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NCI CANCERLIT® Search: Chronic Myelogenous Leukemia - January 2002
National Cancer Institute®
Last Modified: January 1, 2002
Table of Contents
1
UI - 11334367
AU - Bitisik O; Yavuz S; Yasasever V; Dalay N
TI -
Telomerase activity in patients with chronic myeloid leukemia and
lymphoma.
SO - Res Commun Mol Pathol Pharmacol 2000;107(1-2):3-12
AD - Istanbul University, Oncology Institute, Dept. of Basic Oncology.
Telomeres are repeated DNA sequences, positioned at the ends of
chromosomes and are essential for the stable maintenance of chromosomes.
The telomere length serves as a mitotic clock determining the remaining
replicative capacity of the cell. Telomeric sequences are lost during
each cell division, leading to a process thought to contribute to
senescence and cell death. The enzyme telomerase adds 5'-TTAGGG-3'
repeats to the mammalian telomeres and maintains the telomere length.
Telomerase is normally inactive in most somatic cells but telomerase
activity is observed in malignancies. In this study telomerase activity
was analyzed in patients with chronic myeloid leukemia (CML) and
lymphoma by PCR and ELISA. This approach combines highly specific
amplification of the telomerase-mediated elongation products with
nonradioactive detection in a highly sensitive photometric ELISA. The
PCR products were also analyzed by Southern blotting. The
telomerase-specific PCR products were seperated by electrophoresis and
transferred to a nylon membrane with subsequent detection of the
biotinylated amplificates. High activity levels were detected in 17 CML
( 34%) patients. On the other hand, no activity was observed in lymphoma
patients. An increase in the shorter telomeric bands was observed in CML
patients who displayed a high level of telomerase activity. In contrast
to the low enzyme activity, evidence of telomeric repeats were also
found in some lymphoma patients by Southern blotting. This may indicate
that lymphoma cells may make use of different pathways for maintaining
the length of their telomeres.
2
UI - 11410423
AU - Mattei D; Saglio G; Gottardi E; Gallamini A; Mordini N; Bacigalupo A
TI -
Persisting molecular remission ten years after donor lymphocyte infusion
for hematologic relapse in chronic myeloid leukemia.
SO - Haematologica 2001 May;86(5):545-6
3
UI - 11471471
AU - Anonymous
TI -
New drug targets genetic malfunction in chronic myeloid leukemia.
SO - Am J Health Syst Pharm 2001 Jul 15;58(14):1282
4
UI - 11499689
AU - Murgo A; Wood KF; Gravell AE; Cheson BD
TI -
Clinical trials referral resource. ST1571.
SO - Oncology (Huntingt) 2001 Jul;15(7):881-2, 885-6
AD - National Cancer Institute, USA.
5
UI - 11504279
AU - Druker BJ
TI -
Current treatment approaches for chronic myelogenous leukemia.
SO - Cancer J 2001 Jul-Aug;7 Suppl 1():S14-8
AD - Leukemia Program, Oregon Health Sciences University, Portland 97201,
USA.
Chronic myelogenous leukemia (CML) is a clonal hematopoietic stem cell
disorder that progresses through distinct phases characterized by
progressive loss of the differentiation of the malignant clone. Over the
past 4 decades, it has been established that the Bcr-Abl protein,
created as a consequence of a (9:22) chromosomal translocation, is the
cause of the disease. Bcr-Abl functions as a constitutively activated
tyrosine kinase, and this kinase activity is absolutely required for the
transforming function of the Bcr-Abl protein. Thus, a specific inhibitor
of the Bcr-Abl tyrosine kinase would be predicted to be an effective and
selective therapeutic agent for CML. STI571, an Abl-specific tyrosine
kinase inhibitor, has shown remarkable activity in all phases of CML.
The clinical features, molecular pathogenesis, and current treatment
options of CML are reviewed along with the development of STI571, the
phase I clinical results, and the application of this paradigm to other
malignancies.
6
UI - 11529594
AU - Kerridge I; Spencer A; Azzi A; Seldon M
TI -
Response to erythropoietin in chronic myelomonocytic leukaemia.
SO - Intern Med J 2001 Aug;31(6):371-2
7
UI - 11571506
AU - Urbano-Ispizua A; Brunet S; Solano C; Moraleda JM; Rovira M; Zuazu J; de
TI -
La Rubia J; Bargay J; Caballero D; Diez-Martin JL; Ojeda E; Perez de
Oteiza JP; Ferra C; Espigado I; Alegre A; de La Serna J; Torres P; Riu
C; Odriozola J; Rozman C; Sierra J; Garcia-Conde J; Montserrat E;
Spanish Group of Allo-PBT
Allogeneic transplantation of CD34+-selected cells from peripheral blood
in patients with myeloid malignancies in early phase: a case control
comparison with unmodified peripheral blood transplantation.
SO - Bone Marrow Transplant 2001 Aug;28(4):349-54
AD - Depatment of Hematology, Hospital Clinic, University of Barcelona,
Spain.
An allogeneic transplantation of CD34(+)-selected cells from peripheral
blood (allo-PBT/CD34(+)) from HLA-identical sibling donors was performed
in 50 adult patients with acute myeloid leukemia in first complete
remission (AML CR1) (n = 29), myelodysplastic syndrome (MDS) (n = 4), or
chronic myeloid leukemia in first chronic phase (CML CP1) (n = 17).
Clinical results were compared to a concurrent group of 50 patients
transplanted with unmodified peripheral blood progenitor cells
(allo-PBT), matched for age, diagnosis, and disease stage. The median
follow-up period was 29 months (range 1-69). The actuarial probability
of developing acute GVHD clinical grade II to IV was 16% (95%CI: 6-26)
for the allo-PBT/CD34(+) group and 41% (95%CI: 29-57) for the allo-PBT
group (P = 0.002). The actuarial probability of developing extensive
chronic GVHD was 22% (95%CI: 8-36) for the allo-PBT/CD34(+) group and
47% (95%CI: 31-63) for the allo-PBT group (P = 0.02). Recipients of
allo-PBT/CD34(+) had less toxicity associated with the transplant and
better Karnofsky index at the last follow-up. For AML/MDS patients, the
actuarial probability of disease-free survival (DFS) for recipients of
allo-PBT/CD34(+) and allo-PBT was 65% (95%CI: 45-85) vs43% (95%CI:
28-58) (P = 0.05), respectively. These data provide a rationale for a
randomised trial of allo-PBT/CD34(+) vs allo-PBT in AML/MDS patients in
early stage of the disease.
8
UI - 11550277
AU - Wang YL; Bagg A; Pear W; Nowell PC; Hess JL
TI -
Chronic myelogenous leukemia: laboratory diagnosis and monitoring.
SO - Genes Chromosomes Cancer 2001 Oct;32(2):97-111
AD - Department of Pathology and Laboratory Medicine, Hospital of the
University of Pennsylvania, 413b Stellar-Chance Building, 422 Curie
Blvd., Philadelphia, PA 19104, USA.
Rapid developments have occurred both in laboratory medicine and in
therapeutic interventions for the management of patients with chronic
myelogenous leukemia (CML). With a wide array of laboratory tests
available, selecting the appropriate test for a specific diagnostic or
therapeutic setting has become increasingly difficult. In this review,
we first discuss, from the point of view of laboratory medicine, the
advantages and disadvantages of several commonly used laboratory assays,
including cytogenetics, fluorescence in situ hybridization (FISH), and
qualitative and quantitative reverse transcriptase-polymerase chain
reaction (RT-PCR). We then discuss, from the point of view of clinical
care, the test(s) of choice for the most common clinical scenarios,
including diagnosis and monitoring of the therapeutic response and
minimal residual disease in patients treated with different therapies.
The purpose of this review is to help clinicians and laboratory
physicians select appropriate tests for the diagnosis and monitoring of
CML, with the ultimate goal of improving the cost-effective usage of
clinical laboratories and improving patient care. Copyright 2001
Wiley-Liss, Inc.
9
UI - 11575716
AU - Shah NP; Sawyers CL
TI -
Recent success with the tyrosine kinase inhibitor STI-571--lessons for
targeted therapy of cancer.
SO - Curr Opin Investig Drugs 2001 Mar;2(3):422-3
AD - Department of Medicine, University of California, Los Angeles
90095-1678, USA.
10
UI - 11567987
AU - Goldman JM; Druker BJ
TI -
Chronic myeloid leukemia: current treatment options.
SO - Blood 2001 Oct 1;98(7):2039-42
AD - Imperial College School of Medicine, London, United Kingdom.
jgoldman@ic.ac.uk
The choice of primary treatment for patients with chronic myeloid
leukemia (CML) diagnosed in chronic phase has become exceedingly
difficult. There is little doubt that allogeneic stem cell
transplantation can eradicate the leukemia and that a
graft-versus-leukemia effect makes a major contribution to this result;
conversely, only a minority of patients are eligible for
transplantation, which still carries an appreciable risk for death or
protracted illness. For most patients, interferon-alpha (IFN-alpha)
prolongs life to some degree in comparison with hydroxyurea, but it is
associated with considerable toxicity. The newly introduced tyrosine
kinase inhibitor STI571 induces complete hematologic remission in almost
all patients and is associated with a very high rate of cytogenetic
response; its capacity to prolong life in comparison with IFN-alpha is
not yet established. Here are reviewed some factors that predict
survival after nontransplantation therapy and after allografting for CML
in chronic phase. Two contrasting options are considered for managing
the patient with newly diagnosed disease, and it can be concluded that,
for now, allogeneic stem cell transplantation soon after diagnosis
should continue to be offered as an option for selected patients.
Further experience with the use of STI571 as a single agent or in
combination with other antileukemic agents may alter the picture in the
near future.
11
UI - 11570925
AU - Dalton SR; Ririe DW; Neuhauser TS
TI -
Cauda equina syndrome in a 65-year-old man, status post-bone marrow
transplant for chronic myeloid leukemia.
SO - Arch Pathol Lab Med 2001 Oct;125(10):1385-6
AD - Department of Pathology, Wilford Hall Medical Center, Lackland AFB,
Texas, USA.
12
UI - 11571715
AU - Press RD
TI -
Pharmacologic inhibition of the Bcr-Abl kinase with STI571: a novel,
safe, and effective therapy for chronic myeloid leukemia.
SO - Mol Diagn 2001 Sep;6(3):211-3
13
UI - 11579507
AU - Tanaka M; Kanamori H; Kuwabara H; Yamaji S; Kamijo A; Taguchi J; Fujita
TI -
H; Fujisawa S; Matsuzaki M; Mohri H; Ishigatsubo Y
[Successful second transplant from one-locus HLA-mismatched unrelated
donor for graft rejection following initial transplant from another
unrelated donor in a patient with chronic myelogenous leukemia]
SO - Rinsho Ketsueki 2001 Aug;42(8):656-8
AD - First Department of Internal Medicine, Yokohama City University School
of Medicine.
We report a patient with chronic myelogenous leukemia who received a
second transplant from a one-locus HLA-mismatched unrelated donor after
rejection of an initial bone marrow graft. For the first transplant,
HLAs were fully matched, conditioning with busulfan + cyclophosphamide
(CY) was applied, and cyclosporin A + short-term methotrexate (sMTX) was
used for prophylaxis against GVHD. A complete chimera was not obtained,
and the graft was rejected on day 122. For the second transplant, there
was a one-HLA locus (DR) mismatch, conditioning was done with total body
irradiation + cytarabine + CY, and GVHD prophylaxis consisted of FK506 +
sMTX. Engraftment was obtained on day 27, and no graft failure was
occurred at the time of writing. This case suggests that strong
immunosuppression may have prevented rejection of the second bone marrow
graft.
14
UI - 11585707
AU - Ullrich O; Grune T
TI -
Proteasomal degradation of oxidatively damaged endogenous histones in
K562 human leukemic cells.
SO - Free Radic Biol Med 2001 Oct 1;31(7):887-93
AD - Dept. of Cell- and Neurobiology, Institute of Anatomy, Humboldt
University Berlin, Schumannstrasse 20/21, D-10098 Berlin, Germany.
A number of antitumor drugs act via the oxidation of nuclear material in
the tumor cell. It is therefore important to know if tumor cells can
effectively and precisely cope not only with oxidatively induced DNA
damage, but also with nuclear protein oxidation. In this study, we
investigated the endogenous degradation of oxidatively damaged histones
in K562 human leukemic cells after oxidative challenge and demonstrated
a link to the overall cellular stress response pathways by
poly-ADP-ribose-polymerase (PARP). After an oxidative challenge,
endogenous nuclear protein degradation, as well as histone degradation,
was enhanced. Among the histone fractions, histone H1 revealed the
highest degradation rate, and more than 85% of the total degraded H1
disappeared in the first 30 min after oxidative challenge. Short-term
degradation of histones up to 30 min, as well as long-term degradation
up to 48 h after oxidative challenge, was significantly reduced in the
presence of the PARP inhibitor 3-aminobenzamide, and nearly completely
abrogated by the selective proteasome inhibitor lactacystin.
Immunoprecipitation experiments indicated that the proteasome
specifically degraded oxidized histones. Thus, we show that the nuclear
proteosome system in tumor cells is capable of preventing the
accumulation of oxidized proteins in this compartment and may suggest
further treatment strategies to effectively interfere with the protein
"repair" and replacement strategies of tumor cells.
15
UI - 11601004
AU - Su XY; Cao Q; He KL
TI -
[Chromosomal abnormalities in 38 CML cases of various phases]
SO - Zhonghua Yi Xue Za Zhi 1999 Jan;79(1):34-7
AD - Shanghai Institute of Hematology, Rui-Jin Hospital, Shanghai 200025.
OBJECTIVE: To study the genomic abnormality underlying the blast crisis
of chronic myeloid leukemia(CML). METHODS: 15 CML patients in blast
crisis (BC), 3 in accelerated phase (AP) and 20 in chronic phase (CP)
were analyzed by conventional cytogentics, comparative genomic
hybridization (CGH) and dual color chromosomal painting. RESULTS:
Philadelphia (Ph) chromosome was identified in every case studied. Only
5 among 20 CP patients had additional abnormalities while 12 out of 14
patients with disease progression (BC + AP) showed extra numerical
and/or structural chromosmal aberrations. Cytogenetically, the most
common chromosome gains during BC and AP were double or triple Ph
chromosome(5/14), trisomy 8(5/14), trisomy 7(1/14) and 17 (1/14). Three
cases showed the same region being involved in translocations
t(1;17)(q12-21;q10), t(1;10) (q12-21;q26) and t(1;11)(q12-21;p15). CGH
analysis detected genetic imbalances in 8 cases. In one case, a very
complex chromosmal translocation del(3), del(6)(q13-21),
der(6)t(17;3;6), der(17)t(6;17) was characterized by chromosomal
painting. CONCLUSION: We find that the combined use of CGH, chromosomal
painting, and classic cytogenetic analysis allows a better evaluation of
the genomic aberration involved in CML blastic transformation, and
offers new directions for its further molecular investigation.
16
UI - 11601240
AU - Yao B; Guo M; Pian H
TI -
[Cytogenetic analysis and bcr/abl mRNA detection in chronic myeloid
leukemia]
SO - Zhonghua Xue Ye Xue Za Zhi 1999 Mar;20(3):137-9
AD - Affiliated Hospital of Academy of Military Medical Sciences, Beijing
100039.
OBJECTIVE: To define the relationship between Ph chromosome and BCR/ABL
mRNA expression in chronic myeloid leukemia (CML) patients, and compare
cytogenetic analysis and PCR method. METHODS: Marrow or peripheral blood
samples from 33 CML patients were analyzed by R banding technique and
PCR method. Eleven patients who received allogeneic BMT or alpha-IFN +
low dose HU were followed up. RESULTS: In 33 patients, 29 were Ph(+), 30
expressed BCR/ABL mRNA. In 6 patients who received BMT, 4 were Ph(-), 2
were Ph(+). However, 2 patients were (-), 4 were (+) by PCR method. In 5
patients who received alpha-IFN, the percentage of Ph(+) cells reduced
after 6 and 12 months treatment than before treatment in 2 cases
respectively. In 41 samples, 34 cases were consistent by 2 methods.
CONCLUSION: Each method, Cytogenetic analysis or PCR has its advantage
and defect. The better method are integration of 2 methods in diagnosis
and treatment monitoring of CML patients, so that provide real and
beneficial information for clinic.
17
UI - 11489902
AU - Boren J; Cascante M; Marin S; Comin-Anduix B; Centelles JJ; Lim S;
TI -
Bassilian S; Ahmed S; Lee WN; Boros LG
Gleevec (STI571) influences metabolic enzyme activities and glucose
carbon flow toward nucleic acid and fatty acid synthesis in myeloid
tumor cells.
SO - J Biol Chem 2001 Oct 12;276(41):37747-53
AD - Department of Biochemistry and Molecular Biology, Institut
d'Investigacions Biomediques August Pi i Sunyer, University of
Barcelona, Marti i Franques 1, Barcelona 08028, Spain.
Chronic myeloid leukemia cells contain a constitutively active Bcr-Abl
tyrosine kinase, the target protein of Gleevec (STI571)
phenylaminopyrimidine class protein kinase inhibitor. Here we provide
evidence for metabolic phenotypic changes in cultured K562 human myeloid
blast cells after treatment with increasing doses of STI571 using
[1,2-13C2]glucose as the single tracer and biological mass spectrometry.
In response to 0.68 and 6.8 microm STI571, proliferation of
Bcr-Abl-positive K562 cells showed a 57% and 74% decrease, respectively,
whereas glucose label incorporation into RNA decreased by 13.4% and
30.1%, respectively, through direct glucose oxidation, as indicated by
the decrease in the m1/Sigma(m)n ratio in RNA. Based on the in vitro
proliferation data, the IC50 of STI571 in K562 cultures is 0.56 microm.
The decrease in 13C label incorporation into RNA ribose was accompanied
by a significant fall in hexokinase and glucose-6-phosphate
1-dehydrogenase activities. The activity of transketolase, the enzyme
responsible for nonoxidative ribose synthesis in the pentose cycle, was
less affected, and there was a relative increase in glucose carbon
incorporation into RNA through nonoxidative synthesis as indicated by
the increase in the m2/Sigma(m)n ratio in RNA. The restricted use of
glucose carbons for de novo nucleic acid and fatty acid synthesis by
altering metabolic enzyme activities and pathway carbon flux of the
pentose cycle constitutes the underlying mechanism by which STI571
inhibits leukemia cell glucose substrate utilization and growth. The
administration of specific hexokinase/glucose-6-phosphate
1-dehydrogenase inhibitor anti-metabolite substrates or competitive
enzyme inhibitor compounds, alone or in combination, should be explored
for the treatment of STI571-resistant advanced leukemias as well as that
of Bcr-Abl-negative human malignancies.
18
UI - 11590581
AU - Hamidou MA; Boumalassa A; Larroche C; El Kouri D; Bletry O; Grolleau JY
TI -
Systemic medium-sized vessel vasculitis associated with chronic
myelomonocytic leukemia.
SO - Semin Arthritis Rheum 2001 Oct;31(2):119-26
AD - Department of Internal Medicine, Hotel-Dieu, University Hospital Nantes,
Nantes, France. mohamed.hamidou@chu-nantes.fr
OBJECTIVE: To determine the clinical aspects of systemic vasculitis
associated with chronic myelomonocytic leukemia (CMML). METHODS: In this
retrospective study, 8 patients suffering from systemic vasculitis
associated with CMML are described. The French and English literature on
systemic vasculitis associated with myelodysplasia was reviewed.
RESULTS: All 8 patients had a systemic medium-sized vessel vasculitis
which fulfilled the American College of Rheumatology criteria for
polyarteritis nodosa in the setting of active CMML. Antineutrophil
cytoplasmic antibodies (ANCA) were negative in 7 patients. One patient
had cytoplasmic ANCA by indirect immunofluorescence without
antiproteinase 3 or antimyeloperoxydase antibodies on the enzyme-linked
immunosorbent assay. At presentation, 6 patients had fever of unknown
origin, 5 had polymyalgia rheumatica, 3 had sensory hearing loss, and 4
had eosinophilia. None had viral infection or drug-associated
vasculitis. Diagnostic procedures included renal or hepatic angiography
in 6 patients which showed microaneurysms in 4, skin and temporal artery
biopsy in 2 which showed vasculitis, and 1 postmortem examination which
showed gastroduodenal arteritis. All patients were treated with
corticosteroids, and 7 received immunosuppressive drugs. Death was
attributable to vasculitis in 2 cases, infection in 3, and other
vasculitis-related causes in 2. In a review of the French-English
literature, we found 11 similar cases of ANCA-negative systemic
vasculitis, generally associated with refractory anemia, with or without
blast excess. CONCLUSIONS: Systemic ANCA-negative polyarteritis
nodosa-type vasculitis seems closely associated to CMML. Clinical
presentation is nonspecific, and systemic vasculitis should be suspected
when a patient with myelodysplasia develops atypical manifestations.
Renal, gastrointestinal, or hepatic angiography are useful diagnostic
procedures when more invasive biopsies should be avoided because of low
platelet count. The prognosis of CMML-associated systemic vasculitis is
poor. Copyright 2001 by W.B. Saunders Company
19
UI - 11597734
AU - Marley SB; Davidson RJ; Lewis JL; Nguyen DX; Eades A; Parker S; Goldman
TI -
JM; Gordon MY
Progenitor cells from patients with advanced phase chronic myeloid
leukaemia respond to STI571 in vitro and in vivo.
SO - Leuk Res 2001 Nov;25(11):997-1002
AD - Leukaemia Research Fund Centre for Adult Leukaemia, Department of
Haematology, Imperial College School of Medicine, Hammersmith Campus,
DuCane Road, W12 ONN, London, UK.
STI571 targets p210(BCR-ABL) in chronic myeloid leukaemia (CML). In
vitro, STI571 reduces self-replication (replating ability) by
chronic-phase CML CFU-GM. Here, we studied CFU-GM in advanced-phase
(accelerated and blast crisis) CML. The numbers and self-replication of
CFU-GM in advanced phase were greater than in the chronic phase.
Self-replication by CFU-GM from advanced phase patients was reduced by
STI571 or IFN alfa to the same extent as in the chronic phase. The
reduced replating ability induced by STI571 correlated with that induced
by IFN alpha (r=0.73). STI571 treatment in vivo also reduced replating
ability and the numbers of CFU-GM/ml of blood.
20
UI - 11600728
AU - Bjork J; Albin M; Welinder H; Tinnerberg H; Mauritzson N; Kauppinen T;
TI -
Stromberg U; Johansson B; Billstrom R; Mikoczy Z; Ahlgren T; Nilsson PG;
Mitelman F; Hagmar L
Are occupational, hobby, or lifestyle exposures associated with
Philadelphia chromosome positive chronic myeloid leukaemia?
SO - Occup Environ Med 2001 Nov;58(11):722-7
AD - Department of Occupational and Environmental Medicine, Lund University
Hospital, SE-221 85 Lund, Sweden. jonas.bjork@ymed.lu.se
OBJECTIVES: To investigate a broad range of occupational, hobby, and
lifestyle exposures, suggested as risk factors for Philadelphia
chromosome positive (Ph+) chronic myeloid leukaemia (CML). METHODS: A
case-control study, comprising 255 Ph+CML patients from southern Sweden
and matched controls, was conducted. Individual data on work tasks,
hobbies, and lifestyle exposures were obtained by telephone interviews.
Occupational hygienists assessed occupational and hobby exposures for
each subject individually. Also, occupational titles were obtained from
national registries, and group level exposure-that is, the exposure
proportion for each occupational title-was assessed with a job exposure
matrix. The effects of 11 exposures using individual data and two
exposures using group data (organic solvents and animal dust) were
estimated. RESULTS: For the individual data on organic solvents, an
effect was found for moderate or high intensity of exposure (odds ratio
(OR) 3.4, 95% confidence interval (95% CI) 1.1 to 11) and for long
duration (15-20 years) of exposure (OR 2.1, 95% CI 1.1 to 4.0). By
contrast, the group data showed no association (OR 0.69, 95% CI 0.27 to
1.8; moderate or high intensity versus no exposure). For extremely low
frequency electromagnetic fields (EMFs), only individual data were
available. An association with long occupational exposure to EMFs was
found (OR 2.3, 95% CI 1.2 to 4.5). However, no effect of EMF intensity
was indicated. No significant effects of benzene, gasoline or diesel, or
tobacco smoking were found. OR estimates below unity were suggested for
personal use of hair dye and for agricultural exposures. CONCLUSIONS:
Associations between exposure to organic solvents and EMFs, and Ph+CML
were indicated but were not entirely consistent.
21
UI - 11602316
AU - Carella AM; Melo JV; Goldman JM
TI -
Portofino International Conference on Chronic Myeloid Leukemia.
SO - Exp Hematol 2001 Oct;29(10):1147-56
AD - Department of Hematology and Stem Cell Transplantation Unit, Ospedale
Casa Sollievo della Sofferenza--IRCCS, San Giovanni Rotondo FG, Italy.
amcarella@operapadrepio.it
22
UI - 11669299
AU - Hernandez-Boluda JC; Cervantes F; Alvarez A; Costa D; Montserrat E
TI -
Single-agent therapy with oral mercaptopurine for nonlymphoid blast
crisis of chronic myeloid leukemia.
SO - Ann Hematol 2001 Sep;80(9):516-20
AD - Department of Hematology, Postgraduate School of Hematology
Farreras-Valenti, Hospital Clinic, IDIBAPS, University of Barcelona,
Spain.
Currently, no effective treatment is available for the nonlymphoid blast
crisis (BC) of chronic myeloid leukemia (CML) and because of this the
prognosis for such patients remains invariably poor. In an attempt to
determine the results provided by palliative treatment with oral
6-mercaptopurine (6-MP) in the above hematological condition, 30 such
patients were analyzed for hospital stay, days of intravenous (i.v.)
antibiotics, transfusion requirements, response rate, and survival.
Thirty patients with nonlymphoid BC matched for their initial
characteristics and treated with different i.v. regimens were used for
comparison purposes. Patients managed with 6-MP spent less days in
hospital (median: 9, range: 0-46 vs median: 42, range: 5-140; P<0.0001),
needed antibiotics for less days (median: 0. range: 0-46 vs median: 20,
range: 0-57; P<0.0001), and received less platelet transfusions (median:
0, range: 0-20 vs median: 6, range: 0-63; P=0.004) than those treated
with i.v. chemotherapy. Although no complete or partial remission was
achieved by patients receiving 6-MP vs six in the i.v. chemotherapy
group, no significant difference was observed when the survival of both
groups was compared (median: 4.7 months, range: 0.1-22.7 vs median: 3.8
months, range: 0.2-12, respectively). These results indicate that 6-MP
therapy constitutes a good palliative treatment for patients with
nonlymphoid BC of CML. However, new treatment strategies for this
hematological condition are required.
23
UI - 11640869
AU - Chase A; Huntly BJ; Cross NC
TI -
Cytogenetics of chronic myeloid leukaemia.
SO - Best Pract Res Clin Haematol 2001 Sep;14(3):553-71
AD - Wessex Regional Genetics Laboratory, Salisbury District Hospital,
Salisbury, Wilts SP2 8BJ, UK.
The standard Philadelphia (Ph) translocation t(9;22), its variants and a
proportion of Ph-negative cases are positive for the BCR-ABL fusion
gene, as determined by molecular analysis. Extensive deletions of
chromosome 9 and 22 derived sequences around the translocation
breakpoints on the derivative 9 are seen in 10-30% of patients at
diagnosis and may confer a worse prognosis. Additional cytogenetic
changes can occur in the few months before or during disease progression
and are often specific for blast morphology; however, the molecular
basis of the most common additional cytogenetic abnormalities is largely
unknown. Cytogenetics is important for monitoring patient response to
treatment but is increasingly being replaced by the more sensitive and
less invasive techniques of RT-PCR and FISH. Copyright 2001 Harcourt
Publishers Ltd.
24
UI - 11672777
AU - Gonzalez FA; Anguita E; Mora A; Asenjo S; Lopez I; Polo M; Villegas A
TI -
Deletion of BCR region 3' in chronic myelogenous leukemia.
SO - Cancer Genet Cytogenet 2001 Oct 1;130(1):68-74
AD - Department of Haematology, Hospital Clinico San Carlos, Madrid, Spain.
The t(9;22)(q34;q11) produces the BCR/ABL fusion gene which codifies a
210 kb protein with a strong tyrosine kinase activity and is involved in
cellular development and growth. Because this translocation is a
reciprocal event, it could give rise to a second fusion gene, ABL-BCR,
on the derivative 9q+. We analyzed the influence of the 3' M-BCR
deletion on the clinical picture at diagnosis and disease outcome in 57
patients with a clinical diagnosis of CML. Molecular studies were done
on DNA from peripheral blood leukocytes or bone marrow with the
restrictions enzymes BglII, EcoRI, HindIII, and BamHI, and the BCR 3'
probe (transprobe 1) (Oncogene Science Inc.), which encompasses almost
all of the 5.8 Kb of the M-BCR gene area. In 18 patients Southern blot
analysis showed deletion of the 3' end of BCR gene (32.7%). There were
no significant differences between patients with or without deletion,
either in the clinical and laboratory data at the disease diagnosis or
at the disease outcome. The absence of differences between the patients
with and without 3' BCR deletion supports the hypothesis that the hybrid
gene ABL-BCR does not have an important role in leukemogenesis in CML
cases.
25
UI - 11600816
AU - Hochhaus A; Lahaye T; Kreil S; Berger U; Metzgeroth G; Hehlmann R
TI -
[Selective inhibition of tyrosine kinases - a new therapeutic principle
in oncology]
SO - Onkologie 2001 Sep;24 Suppl 5():65-71
AD - III. Medizinische Klinik, Fakultat fur Klinische Medizin Mannheim der
Universitat Heidelberg, Mannheim, Germany. hochhaus@uni-hd.de
Tyrosine kinases are enzymes that regulate mitosis, differentiation,
migration, neovascularization, and apoptosis. Their spectrum and
association with specific malignancies offer multiple targets for
therapeutic intervention. Chronic myelogenous leukemia (CML) represents
an ideal target for a therapy using a selective inhibitor of the BCR-ABL
tyrosine kinase. The 2-phenylpyrimidine derivative STI571 was rationally
designed to inhibit ABL and BCR-ABL tyrosine kinase activities through
competitive ATP-binding pocket interactions. Phase II data demonstrate
hematologic and cytogenetic responses in interferon refractory
chronic-phase, accelerated-phase and blast crisis patients. However,
long-term observation is needed to confirm that response data result in
prolongation of survival. STI571 is being studied in other malignancies,
including leukemias characterized by expression of alternate molecular
forms of BCR-ABL and those expressing protein tyrosine kinases with
ATP-binding pockets structurally similar to ABL, e.g. c-kit and PDGF-R.
Gastrointestinal stromal tumor (GIST) cells overexpress the stem cell
factor receptor CD117, the product of the proto-oncogene c-kit.
Inhibition of c-kit in vivo results in an immediate metabolic change of
the tumor cells, detectable by positron emission tomography. Since c-kit
overexpression is inhibited in small-cell lung cancer cell lines, a
study with STI571 as second-line therapy of c-kit-positive small-cell
lung cancer is in progress. Clinical studies are ongoing in malignancies
associated with an enhanced activity of the PDGF-R, such as highgrade
glioma, prostate cancer and leukemias with rearrangements of PDGF-R. The
development of selective tyrosine kinase inhibitors is considered a
promising approach for the design of new drugs. Clinical responses to
STI571 in various malignancies may stimulate greater interest in the
clinical use of tyrosine kinase inhibitors. Copyright 2001 S. Karger
GmbH, Freiburg
26
UI - 11681414
AU - Yamaguchi H; Inokuchi K; Sakuma Y; Dan K
TI -
Mutation of the p51/p63 gene is associated with blastic crisis in
chronic myelogenous leukemia.
SO - Leukemia 2001 Nov;15(11):1729-34
AD - Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
The p51/p63 gene, a novel member of the p53 gene family, has recently
been identified at 3q27-9. There are at least six major isotypes of
p51/p63 mRNA transcripts. p51A/TAp63gamma has the potential to induce
apoptosis and growth suppression in a manner similar to p53, and other
isotypes may suppress the p53 and p51A1TAp63gamma genes in a
dominant-negative manner. We analyzed the mutation and expression of the
p51/p63 gene in 80 cases of chronic myelogenous leukemia (CML) to
evaluate its role in blastic transformation. Expression of the p51/p63
gene was d
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