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NCI CANCERLIT® Search: Myeloproliferative Disorders - October 2002
National Cancer Institute®
Last Modified: October 1, 2002
- Acute promyelocytic leukemia with marrow fibrosis at initial presentation: possible involvement of transforming growth
- Bone marrow reticulin fibrosis at diagnosis in promyelocytic leukaemia treated with all-trans retinoic acid has no adverse prognosis.
- Cytogenetic and molecular genetic aspects of essential thrombocythemia.
- Constitutional trisomy 8 as first mutation in multistep carcinogenesis: clinical, cytogenetic, and molecular data on three cases.
- Lack of correlation between growth of TF-1 cells and tyrosine phosphorylation signals in response to IL-3, IL-5 and GM-CSF.
- Hyperfibrotic myelodysplasia: a report of three cases showing haematological remission following treatment with prednisolone.
- Proposed classification for the myelodysplasia/myelofibrosis syndromes.
- Transient normal platelet counts and decreased requirement for interferon during pregnancy in essential thrombocythaemia.
- Pregnancy in women with essential thrombocythaemia.
- Myelodysplastic and myeloproliferative syndromes associated with giant cell arteritis and polymyalgia rheumatica: a coincidental coexistence or
- Reactive and clonal thrombocytosis: proinflammatory and hematopoietic cytokines and acute phase proteins.
- Serum proinflammatory cytokines and its relationship to clinical parameters in lung cancer patients with reactive thrombocytosis.
- Thrombocytosis is associated with a significant increase in the cancer specific death rate after radical nephrectomy.
- CD34+ stem cells in chronic myeloproliferative disorders.
- Acute myeloid leukemia (AML) having evolved from essential thrombocythemia (ET): distinctive chromosome abnormalities in patients
- Platelet thromboxane synthesis and release reactions in myeloproliferative disorders.
- Studies of von Willebrand factor in essential thrombocythemia patients treated with alpha-2b recombinant interferon.
- Procoagulant activity of mononuclear cells is increased in myeloproliferative and myelodysplastic diseases.
Table of Contents
1
UI - 11014898
AU - Mori A; Wada H; Okada M; Takatsuka H; Tamura A; Fujimori Y; Okamoto T;
TI -
Takemoto Y; Kanamaru A; Kakishita E
Acute promyelocytic leukemia with marrow fibrosis at initial
presentation: possible involvement of transforming growth
factor-beta(1).
SO - Acta Haematol 2000;103(4):220-3
AD - Second Department of Internal Medicine, Hyogo College of Medicine,
Hyogo, Japan.
Although the occurrence of marrow fibrosis in acute myeloid leukemia has
been described, there have been no reports of acute promyelocytic
leukemia (APL) associated with marrow fibrosis. Here we describe an APL
patient with severe marrow fibrosis at initial presentation. He had the
typical manifestations of APL, except for marrow fibrosis. Complete
remission was achieved by treatment with all-trans retinoic acid plus
chemotherapy, and his marrow fibrosis gradually improved concomitantly
with the decrease in leukemic cells. To clarify the mechanism of marrow
fibrosis in this patient, we investigated the expression of genes for
several cytokines promoting fibrosis by the reverse transcriptase
polymerase chain reaction methods. An overexpression of transforming
growth factor-beta(1) was noted in his leukemic cells at initial
presentation, whereas no increase in expression was observed at the time
of relapse when he no longer had marrow fibrosis. These findings suggest
that overexpression of transforming growth factor-beta(1) was involved
in the development of marrow fibrosis in this APL patient. Copyright
2000 S. Karger AG, Basel
2
UI - 12187033
AU - Losada R; Cabrera H; Hernandez P; Hernandez C; Menendez A; Mesa J;
TI -
Plascencia A; Ramon L; Agramonte O; Espinosa E
Bone marrow reticulin fibrosis at diagnosis in promyelocytic leukaemia
treated with all-trans retinoic acid has no adverse prognosis.
SO - Acta Haematol 2002;108(2):111-2
AD - Instituto de Hematologia e Inmunologia, La Habana, Cuba.
ihidir@hemato.sld.cu
3
UI - 12187022
AU - Steensma DP; Tefferi A
TI -
Cytogenetic and molecular genetic aspects of essential thrombocythemia.
SO - Acta Haematol 2002;108(2):55-65
AD - Division of Hematology and Internal Medicine, Mayo Clinic, Rochester,
Minn. 55905, USA.
Essential thrombocythemia (ET) is a chronic myeloid disorder that is
characterized by thrombocytosis, thrombohemorrhagic and vasomotor
symptoms, a long median survival, and a low risk of transformation to
leukemia. ET can be difficult to distinguish from secondary (reactive)
thrombocytosis, and the diagnosis of ET can only be made after the
exclusion of other marrow disorders with similar features. Although ET
has been assumed to be a clonal process, recent studies have suggested
that a substantial number of cases classified as ET may actually not be
clonal, and nonclonality may be associated with a lower risk of
thrombosis. The lack of a characteristic cytogenetic marker for ET
confounds analyses of clonality and offers no insight into disease
pathogenesis. There is controversy over the proper classification of
thrombocytosis associated with the pathological BCR-ABL gene
rearrangement; such cases are not clearly distinguishable from chronic
myelogenous leukemia (CML) and should be provisionally classified as
CML. New insights are emerging into the role of the megakaryocytopoiesis
regulator thrombopoietin (TPO) and its receptor, c-Mpl, in ET and
related disorders, but TPO-Mpl dynamics appear to be complex. In some
familial thrombocythemic syndromes, mutations in the 5' untranslated
region of TPO have recently been described, but these have not yet been
observed in sporadic ET. In the future, global analysis of gene
expression patterns may help overcome diagnostic dilemmas, refine
disease classification, and lead to an improved understanding of the
pathogenesis of ET. Copyright 2002 S. Karger AG, Basel
4
UI - 8913726
AU - Seghezzi L; Maserati E; Minelli A; Dellavecchia C; Addis P; Locatelli F;
TI -
Angioni A; Balloni P; Miano C; Cavalli P; Danesino C; Pasquali F
Constitutional trisomy 8 as first mutation in multistep carcinogenesis:
clinical, cytogenetic, and molecular data on three cases.
SO - Genes Chromosomes Cancer 1996 Oct;17(2):94-101
AD - Clinica Pediatrica, Universita di Pavia, Italy.
Three patients, with constitutional trisomy 8 mosaicism (CT8M), who
developed a malignancy are reported. The diagnoses were refractory
anaemia, acute lymphoblastic leukaemia, and idiopathic myelofibrosis. In
the child with acute leukaemia, the CT8M was diagnosed at birth due to
severe dysmorphisms and malformations; the other two patients showed a
milder phenotype, and the CT8M was diagnosed only after the finding of
trisomy 8 in neoplastic cells. The review of eight similar, previously
reported cases and the clinical, cytogenetic, and molecular studies
performed in our patients led us to make the following observations: (I)
CT8M predisposes to neoplasms, preferentially to myelo- or
lymphoproliferative diseases; (2) a gene dosage effect for glutathione
reductase in red blood cells was seen in two of our patients; (3) the
wide phenotypic variation of CT8M was confirmed: trisomy 8 in neoplastic
cells of phenotypically near-normal cases may be misinterpreted as
acquired; and (4) molecular studies suggested a postzygotic origin of
the trisomy in our three cases, with the supernumerary chromosome being
of paternal origin in one case and of maternal origin in the other two.
We postulate that the trisomy 8 in neoplasms may often occur by mitotic
nondisjunction in an early embryonic multipotent cell and that what is
usually interpreted as an acquired trisomy 8 may in fact be CT8M. The
constitutional trisomy 8 would act as a pathogenetically important first
mutation in multistep carcinogenesis. Whenever trisomy 8 is found in
malignancies, the patient should be reevaluated clinically to exclude
CT8M, and CT8M patients should be monitored for the possible development
of malignancies.
5
UI - 9325013
AU - Ettinger S; Fong D; Duronio V
TI -
Lack of correlation between growth of TF-1 cells and tyrosine
phosphorylation signals in response to IL-3, IL-5 and GM-CSF.
SO - Cytokine 1997 Sep;9(9):650-9
AD - Department of Medicine, University of British Columbia, Jack Bell
Research Centre, Vancouver, Canada.
The human cell line, TF-1, was used to compare responses to interleukin
3 (IL-3), IL-5 and granulocyte-macrophage colony-stimulating factor
(GM-CSF). TF-1 cells grew well in the presence of any one of the
cytokines in early passages. However, the level of tyrosine
phosphorylation was minimal in response to IL-5, and detection of a
tyrosine phosphorylation signal required high concentrations of IL-5.
When grown for longer periods of time in the presence of one of the
cytokines, there were dramatic difference in the cells' responses. IL-3
or GM-CSF-grown cells showed only half of the original bioassay response
to IL-5. However, cells grown in IL-5 alone kept the same response, and
all cells showed the same response to IL-3 and GM-CSF. IL-5-grown cells
also had an increased tyrosine phosphorylation signal, along with
increased sensitivity to IL-5, yet there was no difference in an IL-5
bioassay. The relative level of detection of tyrosine phosphorylated
JAK-2, STAT-5, SHC, and other substrates corresponded to the overall
tyrosine phosphorylation signal. IL-5-grown cells had approximately
10-fold more IL-5 receptor alpha subunit message compared to IL-3-grown.
These results suggest that response of TF-1 cells to IL-5 may be
deceiving in that a good response in a bioassay can be observed with
relatively little tyrosine phosphorylation, but an increase in tyrosine
phosphorylation can be correlated with an increase in the expression of
IL-5 receptor alpha subunit.
6
UI - 2043466
AU - Watts EJ; Majer RV; Green PJ; Mavor WO
TI -
Hyperfibrotic myelodysplasia: a report of three cases showing
haematological remission following treatment with prednisolone.
SO - Br J Haematol 1991 May;78(1):120-2
AD - Department of Haematology, Orsett Hospital, Grays, Essex.
7
UI - 1772789
AU - Reilly JT; Dolan G
TI -
Proposed classification for the myelodysplasia/myelofibrosis syndromes.
SO - Br J Haematol 1991 Dec;79(4):653
8
UI - 8603023
AU - Shpilberg O; Shimon I; Sofer O; Dolitski M; Ben-Bassat I
TI -
Transient normal platelet counts and decreased requirement for
interferon during pregnancy in essential thrombocythaemia.
SO - Br J Haematol 1996 Feb;92(2):491-3
AD - Institute of Haematology, Chaim Sheba Medical Centre, Tel-Hashomer,
Israel.
We report on the remarkable decrease in the platelet counts during
pregnancy in two women with essential thrombocythaemia following
treatment with recombinant interferon-alpha (r-IFN-alpha). Prior to
pregnancy, the first patient was treated for 10 months with r-IFN-alpha
3 x 10(6) units/d six times per week, and the platelet count ranged
between 750 and 800 x 10(9)/l. Starting from the sixth week of
gestation, the platelet count decreased to normal levels and remained
so, resulting in a lower r-IFN-alpha requirement. Following successful
delivery of a healthy newborn an abrupt rise of the platelet count to
pre-gestation values was observed, necessitating increased r-IFN-alpha
dosage before pregnancy. The second patient when she became pregnant had
been treated with r-IFN-alpha 3 x 10(6) units/d six times per week for
10 weeks. Starting from the 24th week of gestation the platelet count
decreased, and despite reduction in the dose of r-IFN-alpha reached
normal values at the time of delivery. The exact mechanism for the
platelet count normalization during pregnancy is unclear, and several
possibilities are discussed.
9
UI - 8703837
AU - Frezzato M; Rodeghiero F
TI -
Pregnancy in women with essential thrombocythaemia.
SO - Br J Haematol 1996 Jun;93(4):977
10
UI - 12189460
AU - Espinosa G; Font J; Munoz-Rodriguez FJ; Cervera R; Ingelmo M
TI -
Myelodysplastic and myeloproliferative syndromes associated with giant
cell arteritis and polymyalgia rheumatica: a coincidental coexistence or
a causal relationship?
SO - Clin Rheumatol 2002 Aug;21(4):309-13
AD - Service of Autoimmune Diseases, Institut Clinic d'Infeccions i
Immunologia, Institut d'Investigacions Biomediques August Pi i Sunyer
(IDIBAPS), Hospital Clinic, University of Barcelona, Barcelona, Spain.
A variety of systemic autoimmune disorders have been reported in
patients with myelodysplastic and myeloproliferative syndromes. A
possible association with polymyalgia rheumatica and giant cell
arteritis has also been recognised. We report another case of
polymyalgia rheumatica and one of giant cell arteritis associated with a
myelodysplastic syndrome and the two first cases of giant cell arteritis
associated with essential thrombocytaemia and chronic myelomonocytic
leukaemia, respectively. It seems that there is a relationship between
these entities, but the nature of this association is still unknown.
11
UI - 11332909
AU - Araneda M; Krishnan V; Hall K; Kalbfleisch J; Krishnaswamy G; Krishnan K
TI -
Reactive and clonal thrombocytosis: proinflammatory and hematopoietic
cytokines and acute phase proteins.
SO - South Med J 2001 Apr;94(4):417-20
AD - Department of Internal Medicine, James H. Quillen VA Medical Center and
James H. Quillen College of Medicine, East Tennessee State University,
Johnson City 37614-0622, USA.
BACKGROUND: We quantitated proinflammatory and thrombopoietic cytokines
in reactive thrombocytosis (RT) and clonal thrombocytosis (CT) to
identify a cytokine profile that might aid in the distinction of these
two disorders. METHODS: Serum levels of cytokines relevant to platelet
biology--interleukins 3, 6, 11, and 1beta; thrombopoietin; tumor
necrosis factor alpha; and C-reactive protein (CRP)--were measured by
enzyme-linked immunosorbent assay in healthy subjects and in patients
with CT and RT. RESULTS: Interleukin-6 and CRP levels were higher in RT
patients than in controls or CT patients. Interleukin 1beta levels were
higher in the RT group than in the CT and control groups. CONCLUSIONS:
In RT, IL-6, IL-1beta, and CRP levels are elevated. In both RT and CT,
IL-11 is elevated, but thrombopoietin levels are not.
12
UI - 12195834
AU - Alexandrakis MG; Passam FH; Perisinakis K; Ganotakis E; Margantinis G;
TI -
Kyriakou DS; Bouros D
Serum proinflammatory cytokines and its relationship to clinical
parameters in lung cancer patients with reactive thrombocytosis.
SO - Respir Med 2002 Aug;96(8):553-8
AD - Department of Haematology, Medical School University of Crete,
University Hospital of Heraklion, Crete, Greece.
Proinflammatory cytokines Interleukin-1 beta (IL-1 beta) and
Interleukin-6 (IL-6) play a significant role in the pathogenetic
processes related to various malignant and inflammatory conditions.
Leukocytosis, thrombocytosis and increased acute phase protein levels
are part of a systemic inflammatory response. In this study, we measured
the concentrations of IL-1 beta, IL-6 and ferritin as well as
hemoglobin, lactate dehydrogenase (LDH), C-reactive protein (CRP) and
erythrocyte sedimentation rate (ESR) in 23 patients (male 15, female 8,
median age 68 years) with lung cancer and reactive thrombocytosis
(LCRT), in 27 (male 18, female 9, median age 64 years) with benign
inflammatory lung disorder (BILD) and 18 (male 10, female 8, median age
62 years) lung cancer patients with a normal platelet count (LCNP). IL-1
beta levels were significantly higher in the three patient groups in
comparison with control subjects (P < 0.001) but without significant
difference among the three patient groups. IL-6 was higher in all three
patients groups but only in the BILD group it was significantly higher
than the control group (P < 0.05). However, no significant difference in
IL-6 serum levels was found between the two lung cancer groups. CRP and
LDH were significantly higher in the LCRT group in comparison with the
other two patient groups (P < 0.01 and 0.001, respectively), while
ferritin was higher in both lung cancer groups in comparison with the
BILD group (P < 0.001). Our data suggest that in lung cancer patients,
reactive thrombocytosis is part of the systemic inflammatory reaction
for which IL-1 beta and IL-6 may be intermediate but not independent
mediators.
13
UI - 12352397
AU - O'Keefe SC; Marshall FF; Issa MM; Harmon MP; Petros JA
TI -
Thrombocytosis is associated with a significant increase in the cancer
specific death rate after radical nephrectomy.
SO - J Urol 2002 Oct;168(4 Pt 1):1378-80
AD - Department of Urology, Emory University School of Medicine, Emory
Winship Cancer Cener and Atlanta Veterans Affairs Medical Center,
Georgia, USA.
PURPOSE: We have previously reported that patients with advanced renal
cell carcinoma and a normal platelet count of 400,000/mm. have a 64%
increase in life expectancy compared with those with thrombocytosis. We
determined whether thrombocytosis was predictive of death from renal
cell carcinoma after radical nephrectomy was performed with curative
intent for early stage disease. MATERIALS AND METHODS: We reviewed the
records of 204 patients with renal cell carcinoma who underwent radical
Emory University Hospital. Survival, pathological grade and stage were
recorded from the Emory Winship Cancer Institute tumor registry.
Platelet counts were recorded and any patient with at least 1 platelet
count of greater than 400,000/mm. was classified with thrombocytosis.
Those with a platelet count of 400,000/mm. were classified with a normal
platelet count. RESULTS: There were 26 patients with thrombocytosis and
178 patients with persistently normal platelet counts. The overall and
cancer specific death rate in the 26 patients with thrombocytosis was
50% and 42%, respectively. The overall mean time between nephrectomy and
death was 12.1 months in this group. The overall and cancer specific
death rate in the 178 patients with a normal platelet count was 15.2%
and 7.3%, respectively. Mean time to death was 22.6 months in this
group. Differences in the overall and cancer specific death rates were
highly statistically significant as well as clinically significant.
These differences remained significant after controlling for grade,
stage and histological type of cancer. CONCLUSIONS: This study documents
the association of thrombocytosis with decreased survival in patients
with renal cell carcinoma. In those who undergo nephrectomy for early
stage renal cell carcinoma with a perioperative platelet count of
greater than 400,000/mm. the cancer specific death rate from renal cell
carcinoma is greater than 5 times the rate in patients with a
persistently normal platelet counts after radical nephrectomy. The
platelet count appears to be a new and powerful independent
prognosticator in patients with renal cell carcinoma who undergo radical
nephrectomy for presumed localized disease.
14
UI - 11962756
AU - Thiele J; Kvasnicka HM
TI -
CD34+ stem cells in chronic myeloproliferative disorders.
SO - Histol Histopathol 2002 Apr;17(2):507-21
AD - Institute of Pathology, University of Cologne, Germany.
j.thiele@uni-koeln.de
Contrasting the wealth of information that is available about various
biological and therapeutic aspects of human CD34+ stem cells, little
data exist concerning their quantity and dynamics as well as their
mutual relationships with other hematopoietic constituents in the bone
marrow of patients with chronic myeloproliferative disorders. In
comparison with a control group frequency of progenitors is
significantly increased in chronic myeloid leukemia (CML). Following
different therapeutic modalities their quantity reflects therapeutic
efficacy (responder and non-responder patients) and therefore exerts a
predictive value regarding acceleration and blastic crisis. The
significant correlations between fiber content and number of these
precursors elucidates the complex interactions between stroma and
progenitor cell differentiation and maturation. Following allogeneic
bone marrow transplantation there is a rapid recovery of the CD34+ stem
cell population in the first month. A higher number of these cells is
related with graft size, an earlier independence for platelet
transfusion and a more extended regeneration of erythro- and
megakaryopoiesis. The slight increase in reticulin fibers in these
patients may be associated with the complex and so far ill-defined
pathomechanism of homing (adherence to the fibrous matrix). In
idiopathic myelofibrosis (IMF) an increased number of CD34+ stem cells
is found predominantly in the early (prefibrotic or mild fibrotic)
hypercellular stages and probably indicates a higher proliferative
activity of the precursor cell pool. According to sequential biopsies
most patients with early IMF that later evolved into an overt
fibrosclerotic stage usually display a reduction of progenitor cells
during the development of myelofibrosis. The unequal distribution of
CD34+ stem cells in the bone marrow versus spleen in IMF (advanced
fibrosclerotic stage) is in support of the currently discussed
hypothesis of splenic filtration and concentration of precursor cells as
an essential feature of myeloid metaplasia. Regarding prognosis in CML a
higher amount of CD34+ stem cells is significantly associated with an
unfavorable survival and thus confirms the assumed implication of an
accelerated phase of disease at onset. On the other hand, in
polycythemia vera (PV) and IMF a low number of progenitors is probably
due to a decreased proliferation rate (reduced hematopoietic turnover
index) and therefore reflects a reduction in the regenerative capacity
of hematopoiesis. For this reason, a presumptive defect in the recovery
of normal and clonally transformed stem cells is speculated to add to
the worsening of prognosis by causing the well-known bone marrow
insufficiency in terminal stage PV and IMF.
15
UI - 12357360
AU - Bernasconi P; Boni M; Cavigliano PM; Calatroni S; Brusamolino E;
TI -
Passamonti F; Volpe G; Pistorio A; Giardini I; Rocca B; Caresana M;
Lazzarino M; Bernasconi C
Acute myeloid leukemia (AML) having evolved from essential
thrombocythemia (ET): distinctive chromosome abnormalities in patients
treated with pipobroman or hydroxyurea.
SO - Leukemia 2002 Oct;16(10):2078-83
AD - Department of Blood, Heart and Lung Medical Sciences of the University
of Pavia and Division of Hematology, Policlinico San Matteo IRCCS,
Italy.
ET is a chronic myeloproliferative disorder rarely evolving into AML,
sometimes preceded by a myelodysplastic syndrome (MDS). Such
transformations mostly occur in patients treated with radiophosphorous
((32)P) or alkylating agents, especially busulfan. Recently, concern has
also arisen about the long-term safety of hydroxyurea (HU). Pipobroman
(PI), a well tolerated and simple to use drug, constitutes a valid
alternative to those cytoreductive treatments. The present study reports
on 155 ET patients treated at our institution from 1985 to 1995, and
achieved with PI as the only treatment in 106 patients and with HU in 23
patients. Twenty-six patients received no treatment. After a median
follow-up of 104 months, seven patients (four treated with HU, and three
with PI) developed AML whereas one patient treated with PI developed
MDS. A significant difference in progression-free survival was observed
between HU- and PI-treated patients (P = 0.004). A short-arm deletion of
chromosome 17 was most frequently detected in HU-treated patients, while
a long-arm trisomy of chromosome 1 and a monosomy 7q were seen in
PI-treated patients. No TP53 mutation was discovered in the six patients
studied (two HU-treated and four PI-treated). We conclude that these
cytogenetic abnormalities are not linked to the natural history of the
disease, but rather that they might be induced by the cytoreductive
treatment.
16
UI - 6211399
AU - Smith IL; Martin TJ
TI -
Platelet thromboxane synthesis and release reactions in
myeloproliferative disorders.
SO - Haemostasis 1982;11(2):119-27
A group of patients with myeloproliferative disorders was studies with
respect to platelet aggregation responses, release of
beta-thromboglobulin and incorporated 5-hydroxy-tryptamine, and
synthesis of thromboxane b 2. In all patients the resting plasma
beta-thrombo-globulin was elevated. Aggregation responses were
frequently impaired to adrenaline, arachidonic acid, A23187 and the
prostaglandin endoperoxide analogue, U44069. Both 5-hydroxy-tryptamine
and beta-thromboglobulin release were greater with patients' platelets
than with those of controls in response to adrenaline, ADP and U44069.
The patients' platelets produced more thromboxane B2 than did controls,
irrespective of the agonist used, yet those aggregating agents which are
thought to act by generating thromboxane A2 were relatively ineffective
in causing aggregation. This might reflect resistance to thromboxane A2
action in these patients, which is met by increased thromboxane
formation.
17
UI - 1773983
AU - Mazzucconi MG; Ferrari A; Solinas S; Vitale A; Chistolini A; Federici
TI -
AB; Mandelli F
Studies of von Willebrand factor in essential thrombocythemia patients
treated with alpha-2b recombinant interferon.
SO - Haemostasis 1991;21(3):135-40
AD - Department of Human Biopathology, University La Sapienza, Rome, Italy.
The crucial role of the von Willebrand Factor (vWF) and its interaction
with platelets in myeloproliferative disorders (MPD) have emerged in
recent years. Recently, many authors have reported the therapeutical
efficacy of interferon (IFN) in MPD with thrombocytosis in decreasing
platelet number. The purpose of our report is to study the modifications
of vWF in a series of 20 patients affected by essential thrombocythemia
(ET) or MPD with thrombocytosis, treated with alpha 2b recombinant IFN
(alpha 2b-rIFN). Patients were studied before treatment and after
complete or partial response: vWF-related properties, bleeding time (BT)
and ristocetin-induced platelet aggregation (RIPA) were evaluated.
Before treatment, we found prolonged BT in 5 patients (25%), abnormal
RIPA in 8 (40%), reduced factor VIII coagulant activity (VIII:C) in 2
(10%), reduced vWF-related antigen (vWF:Ag) in 5 (25%) and low
vWF:ristocetin cofactor (vWF:Ricof) in 5 (25%). Twelve subjects were
evaluated after hematologic remission: in all patients, BT, VIII:C,
vWF:Ag and vWF:Ricof were within normal range or upper normal limits.
RIPA was abnormal in 7 subjects. Multimer patterns of vWF were performed
in 3 patients before and after treatment: 2 of them showed loss of
high-molecular-weight multimers that seemed to recover at remission. IFN
seems to induce improvement of platelet number and their functions in
MPD with thrombocytosis.
18
UI - 8738590
AU - Bazzan M; Vaccarino A; Stella S; Foli C; Omede P; Gallone G; Tamponi G;
TI -
Pileri A
Procoagulant activity of mononuclear cells is increased in
myeloproliferative and myelodysplastic diseases.
SO - Haemostasis 1996 May-Jun;26(3):157-63
AD - Dipartimento di Medicina ed Oncologia Sperimentale, Universita degli
Studi di Torino, Ospedale Molinette, Italia.
Procoagulant activity (PCA) of peripheral mononuclear cells (PMC) was
evaluated in patients with primary thrombocythemia (PT, group A),
polycythemia vera (PV), idiopathic myelofibrosis (IM) and
myelodysplastic syndromes (group B), and in 15 healthy subjects as
control group. PCA of PMC was assayed under basal conditions and after
agonist-induced stimulation: bacterial lipopolysaccharide, glycosylated
granulocyte-macrophage colony-stimulating factor, recombinant
alpha-interferon. PCA was similar in the control group and group A when
no stimulation was used, while PCA was found significantly higher in
group B patients in the same conditions. In group A patients and in the
control group, but not in group B patients, a lower PCA expression was
found when PMC were simultaneously coincubated with LPS and
alpha-interferon with respect to LPS incubation alone.
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