University Rotterdam and University
Hospital Rotterdam, The Netherlands. vandongen@immu.fgg.eur.nl
Antibody-targeted chemotherapy is a promising therapy in patients with
acute myeloid leukemia (AML). In a phase II study of Mylotarg (CMA-676,
gemtuzumab ozogamicin), which consists of a CD33 antibody linked to
calicheamicin, saturation and internalization by leukemic and normal
myeloid cells were analyzed in 122 patients with relapsed AML.
Peripheral blood samples were obtained just before and 3 and 6 hours
after the start of the first and second Mylotarg treatment cycles.
Within 3 to 6 hours after infusion, near complete saturation of CD33
antigenic sites by Mylotarg was reached for AML blasts, monocytes, and
granulocytes, whereas Mylotarg did not bind to lymphocytes. Saturation
levels prior to the start of the second Mylotarg treatment cycle were
significantly increased compared with background levels before the start
of the first cycle. This apparently was caused by remaining circulating
Mylotarg from the first treatment cycle (approximately 2 weeks earlier).
On binding of Mylotarg to the CD33 antigen, Mylotarg was rapidly
internalized, as determined by the decrease in maximal surface membrane
Mylotarg binding. Internalization of Mylotarg was also demonstrated in
myeloid cells in vitro and was confirmed by confocal laser microscopy.
In vitro studies using pulse labeling with Mylotarg showed a continuous
renewed membrane expression of CD33 antigens, which can significantly
increase the internalization process and thereby the intracellular
accumulation of the drug. Finally, Mylotarg induced dose-dependent
apoptosis in myeloid cells in vitro. These data indicate that Mylotarg
is rapidly and specifically targeted to CD33(+) cells, followed by
internalization and subsequent induction of cell death.
9
UI - 11410481
AU - Bross PF; Beitz J; Chen G; Chen XH; Duffy E; Kieffer L; Roy S; Sridhara
TI -
R; Rahman A; Williams G; Pazdur R
Approval summary: gemtuzumab ozogamicin in relapsed acute myeloid
leukemia.
SO - Clin Cancer Res 2001 Jun;7(6):1490-6
AD - Division of Oncology Drug Products, Center for Drug Evaluation and
Research, Food and Drug Administration, Rockville, Maryland 20852, USA.
brossp@cder.fda.gov
PURPOSE: Gemtuzumab ozogamicin (Mylotarg; Wyeth Laboratories,
Philadelphia, PA) consists of a semisynthetic derivative of
calicheamicin, a cytotoxic antibiotic linked to a recombinant monoclonal
antibody directed against the CD33 antigen present on leukemic
myeloblasts in most patients with acute myeloid leukemia (AML). In this
study, we review the preclinical and clinical profiles of this
immunoconjugate and the regulatory review that led to marketing approval
by the United States Food and Drug Administration. EXPERIMENTAL DESIGN:
From the literature and manufacturer's data, we review the activity,
tolerability, and pharmacokinetics of gemtuzumab ozogamicin in
preclinical and Phase I studies and its activity, efficacy, and side
effects in three Phase 2 trials of 142 patients with relapsed AML.
RESULTS: In Phase I studies, the major toxicity was myelosuppression,
especially neutropenia and thrombocytopenia, resulting from the
expression of CD33 on myeloid progenitor cells. The Phase 2 dose was 9
mg/m(2) infused i.v. over 4 h, repeated on day 14. A minority of
patients experienced acute infusion-related symptoms, usually transient
and occasionally requiring hospitalization. The complete response (CR)
rate with full recovery of hematopoiesis was 16%. A subset of patients
[CRs with incomplete platelet recovery (CRps)] was identified with blast
clearance and neutrophil recovery but incomplete platelet recovery. The
duration of responses of CRps appeared to be similar to those of the
CRs, although the numbers were small. The question of the equivalence of
these response groups was a central issue in the review of this new drug
application (NDA). After considerable discussion, the Oncology Drugs
Advisory Committee recommended allowing inclusion of CRps resulting in
an overall response rate in the Phase 2 studies of 30%. In the subgroup
of patients over 60 years of age, the overall response rate was 26%.
Response duration was difficult to establish because of the high
prevalence of postremission therapies. Tolerability and ease of
administration may be improved compared with conventional chemotherapy,
except for hepatotoxicity, with 31% of patients exhibiting abnormal
liver enzymes. One patient died of liver failure in the Phase 2 trials.
CONCLUSIONS: Marketing approval of gemtuzumab ozogamicin was granted on
May 17, 2000 by the United States Food and Drug Administration under the
Accelerated Approval regulations. Gemtuzumab ozogamicin is indicated for
the treatment of patients with CD33 positive AML in first relapse who
are 60 years of age or older and who are not considered candidates for
cytotoxic chemotherapy. The approved dose was 9 mg/m(2) i.v. over 4 h
and repeated in 14 days. Completion of the ongoing studies of gemtuzumab
ozogamicin in relapsed AML and initiation of randomized clinical trials
comparing the effects of gemtuzumab ozogamicin in combination with
conventional induction chemotherapy to conventional chemotherapy alone
on survival are mandated to confirm clinical benefit under the
accelerated approval Subpart H regulations. Postmarketing reports of
fatal anaphylaxis, adult respiratory distress syndrome (ARDS), and
hepatotoxicity, especially venoocclusive disease (VOD) in patients
treated with gemtuzumab ozogamicin, with and without associated
hematopoietic stem cell transplantation (HSCT), have required labeling
revisions and the initiation of a registration surveillance program.
Tumor lysis and ARDS have been reported in patients with leukocytes
above 30,000/ml treated with gemtuzumab ozogamicin; therefore, the
reduction of leukocyte counts to below 30,000/ml is recommended prior to
treatment. Patients should be carefully monitored for acute
hypersensitivity, hypoxia, and delayed hepatotoxicity following
treatment with gemtuzumab ozogamicin.
10
UI - 11474494
AU - Larson RA
TI -
Current use and future development of gemtuzumab ozogamicin.
SO - Semin Hematol 2001 Jul;38(3 Suppl 6):24-31
AD - University of Chicago, Chicago, IL 60637, USA.
The antigen CD33 is expressed on blast cells in 80% to 90% of acute
myeloid leukemia (AML) cases but, importantly, is not expressed on
pluripotent hematopoietic stem cells or on nonhematologic cells.
Gemtuzumab ozogamicin (CMA-676) uses a recombinant humanized anti-CD33
monoclonal IgG4 antibody to deliver the potent cytotoxin, calicheamicin,
into cells. Three multicenter trials have evaluated the efficacy and
safety of gemtuzumab ozogamicin as a single agent in 142 patients with
CD33+ AML in untreated first relapse. The median age was 61 years
(range, 22 to 84 years), none had prior myelodysplasia, and all had had
a first complete remission lasting > or = 3 months. Two doses of 9 mg/m2
were given 14 days apart by 2-hour intravenous infusion. The overall
response rate was 30% (ie, < or = 5% blasts remaining in the bone
marrow, neutrophils > or = 1,500/microL, and red blood cell and platelet
transfusion independence). There was no significant difference in
response rate between patients less than 60 years of age and those > or
= 60 years old (34% v 26%, respectively) or between patients whose first
remission had lasted less than 12 months or > or = 12 months (28% v 32%,
respectively). Overall survival was 31% at 1 year; median survival was
5.9 months. Median relapse-free survival was 6.8 months. An
infusion-related syndrome (chills, fever, rigors, nausea, hypotension,
and pain) was common. Severe myelosuppression occurred in all patients,
but severe mucositis (4%) and infections (23%) were relatively
infrequent. Severe hyperbilirubinemia (23%) and elevated hepatic
transaminases (18%) were usually transient. Among all 142 patients, the
median total hospitalization was 24 days; 16% of patients required < or
= 7 days in hospital. Additional studies are currently evaluating
gemtuzumab ozogamicin in combination with, or as an alternative to,
other standard AML chemotherapy. Copyright 2001 by W.B. Saunders
Company.
11
UI - 11511025
AU - McGavin JK; Spencer CM
TI -
Gemtuzumab ozogamicin.
SO - Drugs 2001;61(9):1317-22; discussion 1323-4
AD - Adis International Limited, Mairangi Bay, Auckland, New Zealand.
demail@adis.co.nz
Gemtuzumab ozogamicin is a humanised monoclonal IgG4 antibody, linked to
a cytotoxic calicheamicin derivative. It effects cell necrosis by
specifically targeting the CD33 antigen which is expressed on the
surface of leukaemic cell blasts in more than 90% of patients with acute
myeloid leukaemia (AML), but is not present on normal stem cells.
Therapy with gemtuzumab ozogamicin (2 doses of 9 mg/m2) in 3
noncomparative studies produced complete remission in 16% of adult
patients with AML in first relapse, and complete remission with
incomplete platelet recovery in an additional 13% of patients. Rates of
remission did not differ between those aged less than 60 years and older
than 60 years. Many patients were able to receive both doses of
gemtuzumab ozogamicin therapy as outpatients. Survival duration was
similar between those treated as outpatients and those requiring
hospitalisation. About one-third of 11 children and adolescents treated
with 2 doses of 9 mg/m2 gemtuzumab ozogamicin in a phase I study showed
<5% bone marrow blasts after completion of therapy. The most commonly
encountered adverse events in clinical trials with gemtuzumab ozogamicin
were myelosuppression, increased levels of hepatic enzymes, infection,
fever, bleeding, chills, nausea and vomiting and dyspnoea. No
treatment-related renal failure or alopecia was reported.
12
UI - 11673694
AU - Sievers EL; Linenberger M
TI -
Mylotarg: antibody-targeted chemotherapy comes of age.
SO - Curr Opin Oncol 2001 Nov;13(6):522-7
AD - Clinical Research Division, Fred Hutchinson Cancer Research Center,
Seattle, Washington 98109-1024, USA. esievers@fhcrc.org
Mylotarg (gemtuzumab ozogamicin, CMA-676; Wyeth-Ayerst Laboratories,
Philadelphia, PA) recently was approved by the US Food and Drug
Administration for the treatment of patients with CD33-positive acute
myeloid leukemia in first relapse, age 60 years or older, who are not
considered candidates for other types of cytotoxic chemotherapy. In
combined phase II studies of 142 patients with CD33-positive acute
myeloid leukemia in first relapse, Mylotarg monotherapy was associated
with a 30% overall response rate. Although treated patients had
relatively high incidences of myelosuppression, hyperbilirubinemia, and
elevated hepatic transaminases, the incidences of severe mucositis and
infections were low compared with what might be expected in association
with conventional chemotherapeutic treatment. Preliminary data in
pediatric patients also suggest that the immunoconjugate is reasonably
well tolerated. Studies of Mylotarg in combination with anthracycline,
cytarabine, and agents that inhibit P-glycoprotein are underway.
13
UI - 11722411
AU - Petti MC; Pinazzi MB; Diverio D; Romano A; Petrucci MT; De Santis S;
TI -
Meloni G; Tafuri A; Mandelli F; Lo Coco F
Prolonged molecular remission in advanced acute promyelocytic leukaemia
after treatment with gemtuzumab ozogamicin (Mylotarg CMA-676).
SO - Br J Haematol 2001 Oct;115(1):63-5
AD - Department of Cellular Biotechnology and Haematology, University La
Sapienza, Roma, Italy.
We report a patient with acute promyelocytic leukaemia (APL) who
received two doses of gemtuzumab ozogamicin for advanced disease.
Previous treatments included front-line all-trans retinoic acid and
anthracyclines, polychemotherapy consolidation, salvage chemotherapy for
the first relapse followed by autologous stem cell transplantation
(ASCT), arsenic trioxide for the second relapse followed by a second
ASCT and then high-dose methotrexate for more advanced systemic disease
with central nervous system involvement. The patient achieved prolonged
haematological and molecular remission after monotherapy with gemtuzumab
ozogamicin given at the time of the third relapse.
14
UI - 11781652
AU - Tack DK; Letendre L; Kamath PS; Tefferi A
TI -
Development of hepatic veno-occlusive disease after Mylotarg infusion
for relapsed acute myeloid leukemia.
SO - Bone Marrow Transplant 2001 Nov;28(9):895-7
AD - Division of Hematology and Internal Medicine, Mayo Clinic, Rochester, MN
55905, USA.
Mylotarg (gemtuzumab zogamicin) is a conjugated monoclonal antibody that
has recently become available for use in patients with relapsing or
refractory acute myeloid leukemia. Reversible hepatotoxicity is common
after administration. We describe the first report of hepatic
veno-occlusive disease (HVOD) developing after Mylotarg infusion in a
patient who underwent hematopoietic stem cell transplantation 8 months
earlier. Certain antineoplastic agents have been implicated as a cause
of HVOD, but the disease is most commonly seen within 30 days after
hematopoietic stem cell transplantation. The possible association
between Mylotarg infusion and HVOD is discussed.
15
UI - 11899326
AU - Sorokin P
TI -
Mylotarg approved for patients with CD33+ acute myeloid leukemia.
SO - Clin J Oncol Nurs 2000 Nov-Dec;4(6):279-80
Acute myeloid leukemia (AML) is the most common adult leukemia and has
historically been treated with intensive multiagent chemotherapy. In May
2000, the U.S. Food and Drug Administration approved a new agent,
gemtuzumab ozogamicin (Mylotarg) to treat patients who are 60 years and
older in first relapse with CD33+ AML and not considered candidates for
chemotherapy. Gemtuzumab is an antibody-targeted agent that binds
specifically to the CD33 antigen that is found on the surface of more
than 80% of patients with AML. The agent is administered via i.v. over
two hours, and premedication with acetaminophen and diphenhydramine is
recommended. Side effects include fever, chills, neutropenia and
thrombocytopenia, and asymptomatic hypotension. Clinical remissions have
been observed with gemtuzumab, and additional trials with this new agent
currently are being conducted.
16
UI - 11898239
AU - Treish IM
TI -
Targeting leukemia cells with gemtuzumab ozogamicin.
SO - Cancer Pract 2000 Sep-Oct;8(5):254-7
AD - Department of Pharmacy, University of North Carolina Hospitals, Chapel
Hill, North Carolina, USA.
17
UI - 11989187
AU - Anderson S; Files J
TI -
Tumor lysis syndrome secondary to Gemtuzumab Ozogamicin in a patient
with acute myelogenous leukemia.
SO - J Miss State Med Assoc 2002 Apr;43(4):105-6
AD - Department of Medicine, University of Mississippi Medical Center, USA.
18
UI - 12010830
AU - Estey EH; Giles FJ; Beran M; O'Brien S; Pierce SA; Faderl SH; Cortes JE;
TI -
Kantarjian HM
Experience with gemtuzumab ozogamycin ("mylotarg") and all-trans
retinoic acid in untreated acute promyelocytic leukemia.
SO - Blood 2002 Jun 1;99(11):4222-4
AD - Department of Leukemia, The University of Texas MD Anderson Cancer
Center, Houston 77030, USA. ehestey@mdanderson.org
We administered gemtuzumab ozogamycin ("mylotarg"; 9 mg/m(2) day 1 or 5)
and all-trans retinoic acid (ATRA) to 19 patients with untreated acute
promyelocytic leukemia (APL). There were 3 patients who also received
idarubicin because of a white blood cell (WBC) count of more than 30
000/microL. In complete remission (CR), patients were to receive 8
courses of mylotarg (9 mg/m(2) every 4 to 5 weeks) and ATRA; idarubicin
was added only for persistent or recurrent polymerase chain reaction
(PCR) positivity. The CR rate was 16/19 (84%). All 12 patients tested to
date were PCR-negative 2 to 4 months from CR date; none of the 7
patients evaluated subsequently have reverted to PCR positivity (median
follow-up in CR was 5 months, up to 14 months). Mylotarg was well
tolerated. A median of 5 post-CR courses have been given to date with 3
patients having currently received 8 post-CR courses, and 4 patients
receiving 7 post-CR courses. Mylotarg appears active in APL, and
repeated administration is feasible.
19
UI - 2115958
AU - Rhodes AM
TI -
A minor's refusal of treatment.
SO - MCN Am J Matern Child Nurs 1990 Jul-Aug;15(4):261
AD - Finance and University Services, University of Iowa, Iowa City.
20
UI - 11925533
AU - Parisi E; Draznin J; Stoopler E; Schuster SJ; Porter D; Sollecito TP
TI -
Acute myelogenous leukemia: advances and limitations of treatment.
SO - Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002 Mar;93(3):257-63
AD - Department of Oral Medicine, School of Dental Medicine, University of
Pennsylvania, Philadelphia, PA 19104, USA.
Acute myelogenous leukemia (AML) describes a group of related
hematologic malignancies that are being approached therapeutically from
several perspectives. Conventional chemotherapeutic agents, such as
anthracyclines and cytosine arabinoside (Ara-C), are useful in treating
AML but now appear to have reached their maximum potential. Newer
therapeutic approaches to AML have recently focused on immune-based
therapy through monoclonal antibodies that target and destroy malignant
cells via specific cell receptors. One such agent is gemtuzumab
(CMA-676), an agent that targets the CD33 antigen on malignant myeloid
cells. Initial studies have shown significant anticancer activity. We
will discuss traditional and newer therapeutic approaches to AML and
review the role of monoclonal antibody based therapies for patients with
AML. A case of a 30-year-old man with refractory AML who was treated
with gemtuzumab will be mentioned, highlighting potential applications
and possible limitations to this novel therapy. Despite the effective
reduction in the number of malignant cells in bone marrow, gemtuzumab
ineffectively treated extramedullary leukemic gingival infiltrate.
Regardless of limitations, monoclonal-based therapy offers an exciting
and potentially safer adjunctive therapy for patients with AML.
21
UI - 12094255
AU - Porrata LF; Litzow MR; Tefferi A; Letendre L; Kumar S; Geyer SM;
TI -
Markovic SN
Early lymphocyte recovery is a predictive factor for prolonged survival
after autologous hematopoietic stem cell transplantation for acute
myelogenous leukemia.
SO - Leukemia 2002 Jul;16(7):1311-8
AD - Division of Hematology, Department of Internal Medicine, Mayo Clinic,
Rochester, MN 55905, USA.
Absolute lymphocyte count (ALC) recovery correlates with survival after
autologous hematopoietic stem cell transplantation (AHSCT) for patients
with multiple myeloma, non-Hodgkin's lymphoma, and metastatic breast
cancer. The role of ALC recovery in relationship to clinical outcome
after AHSCT in patients with acute myelogenous leukemia is unknown. We
analyzed 45 patients who underwent AHSCT at Mayo Clinic, Rochester,
Minnesota between 1990 and 2000. The ALC threshold was selected at 500
cells/microl on day 15 post-AHSCT based on our previous studies.
Thirty-two females and 13 males were included in the study with a median
age of 45 years (range 12-75). The median follow-up was 14 months with a
maximum of 129 months. The median overall and leukemia-free survival
were significantly better for the 23 patients with ALC at day 15 > or
=500 cells/microl compared with 22 patients with ALC <500 cells/microl
(not yet reached vs 10 months, P < 0.0009; 105 vs 9 months, P < 0.0008,
respectively). In conclusion, ALC > or =500 cells/microl on day 15
post-AHSCT is associated with better survival in acute myelogenous
leukemia and requires further studies.
22
UI - 11899773
AU - Wilkinson K
TI -
Arsenic trioxide.
SO - Clin J Oncol Nurs 2001 Sep-Oct;5(5):237-8
23
UI - 12057059
AU - Douer D
TI -
Acute promyelocytic leukemia.
SO - Curr Treat Options Oncol 2000 Apr;1(1):31-40
AD - Division of Hematology, Norris Comprehensive Cancer Center, University
of Southern California, 1441 Eastlake Ave, Los Angeles, CA 90033, USA.
The treatment of acute promyelocytic leukemia (APL) is different from
other subtypes of acute myelocytic leukemia (AML). All trans-retinoic
acid (ATRA) is an essential component of the standard remission
induction for all newly diagnosed APL patients. Remission induction with
ATRA and chemotherapy given concurrently appears to be associated with
fewer relapses. With further consolidation chemotherapy without
high-dose cytosine arabinoside, the disease-free survival rate can reach
70% to 80%, and many of these patients are cured, more so than in any
other AML subtype. APL is especially sensitive to anthracyclines, which
should be included in the chemotherapy cycles at a higher dose than in
other AML subtypes. Maintenance with low-dose chemotherapy (oral daily
6-mercaptopurine with weekly methotrexate) or ATRA further improves the
long-term outcome. New approaches are also available for relapsing
patients, although the optimal treatment is unknown. Patients who did
not receive oral ATRA in first relapse can be treated with this agent,
as can first relapsing patients who have been off the drug for more than
1 year. Because of poor remission rates, ATRA should not be used in
patients with second or subsequent relapses (whether ATRA was given in
the past), in patients with relapses early after ATRA discontinuation,
or in patients relapsing while on ATRA therapy. Arsenic trioxide can
also be used, especially in patients resistant to ATRA. Because arsenic
trioxide is still experimental and not yet widely available, patients
who are unlikely to respond to ATRA or who unsuccessfully undergo ATRA
reinduction should be treated with chemotherapy. Patients in second or
subsequent remission induced with ATRA or chemotherapy should receive
consolidation chemotherapy. When arsenic trioxide is used for
reinduction, the drug should be continued for several cycles; however,
adding consolidation chemotherapy might improve the results. Because it
is unknown whether APL in second or subsequent remission is curable with
salvage therapy, allogeneic hematopoietic stem cell transplantation is
often considered for patients with a human leukocyte antigen
(HL-A)-identical sibling and autologous transplantation when a donor
does not exist. However, compared with the new treatments, the role of
transplantation for relapse is unclear. In first remission, there is no
role for transplantation. A new liposomal formulation of intravenous
ATRA is being investigated and seems effective in late first relapses,
and it may be able to induce and maintain first remissions in selected
patients without chemotherapy.
24
UI - 12071940
AU - Tamayose K; Sugimoto K; Ando M; Oshimi K
TI -
Mononucleosis syndrome and acute monocytic leukemia.
SO - Eur J Haematol 2002 Apr;68(4):236-8
AD - Department of Hematolgy, Juntendo University School of Medicine, Tokyo,
Japan. tamayose@med.juntendo.ac.jp
The association of infectious mononucleosis and an immunocompromised
host such as occurs in acute leukemia is reported. The most common cause
of infectious mononucleosis is Epstein-Barr virus (EBV) and
cytomegalovirus (CMV). Patients with mononucleosis syndrome caused by
other agents are rare. We report a case of acute monocytic leukemia
(AMoL) who developed varicella zoster virus (VZV) mononucleosis syndrome
in the bone marrow recovery phase after myelosuppression due to
high-dose cytarabine. Mononuclear leukocytes appearing during the
mononucleosis syndrome were very similar to the initial leukemic cells.
Varicella zoster virus mononucleosis syndrome was confirmed by delayed
herpes zoster rash with dermatomal distribution.
25
UI - 12016812
AU - Yang J; Han Z; Pei M; Xiao N
TI -
[Fatal side-effects of all-trans retinoic acid in the treatment of acute
promyelocytic leukemia]
SO - Hunan Yi Ke Da Xue Xue Bao 1999;24(3):293-5
AD - Department of Hematology, Second Affiliated Hospital, Hunan Medical
University, Changsha 410011.
Of 82 patients with acute promyelocytic leukemia (APL) who were treated
with all-trans retinoic acid (ATRA), 35 developed leukocytosis and 22
fatal side-effects(15 with retinoic acid syndrome and 7 intracranial
bleeding). There was a high mortality in the patient with fatal
side-effects. The relationship between leukocytosis and fatal
side-effects was analyzed and the effect of therapeutic interventions on
the development and prognosis of the fatal side-effects was
investigated. The results showed that leukocytosis was a risk factor of
the development of fatal side-effects in APL treated with ATRA. ATRA
combined with small dose of harringtonin in treating APL can reduce the
incidence of intracranial bleeding resulted from leukocytosis and
corticosteroid can decrease the mortality of retinoic acid syndrome.
26
UI - 12111790
AU - Tomonari A; Shirafuji N; Iseki T; Ooi J; Nagayama H; Masunaga A; Tojo A;
TI -
Tani K; Asano S
Acquired pulmonary alveolar proteinosis after umbilical cord blood
transplantation for acute myeloid leukemia.
SO - Am J Hematol 2002 Jun;70(2):154-7
AD - Department of Hematology/Oncology, The Institute of Medical Science, The
University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639,
Japan. atomonar@ims.u-tokyo.ac.jp
Pulmonary alveolar proteinosis (PAP) is a heterogeneous disease that
occasionally develops with hematological malignancy. However, PAP in
association with hematopoietic stem cell transplantation is quite rare.
Here we present the first report of a patient who developed PAP after
cord blood transplantation (CBT). A 45-year-old female with AML
underwent unrelated CBT. On day +2 after CBT she developed congestive
heart failure with diffuse alveolar infiltrates in the bilateral lungs.
Despite treatment, the alveolar infiltrates further increased with
progression of multiple organ failure (MOF). She died from MOF before
hematopoietic recovery on day +27. Post-mortem study revealed that
massive amorphous materials positive for periodic acid-Schiff stain
filled in the pulmonary alveoli. These findings led to a diagnosis of
PAP. The bone marrow was hypocellular without the leukemic cells. The
impaired immunity during the period of leukopenia as well as the
impaired clearance of surfactant proteins might contribute to the
development of PAP. Copyright 2002 Wiley-Liss, Inc.
27
UI - 12060484
AU - Mandelli F; Avvisati G; Lo Coco F
TI -
Advances in the understanding and management of acute promyelocytic
leukemia.
SO - Rev Clin Exp Hematol 2002 Mar;6(1):60-71; discussion 86-7
AD - Department of Cellular Biotechnologies and Hematology, University 'La
Sapienza', Rome, Italy.
Considerable progress has been made over the past decade in the
understanding and management of acute promyelocytic leukemia (APL). At
the laboratory level, molecular mechanisms underlying the arrest of
differentiation that typically features in this malignancy, have been
clarified and currently provide important models for addressing future
investigation aimed at releasing the maturation block in other
malignancies. In the clinic, advances in the management of APL have
converted this rapidly fatal disease into the most frequently curable
leukemia in adults. Use of retinoids in combinatorial protocols with
anthracycline-based chemotherapy for front line treatment currently
results in long-term survival and potential cure in at least 60% of
newly diagnosed patients. Even after relapse, the disease is still
curable in a high percentage of cases by various approaches including
combinations of chemotherapy, retinoids, arsenic trioxide, stem cell
transplantation and antibody-targeted chemotherapy. Genetic testing for
identification of the disease-specific gene rearrangement and monitoring
of residual disease have proved critical in establishing correct
diagnosis and better evaluate the response to therapy at the molecular
level. Current 'hot' issues for clinical investigation include: (i)
better understanding and management of the severe coagulopathy present
at diagnosis in most patients; (ii) the definition of risk categories to
improve identification of patients at highest risk of relapse and (iii)
the translation of successful differentiation therapy to other leukemia
subsets.
28
UI - 12113082
AU - Anonymous
TI -
Encouraging results from phase I trial of GVAX.
SO - Expert Rev Anticancer Ther 2001 Dec;1(4):510
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