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NCI CANCERLIT® Search: Chronic Lymphocytic Leukemia - June 2002
National Cancer Institute®
Last Modified: June 1, 2002
- Rethinking advanced directives.
- Randomized, double-blind, placebo-controlled trial of recombinant human erythropoietin, epoetin Beta, in hematologic malignancies.
- T-cell prolymphocytic leukemia with hemorrhagic gastrointestinal involvement and a new chromosomal abnormality.
- Prognostic relevance of a scoring system based on clinical and biological parameters in early chronic lymphocytic leukemia.
- Therapeutic role of alemtuzumab (Campath-1H) in patients who have failed fludarabine: results of a large international study.
- Notch2 is involved in the overexpression of CD23 in B-cell chronic lymphocytic leukemia.
- Aggressive growth of epithelial carcinomas following treatment with nucleoside analogues.
- Intercellular adhesion molecules (ICAMs) 2 and 3 are frequently expressed in B cell chronic lymphocytic leukemia.
- Alemtuzumab.
- Chronic lymphocytic leukemia B cells are endowed with the capacity to attract CD4+, CD40L+ T cells by producing CCL22.
- Involvement of protein kinase C and phosphatidylinositol 3-kinase pathways in the survival of B-cell chronic lymphocytic leukemia cells.
- The chemokine receptor CCR7 and alpha4 integrin are important for migration of chronic lymphocytic leukemia cells into lymph nodes.
- [Chronic lymphatic leukemia: significance of erythropoietin]
- Production of matrix metalloproteinase-9 in early stage B-CLL: suppression by interferons.
- Phenotypic transformation of CD52(pos) to CD52(neg) leukemic T cells as a mechanism for resistance to CAMPATH-1H.
- B-CLL cells are capable of synthesis and secretion of both pro- and anti-angiogenic molecules.
- Lack of somatic hypermutation of IG V(H) genes in lymphoid malignancies with t(2;14)(p13;q32) translocation involving the BCL11A gene.
- Distinct genomic events in the myeloid and lymphoid lineages in simultaneous presentation of chronic myeloid leukemia and B-chronic
- Fludarabine as second-line therapy for B cell chronic lymphocytic leukaemia: a technology assessment.
- Genetic susceptibility to chronic lymphocytic leukemia.
- Alkylating agents and nucleoside analogues in the treatment of B cell chronic lymphocytic leukemia.
- Multiple cell cycle regulator alterations in Richter's transformation of chronic lymphocytic leukemia.
- Bax expression correlates with cellular drug sensitivity to doxorubicin, cyclophosphamide and chlorambucil but not fludarabine, cladribine or
- Expression profile of 11 proteins and their prognostic significance in patients with chronic lymphocytic leukemia (CLL).
- Autologous and allogeneic stem cell transplantation for chronic lymphocytic leukemia.
- Genetics of chronic lymphocytic leukemia: genomic aberrations and V(H) gene mutation status in pathogenesis and clinical course.
- Lack of BCL10 mRNA mutation in lymphold malignancies.
- Cell surface expression of CD25, CD54, and CD95 on B- and T-cells in chronic lymphocytic leukaemia in relation to trisomy 12, atypical
- Large-cell transformation of chronic lymphocytic leukemia and follicular lymphoma during or soon after treatment with
- Cryopreserved chronic lymphocytic leukemia cells analyzed by multicolor fluorescence in situ hybridization after optimized mitogen stimulation.
Table of Contents
1
UI - 11883499
AU - Feldt KS
TI -
Rethinking advanced directives.
SO - J Gerontol Nurs 2000 Oct;26(10):5
2
UI - 12011126
AU - Osterborg A; Brandberg Y; Molostova V; Iosava G; Abdulkadyrov K; Hedenus
TI -
M; Messinger D; Epoetin Beta Hematology Study Group
Randomized, double-blind, placebo-controlled trial of recombinant human
erythropoietin, epoetin Beta, in hematologic malignancies.
SO - J Clin Oncol 2002 May 15;20(10):2486-94
AD - Department of Oncology (Radiumhemmet), Karolinska Hospital, S-17176
Stockholm, Sweden. anders.osterborg@ks.se
PURPOSE: To investigate the effect of recombinant human erythropoietin
(epoetin beta) on anemia, transfusion need, and quality of life (QOL) in
severely anemic patients with low-grade non-Hodgkin's lymphoma (NHL),
chronic lymphocytic leukemia (CLL), or multiple myeloma (MM). PATIENTS
AND METHODS: Transfusion-dependent patients with NHL (n = 106), CLL (n =
126), or MM (n = 117) and a low serum erythropoietin concentration were
randomized to receive epoetin beta 150 IU/kg or placebo subcutaneously
three times a week for 16 weeks. Primary efficacy criteria were
transfusion-free and transfusion- and severe anemia-free survival
(hemoglobin [Hb] > 8.5 g/dL) between weeks 5 to 16. Response was defined
as an increase in Hb > or = 2 g/dL with elimination of transfusion need.
QOL was assessed by the Functional Assessment of Cancer Therapy scale.
RESULTS: Transfusion-free (P =.0012) survival and transfusion- and
severe anemia-free survival (P =.0001) were significantly greater in the
epoetin beta group versus placebo (Wald chi(2) test), giving a relative
risk reduction of 43% and 51%, respectively. The response rate was 67%
and 27% in the epoetin beta versus the placebo group, respectively (P
<.0001). After 12 and 16 weeks of treatment, QOL significantly improved
in the epoetin beta group compared with placebo (P <.05); this
improvement correlated with an increase in Hb concentration (> or = 2
g/dL). A target Hb that could be generally recommended could not be
identified. CONCLUSION: Many severely anemic and transfusion-dependent
patients with advanced MM, NHL, and CLL and a low performance status
benefited from epoetin therapy, with elimination of severe anemia and
transfusion need, and improvement in QOL.
3
UI - 11999363
AU - Toyota S; Nakamura N; Dan K
TI -
T-cell prolymphocytic leukemia with hemorrhagic gastrointestinal
involvement and a new chromosomal abnormality.
SO - Int J Hematol 2002 Apr;75(3):314-7
AD - Department of Internal Medicine, Yokosuka Kyousai Hospital, Kanagawa,
Japan.
We report a case of T-cell prolymphocytic leukemia in a 56-year-old
woman who exhibited hemorrhaging with gastric involvement as the first
manifestation. This patient's condition was diagnosed as T-cell
prolymphocytic leukemia based on the findings of lymphocytosis, abnormal
immunophenotype, hepatosplenomegaly, lymphadenopathy, and cutaneous
involvement. Endoscopic examination of the upper gastrointestinal tract
revealed hemorrhage from a gastric lesion with histological involvement.
Cytogenetic analysis revealed chromosomal abnormalities, 46,XX,der(1),
add(1)(p36), that have not previously been described in T-cell
prolymphocytic leukemia. In spite of a transient response to
chemotherapy, the patient died 15 months after onset of the disease.
4
UI - 11920207
AU - Leotard S; Chastang C; Travade P; Jaudon MC; Tournilhac O; Baudet S;
TI -
Merle-Beral H
Prognostic relevance of a scoring system based on clinical and
biological parameters in early chronic lymphocytic leukemia.
SO - Hematol J 2000;1(5):301-6
AD - Service d'Hematologie Biologique, Pitie-Salpetriere Hospital, 47
Boulevard de l'Hopital, 75013 Paris, France.
INTRODUCTION: Among patients with indolent form of B-cell chronic
lymphocytic leukemia, some of them will progress into more advanced
stages. To better define this subpopulation of patients, we attempted to
define some parameters capable of predicting a pejorative clinical
outcome. MATERIALS AND METHODS: Eighty-eight previously untreated
patients with B-cell chronic lymphocytic leukemia in Binet stage A were
analysed to study the prognostic value of simple serological variables:
soluble CD23 (sCD23), beta2 microglobulin (beta2m),
lactate-dehydrogenase activities and albumin level. Results were
compared to other conventional clinical and biological parameters by
univariate and multivariate statistical analysis. RESULTS: Our data show
that: (1) among those studied, sCD23 >50 u/ml was the only serological
significant parameter clearly correlated with disease progression and
(2) stage A" patients (hemoglobin level between 100 and 120 g/l and/or
lymphocytosis >30.10(9)/l), axillary lymph nodes and
hypogammaglobulinemia were found to be other variables associated with a
pejorative outcome. These four variables enabled the establishment of a
scoring system, capable of predicting disease progression since 66% of
the patients with a score < or =2 are going to evolve into advanced
stages vs 12% with a score <2. Furthermore, the time to progression is
shortened when the score is increasing. CONCLUSION: Our findings show
the prognostic relevance of a scoring system including sCD23 level. This
score could be taken into account in the treatment strategy of B-cell
chronic lymphocytic leukemia.
5
UI - 11986207
AU - Keating MJ; Flinn I; Jain V; Binet JL; Hillmen P; Byrd J; Albitar M;
TI -
Brettman L; Santabarbara P; Wacker B; Rai KR
Therapeutic role of alemtuzumab (Campath-1H) in patients who have failed
fludarabine: results of a large international study.
SO - Blood 2002 May 15;99(10):3554-61
AD - M. D. Anderson Cancer Center, Houston, TX 77030, USA.
mkeating@mdanderson.org
This study investigated the efficacy, safety, and clinical benefit of
alemtuzumab (Campath-1H) for patients with relapsed or refractory B-cell
chronic lymphocytic leukemia exposed to alkylating agents and having
failed fludarabine therapy. Ninety-three patients received alemtuzumab
in 21 centers worldwide, with the aim to obtain an overall response rate
of at least 20%. Dosage was increased gradually (target 30 mg, 3 times
weekly, for a maximum of 12 weeks). Infection prophylaxis was mandatory,
beginning on day 8, and continuing for a minimum of 2 months after
treatment. Responses were assessed at weeks 4, 8, and 12, and patients
were followed for 34 months. Overall objective response in the
intent-to-treat population (n = 93) was 33% (CR 2%, PR 31%). Median time
to response was 1.5 months (range, 0.4-3.7 months). Median time to
progression was 4.7 months overall, 9.5 months for responders. At data
cut-off, 27 patients (29%) were alive; overall median survival was 16
months (95% CI: 11.8-21.9) and 32 months for responders. Nineteen
responders survived more than 21 months. Clinical benefit was observed
both in responders and in patients with stable disease. The most common
adverse events were related to infusion, generally grade 1 or 2 in
severity, occurring mainly in the first week. Grade 3 or 4 infections
were reported in 25 patients (26.9%). However, only 3 (9.7%) of 31
patients who responded to alemtuzumab treatment developed grade 3 or 4
infections on the study. Alemtuzumab induced significant responses in
these patients with clinical benefit in the majority and with acceptable
toxicity in a high-risk group.
6
UI - 11986231
AU - Hubmann R; Schwarzmeier JD; Shehata M; Hilgarth M; Duechler M; Dettke M;
TI -
Berger R
Notch2 is involved in the overexpression of CD23 in B-cell chronic
lymphocytic leukemia.
SO - Blood 2002 May 15;99(10):3742-7
AD - Department of Hematology, Clinic of Internal Medicine I, University of
Vienna, Vienna, Austria.
Members of the Notch family encode transmembrane receptors that modulate
differentiation, proliferation, and apoptotic programs of many precursor
cells, including hematopoietic progenitors. Stimulation of Notch causes
cleavage followed by translocation of the intracellular domain (NotchIC)
to the nucleus, where it activates transcription of CBF1 responsive
genes. The aim of this study was to elucidate the mechanisms leading to
the overexpression of CD23, a striking feature of B-cell chronic
lymphocytic leukemia (B-CLL) cells. By electrophoretic mobility shift
assays, we identified a transcription factor complex (C1) that binds
sequence specific to one known and 4 newly identified putative CBF1
recognition sites in the CD23a core promoter region. With the use of
Epstein-Barr virus (EBV)-infected B cells as a model for CBF1 mediated
CD23a expression, C1 was found to be EBV inducible. Supershift assays
revealed that the nuclear form of Notch2 is a component of C1 in B-CLL
cells, supporting a model in which NotchIC activates transcription by
binding to CBF1 tethered to DNA. Transient transfection of REH pre-B
cells with an activated form of Notch2 induced endogenous CD23a,
confirming that CD23a is a target gene of Notch2 signaling. Finally,
reverse transcription-polymerase chain reaction and kinetic analysis
demonstrated that the Notch2 oncogene is not only overexpressed in B-CLL
cells but might also be related to the failure of apoptosis
characteristic for this disease. In conclusion, these data suggest that
deregulation of Notch2 signaling is involved in the aberrant expression
of CD23 in B-CLL.
7
UI - 11994981
AU - Larsen CR; Hansen PB; Clausen NT
TI -
Aggressive growth of epithelial carcinomas following treatment with
nucleoside analogues.
SO - Am J Hematol 2002 May;70(1):48-50
AD - Department of Internal Medicine F, Section of Hematology and Oncology,
Hillerod Hospital, Hillerod, Denmark. rifbjerg@dadlnet.dk
Two patients, one with B-cell chronic lymphocytic leukemia (CLL) and one
with hairy-cell leukemia (HCL), were treated with immunosuppressive
chemotherapy. The patient with CLL was a 54-year-old female, who had had
a squamous cell carcinoma (SCC) excised from her forehead 5 months
before receiving the first course of fludarabine. During the fludarabine
treatment, the patient developed a local SCC relapse and metastases in
the neck. The carcinoma was treated by excision and radiotherapy, and
further fludarabine treatment was withheld. Nevertheless, the SCC
metastasized aggressively and the patient died 3 months after the start
of fludarabine treatment, primarily due to respiratory failure. The
autopsy revealed heavy SCC infiltrations involving the lungs, pleura,
mediastinum, pericardium, and liver. The patient with HCL was a
69-year-old male. At the time of diagnosis of HCL, the patient had two
solid tumors in the liver containing poorly differentiated epithelial
carcinoma cells of unknown origin. During treatment with
2-chlorodeoxyadenosine (2CdA), the tumors in the liver rapidly spread in
multiple intrahepatic metastases, followed by liver failure and death
within 1 month. Fludarabine and 2CdA cause a substantial suppression of
all lymphocyte subsets, in particular the T-cell line. T-lymphocytes are
believed to be responsible for the usually slow growth and the low
metastatic rate of the SCC skin lesions. It is therefore assumed that
fludarabine and 2CdA in these two cases triggered an exacerbation of
both tumors due to the T-cell depletion. Copyright 2002 Wiley-Liss, Inc.
8
UI - 8656688
AU - Molica S; Dattilo A; Mannella A; Levato D
TI -
Intercellular adhesion molecules (ICAMs) 2 and 3 are frequently
expressed in B cell chronic lymphocytic leukemia.
SO - Leukemia 1996 May;10(5):907-8
AD - Divisione de Ematologia, Ospedale Regionale, 'A Pugliese', Catanzaro,
Italy.
Using different monoclonal antibodies (moAbs) from the 5th International
Workshop on Leukocyte Differentiation Antigens we studied the expression
of intercellular adhesion molecules (ICAMs) 2 and 3 on a homogeneous
group of 23 B cell chronic lymphocytic leukemia (CLL) patients. Our
results show that either ICAM-2 or ICAM-3 are constitutively expressed
on CD5+ B-CLL cells. Owing to the role of ICAM molecules in governing
the migration and traffic of lymphocytes to lymph nodes, our findings
need to be validated in a more consistent patient series to understand
clinico-prognostic implications of such an expression.
9
UI - 11794950
AU - Anonymous
TI -
Alemtuzumab.
SO - Am J Health Syst Pharm 2001 Dec 15;58(24):2372-3
10
UI - 11981828
AU - Ghia P; Strola G; Granziero L; Geuna M; Guida G; Sallusto F; Ruffing N;
TI -
Montagna L; Piccoli P; Chilosi M; Caligaris-Cappio F
Chronic lymphocytic leukemia B cells are endowed with the capacity to
attract CD4+, CD40L+ T cells by producing CCL22.
SO - Eur J Immunol 2002 May;32(5):1403-13
AD - Department of Oncological Sciences, University of Torino, University
Division of Clinical Immunology and Hematology, Ospedale Mauriziano
Umberto I, Torino, Italy.
The natural history of B-chronic lymphocytic leukemia (CLL) is not
entirely explained by intrinsic defects of the neoplastic cell, but is
also favored by microenvironmental signals. As CLL cells retain the
capacity to respond to CD40 ligand (CD40L) and as CD4(+) T cells are
always present in involved tissues, we asked whether malignant CLL cells
might produce T cell-attracting chemokines. We studied the chemokine
expression of CD19(+)/CD5(+) malignant B cells from peripheral blood
(PB), lymph nodes (LN) or bone marrow (BM) of 32 patients and found a
major difference. LN- and BM-, but not PB-derived cells, expressed a
readily detectable reverse transcription-PCR band for CCL22 and one for
CCL17 of variable intensity. CD40 ligation of PB cells induced the mRNA
expression of both CCL22 and CCL17. CCL22 was also released in the
culture supernatants. These supernatants induced the migration of
activated CD4(+), CD40L(+) T cells expressing the CCL22 receptor, CCR4.
T cell migration was abrogated by anti-CCL22 antibodies.
Immunohistochemistry and cytofluorography studies revealed that a
proportion of CD4(+) T cells in CLL LN and BM expressed CD40L. Our data
demonstrate that malignant CLL cells chemo-attract CD4(+) T cells that
in turn induce a strong chemokine production by the leukemic clone,
suggesting a vicious circle, leading to the progressive accumulation of
the neoplastic cells.
11
UI - 11929788
AU - Barragan M; Bellosillo B; Campas C; Colomer D; Pons G; Gil J
TI -
Involvement of protein kinase C and phosphatidylinositol 3-kinase
pathways in the survival of B-cell chronic lymphocytic leukemia cells.
SO - Blood 2002 Apr 15;99(8):2969-76
AD - Unitat de Bioquimica, Departament de Ciencies Fisioliques II,
Universitat de Barcelona, Spain.
B-cell chronic lymphocytic leukemia (B-CLL) is characterized by the
accumulation of long-lived CD5(+) B lymphocytes. TPA
(12-O-tetradecanoylphorbol 13- acetate) and interleukin-4 (IL-4) inhibit
apoptosis of B-CLL lymphocytes ex vivo. We used specific inhibitors of
protein kinase C (PKC), extracellular-regulated kinase (ERK), and
phosphatidylinositol 3-kinase (PI3-kinase) to study their involvement in
TPA- and IL-4-induced survival of B-CLL lymphocytes. BisI, a specific
inhibitor of PKC, induced apoptosis and inhibited the antiapoptotic
activity of TPA and IL-4. B-CLL cells have a basal PKC activity that was
increased by TPA but not by IL-4. TPA, but not IL-4, induced ERK
activation. However, the inhibition of ERK activation did not affect the
viability of B-CLL lymphocytes, demonstrating that this pathway is not
involved in their survival. Inhibition of PI3-kinase by LY294002 induced
apoptosis of B-CLL cells and inhibited the survival effect of IL-4 and
TPA. In addition, Akt, a downstream effector of PI3-kinase activity, was
phosphorylated by TPA and IL-4 in B-CLL cells, though PI3-kinase had no
effect on PKC-dependent phosphorylation of Akt. Furthermore, the
inhibition of PKC or PI3-kinase increased dexamethasone- and
fludarabine-induced apoptosis ex vivo in the presence of survival
factors. These results demonstrate that PKC and PI3-kinase are involved
in the survival of B-CLL cells and suggest that inhibitors of these
pathways could be combined with the drugs used in the treatment of
B-CLL.
12
UI - 11929789
AU - Till KJ; Lin K; Zuzel M; Cawley JC
TI -
The chemokine receptor CCR7 and alpha4 integrin are important for
migration of chronic lymphocytic leukemia cells into lymph nodes.
SO - Blood 2002 Apr 15;99(8):2977-84
AD - Department of Haematology, University of Liverpool, Liverpool, United
Kingdom. k.j.till@liv.ac.uk
Malignant lymphocyte migration into lymph nodes is an important aspect
of chronic lymphocytic leukemia (CLL), yet little is known about the
processes involved. Here we demonstrate that CLL cells migrate across
vascular endothelium in response to at least 3 chemokines, namely,
CCL21, CCL19, and CXCL12. Moreover, transendothelial cell migration
(TEM) in response to CCL21 and CCL19 was significantly higher for the
malignant B cells of patients who had clinical lymph node involvement as
compared with those of patients lacking such organomegaly. Furthermore,
the expression of CCR7, the receptor for both CCL21 and CCL19,
correlated with clinical lymphadenopathy, and blocking of CCR7 inhibited
CLL cell TEM. By using immunohistochemistry we demonstrated that CCL21
and CCL19, but not CXCL12, are located in high endothelial venules and
are, therefore, in an appropriate location to induce TEM. Regarding the
adhesion receptors involved in TEM, alpha4 (most likely in association
with beta1) and alphaLbeta2 were shown to be important in CLL cell TEM
in vitro, but only the level of alpha4 expression correlated with the
presence of clinical lymphadenopathy. The present studies are the first
to shed light on the factors determining CLL cell entry into nodes and
define the phenotype of circulating malignant cells likely to determine
the pattern of lymph node enlargement in the disease.
13
UI - 11987022
AU - Barthel HR
TI -
[Chronic lymphatic leukemia: significance of erythropoietin]
SO - Dtsch Med Wochenschr 2002 May 3;127(18):982; discussion 982-3
14
UI - 11986939
AU - Bauvois B; Dumont J; Mathiot C; Kolb JP
TI -
Production of matrix metalloproteinase-9 in early stage B-CLL:
suppression by interferons.
SO - Leukemia 2002 May;16(5):791-8
AD - Unite 365 INSERM, Section de Recherche, Institut Curie, Pavillon
Pasteur, 26 rue d'Ulm, 75248 Paris cedex 05, France.
Besides vascular endothelial growth factor (VEGF) and basic fibroblast
growth factor (bFGF), matrix metalloproteinases (MMPs) play critical
roles in angiogenesis, tumor invasion and metastasis. Increased
angiogenesis is observed in chronic B lymphocytic leukemia (B-CLL) and
published data reported VEGF and bFGF production in this disease. The
purpose of this study was to investigate MMP expression in early stage
B-CLL. Elevated MMP-9 concentrations were detected by ELISA in the sera
of B-CLL patients (median level 250 ng/ml) compared with healthy donors
(67 ng/ml) (P < 0.0001), and immunostaining with antibodies against
MMP-9 and B cell antigens (CD19, CD23) substantiated the presence of
MMP-9 in tumoral B lymphocytes. By using RT-PCR, ELISA and zymography
experiments, we confirmed that B-CLL cells expressed and released the
pro-form of MMP-9 with Mr 92 kDa (158-1300 pg/ml/10(6) cells/48 h),
p-aminophenylmercuric acetate generating a 82 kDa active form. In
contrast, the production of MMP-9 by normal counterpart B cells was
significantly low (28-169 pg/ml/10(6)cells/48 h). Moreover, B-CLL
culture supernatants contained bFGF (median levels 17 pg/ml/10(6)
cells/48 h), VEGF (1.4 pg/ml/10(6) cells/48 h) and TNF-alpha (0.2
pg/ml/10(6) cells/48 h). TNF-alpha and VEGF antibodies blocked MMP-9 at
the mRNA and protein levels. Interferons (IFNs) type I or type II
repressed MMP-9 gelatinolytic activity in a dose and time dependency,
and this was reflected by a parallel inhibition of MMP-9 mRNA and
protein. IFNs however did not affect the production of bFGF, VEGF and
TNF-alpha. Together, our data show that B-CLL lymphocytes synthesize
MMP-9 and emphasize the specific inhibitory actions of IFNs on its
expression.
15
UI - 11986948
AU - Birhiray RE; Shaw G; Guldan S; Rudolf D; Delmastro D; Santabarbara P;
TI -
Brettman L
Phenotypic transformation of CD52(pos) to CD52(neg) leukemic T cells as
a mechanism for resistance to CAMPATH-1H.
SO - Leukemia 2002 May;16(5):861-4
AD - Department of Hematology/Oncology, Marshfield Clinic, Marshfield, WI,
USA.
Immunotherapy utilizing CAMPATH-1H for patients with
chemotherapy-refractory chronic lymphocytic leukemia has yielded
encouraging results with many reports of complete remission. Here we
report the outcome of two patients with CD4-positive T cell
prolymphocytic leukemia treated with CAMPATH-1H. Both patients responded
rapidly to treatment and subsequently developed CD4 lymphopenia. One
patient remained in complete remission after 14 weeks of treatment.
Serial peripheral blood flow cytometry revealed that the CD52 antigen
was present throughout treatment. The other patient who was initially
CD52-positive, became CD52-negative after 6 weeks of treatment, and
developed progressive symptoms of T cell prolymphocytic leukemia.
Immunotherapy was stopped, chemotherapy proved futile, and the patient
died. This change in phenotype from CD52-positive to -negative during
CAMPATH-1H therapy points out a need to develop strategies for
maintaining antigenic expression during monoclonal antibody therapy.
16
UI - 11986954
AU - Kay NE; Bone ND; Tschumper RC; Howell KH; Geyer SM; Dewald GW; Hanson
TI -
CA; Jelinek DF
B-CLL cells are capable of synthesis and secretion of both pro- and
anti-angiogenic molecules.
SO - Leukemia 2002 May;16(5):911-9
AD - Department of Medicine, Division of Hematology, Mayo Graduate and
Medical Schools, Mayo Clinic, 200 First Street SW, Rochester, MN 55905,
USA.
Initial work has shown that clonal B cells from B-chronic lymphocytic
leukemia (B-CLL) are able to synthesize pro-angiogenic molecules. In
this study, our goal was to study the spectrum of angiogenic factors and
receptors expressed in the CLL B cell. We used ELISA assays to determine
the levels of basic fibroblast growth factors (bFGF), vascular
endothelial growth factor (VEGF), endostatin, interferon-alpha
(IFN-alpha) and thrombospondin-1 (TSP-1) secreted into culture medium by
purified CLL B cells. These data demonstrated that CLL B cells
spontaneously secrete a variety of pro- and anti-angiogenic factors,
including bFGF (23.9 pg/ml +/- 7.9; mean +/- s.e.m.), VEGF (12.5 pg/ml
+/- 2.3) and TSP-1 (1.9 ng/ml +/- 0.3). Out of these three factors, CLL
B cells consistently secreted bFGF and TSP-1, while VEGF was expressed
in approximately two-thirds of CLL patients. Of interest, hypoxic
conditions dramatically upregulated VEGF expression at both the mRNA and
protein levels. We also employed ribonuclease protection assays to assay
CLL B cell expression of a variety of other angiogenesis-related
molecules. These analyses revealed that CLL B cells consistently express
mRNA for VEGF receptor 1 (VEGFR1), thrombin receptor, endoglin, and
angiopoietin. Further analysis of VEGFR expression by RT-PCR revealed
that CLL B cells expressed both VEGFR1 mRNA and VEGFR2 mRNA. In summary,
these data collectively indicate that CLL B cells express both pro- and
anti-angiogenic molecules and several vascular factor receptors. Because
of the co-expression of angiogenic molecules and receptors for some of
these molecules, these data suggest that the biology of the leukemic
cells may also be directly impacted by angiogenic factors as a result of
autocrine pathways of stimulation.
17
UI - 11986957
AU - Kuppers R; Sonoki T; Satterwhite E; Gesk S; Harder L; Oscier DG; Tucker
TI -
PW; Dyer MJ; Siebert R
Lack of somatic hypermutation of IG V(H) genes in lymphoid malignancies
with t(2;14)(p13;q32) translocation involving the BCL11A gene.
SO - Leukemia 2002 May;16(5):937-9
AD - Institute for Genetics, Department of Internal Medicine I, LFI E4 R706,
University of Cologne, Joseph-Stelzmannstrasse 9, D-50931 Cologne,
Germany.
The t(2;14)(p13;q32.3) involving the BCL11A and IGH genes is a rare but
recurrent chromosomal aberration in B-cell malignancies. Hitherto,
juxtaposition of BCL11A and IGH has only been described in B-cell
chronic lymphocytic leukemia (B-CLL) and immunocytoma. As subgroups of
B-CLL can be distinguished by the pattern of somatic mutation of
immunoglobulin variable (V) genes we investigated four lymphomas with
IGH/BCL11A involvement for IGH hypermutation. Clonal V(H) gene
rearrangements were amplified; in all four cases, sequencing of the
amplificates revealed the rearranged V(H) genes to lack somatic
mutations. These results suggest that t(2;14)(p13;q32.3) is associated
with a subset of B-CLL/immunocytoma characterized by non-mutated IG
genes deriving from pre-germinal center B cells. As the translocations
in both informative cases are targeted to the switch regions of the IGG2
gene, which is mainly used in T cell-independent immune responses, these
translocations presumably occurred in activated B cells in the course of
T cell-independent immune responses outside the germinal center.
18
UI - 11986962
AU - Crescenzi B; Sacchi S; Marasca R; Temperani P; La Starza R; Matteucci C;
TI -
Bonacorsi G; Romoli S; Martelli MF; Mecucci C; Emilia G
Distinct genomic events in the myeloid and lymphoid lineages in
simultaneous presentation of chronic myeloid leukemia and B-chronic
lymphocytic leukemia.
SO - Leukemia 2002 May;16(5):955-6
19
UI - 12022937
AU - Hyde C; Wake B; Bryan S; Barton P; Fry-Smith A; Davenport C; Song F
TI -
Fludarabine as second-line therapy for B cell chronic lymphocytic
leukaemia: a technology assessment.
SO - Health Technol Assess 2002;6(2):1-89
AD - Department of Public Health and Epidemiology, University of Birmingham,
UK.
20
UI - 12040432
AU - Houlston RS; Catovsky D; Yuille MR
TI -
Genetic susceptibility to chronic lymphocytic leukemia.
SO - Leukemia 2002 Jun;16(6):1008-14
AD - Section of Cancer Genetics, Institute of Cancer Research, Sutton, UK.
There is increasing evidence that a subset of chronic lymphocytic
leukemia is caused by an inherited predisposition. Here we review the
evidence for an inherited predisposition, the characteristics of
familial cases and evidence for the involvement of specific genes.
21
UI - 12040433
AU - Robak T; Kasznicki M
TI -
Alkylating agents and nucleoside analogues in the treatment of B cell
chronic lymphocytic leukemia.
SO - Leukemia 2002 Jun;16(6):1015-27
AD - Department of Hematology, Medical University of Lodz, Copernicus
Memorial Hospital, Lodz, Poland.
Chronic lymphocytic leukemia (CLL) is the most common form of leukemia
in the Western world. The natural clinical course is highly variable and
chemotherapy is usually not indicated in early and stable disease.
Treatment is needed in the progressive form of this leukemia.
Chlorambucil, with or without steroids, has been for many years the drug
of choice in the treatment of CLL. More recently, treatment approaches
have included nucleoside analogues, (NA) fludarabine (FAMP) and
cladribine (2-CdA, 2-chlorodeoxyadenosine), which seem to be the
treatment of choice for patients failing standard therapies. Their role
as first line therapy is being investigated in randomized trials and the
results have recently been published. These studies have shown a higher
overall response and complete remission (CR) rate and longer response
duration in patients treated initially with NA than with chlorambucil or
cyclophosphamide-based combination regimens. In contrast, overall
survival is similar in patients treated with NA and alkylating agents.
However, the randomized trials were designed as crossover studies which
may influence survival. Combined use of NA with other cytotoxic drugs,
cytokines, monoclonal antibodies and other agents may increase the CR
and prolong survival time. However, the results of randomized trials
comparing combination treatment with NA alone are not yet available. In
conclusion, alkylating agents still have an important place in the
routine management of the majority of CLL patients. NA should be
routinely used as second line treatment and possibly as first line
therapy in younger patients, who are candidates for potentially curative
treatment such as stem cell transplantation and/or monoclonal
antibodies.
22
UI - 12040434
AU - Cobo F; Martinez A; Pinyol M; Hernandez L; Gomez M; Bea S; Esteve J;
TI -
Rozman M; Bosch F; Lopez-Guillermo A; Montserrat E; Campo E
Multiple cell cycle regulator alterations in Richter's transformation of
chronic lymphocytic leukemia.
SO - Leukemia 2002 Jun;16(6):1028-34
AD - Institute of Hematology and Oncology, Department of Hematology, Institut
d'Investigacions Biomediques August Pi i Sunyer, Hospital Clinic,
University of Barcelona, Barcelona, Spain.
To investigate the role of the cell cycle regulators p21(Waf1),
p27(Kip1), retinoblastoma (Rb), and cyclin D1 in Richter's
transformation of chronic lymphocytic leukemia (CLL), we analyzed 19 CLL
and eight Richter's syndrome (RS) tumors, previously characterized for
p53 and ARF/INK4a abnormalities. p21(Waf1)immunohistochemical expression
was negative in 12 of 15 CLL (80%), whereas it was moderate or strong in
three of seven RS (43%). p21(Waf1) gene was in germline configuration in
all the tumors analyzed. Four immunohistochemical patterns of p53 and
p21(Waf1) expression were observed: (1) p53-/p21- in 10 of 15 CLL (67%),
but only in two of six RS (33%); (2) p53+/p21+ in three CLL (20%) and
two RS (33%); (3) p53-/p21+ in one RS; and (4) p53++/p21- in two CLL and
one RS. Two p53+/p21+ CLL evolved into RS. p53 mutations clustered
around the p53++/p21- (two CLL and one RS) and p53-/p21- (one CLL and
one RS) tumors. While the majority of CLL displayed strong p27
immunoreactivity, RS tumors were constantly p27-negative. p27(Kip1) gene
was in germline configuration in all the tumors analyzed. Most CLL cases
were negative for Rb expression. In contrast, all RS exhibited strong Rb
expression. Cyclin D1 overexpression was only detected in one CLL
evolving into RS and one RS. In conclusion, a p53+/p21-
immunohistochemical pattern is shown exclusively by p53-mutated CLL/RS.
Additionally, our results suggest a possible implication of
moderate/strong p21(Waf1) expression, loss of p27 expression, and cyclin
D1 overexpression in the Richter's transformation of CLL.
23
UI - 12040435
AU - Bosanquet AG; Sturm I; Wieder T; Essmann F; Bosanquet MI; Head DJ;
TI -
Dorken B; Daniel PT
Bax expression correlates with cellular drug sensitivity to doxorubicin,
cyclophosphamide and chlorambucil but not fludarabine, cladribine or
corticosteroids in B cell chronic lymphocytic leukemia.
SO - Leukemia 2002 Jun;16(6):1035-44
AD - Bath Cancer Research, Wolfson Centre, Royal United Hospital, Bath, UK.
In B-CLL, non-proliferating B cells accumulate due to defective
apoptosis. Cytotoxic therapies trigger apoptosis and deregulation of
apoptotic pathways contributes to chemoresistance. Loss of the
apoptosis-promoting Bax has been implicated in resistance to cytotoxic
therapy. We therefore evaluated ex vivo drug sensitivity of CLL,
producing chemoresponse data which are prognostic indicators for B-CLL,
in particular in the case of purine nucleoside analogs. To analyze the
underlying mechanisms of drug resistance, we compared endogenous Bax and
Bcl-2 expression to ex vivo response to eight drugs, and to survival in
39 B-CLL patients. We found that reduced Bax levels correlated well with
ex vivo resistance to traditional B-CLL therapies - anthracyclines,
alkylating agents and vincristine (all P < 0.04). Surprisingly, no such
relationship was observed for the purine nucleoside analogs or
corticosteroids (all P > 0.5). Mutational analysis of p53 could not
explain the loss of Bax protein expression. Levels of Bcl-2 were not
associated with sensitivity to any drug. In contrast to the ex vivo
data, neither Bax or Bcl-2 expression nor doxorubicin sensitivity were
associated with increased survival whereas sensitivity to fludarabine
correlated with better overall survival (P = 0.031). These findings
suggest that the resistance to purine nucleoside analogs and
corticosteroids in B-CLL is due to inactivation of pathways different
from those activated by anthracyclines, vinca alkaloids and alkylating
agents and may be the molecular rationale for the efficacy of purine
analogs in this disease.
24
UI - 12040436
AU - Faderl S; Keating MJ; Do KA; Liang SY; Kantarjian HM; O'Brien S;
TI -
Garcia-Manero G; Manshouri T; Albitar M
Expression profile of 11 proteins and their prognostic significance in
patients with chronic lymphocytic leukemia (CLL).
SO - Leukemia 2002 Jun;16(6):1045-52
AD - Department of Leukemia, The University of Texas, MD Anderson Cancer
Center, Houston, TX 77030, USA.
It has been suggested that the expansion of the leukemic cells in
chronic lymphocytic leukemia (CLL) is due to dysregulation of pathways
of programmed cell death (apoptosis) rather than cell proliferation,
although differences may exist in early vs late and treated vs untreated
patients. In the present study, we analyzed the expression of 11
proteins in CLL cells that are implicated in the control of apoptosis,
proliferation, and differentiation, and correlated this expression
profile with survival. Using a quantitative solid-phase radioimmunoassay
(RIA), we measured the cellular protein levels of Bcl-2, cyclin D1,
PCNA, ATM, Fas, Bax, retinoic acid receptor alpha (RARalpha), retinoic
acid receptor beta (RXRbeta), Flt1, VEGF, and cellular
beta2-microglobulin in 230 samples of CLL. Univariate analysis using the
Cox proportional hazard model showed a correlation with survival of only
the following proteins: Bcl-2 (P < 0.001), cyclin D1 (P = 0.027), Fas (P
= 0.055), PCNA (P < 0.001), and ATM (P = 0.028). In a multivariate
analysis using classification and regression tree analysis (CART), five
groups of patients (nodes) could be generated with significant
differences of survival expectation (P < 0.0001) based on levels of
expression of the above proteins. Based on CART analysis, Bcl-2 levels
emerge as the most important protein in predicting survival between all
11 proteins studied. Patients with marked elevation in Bcl-2 levels had
the worst outcome while patients with intermediate levels, but with high
levels of PCNA and cyclin D1 or abnormal ATM expression had intermediate
survival. These data indicate that intracellular levels of proteins such
as Bcl-2, ATM, cyclin D1, and PCNA can be used as markers to predict
clinical behavior and survival in patients with CLL. The pathways in
which these proteins are involved may also represent possible targets
for future therapeutic trials in CLL.
25
UI - 12040430
AU - Dreger P; Montserrat E
TI -
Autologous and allogeneic stem cell transplantation for chronic
lymphocytic leukemia.
SO - Leukemia 2002 Jun;16(6):985-92
AD - Department of Hematology, AK St Georg, Hamburg, Germany.
Allogeneic and autologous stem cell transplantation (SCT) are
increasingly considered for treatment of patients with chronic
lymphocytic leukemia (CLL). In order to assess the potential therapeutic
value of SCT for CLL, the present article aims at answering the
following crucial questions: (1) Is SCT a curative treatment? (2) Does
SCT improve the prognosis of poor-risk CLL? (3) Do risk factors exist
which are useful for defining prognostic groups in terms of feasibility
and post-transplant outcome? The efficacy of auto-SCT relies exclusively
on the cytotoxic therapy administered. To date, there is only limited
hope that autotransplantation can cure the disease. Nevertheless, the
results of the published series suggest that auto-SCT is capable of
improving the prognosis of CLL with poor-risk features. Well defined
favorable conditions for successful autografting are the status of the
disease (CR or VGPR) and the number of lines of therapy (<2) before
transplantation. The crucial anti-leukemic principle of allo-SCT
consists in the immune-mediated GVL effects conferred with the graft.
The GVL activity explains that allografting seems to be curative for at
least a subset of patients. However, as long as allo-SCT in CLL is still
associated with an excessively high treatment-related mortality, only
selected patients with advanced poor-risk disease should be considered
for allografting. The development of conditioning regimens with reduced
intensity may allow extending the indications of allogeneic SCT for CLL
in the near future.
26
UI - 12040431
AU - Stilgenbauer S; Bullinger L; Lichter P; Dohner H; German CLL Study Group
TI -
(GCLLSG). Chronic lymphocytic leukemia
Genetics of chronic lymphocytic leukemia: genomic aberrations and V(H)
gene mutation status in pathogenesis and clinical course.
SO - Leukemia 2002 Jun;16(6):993-1007
AD - Abteilung Innere Medizin III, University of Ulm, Germany.
The genetic characterization of chronic lymphocytic leukemia (CLL) has
made significant progress over the past few years. While conventional
cytogenetic analyses only detected chromosome aberrations in 40-50% of
cases, new molecular cytogenetic methods, such as fluorescence in situ
hybridization (FISH), have greatly enhanced our ability to detect
chromosomal abnormalities in CLL. Today, genomic aberrations are
detected in over 80% of CLL cases. Genes potentially involved in the
pathogenesis were identified with ATM in a subset of cases with 11q
deletion and p53 in cases with 17p13 deletion. For the most frequent
aberration, the deletion 13q14, candidate genes have been isolated.
Genetic subgroups with distinct clinical features have been identified.
11q deletion is associated with marked lymphadenopathy and rapid disease
progression. 17p deletion predicts for treatment failure with alkylating
agents, as well as fludarabine and short survival times. In multivariate
analysis 11q and 17p deletions provided independent prognostic
information. Recently, another important issue of genetic risk
classification in CLL was identified with the mutation status of the
immunoglobulin variable heavy chain genes (V(H)). CLL cases with
unmutated V(H) show more rapid disease progression and shorter survival
times. Whether CD38 expression can serve as a surrogate marker for V(H)
mutation status is currently discussed controversially. V(H) mutation
status and genomic abnormalities, such as 17p and 11q deletion, have
recently been shown to be related to each other, but were of independent
prognostic information in multivariate analysis. Moreover, genomic
aberrations and V(H) mutation status appear to give prognostic
information irrespective of the clinical stage and may therefore allow a
risk assessment for individual patients early in the course of their
disease.
27
UI - 12017308
AU - Kawano T; Iwase S; Nakayama R; Horiguchi-Yamada J; Kobayashi M; Yamada H
TI -
Lack of BCL10 mRNA mutation in lymphold malignancies.
SO - Anticancer Res 2002 Jan-Feb;22(1A):305-9
AD - Department of Molecular Genetics, Institute of DNA Medicine, Jikei
University School of Medicine, Tokyo, Japan. kawano-t@jikei.ac.jp
BACKGROUND: BCL10, a gene involved in the chromosomal translocation
t(1;14)(p22;q32) found in mucosa-associated lymphoid tissue lymphoma
(MALT lymphoma), has shown mutation in not only MALT lymphomas but also
other lymphold tumors. However, the mutation rate remains controversial.
One possible reason is variation in the source material (DNA or RNA),
with most studies having been done using tumor DNA. Accordingly, we
studied BCL10 mutations using tumor RNA. MATERIALS AND METHODS: Fifty
lymphoid malignancies (26 malignant lymphomas, 10 chronic lymphocytic
leukemias and 14 acute lymphoblastic leukemias) were examined. Total RNA
was extracted from the tumor cells and first-strand cDNA was subjected
to single-strand conformation polymorphism and fragment length analysis.
Then the results were confirmed by direct sequencing. RESULTS: No
mutations of the BCL10 gene were found in the 50 samples. There were
four polymorphisms (3G to T, 24G to C, 485C to T and 638G to A). All
samples showed at least one 24C allele. CONCLUSION: The BCL10 mutations
studied are rare events at the RNA level and may not be associated with
the mechanism of tumorigenesis in most lymphoid tumors.
28
UI - 12068792
AU - Hjalmar V; Hast R; Kimby E
TI -
Cell surface expression of CD25, CD54, and CD95 on B- and T-cells in
chronic lymphocytic leukaemia in relation to trisomy 12, atypical
morphology and clinical course.
SO - Eur J Haematol 2002 Mar;68(3):127-34
AD - Division of Hematology, Department of Medicine, Karolinska Hospital,
Stockholm, Sweden. viktoria.hjalmar@ks.se
BACKGROUND: Surface antigen expression can be used to define subgroups
of patients with different clinical courses in chronic lymphocytic
leukaemia of the B-cell type (CLL). PURPOSE-METHODS: To study the
clinical significance of functional markers linked to proliferation
(CD25), adhesion (CD54), and apoptosis (CD95) on B- and T-cells in 68
patients with CLL using dual colour flow cytometry (FCM). RESULTS: The
mean proportion of CD19+ B-cells expressing CD25 was significantly
higher in CLL patients compared to controls (P=0.02), while CD54+ and
CD95+ B-cells did not differ significantly. In CLL with atypical
morphology and in patients with trisomy 12, the mean percentage of CD25+
B-cells was lower than in typical CLL (P<0.02) and in patients with
disomic tumor cells (P<0.03). Patients with 30% of CD25+ B-cells had a
shorter median time to treatment than CD25-negative cases (P=0.01). A
low CD54 expression was associated with a prolonged median time to
treatment (P=0.004), low WBC counts (P<0.05), and low S-LDH (P=0.03). A
high CD95 expression was correlated with elevated S-LDH (P=0.02) and a
finding of lymphadenopathy (P=0.02). In individual patients there was a
strong correlation between B- and T-cell expression of CD25 (P<0.0001),
CD54 (P=0.0002), and CD95 (P=0.0002), respectively. CONCLUSIONS: CD25
and CD54 expression on CD19+ cells seems to give prognostic information.
The strong correlation between the expression of CD25, CD54 and CD95 on
B-and T-cells suggests that the expression of these antigens is not an
inherent characteristic of the malignant B-cell clone.
29
UI - 12038452
AU - Cohen Y; Da'as N; Libster D; Amir G; Berrebi A; Polliack A
TI -
Large-cell transformation of chronic lymphocytic leukemia and follicular
lymphoma during or soon after treatment with
fludarabine-rituximab-containing regimens: natural history- or
therapy-related complication?
SO - Eur J Haematol 2002 Feb;68(2):80-3
AD - Department of Hematology, Hadassah University Hospital, Jerusalem,
Israel.
Novel therapeutic regimens containing purine analogs and monoclonal
antibodies have led to significant improvement in the course of indolent
lymphoproliferative diseases (LPD). Complete clinical and even molecular
remissions have been achieved in an increasing proportion of patients.
In parallel to their tumor cytotoxic effect, these agents are inevitably
associated with prolonged immunosuppression inherent to their mechanism
of antilymphocytic activity. Until now, attention has been paid mainly
to opportunistic infection occurring as a result of the above
drug-induced immunosuppression and less to other possible complications,
such as malignancy or tumor progression in the immunocompromised host.
Here we briefly report nine patients with previously treated indolent
LPD in whom the onset of large-cell transformation occurred during or
shortly after the initiation of regimens containing these agents before
transformation occurred. One patient had received rituximab alone, three
fludarabine-containing regimens and five received sequential regimens
containing both agents. This
30
UI - 12007196
AU - Karhu R; Vilpo L; Isola J; Knuutila S; Vilpo J
TI -
Cryopreserved chronic lymphocytic leukemia cells analyzed by multicolor
fluorescence in situ hybridization after optimized mitogen stimulation.
SO - Genes Chromosomes Cancer 2002 Jul;34(3):345-8
AD - Laboratory of Cancer Genetics, University of Tampere and Tampere
University Hospital, Tampere, Finland.
We investigated the utility of multicolor in situ fluorescence
hybridization (mFISH) on cryopreserved blood cells from 11 chronic
lymphocytic leukemia (CLL) patients. The results demonstrate that an
individually chosen optimized mitogen combination induces proliferation
of neoplastic B-cells after cryopreservation. Abnormal cells were
detected in eight samples by mFISH, and, in six samples, the abnormality
could be verified by comparative genomic hybridization or interphase
FISH. In addition to typical CLL abnormalities, such as del(11q) or +12,
several balanced translocations and single-cell abnormalities were
found. Thus, mFISH can reveal new prognostically relevant chromosome
aberrations in CLL. Copyright 2002 Wiley-Liss, Inc.
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