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NCI CANCERLIT® Search: Chronic Lymphocytic Leukemia - October 2001
National Cancer Institute®
Last Modified: November 21, 2001
Table of Contents
1
UI - 20480737
AU - Trisolini R; Lazzari Agli L; Poletti V
TI -
Bronchiolocentric pulmonary involvement due to chronic lymphocytic
leukemia.
SO - Haematologica 2000 Oct;85(10):1097
AD - Dipartimento di Malattie del Torace, Azienda USL Citt di Bologna, Italy.
2
UI - 21240485
AU - Vu UE; Pavletic ZS; Wang X; Joshi SS
TI -
Increased cytotoxicity against B-chronic lymphocytic leukemia by
cellular manipulations: potentials for therapeutic use.
SO - Leuk Lymphoma 2000 Nov;39(5-6):573-82
AD - Department of Cell Biology and Anatomy, University of Nebraska Medical
Center Omaha, Nebraska 68198-6395, USA.
B-cell chronic lymphocytic leukemia (CLL) is characterized by profound
immune dysfunction and a marked resistance to apoptosis. Understanding
the cellular biology of immune effector cells from CLL patients as well
as leukemic target cells is essential to developing immune mediated
therapeutic strategies for CLL. In this study, an immortal CLL cell line
called WSU-CLL has been used to study the characteristics of B-cell CLL
as a tumor target for natural killer (NK), activated natural killer, and
lymphokine activated killer (LAK) cells. The WSU-CLL cells were
significantly less (p<0.001) susceptible to NK cell mediated
cytotoxicity compared to K562, a standard tumor target cell line. In
vitro activation of effector cells with either short term, low dose IL-2
or long term, high dose IL-2 significantly increased the susceptibility
of CLL cells for cell mediated killing. The addition of
CD1a+/CD3-/CD4+/CD80+/CD83+ dendritic cells derived from human umbilical
cord blood increased the cytotoxicity of LAK cells against WSU-CLL.
There is an increased expression of Bcl-2 and decreased expression of
Fas on WSU-CLL cells as determined by RT-PCR techniques indicating
possible roles for these genes in exerting resistance to immune cell
mediated lysis. When Bcl-2 expression was downregulated in WSU-CLL cells
using gene specific antisense oligonucleotides, the susceptibility of
WSU-CLL cells to the cytotoxicity of chemotherapeutic agent Fludarabine
was increased. Thus, our results suggest that in vitro activation with
cytokines, addition of accessory cell populations such as dendritic
cells and/or manipulation of key gene expression i.e. down regulation of
Bcl-2 might be potential strategies to increase the antitumor
cytotoxicity against CLL cells.
3
UI - 21240491
AU - Evans HL; Polski JM; Deshpande V; Dunphy CH
TI -
CD5+ true SLL/CLL with plasmacytic differentiation and an unusual 1p36
translocation: case report and review of the literature.
SO - Leuk Lymphoma 2000 Nov;39(5-6):625-32
AD - Department of Pathology, Division of Hematopathology, St Louis
University School of Medicine, St Louis, MO 63104, USA. evanshl@slu.edu
Lymphoplasmacytic lymphoma (LPL) and small lymphocytic lymphoma/chronic
lymphocytic leukemia (SLL/CLL)are distinct clinicopathologic entities.
Although some cases of SLL/CLL may show plasmacytic differentiation and
be associated with monoclonal immunoglobulin in serum, such cases appear
to be very rare, and if plasma cell differentiation were marked,
differentiation of SLL/CLL from LPL could be difficult. We report a rare
case of true CD5-positive small lymphocytic lymphoma/chronic lymphocytic
leukemia with unequivocal plasmacytic differentiation. This case also
showed an abnormality of chromosome 1p36 not previously described in
small lymphocytic lymphoma/chronic lymphocytic leukemia.
4
UI - 21109943
AU - Woodlock TJ; Bethlendy G; Segel GB
TI -
Prohibitin expression is increased in phorbol ester-treated chronic
leukemic B-lymphocytes.
SO - Blood Cells Mol Dis 2001 Jan-Feb;27(1):27-34
AD - Department of Medicine, University of Rochester School of Medicine and
Dentistry, Rochester, New York 14642, USA.
Chronic lymphocytic leukemia (CLL) is characterized by the gradual
accumulation of immature B-lymphocytes. CLL B-lymphocytes mature to a
plasmacytoid phenotype when treated in vitro with phorbol esters. CLL
B-cell apparent maturation is associated with altered expression of
specific plasma membrane and mitochondrial proteins including heightened
expression of a 30-kDa heat shock protein 60 (hsp60) analog. During our
efforts to further characterize this hsp60 analog by mass spectrometry,
we detected the mitochondrial protein prohibitin in
phorbol-ester-matured CLL B-lymphocytes. Prohibitin modulates cell
proliferation and inhibits cell cycle traverse in several systems,
although few data are available for lymphocytes. A twofold increase in
prohibitin concentration was observed in phorbol-ester-matured compared
to resting CLL B-cells as determined by quantitative Western immunoblot
analysis. A similar increase in prohibitin was observed in
phorbol-ester-treated normal human B-lymphocyte populations. An
antisense oligonucleotide complementary to the 5' coding region of the
prohibitin gene blunted the increase in prohibitin protein in
phorbol-ester-treated CLL B-cells by 42%. These data suggest that
increased prohibitin expression is associated with and may facilitate
B-cell maturation. Copyright 2001 Academic Press.
5
UI - 21367250
AU - Bergmann L
TI -
Significance of chromosomal aberrations in CLL.
SO - Onkologie 2001 Apr;24(2):176
6
UI - 21360492
AU - Itala M
TI -
[Current treatment of chronic lymphocytic leukemia]
SO - Duodecim 1997;113(11):1015-22
AD - Department of Internal Medicine, Turku University Central Hospital,
Turku, Finland.
7
UI - 21379340
AU - Matutes E; Polliack A
TI -
Morphological and immunophenotypic features of chronic lymphocytic
leukemia.
SO - Rev Clin Exp Hematol 2000 Mar;4(1):22-47
AD - Academic Department of Haematology and Cytogenetics, Royal Marsden
Hospital and Institute of Cancer Research, Fulham Road, London, SW3 6JJ,
UK. estella@icr.ac.uk
In this review, we summarize the morphological features and
immunophenotypic profile of chronic lymphocytic leukemia (CLL) cells,
discuss the value of these investigations as front line diagnostic
tests, and emphasize their correlation with the clinical features,
disease progression, molecular genetics and pathogenesis of CLL. In CLL,
the morphology of the circulating cells is characteristic and typical in
the majority of cases. However, 15% of patients, either at diagnosis or
during the course of the disease, show atypical morphology reflected by
either (1) an increased (> 10%) number of circulating prolymphocytes,
designated CLL/PL, or (2) an increased (> 15%) number of circulating
lymphoplasmacytic and cleaved cells, designated 'atypical' CLL. There is
strong evidence of a close association between atypical morphology
(CLL/PL) and atypical (CLL) and clinical features, e.g. disease
progression, advanced stage and survival, molecular genetics,
particularly trisomy 12, but also the rare cases with t(11;14) or
t(14;19), p53 abnormalities, unmutated immunoglobulin (Ig) VH genes and
origin of the cell (naive, pregerminal center cell). CLL cells have a
distinct immunological repertoire different from that of other
lymphoproliferative disorders. The typical CLL phenotype is CD5+, CD23+,
FMC7-, weak expression of surface Ig (sIg) and weak or absent expression
of membrane CD22 and CD79b. The latter marker identifies an
extracellular epitope of the B-cell receptor (BCR) beta chain and its
weak or absent expression in CLL may derive from the expression of a
truncated form. This, together with the low expression of CD22, might
explain the abnormal signal transduction of CLL cells similar to that of
anergic B lymphocytes. Because no single marker is specific for CLL, a
composite phenotype considering this set of 5 or 6 markers compounded
into a scoring system helps to distinguish CLL from the other B-cell
malignancies. Immunophenotypic analysis has also been shown to be useful
for minimal residual disease detection and adds valuable prognostic
information because the expression of certain markers, such as FMC7 or
CD38, seems to be associated with a poor outcome. In addition, CLL cells
express a variety of Bcl-2 family proteins with a profile that favors
inhibition of apoptosis which, together with the interaction with
microenvironmental (e.g. stromal) cells and the release of cytokines,
explains the long life span and subsequent accumulation of CLL cells in
various organs. Despite controversies relating to the expression of
adhesion molecules (selectins and integrins) in CLL cells, it appears
that some of these molecules do play a role in the pathogenesis, biology
and clinical patterns of the disease. In conclusion, morphology and
immunophenotype are the two essential investigations, which must be
carried out in all cases of CLL. Both provide relevant information in
terms of diagnosis, course of the disease, prognosis and pathogenesis.
8
UI - 21379341
AU - Stilgenbauer S; Lichter P; Dohner H
TI -
Genetic features of B-cell chronic lymphocytic leukemia.
SO - Rev Clin Exp Hematol 2000 Mar;4(1):48-72
AD - Department of Internal Medicine III, University of Ulm, Germany.
The genetic features of B-cell chronic lymphocytic leukemia (CLL) are
currently being reassessed by molecular cytogenetic techniques such as
fluorescence in situ hybridization (FISH). Conventional cytogenetic
studies by chromosome banding are difficult in CLL mainly because of the
low in vitro mitotic activity of the tumor cells, which leads to poor
quantity and quality of metaphase spreads. Molecular genetic analyses
are limited because candidate genes are known for only a few chromosomal
aberrations that are observed in CLL. FISH was found to be a powerful
tool for the genetic analysis of CLL as it overcomes both the low
mitotic activity of the CLL cells and the lack of suitable candidate
genes for analysis. Using FISH, the detection of chromosomal aberrations
can be performed at the single cell level in both dividing and
non-dividing cells, thus circumventing the need of metaphase
preparations from tumor cells. Probes for the detection of trisomies,
deletions and translocation breakpoints can be applied to the regions of
interest with the growing number of clones available from genome-wide
libraries. Using the interphase cytogenetic FISH approach with a disease
specific set of probes, chromosome aberrations can be found in more than
80% of CLL cases. The most frequently observed abnormalities are losses
of chromosomal material, with deletions in band 13q14 being the most
common, followed by deletions in 11q22-q23, deletions in 17p13 and
deletions in 6q21. The most common gains of chromosomal material are
trisomies 12q, 8q and 3q. Translocation breakpoints, in particular
involving the immunoglobulin heavy chain locus at 14q32, which are
frequently observed in other types of non-Hodgkin's lymphoma, are rare
events in CLL. Genes affected by common chromosome aberrations in CLL
appear to be p53 in cases with 17p deletion and ataxia telangiectasia
mutated (ATM), which is mutated in a subset of cases with 11q22-q23
aberrations. However, for the other frequently affected genomic regions,
the search for candidate genes is ongoing. In parallel, the accurate
evaluation of the incidence of chromosome aberrations in CLL by FISH
allows the correlation of genetic abnormalities with clinical disease
manifestations and outcome. In particular, 17p abnormalities and
deletions in 11q22-q23 have already been shown to be among the most
important independent prognostic factors identifying subgroups of
patients with rapid disease progression and short survival. In addition,
deletion 17p has been associated with resistance to treatment with
purine analogs. Therefore, genetic abnormalities may allow a risk
assessment for individual patients at the time of diagnosis, thus giving
the opportunity for a risk-adapted management.
9
UI - 21379339
AU - Caligaris-Cappio F
TI -
Biology of chronic lymphocytic leukemia.
SO - Rev Clin Exp Hematol 2000 Mar;4(1):5-21
AD - Divisione Universitaria di Immunologia Clinica, Ospedale Mauriziano
Umberto I, Dipartimento di Scienze Biomediche e Oncologia Umana,
Universita di Torino, Torino, Italy.
B-cell chronic lymphocytic leukemia (CLL) lies at the cross-roads of
hematology, immunology and oncology for at least three major reasons:
(a) it is the prototype of human malignancies that primarily involve
defects in the induction of apoptosis; (b) CLL patients develop a severe
immunodeficiency with progressive hypogammaglobulinemia; and (c) they
have a high prevalence of autoimmune phenomena. Recent advances in the
biology of the malignant cell in CLL lead to a scenario comprised of two
basic elements: first, CLL cells are optimally organized to survive in
their niches because their ability to undergo apoptosis is severely
hampered; second, they have a microenvironment-dependence that promotes
their extended survival, a situation that arises most probably through
direct cell-to-cell contacts. In addition, CLL cells themselves are the
major accessory cells in CLL, but are inefficient antigen-presenting
cells. This latter defect may provide a clue to reinterpret the events
of immunodeficiency and autoimmunity.
10
UI - 21379342
AU - Orsini E; Guarini A; Foa R
TI -
Accessory cells, cytokine loops and cell-to-cell interactions in chronic
lymphocytic leukemia.
SO - Rev Clin Exp Hematol 2000 Mar;4(1):73-98
AD - Dipartimento di Biotecnologie Cellulari ed Ematologia, University La
Sapienza, Via Benevento 6, 00161 Rome.
In addition to the extensive work that has been conducted in order to
understand better the biological features of the leukemic population in
B-cell chronic lymphocytic leukemia (CLL), over the years considerable
interest has been directed towards other related studies that may have
important implications for the accumulation of the leukemic clone and
for the immunoparesis typical of this disease. In the present review
article, we discuss some of these areas of investigation and, in
particular, we focus on: (1) the multiple abnormalities recorded within
the T and cytotoxic compartment of patients with CLL; (2) cytokine loops
occurring in this disease, with particular emphasis on the cytokines
that appear to play a more critical role; and (3) the cell-to-cell cross
talk that may be actively operational in CLL. These findings will be
discussed in relation with the possible implications that each of them
have in the expansion and clinical behavior of a disease that is
increasingly proving its heterogeneity.
11
UI - 21383856
AU - Jackle R
TI -
[Myeloproliferative diseases. Sometimes waiting it out is the best
therapy]
SO - MMW Fortschr Med 2001 Apr 26;143(17):6-8
12
UI - 21447301
AU - Kaufmann H; Ackermann J; Nosslinger T; Kromer E; Zojer N; Schreiber S;
TI -
Urbauer E; Heinz R; Ludwig H; Huber H; Drach J
Absence of clonal chromosomal relationship between concomitant B-CLL and
multiple myeloma--a report on two cases.
SO - Ann Hematol 2001 Aug;80(8):474-8
AD - University of Vienna, 1st Department of Internal Medicine, Austria.
B-cell chronic lymphocytic leukemia (B-CLL) and multiple myeloma (MM)
are chronic B-cell malignancies that represent different stages of
B-cell maturation. Occasionally, both diseases are present in the same
patient, and this raises the question of clonal associations between the
two neoplasms. We here report on two patients with concomitant B-CLL and
MM. Clonal chromosomal abnormalities in both lymphocytic cells and
plasma cells were studied by interphase fluorescence in situ
hybridization (FISH) using a panel of 24 chromosome- and region-specific
DNA probes. In the first patient, cytogenetics revealed 47, X,
t(Y;22)(p11;q10), +12, dell4(q21q32). By FISH, +12 was present in
lymphoid cells, but not in plasma cells. MM cells were characterized by
multiple chromosomal gains (1, 11q23) and losses (5q, 10, 13q14, 15,
17p13, Y), which were all undetectable in lymphoid cells. The second
patient, in whom no clonal abnormalities were obtained by conventional
cytogenetic analysis, had lymphoid cells with loss of 8q24 by FISH. In
contrast, evidence for a gain of 8q24 (consistent with amplification of
c-myc) was obtained in 13% of plasma cells. Plasma cells were further
characterized by gains of chromosomes 1, 3, 11, 18, and Y. We thus
conclude that this comprehensive molecular cytogenetic analysis
demonstrates the existence of two clonally distinct B-cell malignancies
in both patients.
13
UI - 21455262
AU - Zent CS; Kyasa MJ; Evans R; Schichman SA
TI -
Chronic lymphocytic leukemia incidence is substantially higher than
estimated from tumor registry data.
SO - Cancer 2001 Sep 1;92(5):1325-30
AD - Division of Hematology/Oncology, Departments of Medicine and Pathology,
Central Arkansas Veterans Healthcare System and University of Arkansas
for Medical Sciences, Little Rock, Arkansas 72205, USA.
zentclives@uams.edu
BACKGROUND: Although chronic lymphocytic leukemia (CLL) often is
described as the most common leukemia in the U.S. and Western Europe, to
the authors' knowledge the true incidence of CLL in the U.S. is unknown.
CLL incidence is estimated from tumor registry reports based on tissue
pathology and cancer treatment data. Tumor registry data may
underestimate the incidence of CLL substantially because CLL can be
diagnosed by flow cytometric analysis of peripheral blood cells, and the
majority of patients do not require treatment at the time of diagnosis.
METHODS: To test the hypothesis that CLL has a higher incidence than
estimated from tumor registry data, the authors compared the actual and
reported incidence of CLL for a 10-year interval at the Central Arkansas
Veterans Healthcare System (CAVHS). The accuracy of surveillance methods
for new diagnoses of CLL was confirmed by reviewing the lymphocyte
counts in 45,009 CAVHS patients over a 4-year period. RESULTS: The tumor
registry correctly reported 58 of 93 patients with CLL (62.4%) who were
diagnosed between January 1, 1990 and December 31, 1999. The tumor
registry correctly reported 100% of patients with CLL diagnosed between
1990-1991 but reported only 34.5% of patients with CLL diagnosed between
1998-1999. CONCLUSIONS: The incidence of CLL in the CAVHS was 37.6%
higher than estimated from tumor registry data due to an increase in the
use of peripheral blood immunophenotype as the only diagnostic test for
CLL over the time period of the study. These data suggest that the true
incidence of CLL may be substantially higher than estimated from tumor
registry data. Copyright 2001 American Cancer Society.
14
UI - 21012800
AU - Basu S; Mitra Basu R
TI -
Theophylline as a therapy for chronic lymphocytic leukemia: a case
report and review of literature.
SO - Haematologia (Budap) 2000;30(3):225-7
AD - Department of Medical Oncology, Chittaranjan National Cancer Institute,
Calcutta, India. cncinst@giasc101.vsnl.net.in
We herein, report that theophylline which can induce apoptosis in
chronic lymphocytic leukemia (CLL) cells both in vitro and in vivo, also
appears to be effective when used clinically to treat an advanced CLL
patient.
15
UI - 21190895
AU - Panasci L; Paiement JP; Christodoulopoulos G; Belenkov A; Malapetsa A;
TI -
Aloyz R
Chlorambucil drug resistance in chronic lymphocytic leukemia: the
emerging role of DNA repair.
SO - Clin Cancer Res 2001 Mar;7(3):454-61
AD - Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish
General Hospital, Montreal, Quebec, Canada. L.Panasci@hotmail.com
Various mechanisms have been implicated in nitrogen mustard drug
resistance. The role of these mechanisms in the development of
chlorambucil drug resistance in chronic lymphocytic leukemia (CLL) is
discussed. We review these mechanisms with emphasis on the emerging role
of DNA repair, and specifically, recombinational repair. Inhibition of
these repair processes may lead to new therapies, not only in CLL, but
in other malignancies as well.
16
UI - 21259479
AU - de Vetten MP; van Gelder M; de Greef GE
TI -
Recovery of erythropoiesis following allogeneic bone marrow
transplantation for chronic lymphocytic leukaemia-associated pure red
cell aplasia.
SO - Bone Marrow Transplant 2001 Apr;27(7):771-3
AD - Department of Hematology, University Hospital Rotterdam/Daniel den Hoed
Cancer Center, 3008 AE Rotterdam, Netherlands.
Pure red cell aplasia is a rare condition, that can be either idiopathic
or associated with a lymphoproliferative disorder. The latter is
considered to result from T cell-mediated suppression of haematopoiesis,
and usually responds well to treatment with immunosuppressive
medication. We describe a patient with B-CLL-associated pure red cell
aplasia who did not respond to several courses of immunosuppressive
treatment. Erythropoiesis was finally restored after allogeneic bone
marrow transplantation.
17
UI - 21241666
AU - Ural AU
TI -
Combination chemotherapy with theophylline in chronic lymphocytic
leukemia.
SO - Haematologia (Budap) 2001;31(1):85-6
18
UI - 21317107
AU - Spalding EM; Watkins S; Warwicker P
TI -
Minimal-change glomerulonephritis and chronic lymphocytic leukaemia.
SO - Nephron 2001 Jul;88(3):283-4
19
UI - 21373763
AU - Miller MK; Strauchen JA; Nichols KT; Phelps RG
TI -
Concurrent chronic lymphocytic leukemia cutis and acute myelogenous
leukemia cutis in a patient with untreated CLL.
SO - Am J Dermatopathol 2001 Aug;23(4):334-40
AD - Departments of Dermatopathology, Mount Sinai School of Medicine, New
York, New York 10029, USA.
Patients who have chronic lymphocytic leukemia (CLL) are known to have a
high frequency of second malignant neoplasms. However, acute myelogenous
leukemia (AML) occurring concurrent with or after a diagnosis of CLL is
extremely rare. In this article we report a case of AML developing in a
55-year-old male with a 6-year history of untreated CLL. The diagnosis
was facilitated by touch preparation of a skin punch biopsy specimen.
The patient presented with a two-week history of fever, weakness,
anasarca, and a skin rash. Physical examination revealed pink to
skin-colored firm papules, which coalesced into indurated plaques on his
trunk, upper extremities, and face. The lesions, in combination with
generalized edema, produced a leonine facies. Touch prep of the biopsy
showed medium to large blasts, large monocytoid cells, and numerous
small mature lymphocytes, providing the preliminary diagnosis of a
second, previously undiagnosed myelomonocytic malignancy in this
patient. The initial diagnosis was subsequently confirmed by histologic,
cytochemical, immunohistochemical and flow cytometry studies. This is
the first reported case of CLL with concurrent AML in which rapid touch
prep of a skin punch biopsy facilitated diagnosis.
20
UI - 21426509
AU - Dearden CE; Matutes E; Cazin B; Tjonnfjord GE; Parreira A; Nomdedeu B;
TI -
Leoni P; Clark FJ; Radia D; Rassam SM; Roques T; Ketterer N;
Brito-Babapulle V; Dyer MJ; Catovsky D
High remission rate in T-cell prolymphocytic leukemia with CAMPATH-1H.
SO - Blood 2001 Sep 15;98(6):1721-6
AD - Royal Marsden NHS Trust, London, United Kingdom.
claire.dearden@ccmail.stgh-tr.sthames.nhs.uk
T-cell prolymphocytic leukemia (T-PLL) is a chemotherapy-resistant
malignancy with a median survival of 7.5 months. Preliminary results
indicated a high remission induction rate with the human CD52 antibody,
CAMPATH-1H. This study reports results in 39 patients with T-PLL treated
received prior therapy with a variety of agents, including 30 with
pentostatin; none achieved complete remission (CR). CAMPATH-1H (30 mg)
was administered intravenously 3 times weekly until maximal response.
The overall response rate was 76% with 60% CR and 16% partial remission
(PR). These responses were durable with a median disease-free interval
of 7 months (range, 4-45 months). Survival was significantly prolonged
in patients achieving CR compared to PR or no response (NR), including
one patient who survived 54 months. Nine patients remain alive up to 29
months after completing therapy. Seven patients received high-dose
therapy with autologous stem cell support, 3 of whom remain alive in CR
5, 7, and 15 months after autograft. Stem cell harvests in these
patients were uncontaminated with T-PLL cells as demonstrated by
dual-color flow cytometry and polymerase chain reaction. Four patients
had allogeneic stem cell transplants, 3 from siblings and 1 from a
matched unrelated donor. Two had nonmyeloablative conditioning. Three
are alive in CR up to 24 months after allograft. The conclusion is that
CAMPATH-1H is an effective therapy in T-PLL, producing remissions in
more than two thirds of patients. The use of stem cell transplantation
to consolidate responses merits further study.
21
UI - 21426544
AU - Hisada M; Biggar RJ; Greene MH; Fraumeni JF Jr; Travis LB
TI -
Solid tumors after chronic lymphocytic leukemia.
SO - Blood 2001 Sep 15;98(6):1979-81
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute,
Bethesda, MD 20852, USA. mh280i@nih.gov
Prior reports indicate that patients with chronic lymphocytic leukemia
(CLL) may be at increased risk of subsequent neoplasms. This study
quantified the risk of second cancers among 16 367 patients with CLL in
the population-based Surveillance, Epidemiology and End Results Program.
Overall, the observed/expected ratio (O/E) was 1.20 (95% confidence
interval [CI], 1.15-1.26). Second cancer risks for patients who received
chemotherapy only as the first course of treatment (O/E = 1.21) were
similar to risks for those who received no treatment initially (O/E =
1.19). Significant excesses were found for Kaposi sarcoma (O/E = 5.09),
malignant melanoma (O/E = 3.18), and cancers of the larynx (O/E = 1.72)
and the lung (O/E = 1.66). Increased risks were also found for brain
cancer among men (O/E =1.91) and for cancers of the stomach (O/E = 1.76)
and bladder (O/E = 1.52) among women. Additional investigations of
cancers after CLL are needed to explore the role of immunologic
impairment and/or other etiologic influences.
22
UI - 21449248
AU - Kunzmann V; Ruediger T; Hallek M; Mueller-Hermelink HK; Wilhelm M
TI -
Tumor cell agglutination and not solely cytokine release as mechanism of
adverse reactions during anti-CD20 monoclonal antibody (IDEC-C2B8,
rituximab) treatment.
SO - Blood 2001 Sep 15;98(6):1991-2
23
UI - 21437185
AU - Andersen MK; Christiansen DH; Jensen BA; Ernst P; Hauge G;
TI -
Pedersen-Bjergaard J
Therapy-related acute lymphoblastic leukaemia with MLL rearrangements
following DNA topoisomerase II inhibitors, an increasing problem: report
on two new cases and review of the literature since 1992.
SO - Br J Haematol 2001 Sep;114(3):539-43
AD - Cytogenetic Laboratory, Section of Haematology/Oncology, Department of
Clinical Genetics, Rigshospitalet, Copenhagen, Denmark. MKA@rh.dk
A highly increased risk of myelodysplasia (MDS) and acute myeloid
leukaemia (AML) is well established in patients previously treated for
other malignancies with alkylating agents or topoisomerase II
inhibitors. More recently, single cases of acute lymphoblastic leukaemia
(ALL), often presenting balanced translocations involving chromosome
band 11q23, have been observed. We present two such cases with
t(4;11)(q21;q23), one of whom had previously received only single-agent
chemotherapy with 4-epi-doxorubicin. A review of the literature since
1992 including these two patients reveals a total of 23 cases of ALL or
lymphoblastic lymphoma after chemotherapy presenting balanced
translocations to 11q23. All 23 patients had previously received at
least one topoisomerase II inhibitor, and in two patients
4-epi-doxorubicin had been administered as single-agent chemotherapy for
breast cancer. The latency period to development of t-ALL was 24 months
or less in 20 out of 22 cases. The MLL gene was found to be rearranged
in 14 out of 14 cases, and in three out of six cases the breakpoint was
at the telomeric part of the gene, as observed in most cases of AML
following therapy with topoisomerase II inhibitors. These results
indicate that patients with ALL and balanced translocations to
chromosome band 11q23 following chemotherapy with topoisomerase II
inhibitors in the future should be included with cases of MDS or AML in
calculations of risk of leukaemia.
24
UI - 21437194
AU - Wickremasinghe RG; Ganeshaguru K; Jones DT; Lindsay C; Spanswick VJ;
TI -
Hartley JA; Wadhwa M; Thorpe R; Hoffbrand AV; Prentice HG; Mehta AB
Autologous plasma activates Akt/protein kinase B and enhances basal
survival and resistance to DNA damage-induced apoptosis in B-chronic
lymphocytic leukaemia cells.
SO - Br J Haematol 2001 Sep;114(3):608-15
AD - Department of Haematology, Royal Free and University College School of
Medicine, London, UK. r.wickremasinghe@rfc.ucl.ac.uk
We have studied the actions of autologous plasma on both basal and DNA
damage-induced apoptosis in B-chronic lymphocytic leukaemia (B-CLL)
cells. Apoptosis was quantified using morphological criteria and Western
blot analysis for the apoptosis-specific p85 fragment of poly(ADP
ribose) polymerase. Cell viability was estimated using the methyl
thiazol tetrazolium bromide dye reduction assay. Plasma cultures showed
lower rates of basal apoptosis as well as a decreased cytotoxic response
to chlorambucil and gamma-radiation compared with cultures in fetal calf
serum. Experiments using neutralizing antibodies suggested that the
protective actions of plasma could not be accounted for by interleukin
4, the interferons alpha or gamma or stromal cell-derived factor 1, each
of which have been shown to protect B-CLL cells from apoptosis in vitro.
Plasma addition to B-CLL cells resulted in rapid activation of the Akt
protein kinase, a key signalling enzyme that has been implicated in
anti-apoptotic signalling. LY294002, an inhibitor of
phosphatidylinositol 3'-kinase, blocked Akt activation by plasma. To the
best of our knowledge, this is the first report to show that factors
present in plasma promote basal survival of B-CLL cells and resistance
to cytotoxic drugs via stimulation of the Akt cytoprotective-signalling
pathway. Pharmacological blockade of this pathway may have potential in
the development of novel therapeutic strategies for B-CLL treatment.
25
UI - 21299417
AU - Wolf S; Mertens D; Schaffner C; Korz C; Dohner H; Stilgenbauer S;
TI -
Lichter P
B-cell neoplasia associated gene with multiple splicing (BCMS): the
candidate B-CLL gene on 13q14 comprises more than 560 kb covering all
critical regions.
SO - Hum Mol Genet 2001 Jun 1;10(12):1275-85
AD - Abteilung Organisation Komplexer Genome (H0700), Deutsches
Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg,
Germany.
Deletions in chromosomal band 13q14.3 occur in >50% of B-cell chronic
lymphocytic leukemias (B-CLL) and mantle cell lymphoma, indicating the
localization of a tumor suppressor gene involved in the pathomechanism
of these diseases. Within a 400 kb recurrently deleted segment at least
two minimally deleted subregions had been reported. For the two genes
residing in the proximal subregion, initially named LEU1 and LEU2, a
pathogenic role has not yet been established. We report here that LEU1
is only a small portion of a large gene, which spans all previously
reported critical subregions including the distal subregion. This gene,
designated B-cell neoplasia-associated gene with multiple splicing
(BCMS), is composed of at least 50 exons spanning >or=560 kb of genomic
DNA and is expressed in more than 20 RNA splicing variants. While
tissue-specific expression of RNA variants was observed, there was no
evidence for the expression of a variant specific for B-CLL. Sequence
analysis of the RNA variants suggests that BCMS transcripts belong to
the group of non-coding RNAs. The alignment of the gene with all
critical subregions provides a strong argument for BCMS being the most
likely candidate for the tumor suppressor gene in 13q14 involved in the
leukemogenesis of B-CLL. Due to the limited understanding of functional
RNAs, however, it remains difficult to prove the pathogenic role of
BCMS.
26
UI - 21469673
AU - Hua XH; Genini D; Gussio R; Tawatao R; Shih H; Kipps TJ; Carson DA;
TI -
Leoni LM
Biochemical genetic analysis of indanocine resistance in human leukemia.
SO - Cancer Res 2001 Oct 1;61(19):7248-54
AD - Department of Medicine and The Sam and Rose Stein Institute for Research
on Aging, University of California, San Diego, La Jolla, California
92093-0663, USA.
Indanocine is a potent tubulin-binding drug that is cytotoxic to
multidrug-resistant cancer cell lines. We demonstrated that indanocine
specifically induces apoptosis in malignant B cells from patients with
chronic lymphocytic leukemia. To address the exact biochemical basis for
indanocine toxicity, an indanocine-resistant clone was selected from
mutagenized CEM human lymphoblastoid cells. The resistant cells
displayed a stable indanocine-resistant phenotype for at least 9 months
in drug-free culture. The cloned cells are cross-resistant to colchicine
and vinblastine, but not to paclitaxel, and do not have increased
expression of the multidrug-resistant p170 glycoprotein. In both
parental cells and cell extracts, indanocine treatment caused tubulin
depolymerization. In contrast, the tubulin in the resistant clone did
not depolymerize under identical conditions. Both extract mixing and
cell fusion experiments suggested that a stable structural change in
microtubules, rather than a soluble factor, was responsible for
indanocine resistance. Sequence analysis of parental and resistant cells
revealed a single point mutation in the M40 isotype of beta-tubulin at
nucleotide 1050 (G-->T, Lys(350)-->Asn) in the indanocine-resistant
clone, in a region close to the putative colchicine binding site.
27
UI - 21351351
AU - Gharagozloo S; Khoshnoodi J; Shokri F
TI -
Hepatitis C virus infection in patients with essential mixed
cryoglobulinemia, multiple myeloma and chronic lymphocytic leukemia.
SO - Pathol Oncol Res 2001;7(2):135-9
AD - School of Public Health, Tehran University of Medical Sciences,
Department of Immunology, Tehran 14155, I.R. Iran.
Increased prevalence of HCV infection in some lymphoproliferative
diseases has been recently reported. In the present study, the frequency
of anti-HCV antibody (Ab) together with hepatitis B surface (HBs)
antigen (Ag) and anti-HBs Ab were determined in 42, 45 and 23 patients
with essential mixed cryoglobulinemia (EMC), multiple myeloma (MM) and
B-cell chronic lymphocytic leukemia (B-CLL), respectively. Thirty
hospitalized patients with chronic rheumatoid arthritis (RA) were also
included as a control. Specific antibodies to HCV antigens were detected
by enzyme linked immunosorbent assay (ELISA) and positive results were
confirmed by a recombinant immunoblot assay (RIBA). Our results
demonstrated anti-HCV positivity in 69%, 11% and 4.3% of the EMC, MM and
B-CLL samples tested, respectively. None of the RA patients were found
to be anti-HCV positive. No significant differences were observed
between the patients groups regarding the frequency of HBs Ag and
anti-HBs Ab. Considering the low incidence of HCV infection in the
control group and the normal population, these results confirm and
extend previous reports on the possible role of HCV infection in the
etiology of EMC and further suggest involvement of this virus in a
subset of MM.
28
UI - 20186685
AU - Dohan MC
TI -
Reflections on a bone marrow transplant.
SO - Ann Intern Med 2000 Apr 4;132(7):589-90
AD - mcdohan@massmed.org
29
UI - 21433716
AU - Dereure O; Navarro R; Rossi JF; Guilhou JJ
TI -
Rituximab-induced vasculitis.
SO - Dermatology 2001;203(1):83-4
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