against. GP lIb/Illa. (CDw4l), one for GP lb (CDw42), and one for. GP lIla. Regarding the expression of myeboid markers on megakaryo- blasts, from our study,.
CORRESPONDENCE
1227
REFERENCES 1. Thiery Hematol
iP,
Bessis
2:167,
2.
Radley
Blood
JM,
56:996,
3.
M:
Mecanisme
Scurfield
G:
The
mechanism
RM,
Yee
M: Megakaryocyte
by whole
and
partially
ma:
model
4.
system
Haemostas Ihzumi
platelet
7.
the
study
of
platelet
H, Nett
release
from
ing
Blood
I: SEM
A, Sanada
M, Muto
iap
electron
40:305,
1977
T: Mechanism
liberation.
Tohuku
M: Studien
zur
thrombocytenbildung Acta
Hematol
x.
AV,
Morphologic
M, Damashek
characteristics
microscopy penic
Stefanini
in normal
purpura.
of megakaryocytes
and
Blood
W: Studies
in patients
8:703,
with
by phase
contrast
IMMUNOLOGIC
they
analyzed
blasts
and
the
the recent
expression
proposed
of
a model
in megakaryoblast
for
immunophenotype
of megakaryoblasts
27 of 240
with
which
a megakaryobbastic
studied
which
included
against GP
with
GP
four
lIb/Illa
specific
like
based
leukemia
other was
a panel
experience
than
lymphoblastic All
one
for GP
the with in
cases
were
antibodies
in
(GP):
two
glycoproteins lb (CDw42),
and
one
for
lIla. Regarding
blasts,
the
from
concluded
study,
and
this
lineage.
clear-cut
antigen
that
granulomonocytic labeling
not
in
are
and granulocytic
(CDI5)
Conflicting
two blast
results
et
27
negative
cases
although
for
there
results
specific
have
reported and
the
Proplatelets
all Res
and
stress
the
as
one
patient,
i15
population negative is not considered.
probably
(BI-3C5)
In one
the
these
In Koike’s
and
indicating These
reactivity
that
GP were
lacking
would
indicate
HLA-DR
marker
of cells,
a
cells
relatively
were the
almost
expression
by the megakaryo-
lIla
in
of the
blast
in a minority
of
with very early
mega-
HLA-DR
CD34
that
in the
cases,
(70%
expressed
dealing
cells
to
megakaryoblastic
lb were
which
at
of HLA-DR.
model
for GP
we were
the
number
point
pure
subse-
occasions
that
twice would
of our
lost
on some
precede
detected which
be
GP
and lIla
is acquired
megakaryoblasts
matura-
a
iF.
SAN
MIGUEL
double-
A. ORFAO
that
E. OJEDA
I 4)
M.C.
H LA-DR of its being
in
Nevertheless,
that
may
HLA-DR.
lIb/Illa
the
suggest
llb/IIa)
a high
antigens, than
in
capillaries
would
the first GP to be acquired
displayed
( I 5%),
which
of megakaryoblasts3;
lIla,
cells
megakaryocytes
pulmonary
is attractive.
bIb/lIla
for
blast,4
GP
lineage, et al,’
FMC25,
ofGP
while
of
in the
patients
(GP
with
cells)
and
1978
in this
ofGP
immature
earlier
21:36,
of our
completely
cells
in
Williams
Development
Occurrence
retention
by Koike
expression
compared
the
RF,
MEGAKARYOBLASTS
as proposed from
platestress
p 405
N:
their
that
in Levine
Megakaryocyte
1986,
Pederson and
Evidence by a physical
function,
(eds):
Liss,
EA:
circulation
M. GONZALEZ
(CD
regarding possibility
that
Thromb
CAN
Division
been
for a theory
implying
DG:
markers.
by megakaryoblasts,24
Evidence
express show
monocytic
Thromb
circulation.
cells,
specific
our
support-
tion.
was
positive
simultaneously
addition,
be
for the CDI 3
(CDw4I)
DN:
Trowbridge and
expressed
karyoblasts.4
it can
to the granulomon-
the
cells
megakaryoal,
negative
JI5
antigens, In
also
of
and
platelet
on
Koike
be restricted
(CDI3)
performed.
megakaryoblasts
expression
thus
individual and
was
markers to
are generally
would
of MY7
suggests
myeboid
according
Nevertheless,
overlap
which
of
and
that megakaryoblasts
antigen, ocytic
expression
our
Penington
DN,
BL
York,
IN
In our
on
on our detected.
Slater
pulmonary
J Haematol
antigen
least,
of markers
to comment
Evatt
vessels
results
megakaryo-
of 22 monocbonal
for platelet
(CDw4l),
on
of appearance
would
component
systematically
et al’ in which
markers
the order We
acute
by Koike
myeboid
maturation.
patients
paper
study lungs.
in the
1987
Slater
Tinggaard
quently,
interest
P.
in the
i,
Scand
first
with
microscope
pulmonary
development
MARKERS
To the Editor:
We read
iF,
New
various man.
OF
1984 megakaryocyte
The
megakaryocytes,
in the
Seth
produced
I 4.
thrombocyto-
1953
EXPRESSION
99:390, iF:
produced
iF, of
69:522,
Martin
Function.
on platelets
idiopathic
M,
Blood
Levin
N, Pisciotta
Martin
electron are
and
1982
megakaryocyte
I 7:160,
I 957 8.
EA,
produced
Tong
lets are
an Megakaryo-
knochenmarkkulturen.
platelets
human
1983
are
13.
in menschlichen
and
all
Biol
Martin
by
on fresh
J Exp
1975 Albrecht
studies
J Cell
fragmentation
platelets.
of platelet
that
physical
12.
Thrombocytopoiesis-analysis
EA,
A light
theory
28:461,
in mouse
5:
freeze-fracture
Trowbridge
I 1 . Trowbridge of
and
study
DN,
Res3l:163,
Thromb
M: Megakaryocyte
microscope
and
megakaryocytes.
Slater
the
observations
megakaryocytes.
Petursson
in thrombocytopenia:
plas-
formation.
mouse
10.
stimulated
thrombocytopenic
P. Bessler
A scanning
Histol
6. Murata I 16:67,
FD, turnover
platelets
T, Hattori
Arch
Zucker
cultured
1, 1979
formation:
cyten
for
of platelet
42:61
spleen.
release.
morphogenesis
fractionated
M, Fishman
mechanism
5.
of platelet
1987
Djaldetti
on the
9.
1980
Leven
69:1046,
Rev
membrane
in vitro A
de la plaquettegenese.
1956
University
the
IZO
of Hematology of Salamanca
Spain
REFERENCES 1. Koike
Imanaka
T,
Aoki
H, Adachi
5,
ing of megakaryoblasts. 2. sors:
D, Rose
Diverse
features
man
N, iM,
Miguel Zola
H,
Catovsky
iF,
69:957,
M, Greaves in four Tavares
McMichael D:
5,
Narita
H, Shibata
Blood
Bevan
3. San Poli
Maruyama
T, Maeda
of platelet
Br i Haematol Bollum
Characterization
T,
phenotyp-
granulocytic
leukaemia
undifferentiated
and terminal
Leukaemia
de Castro Ai,
Ishizuka
1987
M:
cases.
M,
A: Cell surface
J, Matutes Fi, of
5 1 : 147,
1982
E, Rodriguez
B,
Thompson
DS,
blast
in chronic
cells
4.
precur-
Gold-
Erber
transferase. WN,
DY: Detection
logical
malignancies
smears
with
a panel
II. Studies
acute with
Br i Haematol
Breton-Gorius
Mason
I987
in transformation,
leukaemia.
ofcells
i,
and
antibodies
59:297,
1985
iL,
Oscier
DG,
lineage
in haemato-
Villeval
of megakaryocyte
by immuno-alkaline of monoclonal
myelofibrosis
monocbonal
phosphatase antibodies.
labelling
Br i Haematol
Bai
Y, cell
65:87,
