Table of Contents
1
UI - 11843834
AU - Matsubara K; Baba K; Nigami H; Harigaya H; Ishiguro A; Kato T; Miyazaki
TI -
H
Early elevation of serum thrombopoietin levels and subsequent
thrombocytosis in healthy preterm infants.
SO - Br J Haematol 2001 Dec;115(4):963-8
AD - Department of Paediatrics, Nishi-Kobe Medical Centre, 5-7-1 Kojidai,
Nishi-ku, Kobe 651-2273, Japan. kskmatsu@portnet.ne.jp
To verify pathophysiological mechanisms underlying thrombocytosis in
low-birth-weight (LBW) preterm babies, we evaluated kinetic changes in
platelet counts and thrombopoietic cytokines including thrombopoietin
(TPO), interleukin 6 (IL-6) and IL-11 in 24 uncomplicated preterm
infants. Platelet counts in cord blood (CB) (265 +/- 64 x 10(9)/l) were
similar to adult levels, increased by d 14 (473 +/- 140 x 10(9)/l), and
then remained fairly constant. Thrombocytosis (> 500 x 10(9)/l) was
observed in 9/24 (38%) subjects. Mean TPO level in CB was 5.11 +/- 1.51
fmol/ml, peaked at d 2 (7.64 +/- 3.28 fmol/ml), decreased at d 5 (3.93
+/- 1.67 fmol/ml), and thereafter kept fairly constant during the
remaining neonatal period. Compared with term infants, mean TPO levels
of preterm infants in CB and at d 2 were significantly higher (P <
0.01). There was an inverse correlation between platelet counts and TPO
levels (r = 0.45, P < 0.001, n = 88). Preterm neonates with
thrombocytosis had significantly higher TPO values in CB than those
without thrombocytosis (P < 0.05). There was no significant relationship
between platelet counts and IL-6. IL-11 was not detectable. These
results suggest that an early elevation of serum TPO levels is related
to the subsequent thrombocytosis in LBW preterm infants.
2
UI - 11808159
AU - Urabe A
TI -
[Polycythemia vera]
SO - Nippon Rinsho 2001 Nov;59 Suppl 7():498-503
AD - Division of Hematology, NTT Kanto Medical Center.
3
UI - 11872082
AU - Hirri HM; Green PJ
TI -
Skin lesion caused by hydroxyurea.
SO - Eur J Haematol 2001 Nov-Dec;67(5-6):328-9
4
UI - 11850996
AU - Gensini GF; Conti AA
TI -
[Association between hepatocellular carcinoma and polycythemia vera]
SO - Recenti Prog Med 2002 Jan;93(1):25-7
AD - Clinica Medica Generale e Cardiologia, Universita, Firenze.
g.gensini@dfc.unifi.it
The association of hepatocellular carcinoma (HCC) and polycythemia vera
in a middle-aged caucasian man is described for the first time in this
case report. The report underlines the necessity and the importance of a
full, evidence-based investigation of the nature of polyglobuly in the
course of HCC, a condition known to be associated to erythrocytosis, so
far usually considered secondary to HCC, and not primary.
5
UI - 11840268
AU - Marone M; Scambia G; Bonanno G; Rutella S; de Ritis D; Guidi F; Leone G;
TI -
Pierelli L
Transforming growth factor-beta1 transcriptionally activates CD34 and
prevents induced differentiation of TF-1 cells in the absence of any
cell-cycle effects.
SO - Leukemia 2002 Jan;16(1):94-105
AD - Dept of Gynecology, Catholic University, Rome Italy.
A number of cytokines modulate self-renewal and differentiation of
hematopoietic elements. Among these is transforming growth factor beta1
(TGF-beta1), which regulates cell cycle and differentiation of
hematopoietic cells, but has pleiotropic activities depending on the
state of responsiveness of the target cells. It has been previously
shown by us and other authors that TGF-beta1 maintains human CD34(+)
hematopoietic progenitors in an undifferentiated state, independently of
any cell cycle effects, and that depletion of TGF-beta1 triggers
differentiation accompanied by a decrease in CD34 antigen expression. In
the present work, we show that exogenous TGF-beta1 upregulates the human
CD34 antigen in the CD34(+) cell lines TF-1 and KG-1a, but not in the
more differentiated CD34(-) cell lines HL-60 and K-562. We further
studied this effect in the pluripotent erythroleukemia cell line TF-1.
Here, TGF-beta1 did not effect cell growth, but induced transcriptional
activation of full-length CD34 and prevented differentiation induced by
differentiating agents. This effect was associated with nuclear
translocation of Smad-2, activation of TAK-1, and with a dramatic
decrease in p38 phosphorylation. In other systems TGF-beta1 has been
shown to activate a TGF-beta-activated kinase 1 (TAK1), which in turn,
activates p38. The specific inhibitor of p38 phosphorylation, SB202190,
also increased CD34 RNA expression, indicating the existence of a link
between p-38 inhibition by TGF-beta1 and CD34 overexpression. Our data
demonstrate that TGF-beta1 transcriptionally activates CD34 and prevents
differentiation of TF-1 cells by acting independently through the Smad,
TAK1 and p38 pathways, and thus provide important clues for the
understanding of hematopoietic development and a potential tool to
modify response of hematopoietic cells to mitogens or differentiating
agents.
6
UI - 11786204
AU - Lema-Kisoka R; Hayez N; Langer I; Robberecht P; Sariban E; Delporte C
TI -
Characterization of functional VIP/PACAP receptors in the human
erythroleukemic HEL cell line.
SO - Peptides 2001 Dec;22(12):2155-62
AD - Department of Biochemistry and Nutrition, Faculty of Medicine,
Universite Libre de Bruxelles, Brussels, Belgium.
The presence of VIP/PACAP receptors was investigated on the human
erythroleukemic cell line HEL. Specific binding of [125I]-PACAP or
[125I]-VIP on HEL cells or membranes was very low and did not allow to
perform competition curves. At 37 degrees C PACAP transiently increased
cAMP levels in the presence of the non-specific phosphodiesterase
inhibitor IBMX, suggesting rapid desensitization. Kinetic studies
revealed that optimal conditions to measure the EC(50) of PACAP(1-27)
were 10 min at 20 degrees C. Under those conditions, PACAP-related
peptides increased cAMP levels with EC(50) in agreement with the
pharmacological profile of the VPAC(1) receptor subtype: PACAP = VIP >
[K(15), R(16,) L(27)]VIP(1-7)/GRF(8-27) = [R(16)]ChSn (two VPAC(1)
agonists) >> helodermin = secretin. RO 25-1553, a selective activator of
VPAC(2) receptor was inactive at 1 microM. Dose-response curves of
VPAC(1) agonist molecules (PACAP, VIP, [K(15), R(16),
L(27)]VIP(1-7)/GRF(8-27), [R(16)]ChSn) were shifted to the right by the
VPAC(1) receptor antagonist [AcHis(1), D-Phe(2), Lys(15),
Leu(17)]VIP(3-7)/GRF(8-27), with a K(i) of 3 +/- 1 nM (n = 3). The
presence of VPAC(1) receptor mRNA was confirmed by RT-PCR. Preincubation
with PACAP or PMA showed that VPAC(1) receptors underwent homologous and
heterologous desensitization.This study provides the first evidence for
the expression of functional VPAC(1) receptors undergoing rapid
desensitization in HEL cells.
7
UI - 11400658
AU - Bakkaloglu SA; Soylemezoglu O; Karadeniz C; Oguz A; Buyan N; Hasanoglu E
TI -
Pseudohyperkalemia due to reactive thrombocytosis in an infant with yolk
sac tumor.
SO - Pediatr Hematol Oncol 2001 Jun;18(4):303-5
AD - Department of Pediatric Nephrology, Gazi University Faculty of Medicine,
Ankara, Turkey. sevcan@med.gazi.edu.tr
8
UI - 11860444
AU - Allen AJ; Gale RE; Harrison CN; Machin SJ; Linch DC
TI -
Lack of pathogenic mutations in the 5'-untranslated region of the
thrombopoietin gene in patients with non-familial essential
thrombocythaemia.
SO - Eur J Haematol 2001 Oct;67(4):232-7
AD - Department of Haematology, University College London, London, UK.
Thrombopoietin (TPO) is thought to be the major physiological regulator
of thrombopoiesis, and, in general, circulating levels are inversely
proportional to megakaryocyte and platelet mass. However, normal or
elevated TPO levels are found in patients with essential
thrombocythaemia (ET) and the reason for this is not fully understood.
Recent studies have shown that four kindreds with hereditary
thrombocythaemia (HT) have point mutations in the 5'-untranslated region
(UTR) of the TPO gene which lead to increased TPO translation. In order
to determine whether similar mutations are present in apparently
acquired ET, in particular in those patients with polyclonal
myelopoiesis, we have studied this region in 50 ET patients using
neutrophil DNA. The known HT mutations were investigated using
polymerase chain reaction with mismatch primers and restriction enzyme
digestion; only wild-type alleles were detected. Single-stranded
conformation polymorphism (SSCP) analysis of exons 1-4 identified a
C-->T substitution at nucleotide 3767. However, this appears to be a
common polymorphism, as it was present at the same frequency in
haematologically normal controls and is unlikely to be of pathological
significance. These results demonstrate that mutations in the 5' UTR of
the TPO gene are not the cause of the normal or elevated TPO levels in
acquired ET.
9
UI - 11841424
AU - Spivak JL
TI -
The optimal management of polycythaemia vera.
SO - Br J Haematol 2002 Feb;116(2):243-54
AD - Division of Hematology, Johns Hopkins University School of Medicine,
Baltimore, MD, USA. jlspivak@mail.jhmi.edu
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