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EDITORIAL
Chromosomes
By
D
to
W.
FREDERICK
ISTURBANCES
of the
occur
in
and
GUNZ
mitotic
leukemia,
abnormal
mitoses
and polyploid
ments
in favor
of the neoplastic
tion
of the
human
development,
ment
diploid
by
Tjio
number
stituted
as
turn
to
Levan,’
46-and
at
impressive
of
of
methods,
and
cases
there
of
although
not
necessarily
leukemia
their
on
will
readily
and
following
solutions
under
ordinary
glutinin
( PHA
of causing
small
much
larger,
yet no
)
may
seen
be
present
tures
in
good
some
blood.
of
without
PHA,
difficult;
the
Submitted
the
as
there
are
the
of
B.E.C.C.
July
with
of
short-term
the
myelocytes
as
and
treatment
they
cytogenetic
findings,
cultures
in
are
of
chronic
transferred
with
obtained
in
to
coichicine
which
the
in-
blood
no mitoses
do lymphocytes
only
derived
normal
of
of marrow
and
Cytogenetics
mitoses.
accepted
to
from
in
findings
may
each
line
Hospital,
Sept.
such
so
the
or
Not
either
leukemic
alternatively
cells.
leukemic
1-
cul-
lines.
be
or
blood
are
cells,
for publication
in
which
mitoses
in
cell
divide;
come
ChrLrtchurch
any
have
lymphocytes
lymphocytes,
obtained
cultures
PHA,
This
there
to
quantity
be
the
which
normal
have
leukemic
Unit,
of
from
in
normal
may
for
suggested
to leukemic
failed
may
cells
interpretation
normal
or
occurring
from
effect
lately
as belonging
mitoses
is true
an
addition
cells
mitoses
are
leukemic
30, 1963;
the
leukemias-having
normal
same
in
Some
important
soon
are
leukemic
interpreted
acute
of
mixtures
From
as
preparations
Abnormal
them
apparently
divisions
by
more
at first
culture
from
be
in many
though
tam
either
however,
all
led
circumstances.
The
addition,
however,
of a phytohemagextracted
from
Canadian
red beans
has the surprising
effect
“mature”
lymphocytes
in culture
to become
transformed
to
reasonably
cells-as
and
leukemias.
studied
the
the
of the normal
decades-con-
biology
the
can be identified.
In cultured
normal
granulocytes
do not divide
and neither
derived
infrequently,
because
been
such
divide
basis.#{176}
blood
is cultured
the
may
in
in
on
until
establish-
colleagues2
taught
for
immature,
mitotically
active
cells,35
clear
explanation,
although
it has
been
immunologic
When
leukemic
an
one of the arguaccurate
examina-
subsequent
seen
known
existence
possible
The
now
opinion
been
the
interpretations.
leukemia
hypotonic
and
however,
been
used
in this work
consisted
and of blood.
Immature
cells
dividual
chromosomes
occur
because
mature
years
chromosomes
by
of
medium,
is as
has
have
an
and
was,
technics.
the
is a consensus
many
forms,
forms
has furnished
of the disease.
No
as
of
granulocytic
artificial
for
acute
and by Ford
and
his
not 48, as had
been
examination
hundreds
the
new
a volte-face
a detailed
The
technics
bone
marrow
ago,
FIrZGERALD
have
in
complement
7 years
and
process
cell
nature
chromosome
some
P. H.
AND
especially
ot
Leukemia
2-day
cultures
likewise
is
apt
capable
of
Christchurch,
Al-
cultures
New
to
often
con-
mitotic
Zealand.
17, 1963.
394
Bi.ooi:.
Voi..
23. No.
3
(
NiAllell
1, 1964
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
AND
(:HHOMOSOMES
division.
Moreover
all
malities,
if found,
may
ditions.
This
but
commended
itself
The
cultures
be
have
artifacts
the
disadvantage
induced
by
that
the
mitotic
artificial
abnor-
growing
con-
disadvantage
can
be overcome
by examining
the
mitoses
in
preparations
of marrow,
a method
technically
more
difficult
than
which,
because
of its relative
freedom
from
artifacts,
has lately
uncultured
culture
395
LEUKEMIA
to increasing
principal
agreed
numbers
results
of
of workers
in the
cytogenetic
field.
studies
in
leukemia
are
as
follows:
In
tile
acute
as
forms
consisting
nlahties
structure.
These
tion
and
other
are
found
in
It
Ilas
is
few
may
may
differ
chronic
affairs.
Here
an
by
chromosome,
normal
chromosome
it
was
chronic
be
fore
Tile
Ph’
or
in
been
toms
of
tile
the
in
a
in
well
has
entirely
the
disease.
acute
leukemia
for
before
over
abnormal
this
state
consists
one
small
of
classification,
tile city
per
been
cent
than
in
CGL.
condition.
in
of
found
It
of full
reported
of whom
of
the
acro-
the abwhich
all
cases
may
there-
Ph’
cells
clinical
resembling
chromosome
in
seemingly
Occasionally
development
been
all
fathers,
It
70
yet
other
the
has
different
segment
not
condition
Y chromosome,
and
in their
infants,
a
and
specific
An
an
is found.la16
in the
Denver
after
Philadelphia,
present
marrow
leiikemia.2#{176}
be
to
mongol
termed
found
is
translocation-of
abnormal
any
of
of
estab-
of aneuploidy.
abnormality
is
ap-
once
course
types
differmost
The
being
However,
the
various
there
leukemia17’#{176}
provisionally
have
lieved
or
granulocytic
people
degree
probably
No. 21
being
termed
Ph’
discovered.
normal
tile
incidence;
technic.
variable,
case.
as
translocaabnormalities
there
is a lower
by matters
of
throughout
leukemia
constant
such
deletion,
extremely
well
as
abnormalities
series7#{176} chromosome
each
abnor-
)
polyploidy
mitotic
are
that
chromosome
chromosome
in
present
in the
deletion
centric
some
unique
suggested”
almost
by
abnormalities
granulocytic
loss-either
of
tile
extent
by
and
In
of
( aneuploidy,
in others103
for mainly
constantly
to some
In
failure,
exceptions,
been
incidence
produced
change.
that
be
recently
probably
of
high
in number
all cases,
accounted
with
they
lisiled
types
nearly
feature
parently,
is a very
spindle
probably
are
striking
are
and
non-disjunction
ences
there
of alterations
Ph1,
recently21
in
were
without
sympbut
be-
two
male
signs
of
leukemia.
Ill
chronic
great
lymphocytic
majority
unaffected
members
ilerited
are
leukemia
of cases,
of
abnormal
small
This
missing.
but
no
two
abnormalities
siblings
the same
acrocentric
chromosome
with
have
the
family,
have
chromosome
is also
been
from
probably
been
disease,
No.
found
as well
shown
which
and
21,
in
as
the
several
to have
an inthe short
arms
has
been
called
Ch1.22
These
are
some
of chromosome
has
been
The
Ford’s23
of
considered
chief
findings.
to the
recently
possibilities
words,
the
abnormalities
are
he
by
essentially
primary
and
What
onset
Ford23
three:
causal,
is their
of leukemia
and
The
meaning?
The
and
malignancies
other
relation
Hauschka.24
chromosome
secondary
hut
changes
contributory,
may,
or
in
ir-
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396
GUNZ
relevant.
Taking
the
changes
arising
more
last
possibility
or
epiphenomena25
of
further
in the
development.
acute
leukemias
abnormalities
are
persist,
kemia,
often
unchanged,
with
its constant
cannot
apply.
Should
changes
causative
tions
have
esses,
and
should
not
be
to lead
at
times
age.
tions
in
this
Ph’
all
will
necessarily
shown
cases
to
blood,26
the
leukopoietic
to
incidence
nearly
( Ph1
which
)
that
this
of
one
family,
the
No.
only
to other
One
Ch’
higher
chromosome,
appears
to
may
one
loci.
example
this
may
associations:
of
the
chromosomal
leuthat
chromosome
an
etiologic
not
mean
factor
has
the
lymphocytes
also
be
been
of
the
case
of
chromo-
persistence
to
in
peculiar
so,
it
might
most
to
of
a gene
The
there
could
be
imbalance,
that
or
in mongolism,
been
suggested
regulating
also
be
changes
and
granulocytic
or
the
that
is
at
leukemia.
chronic
genes
other
which,
lymphocytic
mutations
anto
a leukemia
abnormality,
both
most
is char-
have
population.28
in
from
is
clearly
appear
instances,
and
is reduplicated
condition,
it has
result
be
leukemia
therefore
which
mongols
chronic
abnormal
locus
then
in
and
inherited
predispose
the
exposure
does
and
general
leukemia
a preleukemic
be
follows
a mechanism
this,
an
is
would
Though
observed
may
the
21,
( Ch’ )
chromosome
the
than
chromosome
damaberra-
damage
in
this
known
tissues.
No.
times
are
this
as
from
aberrations
granulocytic
exposure,
and
Chromosome
is mongolism:
the
submicroscopic
of simple
radiation
result
chromosome
called
these
result
abnormalities
20
Leukemia
it
as
Mutaproc-
chromosome
although
However,
may
either
chromosome
are congenital
in origin
and
is so in at least
two
conditions
of
21
the
that
marrow.
to
chronic
radiation
after
after
and
leuclearly
regarded
instance,
is suspected
chromosome
and lymphocytic
might
also be
poiesis.22’29
at
the
former
This
that
radiation,
years
lymphocytes
trisomy
presence
in
of
leukemia.
by
Since
that
when
suggested26
inapplicable
when
the
the disease.
least
been
between
acterized
for
it has
in
and
predispose
to postulating
of leukemia
chromosome.
or
onset
chromosome
produces
radiation
Ph’
months
cells
relation
obvious
tedate
the
for
and
cells27
The
in which
show
aberrations
these
the
CGL
persist
the
some
of
disease
for the
charac-
granulocytic
suggestion
refers
also
by
clinical
then
for
is probably
caused
the
in leukemogenesis?
to initiate
malignant
grosser
radiation
abnormality
as is readily
tile
radiations,
It may
therefore
be significant
of the forms
known
to occur
such
that
and
only
a short
step
in the
causation
its characteristic
be
event
years
the
of
mean
leukemia,
explanation
lines
with
chronic
the
used,
why
Ionizing
leukemia,
It is therefore
are involved
breakage
it.
at
apparatus
commonly
the
origination
present
causative
for many
reason
in
the
of
an unlikely
distinct
cell
FITZGERALD
would
course
its course;
in
Ph1 chromosome,
as
is no
“irrelevant”
the
in
appears
in which
chromosome
included
to
in
constantly
term,
there
to radiation.
kemia
is one
almost
the
a beginning,
either
This
with
the
been
thought
though
changes,
consequence
throughout
and uniform
or associated
of course
“point”
as
accidentally
or in its
findings
teristic
no
less
AND
leuko-
other
a wider
changes
explanation
in
imbalance
No.
21
however
are
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CHROMOSOMES
AND
produced
might
associations
and
predispose
observed
ieukemia293’
stable
and
and
could
a
be
may
kemias
well
normal
and
the
that
J
tile
for
Such
rather
be
an
Ph1
many
of
which
chromosome
as
it occurs
in
the
in
be
as important
to
demonstrate
to
ask
that
the
may
be
of
as
be
in
21
In
no
other
may
to
type
Ph1
regard
most
chromosome
other
on
development
Whatever
some
aberrations
form
excellent
be
of tile
the
in
markers
this
be
type
penultimate
evidence
the
may
may
point
in leukemogenesis,
the
and
of
indirect
in
of
probably
only
evidence,
it
erythroid
cells
and
and
apparent
specito
type
step
which
position
abnormality;
cells,
the
of
in
suggestion
leukemia.
the
It
production
is neither
when
In
de-
correspond
causative
is accumulating18’29’4’
leukemia.
of
the
acquired.
Ch’
cause
superadded
of
one
for
three
acute
leukemia,
submicroscopic
essential
The
cogent
in
that
this
a step
for
and
chromosome
to
one
necessary
present
incidence
it.
and
adduced
connection
given
changes
cause
has
strength
of
animal
the
terms
mutations
that
acute
“blastic”
of
Burch’s
necessary
for
thesis,
the
full
disease.
precise
and
final;
may
the
only
proliferation,
changes
only
has
in other
and
somatic
related
chromosomal
initiation
changes
this
the
causally
as
as
acquired
leukemia
it
cases,
occurs
may
be
leukemic
of
in
transformation
the
granulocytic
of
as
visible
an
to
than
inherited
trisomy
leulocus
chromosome
stage
abnormalities,
it be forgotten
as grossly
but
abnormality
nor,
of
many
unknown
experimental
rather
mutations
may
( although
series
preferable
itself
mother
pleomorphism
Burch39
four
is certainly
hematopoietic
cllrOflic
a specific
by
unin
alterations
if these
.
in
an
Ph1-positive
in
an
leads
in some
a
directly.
This
granulocytic
as
has lately
been
surmised
that
it may
also be
perhaps
in megakarocytes’#{176}”#{176} ) Its very
high
ficity
same
and
instability
the
change
astonishing
leukemia
one
alterations
is of interest.
the
oversimplification.
as
impossible
the
other
to
have
in
this
carcinogenesis,
the first of these,
and acquired
be next in sucil a series;
nor should
l)ut
to
encourage
well
of
postulating
may
to
naive
of
that
in turn
as
to
mutations
genetic
thus
us
acquired,
general,
may
leukemia,
of leukemia
visible
the
or
eventually
concept
may
velopment
in
changes
development
two-stage
reasons
by
of
inherited
division
such
is perhaps
promotion,
point
Such
parent;
found
the
non-disjunction
offspring.
in the
recently
mechanism
in acute
further
classical
of
the
leading
abnormalities
merely
in the
to leukemia
was
cell
thus
leukemias.38
defects
may
causing
to leukemia
either
that
chromosomes,
congenital
leukemia32
chromosomes
to lead
is a disturbance,
imbalance,
are
abnormalities
leukemia.
be
regulating
a concept
chromosome
major
and
parental
mongol
granulocytic
It
of such
sex
and
miscarriages
also
trisomic
chronic
leukemia
predisposing
expected
typical
favor
between
same
patient.32
Further,
the occurrence
in the
and
leukemia,33’3#{176} sex chromosome
abnormalities
the
and
In
cases
between
the
of
cells
several
multiple
condition
germinal
to leukemia.
in
than
mongolism
in
sibship
of mongolism
leukemia35’37
397
LEUKEMIA
relationship
the
onset
for
many
between
of
leukemia,
types
of
the
newly
there
is
study.
discovered
no
Thus
question
it
is
chromothat
possible,
these
by
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
398
(;UNZ
tracing
in the
locytic
leukemia
gain
a clear
course
of
blood
and
or
picture
new
may
insights
factors
as
by
comparing
by
cytogenetic
understanding
1.
1,
1956.
Ford,
C.
3.
4.
and
of
Carstairs,
K.:
cyte:
its
ity.
Lancet
The
Brecher,
in
blood.
H.,
of
G.,
13.
R.
Hale,
J.
and
Fitz-
induced
leucocytes.
15.
T.
T.,
S. :
Miwa,
The
constitution
of
T.,
ifl-ViV()
in
and
blood
Cancer
Fitzgerald,
F.
W.:
and
marrow
of acute
leukemia.
Res. 22:748,
1962.
P. H., Adams,
A., and Gunz,
Chromosome
studies
in
Baikie,
Inst.
C. :
27:
Chromosome
III.
Acute
J. Nat.
Ishihara,
Canccr
T.,
L.
Kikuchi,
H. : Chronlo-
chromosome
C.,
P.
A.,
tution
and
orders.
Fitzgerald,
Gunz,
and
chronic
A.,
len-
T.,
Cross-
Haushka,
T.
myelocytic
20:393,
P.
\V.:
H.,
S.:
constileukemia
nlyeloprohferative
Blood
A
ab-
chronlosonte
in chronic
G.,
\1.:
188:1165,
Ishihara,
and
of
F.
I.
myeloid
London
H.,
other
\l.,
I).
chromosome
in
A.
W.
Harnclen,
Tough,
Nature,
L.
human
lcukemia.
Brown,
E.,
specific
1960.
Sandberg,
in
Court
K.
Comparison
18.
studies
granulocytic
1960.
A.
white,
adult
acute
leukemia.
J. Nat.
Cancer
Inst.
In press,
1964.
Kinlough,
M. A., and Robson,
H. N.:
Study
of chromosomes
in human
len-
\I.
leukemia
leukeiuia
Crosswhite,
kaemia.
17.
Brit.
1962
minute
normality
Crosswhite,
L. H., and HauschT. S.: Chromosomal
dichotomy
in
McBride,
Cancer
P.
A.,
possible
1961.
Nat.
leukemia.
A.
678,
-,
\l.
Cytogenetic
1. Acute
hllfllan
29:545,
Jacobs,
-,
A.,
\l.:
A. : Chronlosonle
J.
Buckton,
marrow
Brit.
leukaemia.
leukenia
Sciencel32:1497,
16.
P.
acute
1961.
chronic
A. A., Ishihara,
Hauschka,
nlethod.
S)I)IaI
differences
amuong
the
acute
leukemias.
Proc. Am. A. Cancer
Res.
4:60,
1963.
NowelI,
P. C., and
Hungerford,
1). A.:
A
1963.
to the bettreatment.
I.
Nowell,
Sandberg,
Y.,
those
leukemias
1961.
Inst
1 4.
in
the
Jacobs,
granulocytic
1962.
of
Tough,
D.
Stu(lies
proliferacultured
R.,
C.,
and
and
-,
group
and
a direct
Hungerford,
983,
chemi-
1961.
A.
A.,
from 34 human
leukemias
and 80 nonleukemic
controls.
Cancer
Res.
21:
ka,
10.
cell
and
H.:
1:637,
chromosome
9.
Lycette,
Lancet
and
of
Brit.
Tuberculin
in peripheral
blood
P.
Jr.,
1963.
gerald,
mitosis
7. Sandherg,
8.
P.,
on the
leucocytes
by
in human
in children.
human
of
19:349,
Barkhan,
9:101,
12.
F.,
kinetics
study
studies
in
J. 1:1564,
qual-
phytohaenlagglutinin.
Pearmain,
Baikie,
of
and
blood
cells
2:1052,
J.
some
materially
as its successful
kaemia
J.
The
lympho-
Stohiman,
The
the
survival
of certain
or
contributing
as well
Lon-
small
cultures
Blood
human
Haemat.
6.
of
of leukemia,
the
normal
21.
to
in
recipients;4
control
in
granu-
leukemias,
produced
leukopenic
phosphatase,
FITZGERAL!)
in chronic
acute
are
genetic
or trisomy
promise
Nature,
C. : The
E.
with
the
1962.
A. A., Jr.,
tion
Ph’
the
pluripotential
J. : Observations
A.
in
concentrations
J. L.:
human
1:829,
Mackinney,
Cooper,
into
Ph’
in
experiments
followed
alkaline
holds
nature
man.
of the
remissions
1956.
possible
proliferation
peripheral
5.
be
their
Hamerton,
178:1020,
and
which
11.
E.,
chromosomes
don
by
neutrophil
like
fall
REFERENCES
Levan, A.: The chronlof man. Hereditas
42:
number
osome
2
obtained
of the
and
abnormalities
cross-transfusion
be
technics
J. H., and
Tjio,
by
can
abnormalities
ter
rise
means
cells
well
such
substances,
carrying
the
therapy;18”#{176}’42
leukemic
the
characteristic
of
homologous
cal
marrow
the
AND
dis-
1962.
Adams,
Chronic
A.,
granulocytic
and
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
CHROMOSOMES
AND
leukemia
and
19.
Tough,
the
Blood
chromosome.
I.
M.,
Brown,
\V
studies
on
myeloid
1963.
P.
s1.,
Baikie,
E.
R.
bone
1961.
Philadelphia
21 : 183,
Jacobs,
\Villiamson,
399
LEUKEMIA
A.,
A.
D. :
Miller,
Court
G.,
and
in
Kemp,
N.
ner,
cet
21.
H.,
33.
morphological
chromosome.
Lancet
delphia
1963.
22.
Cunz,
F.
\V.,
Adams,
in
chronic
Brit.
Ford,
24.
Hauschka,
C.
lymphocytic
rev.
franc.
T.
ontogeny
and
21:957,
1961.
Bayreuther,
don
K.
E.,
P.
spondylitis.
Lancet
Fitzgerald,
P.
role
and
pri-
LonCourt
sex
38.
J.
A
29.
Brit.
Tough,
M.
(len,
A.
D.
C.,
C.,
and
Buckton,
Jacobs,
acute
26,
31.
Kemp,
ner,
myeloid
In
I).:
for
M.,
1:411,
Lapidus,
P.
S.: Acute
syndrome.
R.
Klinefelter’s
H.,
K.:
Frci
III,
its
converse:
with
1961.
42.
leukaemia
Stafford,
J. L., and
Acute
syndrome.
leukaemia
L:incet
Brown,
Adams,
W.
ity
in
2:
Tanand
2:434,
XI.,
D. C.:
and
a case
of
in
2:1003,
the
1961.
changes
Mole,
in pri-
reticular
neo-
J. Cell. & Comp.
1 ), 235,
1958.
biological
principle
implications
J. H.,
London
distribution
chromosome
chronic
and
Sc.
J., and
\Vhang,
P. : Tissue
Conf.
A.,
F.
W.
Nature,
Tjio,
P.
with
pa-
myelogenous
on
In press,
len-
Leukopoiesis
Disease.
Fitzgerald,
of
in
Ann.
in
New
York
1964.
P.
: A new
chromosome
chronic
granulocytic
H.,
and
Gunz,
abnormalleukaemia.
J. 2:1474,
1961.
Tough,
I. NI., Court
Brown,
\V. XI.,
Baikie,
A. C., Buckton,
K. E., Hamden, D. C., Jacobs,
P. A., and %Vilhams,
J. A.: Chronic
myeloid
leuBrit.
Abbot,
Lancet
Canad.
Harnden,
some
Philadelphia
Acad.
41.
leukaemia
Lit-
mongo-
1962.
Health
XI.
Cytogenetic
H.,
and
J. L., and
( suppl.
J.: A
R.
E.,
tients
and
females.
abnormality
P.
kemia.
1961.
N.
40.
Ham-
King,
male
R. E.,
Hamerton,
Carbone,
\V.
E.,
mal-
21-trisomic
carcinogenesis.
the
associated
Lancet
J. A., and Roath,
and Klinefelter’s
A.,
J. A.:
leukaemia
P.,
Mamunes,
K.
P.
McBride,
mongolism.
:30.
1958.
Brown,
in chronic
studies
and
and
malignancies.
1:1495,
M., Court
Bell,
Lancet
E.,
52
Burch,
small
Hewitt,
childhood
J.
I.
Baikie,
J., and
Webb,
of
childhood
R. \V. : Chromosomal
mary
and transplanted
plasms
of the mouse.
39.
Biol.
of
1961.
sibship.
C.
195:241,
A.,
survey
J.,
Theoret.
sibship.
mongoloid
chromosome
Ford,
1963.
Stewart,
A. S.:
Physiol.
of
same
Baikie,
A. G., Court
Buckton,
K. E., and
Two cases
of leukaemia
1962.
life-span
the
coexistent
with leukemia.
XI. A. J. 88:893,
1963.
37.
immunological
The
long
lymphocytes.
press,
28.
2:676,
H. :
Baikie,
Mongolism
lisfll
Res.
A.,
C.,
E.:
leukaemic
Familial
Brown,
W. M., and Doll, R.: A study
of the chromosome
damage
persisting
after
X-ray
therapy
for ankylosing
27.
2:78,
same
Jacobs,
male,
2 1-trisomic
tie,
in
in
in
Aetiology
XI. W.,
1961.
Nature,
D.
G.
congenitally
Lancet
leuc#{233}mie.
Cancer
len-
1961.
Thompson,
1960.
186:6,
Buckton,
two
chromosomes
growth.
A.:
xxxxY
and
36.
Chromosomes
neoplastic
35.
of
J. Med.
determined
leukaemias.
Bnt.
M. J. 1:452,
1961.
Miller,
0. J., Breg,
W. R., Schmickel,
R. D., and Tretter,
W. : Family
with
leukaemia.
oncogeny.
K. :
mary
H.,
h#{233}mat. 1:165,
S. : The
Harnden,
ignancies:
1962.
et
E.,
1:171,
Stewart,
chromosome
E. : Chromosomes
Nouv.
26.
P.
abnormal
J. 2:1097,
M.
2:3.
25
Fitzgerald,
A. : An
K.
Lancet
Phila1:558,
sibs
England
1963.
Buckton,
Lan-
( mongo-
syndrome
malforma-
among
New
Tan-
34.
B.: I)own’s
) with
a
lisnl
and
leukaemias.
cancers
A. C., and Woods,
and leukaenlia
1963.
2:95,
Hall,
of
( moi-
syndrome
congenital
children.
268:393,
1:844,
J. L.,
Stafford,
R. : Aetiology
other
and
kemic
1963.
20.
W. : Down’s
),
tions
chronic
Lancet
R.
golisnl
Cytogenctic
marrow
leukaemia.
32.
XI.
kaemia:
and
cytogenetic
after
splenic
studies
irradiation.
before
Lancet
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
400
43.
CUNZ
2:115,
Freireich,
R.
1962.
E. J., Carbone,
H.,
of
W.:
transfused
Frederick
terbury
P.
J.,
Whang,
Bronson,
H.
Unit,
leukocytes
W.
E.
function
Gunz,
Hospital
Fitzgerald,
Christchurch
E.,
and
and
fate
from
donors
M.D.,
Board,
FITZGERALD
with
chronic
myelocytic
leukemia
in
leucopenic
recipients.
Conf. on Leukopoiesis
in Health
and Disease.
Ann.
New
York Acad.
Sc. In press,
1964.
P. P., Levin,
Morse,
The
AND
Ph.D.,
Haematolo
Christchurch
New
Zealand
M.Sc.,
Hospital,
Associate
Hospital,
gist,
North
Chrietchurch,
Director,
Christchurch,
Cytogenetics
New
Zealand
Can-
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
1964 23: 394-400
Editorial: Chromosomes and Leukemia
FREDERICK W. GUNZ and P. H. FITZGERALD
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