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NCI CANCERLIT® Search: Chronic Myelogenous Leukemia - July 2002
National Cancer Institute®
Last Modified: July 1, 2002
- Cultured autografting for juvenile myelomonocytic leukaemia.
- Lymphoid preponderance and the absence of basophilia and splenomegaly are frequent in m-bcr-positive chronic myelogenous leukemia.
- [Current pharmacotherapy of chronic myeloid leukemia]
- Interleukin-2 activation of haematopoietic stem cells.
- Homoharringtonine effective in CML patients.
- Chronic myelogenous leukemia in chronic phase.
- Chronic myelomonocytic leukemia.
- Imatinib mesylate--a new oral targeted therapy.
- [Tyrosine kinase inhibitors as the targeted therapy for leukemia]
- Derivative chromosome 9 deletions in chronic myeloid leukemia: poor prognosis is not associated with loss of ABL-BCR expression, elevated
- Not so NICE for CML.
- Imatinib and chronic-phase leukemias.
- Chronic myeloid leukaemia in megakaryocytic crisis.
- Therapy-related chronic myelogenous leukaemia following autologous stem cell transplantation for Ewing's sarcoma.
- Low concentrations of STI571 in the cerebrospinal fluid: a case report.
- Human leucocyte antigen alloimmunization after bone marrow transplantation: an association with chronic myelogenous leukaemia.
- Mylotarg (gemtuzumab ozogamicin) therapy is associated with hepatic venoocclusive disease in patients who have not received stem cell
- Spectral karyotyping refined the identification of a der(Y)t(Y;1)(q11.1 or.2;q12) in the blast cells of a patient with atypical chronic myeloid
- Chemotherapy for mobilisation of Ph-negative progenitor cells from patients with CML: impact of different mobilisation regimens.
- Chronic neutrophilic leukemia evolving from polycythemia vera with multiple chromosome rearrangements: a case report.
- Mediastinal immature teratoma with yolk sac tumor and myelomonocytic leukemia associated with Klinefelter's syndrome.
- Chronic myelogenous leukemia.
- Insights from pre-clinical studies for new combination treatment regimens with the Bcr-Abl kinase inhibitor imatinib mesylate
- Safety and efficacy of STI-571 (imatinib mesylate) in patients with bcr/abl-positive chronic myelogenous leukemia (CML) after autologous
- Clonal Ph-negative hematopoiesis in CML after therapy with imatinib mesylate is frequently characterized by trisomy 8.
- Mini-ice protocol is better than high-dose hydroxyurea to mobilize Ph-negative cells in earlier phases of chronic myelogenous leukemia.
- Unable to resist.
- Chronic myelogenous leukemia: an overview.
- Heterogenic molecular basis for loss of ABL1-BCR transcription: deletions in der(9)t(9;22) and variants of standard t(9;22) in
- Accelerated and blastic phase of chronic myeloid leukemia.
- Immune-mediated complications during interferon alpha therapy in chronic myelogenous leukemia.
- Persistence of lymphoblasts in bone marrow on day 15 and days 22 to 25 of remission induction predicts a dismal treatment outcome in children
- Multiple sclerosis associated with interferon-alpha therapy for chronic myelogenous leukemia.
- [Association between phakomatosis and neoplasia in children pathology. IV Pediatric Clinic experience]
- Immune haemolytic anaemia following T cell-depleted allogeneic bone marrow transplantation for chronic myeloid leukaemia: association with
- Chronic myelogenous leukemia in T cell lymphoid blastic phase achieving durable complete cytogenetic and molecular remission with imatinib
Table of Contents
1
UI - 11972535
AU - Grainger JD; Will AM; Stevens RF
TI -
Cultured autografting for juvenile myelomonocytic leukaemia.
SO - Br J Haematol 2002 May;117(2):477-9
AD - Royal Manchester Children's Hospital, Hospital Road, Pendlebury,
Manchester M27 4HA, UK.
A case of juvenile myelomonocytic leukaemia (JMML) associated with a
chromosomal translocation (1;5) is described. Initial cytoreductive
therapy failed to control the disease. In the absence of a matched
family or unrelated donor, a Dexter-type long-term bone marrow culture
(LTBMC) was established. The LTBMC showed preferential growth of normal
stem cells over the abnormal clone, allowing a cultured autologous stem
cell transplantation to be performed. Despite detection of the t(1;5)
from 5 months to 7 years following cultured autograft, the patient
remained in haematological remission. Currently the patient is alive and
well at 10 years in full cytogenetic remission.
2
UI - 11976825
AU - Hur M; Song EY; Kang SH; Shin DH; Kim JY; Park SS; Cho HI
TI -
Lymphoid preponderance and the absence of basophilia and splenomegaly
are frequent in m-bcr-positive chronic myelogenous leukemia.
SO - Ann Hematol 2002 Apr;81(4):219-23
AD - Department of Clinical Pathology, Seoul National University College of
Medicine, Korea.
Chronic myelogenous leukemia (CML) with a minor bcr-abl transcript is a
rare entity. We describe a 66-year-old female who was diagnosed with CML
in the chronic phase. Molecular analysis of her Philadelphia chromosome
using the reverse transcriptase polymerase chain reaction and subsequent
sequencing revealed a minor bcr-abl transcript. Monocytosis resembling
chronic myelomonocytic leukemia was observed without splenomegaly and
basophilia. Her clinical course was indolent and maintained the chronic
phase of CML for nearly 3 years under hydroxyurea treatment. A review of
the 23 cases of m-bcr CML including this case showed the presence of
monocytosis and the absence of basophilia and splenomegaly in 55.0%,
55.0%, and 70.0% of patients, respectively. The absence of basophilia
was a significant finding in patients without monocytosis ( P=0.01).
Although the hematological features or clinical outcomes were variable
in m-bcr CML cases, all three cases at the onset of the blastic phase
showed lymphoid crisis, implying an increased lymphoid leukemogenicity
of minor bcr-abl transcripts.
3
UI - 11963764
AU - Hochhaus A; Berger U; Reiter A; Hehlmann R
TI -
[Current pharmacotherapy of chronic myeloid leukemia]
SO - Internist (Berl) 2002 Feb;43(2):270-83
AD - III. Medizinische Universitatsklinik, Fakultat fur Klinische Medizin
Mannheim der Universitat Heidelberg, Wiesbadener Strasse 7-11, 68305
Mannheim.
4
UI - 12050948
AU - Hajek R; Koristek Z; Vinklarkova J; Janovska E; Klabusay M; Doubek M;
TI -
Dvorakova D; Bourkova L; Dusek L; Buchler T; Adler J; Adam Z; Penka M;
Mayer J; Vorlicek J
Interleukin-2 activation of haematopoietic stem cells.
SO - Acta Med Austriaca 2002;29(2):61-7
AD - Department of Internal Medicine-Hematooncology, Department of Clinical
Hematology, University Hospital Brno, Bohunice, Jihlavska 20, CZ-639 00
Brno, Czech Republic. r.hajek@fnbrno.cz
BACKGROUND: Recent findings concerning the role of immunity in the
eradication of residual malignant disease after autologous
haematopoietic stem cell transplantation have led to extensive studies
of T-cell and natural killer (NK) mediated anti-tumour effects.
Interleukin 2 (IL-2) activation of autologous bone marrow (BM) or
peripheral blood stem cells (PBSC) before transplantation is one of the
methods of adoptive cell therapy. METHODS: Autologous BM of patients
with chronic myelogenous leukaemia (n = 11) and PBSC of patients with
multiple myeloma (n = 14) were activated by IL-2 in laboratory
conditions with the aim of evaluating the feasibility of this method,
the activation of T and NK cells, recovery of active progenitor cells,
microbial contamination, and reduction of malignant cell content.
RESULTS: Samples of BM (mean 2.6 x 10(6) cells) and PBSC (mean 10.3 x
10(6) cells) were cultured in complete culture medium with IL-2 (6000
Ul/ml) for 24 h. The recovery of CD34+ cells and CFU-GM was 82.5% and
51.5%, respectively, for BM, and 85% and 86%, respectively, for PBSC
(mean values). No purging effect was detected by flow cytometry and a
small decline in malignant cell contamination was observed by
quantitative PCR in BM samples. No microbial contamination occurred
during the sample processing. CONCLUSIONS: The described in vitro
activation of BM and peripheral blood stem cells using IL-2 was
evaluated as a safe and reliable method suitable for clinical
application.
5
UI - 12067785
AU - Hitt E
TI -
Homoharringtonine effective in CML patients.
SO - Lancet Oncol 2002 May;3(5):259
6
UI - 12057124
AU - Kurzrock R; Kantarjian H; Talpaz M
TI -
Chronic myelogenous leukemia in chronic phase.
SO - Curr Treat Options Oncol 2001 Jun;2(3):245-52
AD - Department of Bioimmunotherapy, Box 422, MD Anderson Cancer Center, 1515
Holcombe Boulevard, Houston, TX 77030, USA.
Chronic myelogenous leukemia (CML) is a clonal myeloproliferative
disorder characterized by genomic instability leading to its inevitable
clinical evolution from an easily controlled chronic phase to a terminal
blastic phase. The molecular abnormality responsible for this
disease--BCR-ABL--and the critical biochemical aberrations resulting
from it have been studied in depth. These discoveries have led to the
development of a molecule, STI571, that specifically inhibits the
abnormal kinase enzymatic activity exhibited by BCR-ABL. Early results
of clinical trials using STI571 have shown responses even in blast
crisis. There has also been striking hematologic and cytogenetic
remission rates in patients with advanced chronic phase disease, with
very little toxicity. It is our opinion that this molecule will
revolutionize the treatment of CML. Furthermore, the path leading to its
discovery will become a paradigm for cancer therapeutics. At the time of
this writing, STI571 remains investigational (although it is widely
believed that it will be approved for clinical use in the United States
this year ). Although suggested therapy for a disease does not generally
incorporate medications that are still investigational, in this case,
the impact of a still investigational agent cannot be ignored. The
current data suggest that STI571 will be the treatment of choice for
patients with advanced or resistant chronic phase. To date, STI571 has
not been studied adequately in untreated CML patients. Even so, it is
our feeling that, based on its compelling success in patients with
interferon-refractory and advanced disease and on its benign side effect
profile, it will quickly become the front-line therapy for CML once it
becomes available. Despite the ease of administration of STI571,
patients should continue to be encouraged to participate in clinical
studies so that several vital issues can be resolved: 1) the percentage
of untreated CML patients who will eventually develop molecular
remissions; 2) the proportion of patients in whom resistance to STI571
will emerge; 3) the optimum length of treatment; and 4) the impact on
survival. Because interferon-alfa can also result in cytogenetic
remissions, albeit in a small percent (less than 20%) of early chronic
phase patients, it seems reasonable to suggest that patients who do not
attain cytogenetic/molecular remissions with STI571 alone be treated
with a combination of STI571 and interferon-alfa. Patients who are
resistant to STI571 with or without interferon-alfa should undergo
allogeneic hematopoietic cell transplant. Salvage therapy after
transplant may include donor lymphocyte infusions, interferon-alfa,
additional transplant, and perhaps STI571. Medications such as
hydroxyurea appear destined to play a very limited role in CML. They may
be used in the palliative treatment of older STI571-resistant patients
or those without a transplant donor, although these patients may be best
served by being considered for clinical trials of molecules, such as
polyethylene glycol-interferon-alfa, on other novel agents.
7
UI - 12057067
AU - Bennett JM
TI -
Chronic myelomonocytic leukemia.
SO - Curr Treat Options Oncol 2002 Jun;3(3):221-3
AD - University of Rochester Medical Center, James P. Wilmot Cancer Center,
601 Elmwood Avenue, Rochester, NY, 14642, USA.
john_bennett@urmc.rochester.edu
Chronic myelomonocytic leukemia (CMML) has dysplastic and proliferative
features. The median age of patients with CMML is 70 years; the median
survival is approximately 2 years. Various chemotherapy regimens have
been used with only modest success. When the proliferative phase
prevails, hydroxyurea is the treatment of choice. For younger patients
with high-risk CMML, an allogeneic bone marrow transplantation should be
considered. If a donor cannot be identified, then combination acute
myeloid leukemia-type therapy followed by an autologous stem cell or
marrow transplant should be offered. Clinical trials should be
considered if available because the overall results of therapeutic
interventions are far from optimal.
8
UI - 11870247
AU - Savage DG; Antman KH
TI -
Imatinib mesylate--a new oral targeted therapy.
SO - N Engl J Med 2002 Feb 28;346(9):683-93
AD - Herbert Irving Comprehensive Cancer Center, Columbia University College
of Physicians and Surgeons, New York, NY, USA.
9
UI - 12017607
AU - Heikinheimo M
TI -
[Tyrosine kinase inhibitors as the targeted therapy for leukemia]
SO - Duodecim 2000;116(18):1943-4
10
UI - 12036887
AU - Huntly BJ; Bench AJ; Delabesse E; Reid AG; Li J; Scott MA; Campbell L;
TI -
Byrne J; Pinto E; Brizard A; Niedermeiser D; Nacheva EP; Guilhot F;
Deininger M; Green AR
Derivative chromosome 9 deletions in chronic myeloid leukemia: poor
prognosis is not associated with loss of ABL-BCR expression, elevated
BCR-ABL levels, or karyotypic instability.
SO - Blood 2002 Jun 15;99(12):4547-53
AD - Department of Hematology, University of Cambridge, United Kingdom.
Deletions of the derivative chromosome 9 have recently been reported in
chronic myeloid leukemia. These deletions are large, occur at the time
of the Philadelphia (Ph) translocation, span the translocation
breakpoint, and represent a powerful prognostic indicator. However, the
molecular mechanisms responsible for the poor prognosis associated with
deletions are obscure, and several possible models are investigated
here. First, we demonstrate that all derivative chromosome 9 deletions
detected by fluorescence in situ hybridization were associated with an
absence of ABL-BCR expression. However, loss of ABL-BCR expression also
occurred without an overt deletion, suggesting the existence of other
mechanisms by which ABL-BCR transcription can be abolished. Furthermore,
analysis of survival in 160 patients demonstrated that loss of ABL-BCR
expression, in contrast to deletion status, was not an indicator of poor
prognosis. Second, we addressed the possibility that concomitant small
deletions of the Ph chromosome modulate BCR-ABL transcription. Real-time
reverse-transcription polymerase chain reaction was used to demonstrate
that derivative chromosome 9 deletions were not accompanied by altered
levels of BCR-ABL transcripts. Third, deletions may represent a
consequence of genetic instability within the target cell at the time of
the Ph translocation, with the poor prognosis reflecting a
predisposition to subsequent additional genetic alterations. However,
patients with deletions do not exhibit an increased frequency of
secondary cytogenetic changes following disease progression. Taken
together, these data support a model in which deletions of the
derivative chromosome 9 result in rapid disease progression as a result
of the loss of one or more genes within the deleted region.
11
UI - 12076575
AU - Goldman J; Apperley J; Clark R; Green T; Holyoake T; O'Brien S; Shepherd
TI -
P
Not so NICE for CML.
SO - Lancet 2002 Jun 8;359(9322):2036
12
UI - 12097546
AU - Boros LG; Lee WN; Cascante M
TI -
Imatinib and chronic-phase leukemias.
SO - N Engl J Med 2002 Jul 4;347(1):67-8
13
UI - 12028013
AU - Ranjitkumar S; Lindeman R
TI -
Chronic myeloid leukaemia in megakaryocytic crisis.
SO - Br J Haematol 2002 Jun;117(3):487
AD - Prince of Wales Hospital, Randwick, NSW, Australia. sumibob@hotmail.com
14
UI - 12028029
AU - Numata A; Shimoda K; Gondo H; Kato K; Aoki K; Ito Y; Takase K; Asano Y;
TI -
Okamura T; Niho Y; Harada M
Therapy-related chronic myelogenous leukaemia following autologous stem
cell transplantation for Ewing's sarcoma.
SO - Br J Haematol 2002 Jun;117(3):613-6
AD - Medicine and Biosystemic Science, Kyushu University Graduate School of
Medical Sciences, 3-3-3 Maidashi, Higashi-ku, Fukuoka city, Fukuoka
812-8582, Japan.
A 17-year-old Japanese woman with Ewing's sarcoma was initially treated
with conventional chemotherapy and local irradiation, and then with
high-dose chemotherapy supported by autologous peripheral blood stem
cell transplantation. Four years later she was diagnosed with chronic
myelogenous leukaemia (CML). The BCR/ABL fusion gene was detected in
both peripheral blood and bone marrow cells by reverse
transcription-polymerase chain reaction, but not in the harvest product
of peripheral blood stem cells which were infused at the time of
transplantation. This case adds to the accumulating evidence of
therapy-related CML developing after high-dose chemotherapy and
autologous stem cell transplantation.
15
UI - 12028032
AU - Petzer AL; Gunsilius E; Hayes M; Stockhammer G; Duba HC; Schneller F;
TI -
Grunewald K; Poewe W; Gastl G
Low concentrations of STI571 in the cerebrospinal fluid: a case report.
SO - Br J Haematol 2002 Jun;117(3):623-5
AD - Abteilung fur Hamatologie & Onkologie, Universitatsklinik Innsbruck,
Anichstrasse 35, A-6020 Innsbruck, Austria. andreas.petzer@uibk.ac.at
We report a 53-year-old man with lymphoid blast crisis of Ph+ chronic
myeloid leukaemia who was treated with STI571, a selective inhibitor of
the enzymatic activity of BCR-ABL. He responded excellently to STI571
(600 mg/d), obtaining a complete cytogenetic remission after 3 months of
therapy. Although remission in the bone marrow was sustained, the
patient developed an isolated central nervous system relapse. Subsequent
analyses of STI571 concentrations in the cerebrospinal fluid (CSF)
revealed 2-log lower CSF levels of STI571 than corresponding plasma
levels. These are the first data demonstrating a low penetration of
orally administered STI571 into the CSF in humans.
16
UI - 12028035
AU - Geiger TL; Woodard P; Tong X; Srivastava DK; Johnson R; Turner V; Hale
TI -
G; Richardson S
Human leucocyte antigen alloimmunization after bone marrow
transplantation: an association with chronic myelogenous leukaemia.
SO - Br J Haematol 2002 Jun;117(3):634-41
AD - Department of Pathology, Mail Stop 341, St. Jude Children's Research
Hospital, 132 North Lauderdale Street, Memphis, TN 38105-2794, USA.
terrence.geiger@stjude.org
Platelet refractoriness due to human leucocyte antigen (HLA)
alloimmunization is a significant risk to allogeneic bone marrow
transplant recipients. To identify factors contributing to this risk, we
reviewed the records of 317 consecutive, paediatric, allogeneic bone
marrow transplant recipients at a single institution. The 6-year
estimated cumulative incidence of platelet refractoriness due to HLA
alloimmunization was 2.6% +/- 0.9%. The incidence among patients with
chronic myelogenous leukaemia (CML) 12.5% +/- 5.3% was significantly
greater than that of other patients (1.1% +/- 0.6%, P < 0.001). Graft
rejection (P = 0.003) and the number of platelet transfusions during the
first 90 d after bone marrow transplantation (BMT) (P = 0.0025) were
also significantly associated with alloimmunization. The association
with CML and with graft rejection was not seen among patients
alloimmunized before transplantation. Eight patients developed
alloimmunization, of whom three had mismatched grafts and four had
unrelated grafts. Alloantibody specificities, identified in seven
patients, were unrelated to host or graft major histocompatibility
complex (MHC). Host recognition of alloantigens in transfused blood
products, not graft-host recognition, therefore seems predominantly
responsible for the alloimmunization. These results show that paediatric
CML patients have a significantly increased risk of platelet
refractoriness due to HLA alloimmunization after BMT. Identifying the
mechanism for the increased alloimmunization risk may assist in the
development of therapies to prevent platelet refractoriness.
17
UI - 11466696
AU - Giles FJ; Kantarjian HM; Kornblau SM; Thomas DA; Garcia-Manero G;
TI -
Waddelow TA; David CL; Phan AT; Colburn DE; Rashid A; Estey EH
Mylotarg (gemtuzumab ozogamicin) therapy is associated with hepatic
venoocclusive disease in patients who have not received stem cell
transplantation.
SO - Cancer 2001 Jul 15;92(2):406-13
AD - Department of Leukemia, The University of Texas M. D. Anderson Cancer
Center, Houston, Texas 77030-4095, USA. fgiles@mdanderson.org
BACKGROUND: Mylotarg (Wyeth-Ayerst Laboratories, St. Davids, PA) is the
brand name for a calicheamicin-conjugated humanized anti-CD33 monoclonal
antibody (gemtuzumab ozogamicin, CMA-676) and has been approved recently
for the treatment of a subset of elderly patients who have relapsed
acute myeloid leukemia (AML). Mylotarg is associated with an incidence
of approximately 20% Grade 3 or 4 hyperbilirubinemia and liver
transaminitis in this patient population. Hepatic venoocclusive disease
(VOD) has been reported in patients who have undergone stem cell
transplantation (SCT) after Mylotarg therapy. Outside of the SCT
setting, VOD has been associated very rarely with cytotoxic therapy.
METHODS: The authors assessed the incidence of VOD in 119 patients who
were receiving Mylotarg-containing non-SCT regimens. VOD was diagnosed
through the use of standard Seattle and Baltimore criteria. RESULTS: A
cohort of 119 (61 previously untreated, 58 with relapsed disease)
patients with AML (92 patients), advanced myelodysplastic syndrome (25
patients), or chronic myeloid leukemia in blast phase (2 patients),
received Mylotarg-based regimens. Fourteen (12%) developed VOD. The
diagnosis of VOD was supported by histology in 2 patients and radiologic
studies in a further 10 patients. Five (36%) of 14 patients with VOD had
received no prior antileukemic cytotoxic therapy, including 2 patients
who received single-agent Mylotarg therapy. CONCLUSIONS: Mylotarg was
shown to be associated with the development of potentially fatal VOD in
patients with leukemia who had not received SCT. VOD occurred when
Mylotarg was used either as a single agent or when it was given with
other cytotoxic agents. VOD occurred in Mylotarg-treated patients who
had received no prior cytotoxic therapy. The current study concluded
that risk factors for VOD should be assessed when considering Mylotarg
therapy, and that attempts to avoid and treat VOD are warranted in
patients who receive Mylotarg therapy. Copyright 2001 American Cancer
Society.
18
UI - 12053151
AU - Ohsaka A; Hisa T
TI -
Spectral karyotyping refined the identification of a der(Y)t(Y;1)(q11.1
or.2;q12) in the blast cells of a patient with atypical chronic myeloid
leukemia.
SO - Acta Haematol 2002;107(4):224-9
AD - Department of Transfusion Medicine, Juntendo University School of
Medicine, Tokyo, Japan. ohsaka@med.juntendo.ac.jp
We report a case of atypical chronic myeloid leukemia who showed
leukocytosis with immature granulocytes and dysplastic features but no
monocytosis or basophilia. Cytogenetic analysis by conventional
G-banding showed an abnormal clone, which was interpreted as
46,X,-Y,+der(?)t(?;1)(?;q?1), and no Philadelphia chromosome. Reverse
transcription-polymerase chain reaction did not show either major or
minor BCR-ABL chimeric mRNA. Spectral karyotyping (SKY) and fluorescence
in situ hybridization (FISH) refined the karyotype to
46,X,der(Y)t(Y;1)(q11.1 or.2;q12). The der(Y)t(Y;1) abnormality was
reported previously in 9 cases and associated with myelodysplastic
syndrome or chronic myeloproliferative disorders. SKY in combination
with the standard banding method and FISH may be useful for exploring
undefined chromosome abnormalities in hematological disorders. Copyright
2002 S. Karger AG, Basel
19
UI - 11551022
AU - Deininger M; Ponisch W; Krahl R; Leiblein S; Edel E; Lange T; Fiedler F;
TI -
Freund M; Franke A; Pasold R; von Grunhagen U; Herold M; Dolken G;
Hoffmann FA; Uhle R; Schultze W; Steglich J; Schwarzer A; Richter P;
Winkelmann C; Kettner E; Dachselt K; Subert R; Schwalbe E; Doepper J;
Helbig W; Niederwieser D; East German Study Group Haematology/Oncology
(OSHO)
Chemotherapy for mobilisation of Ph-negative progenitor cells from
patients with CML: impact of different mobilisation regimens.
SO - Bone Marrow Transplant 2001 Jun;27(11):1125-32
AD - Department of Hematology, University of Leipzig, Germany.
Mobilised peripheral blood stem cells are widely used for autografting
in patients with chronic myeloid leukaemia (CML) and it is generally
thought that a high proportion of Ph-negative progenitor cells in the
graft is desirable. We report here the results of 91 stem cell
mobilisations performed with various chemotherapy regimens followed by
G-CSF. We show that mobilisation of Ph-negative cells is possible after
diagnosis as well as in advanced stages of the disease. The yield of
Ph-negative cells is highly dependent on the chemotherapy regimen: while
the combination of idarubicin and cytarabin for 3-5 days (IC3-5)
mobilised Ph-negative cells in most patients, high-dose cyclophosphamide
was ineffective. Mobilisation of Ph-negative progenitor cells after IC3
was at least as effective as after IC5; however, less apheresis sessions
were required, and toxicity was much reduced after IC3. Compared to
historical controls, IC was equally effective as the widely used
ICE/miniICE (idarubicin, cytarabin, etoposide) protocol. No correlation
was found between graft quality and the cytogenetic response to
subsequent treatment with interferon-alpha. We conclude that IC3 is an
effective and well-tolerated regimen for mobilising Ph-negative cells
that compares well with more aggressive approaches such as IC5 and
ICE/miniICE.
20
UI - 11694412
AU - Billio A; Venturi R; Morello E; Rosanelli C; Pescosta N; Coser P
TI -
Chronic neutrophilic leukemia evolving from polycythemia vera with
multiple chromosome rearrangements: a case report.
SO - Haematologica 2001 Nov;86(11):1225-6
21
UI - 12075411
AU - Govender D; Pillay SV
TI -
Mediastinal immature teratoma with yolk sac tumor and myelomonocytic
leukemia associated with Klinefelter's syndrome.
SO - Int J Surg Pathol 2002 Apr;10(2):157-62
AD - Department of Pathology, Nelson R. Mandela School of Medicine,
University of Natal, Durban, South Africa.
A 14-year-old male presenting with a short history of right
subclavicular chest pain was found to have a mediastinal tumor.
Hematologic investigations and bone marrow examination showed features
of myelomonocytic leukemia. The mediastinal tumor was excised, but the
surgery was complicated by massive hemorrhage. The patient's condition
deteriorated postoperatively and he died a week later. The histology of
the mediastinal tumor showed the typical features of an immature
teratoma with a yolk sac tumor. A prominent infiltrate of leukemic blast
cells was present within blood vessels and in close proximity to the
yolk sac component. The karyotypic analysis of leukemic cells isolated
and cultured from the bone marrow showed 50XXY, +8, +21, +iso G-group
marker chromosome karyotype.
22
UI - 11722980
AU - Druker BJ; Sawyers CL; Capdeville R; Ford JM; Baccarani M; Goldman JM
TI -
Chronic myelogenous leukemia.
SO - Hematology (Am Soc Hematol Educ Program) 2001;():87-112
AD - Oregon Health and Science University, Portland, OR 97201-3098, USA.
The treatment recommendations for chronic myelogenous leukemia (CML) are
evolving rapidly. In the past year, pegylated interferon and STI571
(Gleevec, imatinib mesylate), a Bcr-Abl tyrosine kinase inhibitor, have
become commercially available and non-myeloablative stem cell
transplants continue to be refined. Clinicians and patients face a
bewildering array of treatment options for CML. In this article Dr.
Sawyer reviews the clinical results with STI571 and ongoing
investigations into mechanisms of resistance to STI571. Given the
newness of STI571, a practical overview on the administration of STI571
is presented by Drs. Druker and Ford, focusing on aspects such as
optimal dose, management of common side effects, and potential drug
interactions. The most recent data on interferon-based regimens are
reviewed by Dr. Baccarani in the third section. In the last section Dr.
Goldman presents recent results of allogeneic stem cell transplants,
including the reduced intensity conditioning regimens. Lastly, the
proposed place of each of these treatments in the management of CML
patients is addressed to assist in deciding amongst treatment options
for CML patients.
23
UI - 12094245
AU - La Rosee P; O'Dwyer ME; Druker BJ
TI -
Insights from pre-clinical studies for new combination treatment
regimens with the Bcr-Abl kinase inhibitor imatinib mesylate
(Gleevec/Glivec) in chronic myelogenous leukemia: a translational
perspective.
SO - Leukemia 2002 Jul;16(7):1213-9
AD - Oregon Health and Science University, Division of Hematology and Medical
Oncology, Portland 97201, USA.
Clinical phase I/II studies with the Abl kinase inhibitor imatinib
mesylate (Gleevec/Glivec, formerly STI571) for the treatment for chronic
myelogenous leukemia (CML) demonstrated the safety and the remarkable
efficacy of this molecularly targeted agent. However, a significant
proportion of patients treated in the chronic phase of the disease after
having failed interferon alpha (IFN) remain predominantly Philadelphia
chromosome positive (Ph(+)), suggesting a risk of later relapses.
Furthermore, results in blast crisis patients revealed a high frequency
of relapses or resistance to imatinib. To circumvent resistance, improve
response rates, or prolong survival, pre-clinical evaluations of
combinations of imatinib with other agents have been pursued. Some of
these have already been translated into clinical studies. Here, we first
summarize evidence from pre-clinical studies on new combination regimens
with imatinib in the treatment of CML. Second, we analyze preliminary
clinical data of ongoing combination studies. Finally, we provide a
summary of approaches that use novel antileukemic agents with
molecularly characterized modes of action.
24
UI - 12094246
AU - Fischer T; Reifenrath C; Hess GR; Corsetti MT; Kreil S; Beck J;
TI -
Meinhardt P; Beltrami G; Schuch B; Gschaidmeier H; Hehlmann R; Hochhaus
A; Carella A; Huber C
Safety and efficacy of STI-571 (imatinib mesylate) in patients with
bcr/abl-positive chronic myelogenous leukemia (CML) after autologous
peripheral blood stem cell transplantation (PBSCT).
SO - Leukemia 2002 Jul;16(7):1220-8
AD - 3 rd Medical Department, Johannes Gutenberg-University, Mainz, Germany.
We examined safety and efficacy of STI-571 in 24 bcr/abl-positive
patients with CML post PBSCT. At start of STI-571 therapy, nine patients
presented in blast crisis (BC) or in accelerated phase (AP), and 15 in
chronic phase (CP). Patients were evaluated for hematologic, cytogenetic
and molecular response, survival and toxicity. In general, STI-571 was
well tolerated in this heavily pretreated group of patients with a
non-hematologic and hematologic toxicity profile similar to that
observed in a previous phase I trial at comparable doses. Five of nine
patients with CML in transformation (AP, BC) were evaluable for
hematologic response. Two of five patients had transient reductions in
WBC and blasts, and three patients achieved a sustained hematologic
response (>4 weeks). Cytogenetic analysis in these patients revealed
numerical and/or structural responses. In CML chronic phase, STI-571
induced complete hematologic responses in all patients and major
cytogenetic responses in 61% of patients with a complete cytogenetic
response rate of 46%. This report indicates that STI-571 is a safe and
effective drug in heavily pretreated patients. No apparent additional
side-effects were noted in this patient cohort. The high rate of
complete hematologic and complete cytogenetic responses in CP patients
is remarkable, as intensive treatment approaches plus IFN-alpha failed
to be efficient in achieving long-term stabilization of CML in this
patient cohort.
25
UI - 12094265
AU - Andersen MK; Pedersen-Bjergaard J; Kjeldsen L; Dufva IH; Brondum-Nielsen
TI -
K
Clonal Ph-negative hematopoiesis in CML after therapy with imatinib
mesylate is frequently characterized by trisomy 8.
SO - Leukemia 2002 Jul;16(7):1390-3
26
UI - 11426572
AU - Carella AM
TI -
Mini-ice protocol is better than high-dose hydroxyurea to mobilize
Ph-negative cells in earlier phases of chronic myelogenous leukemia.
SO - Leuk Lymphoma 2001 Jan;40(3-4):447-8
27
UI - 12001985
AU - Brooksbank C
TI -
Unable to resist.
SO - Nat Rev Cancer 2002 Apr;2(4):248
28
UI - 11899767
AU - Tennant L
TI -
Chronic myelogenous leukemia: an overview.
SO - Clin J Oncol Nurs 2001 Sep-Oct;5(5):218-9
Important advances have been made in the treatment of chronic
myelogenous leukemia (CML). In the past two decades, treatment of this
disease has changed and now includes the use of hydroxyurea, interferon,
tyrosine kinase inhibitors, and high-dose chemotherapy followed by
hematopoietic stem cell transplantation. Because several relatively
effective forms of therapy now exist, the care and management of
patients with CML has become more complex. Through continued research
and drug development, additional therapies are expected to emerge
offering new hope and expanded treatment options for patients with CML.
29
UI - 11979553
AU - Loncarevic IF; Romer J; Starke H; Heller A; Bleck C; Ziegler M; Fiedler
TI -
W; Liehr T; Clement JH; Claussen U
Heterogenic molecular basis for loss of ABL1-BCR transcription:
deletions in der(9)t(9;22) and variants of standard t(9;22) in
BCR-ABL1-positive chronic myeloid leukemia.
SO - Genes Chromosomes Cancer 2002 Jun;34(2):193-200
AD - Institute for Human Genetics and Anthropology, FSU, Jena, Germany.
ilon@mti-n.uni-jena.de
The objective of this study was to characterize the ABL1-BCR fusion gene
in 76 BCR-ABL1-positive chronic myeloid leukemia (CML) patients
regarding expression as well as genomic status, to assess the frequency
of ABL1-BCR gene deletion in these patients, which has been reported to
be an adverse prognostic factor in Philadelphia chromosome-positive CML.
Patients were analyzed for ABL1-BCR 1b-b3 and/or 1b-b4 transcription by
RT-PCR analysis. ABL1-BCR gene status was analyzed by FISH in 16 CML
patients with no ABL1-BCR transcript. FISH revealed a partial or total
deletion of the ABL1-BCR gene in 9/16 and localized the 5' portion of
ABL1 and the 3' portion of BCR at separated loci in 5/16 patients. The
latter FISH pattern resulted from a nonreciprocal translocation in two
and a complex translocation in three individuals. In 2/16 patients, FISH
could not exclude an intact ABL1-BCR fusion gene. Thus, most CML
patients without ABL1-BCR transcript could be characterized
cytogenetically to belong to two major subgroups: a silent ABL1-BCR gene
was attributed to a deletion in der(9)t(9;22) in 56% of the investigated
patients or to variants of a standard t(9;22) (approximately 31%).
Conversely, none of the 50 patients with an ABL1-BCR transcript
exhibited a variant t(9;22) in GTG-banding analysis. Thus, genomic
aberrations such as deletions or complex genomic rearrangements are the
basic and most frequent cause for ABL1-BCR RNA negativity in CML. The
heterogeneity of the underlying molecular mechanisms may explain
divergent clinical implications described for patients with an ABL1-BCR
deletion and those with no ABL1-BCR transcript. Copyright 2002
Wiley-Liss, Inc.
30
UI - 12057061
AU - Dutcher JP; Wiernik PH
TI -
Accelerated and blastic phase of chronic myeloid leukemia.
SO - Curr Treat Options Oncol 2000 Apr;1(1):51-62
AD - Our Lady of Mercy Cancer Center/New York Medical College, 600 East 233rd
Street, Bronx, NY 10466, USA.
There is currently no standard treatment for the blastic phase of
chronic myeloid leukemia (CML-BC), which is a chemoresistant form of
acute leukemia. Current approaches include using standard acute myeloid
leukemia (AML) regimens in an effort to induce remission, variations of
these approaches with drugs that seem more active in this specific
leukemia, and the direct entry of patients into studies of
investigational agents. Although the likelihood of achieving remission
is small, immediate bone marrow transplantation in remission should be
considered because it provides the only opportunity for long-term
survival at this time. Allogeneic transplantation is preferred, but
autologous transplantation of an early chronic phase marrow may provide
benefit. Often, however, the duration of chemotherapy-induced remission
of blast crisis is very short and may preclude entry into a transplant
program. In addition, the patient may not be a candidate due to donor
issues, age, or medical problems. If transplant is not an option,
maintenance interferon is often used, although its benefit is uncertain.
For patients in the accelerated phase of the disease, which is
characterized by a variety of clinical presentations and cytogenetic
abnormalities, the possibility of favorably manipulating the disease is
greater. Again, there is no standard treatment, and clinical trials are
recommended as first-line therapy. Treatment in the accelerated phase
includes standard AML chemotherapy regimens, combinations of new agents,
and the combination of cytostatic agents with interferon. Patients whose
accelerated phase reverts to chronic phase after treatment may become
candidates for bone marrow transplantation. However, current new
approaches to the chronic phase applied in accelerated phase as well as
new approaches directed specifically toward accelerated phase may lead
to prolonged stabilization without bone marrow transplantation. In view
of a median age of 55 at diagnosis of chronic phase, nontransplant
regimens for accelerated phase that produce long-term benefit are
urgently needed.
31
UI - 12088112
AU - Tothova E; Kafkova A; Stecova N; Fricova M; Guman T; Svorcova E
TI -
Immune-mediated complications during interferon alpha therapy in chronic
myelogenous leukemia.
SO - Neoplasma 2002;49(2):91-4
AD - Department of Hematology, Medical Faculty Hospital and UPJS Kosice,
Slovak Republic. etothova@post.sk
Several prospective randomized studies have shown that the treatment of
chronic myeloid leukemia with interferon alpha (IFNalpha) prolongs the
survival by comparison with conventional chemotherapy. However,
long-term treatment with Interferon alpha can produce or exacerbate
immune-mediated complications (IMC). The purpose of this study was to
analyze the experience with IMC in patients with chronic myelogenous
leukemia (CML) undergoing IFNalpha treatment. The occurrence of IMC was
evaluated in 76 patients (47 male; 29 female) with Philadelphia
chromosome (Ph)-positive CML. Diagnostic criteria of IMC were performed
in patients with symptoms suggestive of particular disorders.
Well-documented and clinically evident complications developed in 7
patients after a median of 19 months (range 1-84) of IFNalpha treatment.
These included 9.2% patients with Ph-positive CML treated with
IFNalpha-containing regimens. Hypothyroidism (H) occurred in 1 patient
(1.3%), immune-mediated hemolysis (HEM) in 2 patients (2.6%) and
connective tissue disorders (CTD) in 4 patients (5.3%) (2 systemic lupus
erythematosus--SLE, 1 Raynaud's phenomena and 1 mixed connective tissue
disease--MCTD). IFNalpha was discontinued in 3 patients and the dose was
reduced in 2 patients. Five of 7 patients (75%) with immune-mediated
complications had some degree of cytogenetic response at the time of the
event. The association with female sex was strong and significant (86%
vs 33.6%, x2; 48; p = 0.02). The frequency of IMC of clinical relevance
with interferon alpha therapy in CML increased (long-term therapy). The
patients treated with interferon alpha should be monitored for signs and
symptoms of autoimmunity.
32
UI - 12070006
AU - Sandlund JT; Harrison PL; Rivera G; Behm FG; Head D; Boyett J; Rubnitz
TI -
JE; Gajjar A; Raimondi S; Ribeiro R; Hudson M; Relling M; Evans W; Pui
CH
Persistence of lymphoblasts in bone marrow on day 15 and days 22 to 25
of remission induction predicts a dismal treatment outcome in children
with acute lymphoblastic leukemia.
SO - Blood 2002 Jul 1;100(1):43-7
AD - Department of Hematology-Oncology, St Jude Children's Research Hospital,
and the University of Tennessee, College of Medicine, Memphis, TN 38105,
USA. john.sandlund@stjude.org
We determined the prognostic importance of morphologically identifiable
persistent disease at day 15 and days 22 to 25 of remission induction in
childhood acute lymphoblastic leukemia (ALL). Among 546 patients entered
on 2 consecutive protocols, 397 patients had evaluable bone marrow (BM)
examinations on day 15 (+/- 1 day) and 218 on days 22 to 25 (+/- 1 day).
Fifty-seven patients (14%) had persistent lymphoblasts (> or = 1%) in
the BM on day 15 and 27 patients (5.5%) had persistent lymphoblasts on
days 22 to 25. The 5-year event-free survival (EFS) was significantly
worse for patients with lymphoblasts on day 15 (40% +/- 6%) or on days
22 to 25 (4% +/- 3%) as compared to those without lymphoblasts on these
dates (78% +/- 2% and 76% +/- 2%, respectively, P <.001 for both
comparisons). A worse prognosis was observed even for patients with a
low percentage of lymphoblasts (ie, 1%-4%) at either day 15 (5-year EFS
= 56% +/- 8%) or days 22 to 25 (5-year EFS = 0%) compared to those
without morphologically identifiable persistent lymphoblasts at these
times (P <.001 for both comparisons). The prognostic impact of
persistent lymphoblasts on both dates remained significant after
adjusting for other known risk factors, including treatment protocol,
age, white blood cell count, DNA index, cell lineage, and central
nervous system status, and National Cancer Institute/Rome criteria
simultaneously. Hence, persistence of lymphoblasts (even 1%-4%) on day
15 of remission induction was associated with a poor prognosis and on
days 22 to 25 signified a particularly dismal outcome; these very
high-risk patients require novel or more intensive therapy to improve
outcome.
33
UI - 12111789
AU - Kataoka I; Shinagawa K; Shiro Y; Okamoto S; Watanabe R; Mori T; Ito D;
TI -
Harada M
Multiple sclerosis associated with interferon-alpha therapy for chronic
myelogenous leukemia.
SO - Am J Hematol 2002 Jun;70(2):149-53
AD - Department of Internal Medicine II, Okayama University Medical School,
2-5-1 Shikata-cho, Okayama 700-8558, Japan.
We report a chronic myelogenous leukemia (CML) patient in chronic phase
(CP) who developed multiple sclerosis (MS) in association with
interferon-alpha (IFN-alpha) administration. In our patient, recombinant
IFN-alpha2b therapy induced hematologically complete and cytogenetically
major partial response for CML first, and sequential central nervous
system dysfunction evolved, which subsided shortly after the cessation
of its administration. Restarting IFN-alpha therapy by changing to a
natural type of IFN-alpha resulted in rapid exacerbation of MS. The
patient's neurological symptoms progressed gradually, but partial
hematologic response persisted without any IFN-alpha derivatives or
anti-cancer agents until a matched unrelated donor transplant procedure
was performed. Myeloablative therapy led to lasting stable state of MS
and finally to complete cytogenetic remission of CML. This patient's
presenting clinical course and laboratory data suggest that both
exertion of anti-leukemic activity and autoimmune process of MS might be
mediated by mutual mechanisms, such as enhancement of specific cellular
immunity induced by IFN-alpha. Copyright 2002 Wiley-Liss, Inc.
34
UI - 12089980
AU - Brumariu O; Miron I; Munteanu M; Enache G; Stan G; Mihailiuc C; Dimov V;
TI -
Dumitrescu G; Rusu C; Mihaila D
[Association between phakomatosis and neoplasia in children pathology.
IV Pediatric Clinic experience]
SO - Rev Med Chir Soc Med Nat Iasi 2000 Apr-Jun;104(2):143-9
AD - Facultatea de Medicina, Universitatea de Medicina si Farmacie Gr. T.
Popa, Iasi.
The risk to developing a neoplasm is increased when associated to a
patient phakomatosis (Recklinghausen neurofibromatosis, Bourneville's
tuberous sclerosis). We analysed 6 cases with phakomatosis and tumours,
admitted in the Department of Oncopediatry, between 1993-1998; five of
these children had neurofibromatosis and one Bourneville's disease. The
associated tumours were hematologic malignancies (juvenile myeloid
chronic leukemia) and solid tumors (rhabdomyosarcoma, hepatic carcinoma,
CNS tumour, NHL optic glioma). The diagnosis was confirmed by
microscopic examination of the bioptic material in all cases. Tumoral
staging was performed by clinics, biology and imagistic investigations.
All cases had extensive and aggressive tumours at the moment of
diagnosis, We noticed a poor response and an early relapse after
chemotherapy. A special follow-up and a different management has to be
established for the patients with phakomatosis, in order to have a good
oncological prophylaxis.
35
UI - 11607771
AU - Cwynarski K; Goulding R; Pocock C; Dazzi F; Craddock C; Kaeda J;
TI -
Olavarria E; Kanfer E; Apperley J; Lawler M; Goldman JM
Immune haemolytic anaemia following T cell-depleted allogeneic bone
marrow transplantation for chronic myeloid leukaemia: association with
leukaemic relapse and treatment with donor lymphocyte infusions.
SO - Bone Marrow Transplant 2001 Sep;28(6):581-6
AD - Department of Haematology, Hammersmith Hospital, ICSM, London, UK.
Immune haemolytic anaemia (IHA) is a recognised complication after
allogeneic stem cell transplantation (SCT) and occurs more frequently if
marrow cells have been subjected to T cell depletion (TCD). Among 58
consecutive patients who underwent TCD-allogeneic SCT from volunteer
unrelated donors for the treatment of CML at the Hammersmith Hospital
nine cases of IHA. All patients had a strongly positive direct and
indirect antiglobulin test and in eight patients the serological
findings were typical of warm-type haemolysis often with antibody
specificities within the Rh system. All nine cases had clinically
significant haemolysis and were treated initially with prednisolone and
immunoglobulin. The onset of IHA coincided with the occurrence of
leukaemic relapse in six cases, and the presence of host haemopoiesis
confirmed by lineage-specific chimerism in all four cases studied. Five
patients received donor lymphocyte infusions (DLI); in three molecular
remission and the restoration of full donor chimerism coincided with
resolution of haemolysis. We conclude that in the context of leukaemic
relapse, DLI is an effective therapy for IHA following allografts
involving TCD.
36
UI - 12115389
AU - Atallah E; Talpaz M; O'brien S; Rios MB; Guo JQ; Arlinghaus R;
TI -
Fernandes-Reese S; Kantarjian H
Chronic myelogenous leukemia in T cell lymphoid blastic phase achieving
durable complete cytogenetic and molecular remission with imatinib
mesylate (STI571; Gleevec) therapy.
SO - Cancer 2002 Jun 1;94(11):2996-9
AD - Department of Leukemia, University of Texas M. D. Anderson Cancer
Center, Houston, Texas 77030, USA.
BACKGROUND: A T cell lymphoid blastic phase of chronic myelogenous
leukemia (CML) is a rare occurrence, with only a few reported cases
worldwide. Standard therapy for such patients is undetermined. Imatinib
mesylate, a Bcr-Abl tyrosine kinase inhibitor, has shown activity in
CML. METHODS: The authors report on a patient with CML and marrow as
well as extramedullary nodal T cell lymphoid blastic phase who was
treated with imatinib mesylate. RESULTS: The patient achieved complete
morphologic and cytogenetic remission within two months of therapy.
Competitive quantitative polymerase chain reaction analysis of marrow
cells was negative after 15 months. Response had lasted for 26+ months
at the time of writing. CONCLUSIONS: The current data suggest that
imatinib mesylate may produce long-term event free survival in patients
with T-cell lymphoid blastic phase CML. Its potential role alone or in
combinations should be further explored in this condition. Copyright
2002 American Cancer Society.
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