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NCI CANCERLIT® Search: Myeloproliferative Disorders - June 2002
National Cancer Institute®
Last Modified: June 1, 2002
- Mesenteric inflammatory pseudotumor: unusual presentation with leukemoid reaction and massive calcified mass.
- Poor prognosis associated with thrombocytosis in patients with gastric cancer.
- High reliability and sensitivity of the BCR/ABL1 D-FISH test for the detection of BCR/ABL rearrangements.
- Management of essential thrombocythemia during pregnancy with aspirin, interferon alpha-2a and no treatment. A comparative analysis of the
- Idiopathic myelofibrosis with nodal, serosal and parenchymatous infiltration. Case report and review of the literature.
- A pleural effusion caused by fibrous hematopoietic tumor successfully treated with prednisolone in a patient with agnogenic myeloid metaplasia
- The 8p11 myeloproliferative syndrome: a distinct clinical entity caused by constitutive activation of FGFR1.
- Myeloproliferative disorders with translocations of chromosome 5q31-35: role of the platelet-derived growth factor receptor Beta.
- Sequential transformation of t(8;13)-related disease: a case report.
- A fourth case of 8p11 myeloproliferative disorder transforming to B-lineage acute lymphoblastic leukaemia. A case report.
- [Pathological analysis of myelodysplastic syndrome with myelofibrosis]
- The role of T cell costimulation by CD80 in the initiation and maintenance of the immune response to human leukemia.
- Towards a molecular understanding of polycythemia rubra vera.
- K562 cells produce and respond to human erythroid-potentiating activity.
- High platelet count multiplies risk following renal cell carcinoma treatment.
- Thrombopoietin administered during induction chemotherapy to patients with acute myeloid leukemia induces transient morphologic changes that
- Acute erythroleukemia--M6B.
- Simultaneous measurement of serum thrombopoietin and expression of megakaryocyte c-Mpl with clinical and laboratory correlates for
- Induction of human aquaporin-1 gene by retinoic acid in human erythroleukemia HEL cells.
- Comparison of four serum-free, cytokine-free media for analysis of endogenous erythroid colony growth in polycythemia vera and essential
- Leukemic transformation with trisomy 8 in essential thrombocythemia: a report of four cases.
Table of Contents
1
UI - 11990706
AU - Kutluk T; Emir S; Karnak I; Gaglar M; Buyukpamukcu M
TI -
Mesenteric inflammatory pseudotumor: unusual presentation with leukemoid
reaction and massive calcified mass.
SO - J Pediatr Hematol Oncol 2002 Feb;24(2):158-9
AD - Department of Pediatric Oncology, Hacettepe University Faculty of
Medicine, Ankara, Turkey.
The authors describe a child with an unusual presentation of mesenteric
inflammatory pseudotumor in association with leukemoid reaction. An
11-year-old-boy admitted with short stature was found to have an
abdominal mass localized in the right lower quadrant. The leukocyte
count was 92,000/mm3 with neutrophilic leukemoid reaction. Abdominal
ultrasonography and computed tomography revealed a massive calcified
mass in the pelvis. Total resection of the mass was performed and the
pathologic diagnosis of inflammatory pseudotumor of the mesentery was
made. Leukemoid reaction dramatically resolved within a few days after
surgical resection. Physicians should be aware of the association of
inflammatory pseudotumor, leukemoid reaction, and massive calcification.
2
UI - 11923136
AU - Ikeda M; Furukawa H; Imamura H; Shimizu J; Ishida H; Masutani S; Tatsuta
TI -
M; Satomi T
Poor prognosis associated with thrombocytosis in patients with gastric
cancer.
SO - Ann Surg Oncol 2002 Apr;9(3):287-91
AD - Department of Surgery, Sakai Municipal Hospital, Sakai, Japan.
mikeda@surg2.med.osaka-u.ac.jp
BACKGROUND: Thrombocytosis is commonly associated with malignant disease
and has recently been suggested to be a poor prognostic indicator in
patients with lung cancer and gynecological cancers. The prevalence of
thrombocytosis in patients with gastric cancer was reviewed, and its
association with poor prognosis was investigated. METHODS: Platelet
count (PLT) and hemoglobin concentrations (Hb) were reviewed in 369
consecutive patients with histologically verified gastric cancer from
1994 to 2000. Differences between categories were analyzed with analysis
of variance, and survival was compared by using the log-rank test on the
Kaplan-Meier life table. Multivariate Cox regression analysis was used
to evaluate whether thrombocytosis is an independent prognostic marker.
RESULTS: Thrombocytosis was found in 42 patients, and anemia was found
in 200 patients. PLT was negatively correlated with Hb. Mean PLT was
significantly increased in patients with noncurative operations. There
was a positive correlation between the depth of tumor invasion and PLT.
One- and 3-year survival expectancies in patients with or without
thrombocytosis were 52.4% and 23.4% and 85.7% and 72.9%, respectively.
PLT was identified as an independent prognostic factor after lymph node
metastasis and depth of tumor invasion. CONCLUSIONS: Thrombocytosis is
an independent prognostic indicator of survival in patients with gastric
cancer.
3
UI - 11904740
AU - Pelz AF; Kroning H; Franke A; Wieacker P; Stumm M
TI -
High reliability and sensitivity of the BCR/ABL1 D-FISH test for the
detection of BCR/ABL rearrangements.
SO - Ann Hematol 2002 Mar;81(3):147-53
AD - Institut fur Humangenetik, Universitatsklinikum Magdeburg, Leipziger
Strasse 44, H. 26, 39120 Magdeburg, Germany.
Antje-Friederike.Pelz@Medizin.Uni-Magdeburg.de
The BCR/ABL1 fusion gene is mainly caused by the t(9; 22)(q34; q11.2)
translocation, which results in the Philadelphia (Ph) chromosome. The Ph
chromosome is the typical hallmark in chronic myeloid leukemia (CML),
but can also be present in acute lymphoblastic leukemia (ALL) and acute
myeloid leukemia (AML). The BCR/ABL1 rearrangement is an important tumor
classification marker and a useful prognostic factor allowing an
adequate therapy management. Ph chromosome detection by conventional
cytogenetics (CC) can be hampered by low quantity and quality of
metaphases from tumor cells. Furthermore, BCR/ABL1 rearrangements may be
hidden due to cryptic rearrangements or complex aberrations. Therefore,
molecular cytogenetic methods turned out to be useful tools for the
detection of BCR/ABL1 rearrangements. We performed fluorescent in situ
hybridization (FISH) with the recently developed BCR/ABL1 D-FISH probe
(QBIOgene, Illkirch, F) on cultured bone marrow and peripheral blood
cells of 71 patients with CML, ALL, AML, and myeloproliferative disorder
(MPD). FISH results and the results of banding methods were directly
compared. Based on the analyses of >200 nuclei per patient, D-FISH
correlated closely with CC and allowed an accurate quantification of
BCR/ABL1 rearrangements even in a low percentage of aberrant cells. No
false-positive or false-negative results were obtained. Furthermore, the
D-FISH probe detected three cryptic and one complex BCR/ABL1
rearrangement, which were not visible by CC. We conclude that D-FISH
reliably detects standard Ph chromosomes as well as its variant
translocations and accurately quantifies BCR/ABL1 rearrangements prior
and during cancer treatment as well as in the phase of remission, in
daily routine tumor cytogenetic diagnostics.
4
UI - 11978937
AU - Vantroyen B; Vanstraelen D
TI -
Management of essential thrombocythemia during pregnancy with aspirin,
interferon alpha-2a and no treatment. A comparative analysis of the
literature.
SO - Acta Haematol 2002;107(3):158-69
AD - Department of Internal Medicine, UZ Leuven, Leuven, Belgium.
It is advisable to treat essential thrombocythemia (ET) during
pregnancy, because elevated platelet counts can lead to maternal and
fetal complications. In order to establish which therapy is more
favorable, we undertook a review of the literature. In addition to our
own case, we found 27 reports which described 75 cases with 143
pregnancies. We discussed the complications of ET during pregnancy and
postpartum, fetal outcome and the therapeutic strategies. Considering
the clear risk of complications during pregnancy -- especially the
occurrence of spontaneous abortion in the first trimester -- and the
risk of intrauterine fetal death, we believe all patients should at
least be treated with aspirin unless there is a contraindication.
Platelet reduction with interferon-alpha (IFN-alpha) might be able to
further reduce the complications of ET during pregnancy and to improve
fetal outcome (data from 14 patients). After treatment with IFN-alpha,
sufficient numbers of umbilical cord blood stem cells can be collected.
Copyright 2002 S. Karger AG, Basel
5
UI - 11978939
AU - Tzankov A; Krugmann J; Steurer M; Dirnhofer S
TI -
Idiopathic myelofibrosis with nodal, serosal and parenchymatous
infiltration. Case report and review of the literature.
SO - Acta Haematol 2002;107(3):173-6
AD - Institute of Pathology, University of Innsbruck, Austria.
alexander.tzankov@uibk.ac.at
Idiopathic myelofibrosis (IMF) is a breakpoint cluster region
rearrangement-negative chronic myeloproliferative disease with
progressive bone marrow fibrosis. We report a female patient (65 years
old) who was admitted to our hospital in 1996. Trephine bone marrow
biopsy revealed diffuse fibrosis with atypical multilobulated
megakaryocytes. A cellular phase of IMF was diagnosed. Three years
later, despite being at intermediate risk, the patient developed
generalized lymphadenopathy and multiple sclerosing tumors throughout
the peritoneum and retroperitoneum. Biopsy specimens from these tumors
revealed sclerosing hematopoietic infiltrates. The present case
demonstrates that IMF not only can progress to acute leukemia but can
also spread uncontrollably, or 'metastasize' with extensive sclerosing
hematopoietic tumors throughout the body. Copyright 2002 S. Karger AG,
Basel
6
UI - 11999361
AU - Hirayama Y; Koyama R; Nagai T; Matsunaga T; Kogawa K; Sakamaki S; Kokai
TI -
Y; Niitsu Y
A pleural effusion caused by fibrous hematopoietic tumor successfully
treated with prednisolone in a patient with agnogenic myeloid metaplasia
with myelofibrosis.
SO - Int J Hematol 2002 Apr;75(3):305-8
AD - Department of Internal Medicine, Higashi Sapporo Hospital, Japan.
yhirayama@hsh.or.jp
A 46-year-old woman suffering from agnogenic myeloid metaplasia (AMM)
exhibited respiratory failure caused by massive pulmonary effusion,
which was speculated to have been produced by chest tumors. A biopsy
specimen revealed findings compatible with fibrous hematopoietic tumor
(FHT): prominent fibroblasts and fibrosis with scantv megakaryocytes.
Serum concentrations of transforming growth factor (TGF)-beta and
platelet-derived growth factor (PDGF) were significantly higher than
those of other cases of AMM without FHT. The effusion did not respond to
administrations of various chemotherapeutic agents, but after
prednisolone administration, the effusion disappeared and the tumors
also diminished. TGF-beta and PDGF were the possible causes of FHT
formation, and for such fibrotic extramedullary regions, the
administration of prednisolone should be considered.
7
UI - 11919391
AU - Macdonald D; Reiter A; Cross NC
TI -
The 8p11 myeloproliferative syndrome: a distinct clinical entity caused
by constitutive activation of FGFR1.
SO - Acta Haematol 2002;107(2):101-7
AD - Department of Haematology, Faculty of Medicine, Imperial College of
Science, Technology and Medicine, Charing Cross Hospital, London, UK.
Several recurrent translocations that involve chromosome band 8p11 have
been described in myeloid malignancies. These translocations target two
distinct genes: (1) FGFR1, a receptor tyrosine kinase for fibroblast
growth factors, and (2) MOZ, a putative histone acetyltransferase whose
precise function remains to be defined. Disruption of FGFR1 is
associated with a disease entity known as the 8p11 myeloproliferative
syndrome (EMS)/stem cell leukemia-lymphoma syndrome, a chronic
myeloproliferative disorder that frequently presents with eosinophilia
and associated T-cell lymphoblastic lymphoma. The disease is aggressive
and rapidly transforms to acute leukaemia, usually of myeloid phenotype.
Currently, only allogeneic stem cell transplantation appears to be
effective in eradicating or suppressing the malignant clone. To date,
four gene fusions associated with distinct translocations have been
described in EMS: the t(8;13)(p11;q12), t(8;9)(p11;q33), t(6;8)(q27;p11)
and t(8;22)(p11q22) fuse ZNF198, CEP110, FOP and BCR, respectively, to
FGFR1. The resulting fusion proteins have constitutive tyrosine kinase
activity and activate multiple signal transduction pathways. These
pathways and the fusion proteins are attractive targets for targeted
signal transduction therapy. Copyright 2002 S. Karger AG, Basel
8
UI - 11919393
AU - Steer EJ; Cross NC
TI -
Myeloproliferative disorders with translocations of chromosome 5q31-35:
role of the platelet-derived growth factor receptor Beta.
SO - Acta Haematol 2002;107(2):113-22
AD - Wessex Regional Genetics Laboratory, Salisbury District Hospital, UK.
Acquired reciprocal chromosomal translocations that involve chromosome
bands 5q31-33 are associated with a significant minority of patients
with BCR-ABL-negative chronic myeloid leukemias. The most common
abnormality is the t(5;12)(q33;p13), which fuses the ETV6/TEL gene to
the platelet-derived growth factor receptor-beta (PDGFRB), a receptor
tyrosine kinase that maps to 5q33. PDGFRB is disrupted by other
translocations and to date four additional partner genes (H4, HIP1,
CEV14 and Rab5) have been reported. Clinically, most patients present
with a myeloproliferative disorder (MPD) with eosinophilia, eosinophilic
leukemia or chronic myelomonocytic leukemia and thus fall into the
broader category of myeloproliferative disorders/myelodysplastic
syndromes (MPD/MDS). With the advent of targeted signal transduction
therapy, patients with rearrangement of PDGFRB might be better
classified as a distinct subgroup of MPD/MDS. Copyright 2002 S. Karger
AG, Basel
9
UI - 11919389
AU - Roy S; Szer J; Campbell LJ; Juneja S
TI -
Sequential transformation of t(8;13)-related disease: a case report.
SO - Acta Haematol 2002;107(2):95-7
AD - Royal Melbourne Hospital, Melbourne, Australia.
We report a case of an atypical myeloproliferative disorder with t(8;13)
that presented as B-lineage acute lymphoblastic leukaemia (B-ALL).
Following induction chemotherapy, the disease manifested as chronic
myeloproliferative state, which responded to hydroxyurea. Terminally,
the disease transformed into acute myeloid leukaemia (AML) with
additional chromosomal abnormalities including monosomy 7. To our
knowledge, this is the first case of this rare atypical
myeloproliferative disorder with t(8;13) that presented as B-ALL and
terminally transformed to AML with additional chromosomal abnormalities.
Copyright 2002 S. Karger AG, Basel
10
UI - 11919390
AU - JabbarAl-Obaidi M; Rymes N; White P; Pomfret M; Smith H; Starczynski J;
TI -
Johnson R
A fourth case of 8p11 myeloproliferative disorder transforming to
B-lineage acute lymphoblastic leukaemia. A case report.
SO - Acta Haematol 2002;107(2):98-100
AD - Department of Haematology, Birmingham Heartlands Hospital, Birmingham,
UK.
A 56-year-old male presented with inguinal lymphadenopathy and
leucocytosis (WBC 98 x 10(9)/l). Bone marrow morphology showed myeloid
hyperplasia, with eosinophilia. Cytogenetic analysis showed no evidence
of the Philadelphia chromosome, and fluorescence in situ hybridisation
studies for the BCR/ABL fusion were negative. All cells examined showed
the t(8;13)(p11;q12) translocation. Six weeks after presentation, the
disease progressed to an acute lymphoblastic leukaemia (ALL). The
lymphoblasts were CD19/CD10 dual positive. Cytogenetic analysis again
showed the t(8;13) translocation, with no additional abnormalities.
There have been at least 14 reported cases of the t(8;13)
myeloproliferative disorder to date, of which only 3 transformed to
B-lineage ALL: our case is the 4th. Copyright 2002 S. Karger AG, Basel
11
UI - 12043202
AU - Matsunaga T; Kato J
TI -
[Pathological analysis of myelodysplastic syndrome with myelofibrosis]
SO - Rinsho Ketsueki 2002 Apr;43(4):252-7
12
UI - 10609780
AU - Matsumoto K; Anasetti C
TI -
The role of T cell costimulation by CD80 in the initiation and
maintenance of the immune response to human leukemia.
SO - Leuk Lymphoma 1999 Nov;35(5-6):427-35
AD - Clinical Research Division, Fred Hutchinson Cancer Research Center,
Seattle, WA 98109, USA.
Most human myeloid leukemias express both class I and class II HLA and
it has been postulated that leukemia-associated peptides are presented
by those molecules. It is possible, however, that leukemia cells escape
the immune surveillance by lacking expression of "costimulatory"
molecules required for activating the immune response. Human
erythroleukemia line (HEL) has been the subject of previous detailed
studies demonstrating surface expression of bona fide HLA molecules but
inability to stimulate allogeneic response of proliferative or cytolytic
T cells. We found that an HLA-DR+ subclone (HEL-DR+) expresses LFA-1,
LFA-3, ICAM-1, ICAM-3, but neither CD80 nor CD86 on the surface.
Transfection of CD80 cDNA into HEL-DR+ cells induced the allogeneic
response of purified T cells from both cord blood and peripheral blood
of adult donors, demonstrating that CD80 expression could lead to
accessory cell-independent activation of naive T cells. Priming
allogeneic peripheral blood T cells by HEL-DR+/CD80+ also lead to
generation of cytotoxic T lymphocytes that lysed both HEL-DR+/CD80+ and
wild type HEL-DR+ equally well, confirming CD80 expression is required
only in the CTL induction phase but not in the CTL effector phase. We
established and maintained alloproliferative T cell clones from adult
blood by stimulation with the HEL-DR+/CD80+ line. The clones could
respond not only to HEL-DR+/CD80+ line but also to the HEL-DR+ line;
however, the proliferative response to HEL-DR+/CD80+ was amplified and
sustained compared to the short-lived response to wild type HEL-DR+
cells. Therefore, expression of CD80 by HEL-DR+ cells was determinant
both to initiate and sustain the T cell response. These experiments
support the hypothesis that lack of expression of "costimulatory"
molecules for T cells contributes to leukemia escape from immune
surveillance, and provide preliminary data for the use of CD80
transfection in the immunotherapy of human leukemia.
13
UI - 10848954
AU - Pahl HL
TI -
Towards a molecular understanding of polycythemia rubra vera.
SO - Eur J Biochem 2000 Jun;267(12):3395-401
AD - Division of Experimental Anaesthesiology, University Hospital Freiburg,
Center for Tumor Biology, Germany. pahl@uni-freiburg.de
Polycythemia rubra vera (PV) is one of four diseases collectively called
the myeloproliferative disorders (MPDs). Each disorder leads to an
increased production of one or several hematopoietic cell lineages. MPDs
arise from acquired mutations in a pluripotent hematopoietic stem cell.
However, the molecular mechanisms leading to the development of these
diseases are poorly understood. This review will summarize and evaluate
recent advances in our understanding of one particular MPD, PV.
14
UI - 2836003
AU - Avalos BR; Kaufman SE; Tomonaga M; Williams RE; Golde DW; Gasson JC
TI -
K562 cells produce and respond to human erythroid-potentiating activity.
SO - Blood 1988 Jun;71(6):1720-5
AD - Department of Medicine, UCLA School of Medicine.
Human erythroid-potentiating activity (EPA) is a 28,000 mol wt
glycoprotein that stimulates the growth of erythroid progenitors in
vitro and enhances colony formation by the K562 human erythroleukemia
cell line. EPA has potent protease inhibitory activity, and is also
referred to as tissue inhibitor of metalloproteinases (TIMP). We
observed that colony formation by K562 cells in semi-solid medium
containing reduced fetal calf serum (FCS) is not directly proportional
to the number of cells plated, suggesting production of autostimulatory
factors by K562 cells. Using radioimmunoprecipitation and a bioassay for
EPA, medium conditioned by K562 cells was found to contain high levels
of biologically active EPA; Northern hybridization analysis confirmed
the expression of EPA mRNA. Radiolabeled EPA was used to identify cell
surface receptors on K562 cells. Together, these results suggest that
EPA may act as an autocrine growth factor for K562 cells.
15
UI - 11998657
AU - Anonymous
TI -
High platelet count multiplies risk following renal cell carcinoma
treatment.
SO - Urol Nurs 2001 Jun;21(3):224-5
16
UI - 12047134
AU - Douglas VK; Tallman MS; Cripe LD; Peterson LC
TI -
Thrombopoietin administered during induction chemotherapy to patients
with acute myeloid leukemia induces transient morphologic changes that
may resemble chronic myeloproliferative disorders.
SO - Am J Clin Pathol 2002 Jun;117(6):844-50
AD - Department of Pathology, Immunology, and Laboratory Medicine, University
of Florida College of Medicine, Gainesville 32610-0275, USA.
Thrombopoietin (TPO), a potent stimulator of megakaryocyte and platelet
production, has been used in clinical trials to reduce thrombocytopenia
after chemotherapy in patients with acute myeloid leukemia (AML). We
report that TPO therapy is associated with peripheral blood and bone
marrow findings that can mimic myeloproliferative disorders. Peripheral
blood and bone marrow samples of 13 patients with AML who received TPO
were examined. A subset of bone marrow samples exhibited
hypercellularity, megakaryocytic hyperplasia, and reticulin fibrosis
after TPO administration. Cases demonstrated as many as 58.4
megakaryocytes per high-powerfield (MHPF) compared with 3.7 MHPF in the
control group. Megakaryocytic atypia, increased mitoses, emperipolesis,
intrasinusoidal megakaryocytes, and thickened trabeculae also were seen.
Peripheral blood findings included leukoerythroblastosis, leukocytosis,
thrombocytosis, and circulating megakaryocyte nuclei. Changes resolved
within 3 months after discontinuation of TPO. This rapid resolution of
the morphologic abnormalities induced by TPO distinguishes these
findings from those seen in true chronic myeloproliferative disorders.
17
UI - 12035366
AU - Mohanty R; Dash B; Chawla SC; Paul HS
TI -
Acute erythroleukemia--M6B.
SO - Indian J Pathol Microbiol 2001 Oct;44(4):461-2
AD - Department of Pathology, Tata Main Hospital, Jamshedpur.
Acute Erythroleukemia is a rare disorder of hematopoietic system,
accounts for 1-3% of all acute leukemia and 15% of myeloid leukemia.
Recently, the World Health Organisation & Society of Haematopathology
proposed a change in the categorization, with M6a and M6b subgroups of
the original FAB classification. Hereby we report a case of acute
erythroleukemia--M6b subtype, presented with pain abdomen and vomiting.
The patient died within two days. The case is being reported for its
rarity and uncommon presentation.
18
UI - 12068799
AU - Elliot MA; Yoon SY; Kao P; Li CY; Tefferi A
TI -
Simultaneous measurement of serum thrombopoietin and expression of
megakaryocyte c-Mpl with clinical and laboratory correlates for
myelofibrosis with myeloid metaplasia.
SO - Eur J Haematol 2002 Mar;68(3):175-9
AD - Division of Hematology and Internal Medicine, Mayo Clinic, Rochester,
Minnesota 55905, USA.
OBJECTIVES: We sought to investigate potential mechanisms of increased
serum thrombopoietin (TPO) concentrations in myelofibrosis with myeloid
metaplasia (MMM) by simultaneously measuring serum TPO, platelet and
megakaryocyte (MK) numbers, and MK c-Mpl expression. METHODS: We studied
17 consecutive patients who had MMM and were not receiving therapy at
the time of evaluation. Serum TPO was measured by a two-site
immunochemiluminometric assay. Immunohistochemical staining of c-Mpl was
accomplished with an immunoperoxidase method on simultaneously obtained
bone marrow specimens. RESULTS: Our findings confirmed the presence of
inappropriately increased serum TPO despite mostly normal or increased
peripheral platelet counts and markedly increased bone marrow MK
numbers. In addition, we found an inverse correlation between platelet
count and serum TPO (P<0.03) and splenic size (P<0.04). However, serum
TPO did not correlate with either bone marrow MK number or c-Mpl
expression. The lack of correlation of serum TPO and bone marrow
megakaryocyte number may be accounted for by the unavoidable
inaccuracies in quantifying megakaryocytopoiesis in a disorder of known
altered hematopoietic progenitor cell distribution, both intramedullary
and extramedullary. The significant inverse correlation between serum
TPO and spleen size suggests that this site of extramedullary
megakaryocytopoiesis may assume a role in the dysfunctional TPO
regulatory axis. CONCLUSIONS: These observations suggest some
preservation of the negative feedback regulation that appears to be
dysfunctional at the MK c-Mpl level. Consistent with previous
observations in animal models, our observations suggest the possibility
that altered TPO regulation resulting in sustained ligand excess may
have pathogenetic relevance in MMM.
19
UI - 12051745
AU - Umenishi F; Schrier RW
TI -
Induction of human aquaporin-1 gene by retinoic acid in human
erythroleukemia HEL cells.
SO - Biochem Biophys Res Commun 2002 May 10;293(3):913-7
AD - Division of Renal Diseases and Hypertension, Department of Medicine,
University of Colorado Health Sciences Center, Denver, CO 80262, USA.
fuminori.umenishi@uchsc.edu
Retinoids have been implicated in the control of cell proliferation,
differentiation, and developmental processes. We report here that
aquaporin-1 (AQP1) is specifically induced by retinoic acid (RA) in
human erythroleukemia HEL cells. Both all-trans-RA (ATRA) and 9-cis-RA
(9CRA) strongly induced the AQP1 mRNA and protein in a dose-dependent
manner. AQP1 protein was mainly expressed in plasma membrane in cells
induced by RAs. To identify the RA response element (RARE) in the human
AQP1 promoter, the 5(')-flanking region of AQP1 promoter was isolated
and transient transfection experiment in HEL cells was performed.
Deletion analysis of the AQP1 promoter revealed that one putative
DR5-like RARE with five spaces was located in the region from -2218 to
-2202; AGGGCAgggacAGGTGA. Electrophoretic mobility shift assay (EMSA)
experiment demonstrated that two slowly migrated complexes (C1 and C2)
capable of binding the RARE sequence were present in nuclear extracts
prepared from cells and the complex C1 was strongly increased in nuclear
extracts by RA stimulation. The complexes C1 and C2 were significantly
abolished by an excess unlabeled probe. These results indicate that RAs
strongly stimulate the human AQP1 gene expression through the RARE and
define a novel role in the regulation of erythropoiesis. (c) 2002
Elsevier Science (USA).
20
UI - 11920280
AU - Dobo I; Mossuz P; Campos L; Girodon F; Allegraud A; Latger-Cannard V;
TI -
Boiret N; Pineau D; Wunder E; Zandecki M; Praloran V; Hermouet S
Comparison of four serum-free, cytokine-free media for analysis of
endogenous erythroid colony growth in polycythemia vera and essential
thrombocythemia.
SO - Hematol J 2001;2(6):396-403
AD - Laboratoire d'Hematologie, Centre Hospitalier Universitaire d'Angers,
Angers, France.
INTRODUCTION: The assay of endogenous erythroid colony formation (EEC),
a characteristic of polycythemia vera and essential thrombocythemia, is
not standardized. In this multicentric study, we tested four semisolid,
serum-free, cytokine-free media based on either methylcellulose (M1, M2)
or collagen (C1, C2) commercialized for the EEC assay. MATERIALS AND
METHODS: Bone marrow mononuclear cells (BMMC) from 73 individuals (62
patients with either polycythemia vera (26), essential thrombocythemia
(19), secondary polyglobuly (17) or chronic myeloid leukemia (2) and 11
healthy donors) were grown in parallel in the four media without, or
with 0.01 U/ml erythropoietin (EPo). RESULTS: In all four media EEC
formation was specific, as it was not observed in cultures of patients
with secondary polyglobuly or chronic myeloid leukemia, nor of healthy
donors. Analysis of fresh or MGG-stained collagen gel cultures allowed
detection of EEC formation significantly more frequently than
methylcellulose-based media; addition of 0.01 U/ml of EPo had little or
no effect on EEC formation. Collagen-based medium C1 gave better results
than the other media tested: the 'C1' EEC assay was positive for 68.2%
of polycythemia vera cultures with significantly higher median EEC
numbers (6.5/10(5) BMMC for patients with one major criteria of
polycythemia vera and 19 and 21/10(5) BMMC for patients with two or
three major criteria, respectively). Medium C1 was also better for
essential thrombocythemia cultures with 47.4% of positive results but
with a low median EEC number (6.7/10(5) BMMC). When associated with the
ELISA dosage of serum EPo, the 'C1' EEC assay allowed confirmation or
elimination of the diagnosis of polycythemia vera for 91% (20/22) of
polyglobulic patients. CONCLUSION: We propose that serum-free
collagen-based culture systems be considered to standardize the EEC
assay, now part of the new criteria of polycythemia vera.
21
UI - 12061320
AU - Hirose Y; Masaki Y; Sugai S
TI -
Leukemic transformation with trisomy 8 in essential thrombocythemia: a
report of four cases.
SO - Eur J Haematol 2002 Feb;68(2):112-6
AD - Division of Hematology and Immunology, Department of Internal Medicine,
Kanazawa Medical University, Ishikawa, Japan.
Karyotype analysis of bone marrow samples was performed in 20 cases of
essential thrombocythemia (ET) at the time of diagnosis. Three patients
had karyotype abnormalities at the time of diagnosis; trisomy 8,
deletion of Y, and del(9)(q?) in each. The patient who had trisomy 8 at
the time of diagnosis underwent myeloid blastic transformation in 35
months. Three patients whose karyotypes were normal at the time of
diagnosis developed a chromosome abnormality with trisomy 8 when they
developed myeloid blastic transformation 38, 79 and 86 months after
initial diagnosis of ET. Two patients with blastic transformation had
been treated with busulfan, one with hydroxyurea and one with
methyl-6-[3-(2-chloroethyl)-3-nitorosoureidol]-6-deoxy-alpha-D-glucopyra
noside (MCNU). It is suggested that progression of the disease may have
increased the incidence of trisomy 8 and the development of leukemic
transformation.
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