E, Clayton. 5,. Karabyn. A,. Dalgleish. A, Gates .... Harbott. J, Engel. R, Gerein. V, Schwamborn. D, Rudolph. R,. Lampert. F: 1 1;l4 translocation in three boys with.
From bloodjournal.hematologylibrary.org by guest on July 10, 2011. For personal use only.
1987 70: 926-931
Cytogenetic studies on prolymphocytic leukemia. II. T cell prolymphocytic leukemia V Brito-Babapulle, M Pomfret, E Matutes and D Catovsky
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Blood (print ISSN 0006-4971, online ISSN 1528-0020), is published weekly by the American Society of Hematology, 2021 L St, NW, Suite 900, Washington DC 20036. Copyright 2011 by The American Society of Hematology; all rights reserved.
From bloodjournal.hematologylibrary.org by guest on July 10, 2011. For personal use only.
Cytogenetic
Studies H. T Cell
By Vasantha We
report
chromosome
prolymphocytic terized
by
clinical.
analysis.
The
inv(14)(ql
1 q32)
(TCR) had
gene
gene
translocations
for
8q
deletion
from
P
was
described characterized and
minimal
by
the
lymph
identification
blood
(PB)
form
of the disease
(T-PLL)
has
been
recognized
membrane
1q32)
acteristic
of T-PLL.
and a
a 1987
was
studies
phenotype,
cases
whereas
chronic
(ATLL),
lymphocytic
cases
react
irregular
prominent
philic
granules.3
ences
from also
the
this
nucleus,
single
has
leukemia
with
with These
may
show
mean
T-PLL
survival was
cases
studies.57
in
found
We of T-PLL,
of
l4ql
I to which
the
mapped,8
and
of 7q35
to which
the
two
of the
by
40
disease,
patients
reported
(ICR) five
gene
in
of
total patients;
Council
6, /986;
accepted
from
the
our
Unit,
requests
to
Daniel
May
23,
Address
reprint Unit,
London
W12
Royal
Postgraduate
OHS,
The publication charge payment.
is
“advertisement” indicate this fact. (C) 1987 by Grune
in
accordance
with
Fund
MRC
Leu-
DuCane
Rd.
were defrayed in part by page therefore be hereby marked 18
U.S.C.
§1734
& Stratton,
Inc.
during
peripheral
ofl-PLL
the
diagnosis
over
90%
1 ). This nos.
The
of
technique
had
a high
a prominent granules
(Fig
in all cases
4 and
May-
of cells
chromatin,
was confirmed
12
(COP,
namely,
devoid
(Fig
follow-up.
was poor overall. examination of
nuclear
of cases
in
chemotherapy
that
a cytoplasm
examination
for
showed
The
x 109/L)
the short of
in
patients.
48 to 50 x l09/L),
of prolymphocytes,’3
and
diagnosis
1,
by electron
was
particularly
7, small-cell
variant
of
T-PLL.3
Diagnostics,
solely
to
Westwood,
MA),
OKI6(CD1),
0K18(CD8)
(Orthoclone), OKI17,’#{176}3A1(CD7),” and anti-Tac (CD25) against the receptor for interleukin-2 (IL-2)’2 (gift from Dr I. Uchiyama). The reactivity with anti-Tac was assessed on fresh leukemic cells and also after 72 hours’ culture at 37#{176}C in RPMI 1640 medium (GIBCO, Grand Island, NY) without added mitogens. E rosettes were performed by using standard techniques, and the presence of deoxynucleotidyl
trifuge
slides
a rabbit
20%
conditioned
fetal
(IdI)
by indirect
was
tested
on cytocen-
immunofluorescence
using
antibody.’3
Mononuclear
Cytogenetics. with
transferase
fixed in acetone
anti-IdI
of 1.5 to 2.0
0006-4971/87/7004-O0l0$3.00/O
926
The
terminal
article must
ratio,
nucleolus,
thoclone,
Royal
UK.
costs ofthis This article
nucleocytoplasmic
useful
1987.
MD, School,
(>100 (WBC,
modalities
features
or lymphadenopa-
Membrane marker analysis. The immunophenotype was assessed by indirect immunofluorescence with a battery of MoAb, and a fluorescein-conjugated F(ab)2 antimouse immunoglobulin was used as second layer. The following MoAb were used: UCHI1(CD3) (gift from Dr P.C.L. Beverley), OKT4(CD4) (Or-
Research
Catovsky, Medical
raised
to increase various
all
symptoms
hepatosplenomegaly in nine
patients
films
characteristic
microscopy
1 5 new
gene
three
tended to
rash,
markedly
M. in all
1 . Briefly,
effusions,
skin
Dr
negative
in Table
lymphadenopathy
was
and
were
to
HILV-I
Haynes
with systemic
massive
on con-
of the
against
B.F.
summarized
was
antibodies
12) presented revealed
remaining
count
Dr
mononu-
reactivity
(MoAb)
from
are
PB
was based
Serum
seven days’ culture,
generalized
response
inset).
(EM.). kaemia
the WBC
the
rearrangements
Leukaemia
char-
and
and
after
anemia,
count
studies.3 (HILV-1)
antibodies
These
on
features
(gift
(nos. 9 and
in the
out
The diagnosis
p24
examination
WBC
carried
immunologic virus
GrUnwald-Giemsa-stained
London.
grant
two
abnormalities
CHOP, M-BACOP, and deoxycoformycin) Light and electron microscopy. PB
is mapped.9
Leukaemia
of which
METHODS
were
monoclonal and
tested
and
clinical
involving
a chain
had
are
with T-PLL. and
anorexia,
an
cytogenetic
rearrangements
/3 chain
School,
with
with
Physical
I I patients
and
from
abnormalities had
receptor
Research
a
of T-PLL
AND
leukemia
p19
Robert-Guroff), the samples.
vesicular
remaining
the TCR
November
Supported
of
been
ten
T cell
Medical
variant
cells
thy).
a differ-
cell
proteins
(malaise,
of azuro-
morphological
aggressive
cases.
Inc.
studies
Clinicalfeatures.
6 months.4
chromosome which
Medical
Submitted
is an
series
have
describe
cases
Postgraduate
a
to be
of T-PLL
some
devoid
8q
one by ultrastructural
I
but two patients
condensation,
a cytoplasm
a small-cell
described.3
have
in each
human
T-
10% to 35%
chromatin
and cells
only
Laboratory
leukemic
a
and
prolymphocytes
peripheral
nucleolus,
been
From
I
B prolymphocytes;
institution
Few
(T-CLL)
antibody.4
(SS),
the core
have
others
S#{233}zarysyndrome
for
& Stratton.
morphological,
firmed
a
be CD4-, CD8+ or react with CD4 and CD8.3 The prolymphocytes from 95% of T-PLL cases react strongly with the CD7(3A1) antibody, whereas in adult T cell lymphoma-leukemia
Grune
trisomy
cells from I 5 patients
clinical,
a distinct
T-PLL
by
Patients.
clear
cell is of T cell origin
represents
in four
MATERIALS
made
peripheral
of
observed
and
first
in
thirds
was
inv(14)(ql
of cell marker and
Two
7q
Catovsky
partial
was
prolymphocyte
the leukemic
entity.2
CD8-
(PLL)
Diagnosis
the advent
where
clinicopathologic
CD4+,
the
With
or
for
and Daniel
with
a series of patients high WBC count,
enlargement.
of
films.’
also
cases.
Trisomy
et al’ in splenomegaly,
node
immunecases
or multisomy
in nine
cases.
LEUKEMIA
by Galton by marked
an
receptor
rearrangements
observed
in four
ROLYMPHOCYTIC
Four
1 . Trisomy
or from
was
T cell
1 4q32.
14q1
found
The
to 14q1 1 and the
an i(8q)
breakpoint
of 6q
cases.
to region
involving
resulting
8pl 2 as the
in nine
Matutes,
had abnormalities of band 1q35 to which the TCR /3 chain gene is mapped. The expression of Tac antigen. investigated in 27 cases of human T cell leukemia virus I-negative chronic T cell leukemia. which included the 1 5 cases of T-PLL, showed a good correlation with abnormalities of 1q35. Our studies on chronic T leukemias suggest that
marker was
Estela trisomy
charac-
membrane
Leukemia
Pomfret,
of T cell
were
abnormality
is localized
heavy-chain
cases
and
frequent
observed
a chain
globulin
All
morphological. most
Mark
in 1 5 cases
(T-PLL).
Leukemia.
Prolymphocytic
Brito-Babapulle,
abnormalities
leukemia
on Prolymphocytic
x
106
calf medium
cells/mL serum.
The
containing
Blood,
cells were seeded in medium cells IL-2
RPM!
were (1
at a concentration 1640
supplemented
cultured
in the
mL/10
mL
Vol 70, No 4 (October),
presence
culture)
of with
1987: pp 926-93
1
From bloodjournal.hematologylibrary.org by guest on July 10, 2011. For personal use only.
CYTOGENETIC
STUDIES
ON T CELL
PLL
927
Table
1 . Clinical
Data
on 1 5 T-PLL
Cases Response to
Age/Sex
Spleen
1
90/M
++
-
450
NR
6wk
2
60/M
++
-
500
NA
3mo
3
83/F
++
-
114
NA
2mo
4#{149}
77/M
-
-
104
PR
3wk
5
48/M
++
++
328
NA
Alive
6
69/M
-
++
400
NA
4mo
7*
46/M
-
+ +
Case
Lymph
WBC
Nodes
lx
1 09/L)
Treatment
48
Survival
Alive-not
Follow-up
3yr
treated
18 mo
(rising) 8
58/M
9
77/F
++
++
-
-
400
PR
6mo
NA
Alive
5 mo
Alive
5 mo
48 (rising)
10
73/F
+ +
+ +
800
PA
11
56/M
+ +
+ +
495
No follow-up
12
80/F
+
50
-
data
Alive-not
treated
3 mo
(rising) 13
33/M
+ +
+ +
207
No follow-up
data
14
58/F
+ +
+
346
No follow-up
data
15
62/M
+
+
In all cases except Abbreviations: Small-cell
NA,
no. 5, ch romosome no response;
stud ies were
PA, partial
perform
96.7 ed at diagnosis
before
Recently
diagnosed
(P1-IA)
at
treatment.
response.
variant.3
phytohemagglutinin
zg/mL) bol
together
ester)
with
at 107/mL
harvested
after
one
followed
hour,
glacial was
with
by
acid out
tg/mL
as mitogens
incubation
acetic carried
0.2
only
and
I 2-0-tetradecanoylphorbolfor 0.05
hypotonic
to three
3, 5, and
zg/mL
and
methanol.
slides
7 days.
colcemid
treatment,
parts
on air-dried
PHA
(0.1
1 3-acetate Cells
were
(GIBCO) fixed
Trypsin
by standard
(phorfor
in one
Giemsa
part
banding
methods.
RESULTS Cell
that
T cell 0
The
markers.
vealed
cells
phenotype
OKTI7+); CD4
antigen
(case
(TdT-,
nos.
3
and
was
not
expressed
and
10),
in Table
in
summarized various and
in
15.
cytoplasm
1 .400;
devoid
current
of azurophil
magnification
granules
x 700).
(original
magnification
x
An
(sd2)
subclone
(sd1
ofinv(14).
(case
in
to the
three
CD4-,
from
(Tac) nos.
3.
Region
in case
two
was
of
expressed
inv(14)
Table
that
chromosome
resulted
in a
Trisomy
or
2B,
had
l;ql
no. was
no.
2, Fig
case
was
6) C,
D,
E,
a t(1 3;14)(q34;ql
1) was
2F).
in
it was
present
Case
1 1 and
no.
both
2, 3, 4, and
trisomy 5),
and
for
7q
in two
was
11,
in 12,
nine
13,
cases,
in a minor
F).
The
major
I ) instead to an
case no. 11 a (sd,) in addi-
12 had
homologues
rearrangement
of
1 4 that
(Fig
observed
of these
were are
these
in addition
t(1I;l4)(14;14)(p13;q11q32;qll)
partial
in
1 3) (data
involved
observed
10 (Fig 2E). In present in a subclone
(Fig
between
(case
1
1, 4, 6, 8, 10,
was
them
(see
case 1;q24)
The
patients
2, 3, 6, and
14q1 nos.
inv(14)(q11q32)
) of
coex-
CD8+.
2).
A t(X;14)(pl
inv(14) t(14;17)(ql
(nos.
CD25
Table
in one
subclone
tion
and
rearrangements
although
was
in cells
cases
CD7+,
CD8-;
Clonal chromosome abnormalities 14 out of 15 cases of T-PLL, and
Cytogenetics.
observed
one
analysis repostthymic
E rosettes+,
-,
CD4+,
CD8;
of four
summarized
Fig 1 . Electromicrograph of a cell from case no. 10 showing an irregular nucleus with the heterochromatin distributed in the periphery and a central prominent nucleolus (original magn’ification x 1 9.000; current magnification x 9.500; uranyl acetate and Reynold’s lead nitrate stain). (Inset) Light microscopy from a PB film from a T-PLL showing cells with a high nucleocytoplasmic ratio. irregular nucleus with a single vesicular nucleolus. and a
CD1 were
and
prolymphocytes
14,
immunophenotyping all the cases had a mature
11 of them
pressed
CD3
from
(nos.
2G).
in four
cases
2 and
3) the
From bloodjournal.hematologylibrary.org by guest on July 10, 2011. For personal use only.
928
BRITO-BABAPULLE
Table
2.
Immunophenotype
of 1 5 Cases
Table
of T-PLL Tac
ities
in 1 5 Cases
CD4 +
-
-
2
+
-
+
+
3
-
+
-
+
4
+
+
-
-
5
+
+
+
-
dup(7)(q21 -+ 35),t(7;15)(q35; q13),+i(8q),dup(X)(q12 -‘
6
+
+
-
+
(Fig 2A)
+
+
+
-
+
+
-
-
9
46,XY,-8,
2
5/5
46,Xq+Y,-8,inv
idic(8q),
3/6
4
+
-
-
+
+
-
-
11
+
+
-
-
12
+
+
-
-
13
+
+
+
+
14
+
+
-
-
15
+
+
-
-
+1
5/8
42,X,
9/15
rearrangements
somy
or partial
(nos.
I, 2, 5, 6, and
affected
tnisomy
for
7q35
8q was
1 1), and
(Fig
observed
in one
case
5
qter)
1),t(?;7)
7, -8,+i(7q),
-
+t(8;20) 1q32),
t(14;21)(pl 1;ql 1) (Fig. 2B) 44,XY,-7,-8,lp+,lq-,4p+,int
18/18
6
42/50
46,XY,
mv q33),i(8q)
8,del(6)(q2
-
1), +t(8;8)(pl
2;
-.
(13;14)(q34;ql
2A).
45,X,
1) (Fig2C)
-8+t(8;8)(pl
2;ql
1),
mnv(14)(ql
1
q32) (Fig2C)
cases was
to the presence of three copies of i(8q) 6 was involved in abnormalities in
five cases.
Four
(nos.
deletions,
-Y,
t(1 1;12)(q21;q24),
Tn-
8) there
I I ) had
.del(6)(q2
del(6)(ql 5q22) dup(7)(q22 .-+
for 8q due Chromosome
3, 5, 6, and
1q32)
(q13;p13),inv(14)(ql
multisomy (Fig 2D).
cases
lp+
,inv(14)(ql
qi 1)t(1 1;12)(q21;q24),derl3t
in eight (no.
-V.
46.XY,
5/50
chromosome
1 2q+
(7;?)(?;p22;q35;?)
-
dT-,CD1-,CD5+,CD7+,Erosettes
Karyotype
1
3
10
AllcaseswereT
Cells
of T-PLL
+
7
No. of Abnormal
Abnormal
CD3
8
Case No.
Chromosome
1
Case
CD8
3.
ET AL
8/20
47.XY,
+22,t(3;
30/30
49,XY,
-
1 1)(q25;ql
8, +i(8q),
3)
+i(8q),
lOq-,mnv(14)(ql
+i(8q),
1q32),+minute
(Fig 2D)
and
one (case no. 10) had a translocation t(5;6)(qI 3;q27). Case had random abnormalities in a few of the 25 cells analyzed.
7 8
Random
25 cells analyzed
9 9
46X.
18/20
10
abnormalities
-X.
-9,
+t(X;9)(p24;pl
+der(X)t(X;14)(pl
1),
1;ql
(qi 3;q27),mnv(14)(ql
1),t(5;6)
1q32)
(Fig 2E) DISCUSSION
Ten out of the I 5 cases abnormalities involving band
to which
TCR
inv( 14)(q I 1q32), ties were secondary inv(14)(qI 1q32) between resulted with
l4q32.
a chain
Thus,
gene
is localized.8
in ten
cases
abnormalities
l4qll
leukemia in
six
For
had
were
in T
cell
acute has
t(lO;l4)(q24;qI
1)
in
four
and
14q32
resulting
in the adjacency
frequent
the majority
of chromosome the
significance
in many
13
10/10
such
1),inv(14)
lt(1 1;14)(14;14)
q32;qll),20q+
(Fig
-
22,i(8q),mnv(14)(ql
1q32)
psu dic(16)t(16;16) 14
6/10
43,X,-X,-7,-
16,-
17,-22,+3,
+ M,mnv(3)(q22q29),i(8q+),inv
(14)(ql 1q32) 15
1) in or
in
T-ALL. also
of 14q1 I with
an
14,derl
45,XY,
ql 1 as
have
of the T cell disorders. abnormalities
of
1)(p 12;
2G)
20/20
A been respecI cell
cases
only
described
lymphocytes
45,XY,
l4q32
inv(14)(qI between (IgV
Because
are not absolutely abnormality
can
gives
be
in the
results an
) and rise
its
-
22,i(8q),mnv(14)(ql
incidence
as T-CLL.25
1q32)
are common
by
1q32)
The
cell
from
lg-TCR
signal
morphology
line
joining
hybrid
sequences
a
given
disease.
SUP-TI
two studies. derived
gene.
from
recombination
heavy-chain segment
present
present cases of of three of eight
of the leukemic
in the latter
a site-specific
immunoglobulin a TCR a chain
to an
in
in 60% of cases in the described in two of 2 1 case of T-PLL6 in two leukemia,24 and seven
was not described
lymphoma
are not very specific,
I
t(10;l4)(q24;qll)
1q24)+t(8;2
(p13;qll
Inv(14)(ql 1q32) was found series of T-PLL and has been T lymphoma,22’23 in another cases described as chronic T
in a case of SS22 and in a T lymphoma, and a t(14;17) has been described in a chronic
leukemia.23 Inversions
45XX,-
62/66
determined
involving
described tively,’9
12
described
inversions
14q1
2;
1;q25),mnv
qi 1),+t(8;21)(p12;ql (q11q32)(Fig2F)
cases,’9’2#{176}
1) in four cases,’6’2’ and t(9;14)(q34;ql We are not aware of tandem translocations and
1 7, +t(8;8)(pl
-
lymphocytic been
t(8;l4)(q24;ql one case.’5 t(9;l4)(q34;qll)
del(6)(q2
made
no. 14 with
1 3,
-
44,XY,-8,-13,-17,-21,int
an
in many T cell disorders, between no. 14 and other
a t(11;14)(pI3;qll)
cases,’68
q32
-8,
(14)(ql 1q32) (Fig2F) 19/26
heavy-chain to 14q32.’4”5
of chromosome
example,
(T-ALL)
and
immunoglobulin are localized
the breakpoint have been described these are usually translocations chromosomes.
Nine
44,XY,
1 1 and both homologues of no. 14 of I I p1 3 with l4ql 1 and l4ql I
to each other. The the AKT-1 oncogene
Although
7/26
qi 1)der(17)t(14;17)(ql
although in one (case no. 6) the abnormaliwith a t(13;l4)(q34;ql 1) in the sd, and in the sd2. In case no. 12 translocations
chromosome no. in the juxtaposition
adjacent gene and
11
of T-PLL studied had chromosome l4ql I, which is the chromosomal
This
suggests
TCRa
a T event
variable (TCRaJ),
in both
The
gene which
that
and
there
IgH
From bloodjournal.hematologylibrary.org by guest on July 10, 2011. For personal use only.
CYTOGENETIC
STUDIES
ON T CELL
929
PLL
Fig 2. Abnormalities involving 14q1 1 or 7q35 and/or nos. 2 (A). 4 (B). 6 (C). 8 (D). 10 (E). 1 1 (F), and 12 (G).
loci
that
make
However,
the
possible
them
sequence
from
14q32
excluded
and
has
Trisomy,
tnisomy
eight
tnisomy,
described
by
had
ing
inversions or
of 1 5 patients
been
malignancies
55
in the
same
recombinases.26
of an
oncogenic
in T-PLL
Zech
cannot
sive
be
al.25
Of
for the whole
cases
multisomy
for
in the present
described
these,
one
out
chromosome
T lymphoid
some
of
Tac
four
with
8. Of the remain-
in
the
absence
partial tnisomy for the q arm of no. 8 by formation of an i(8q) or a t(8p;8q). All cases of trisomy or partial trisomy of 8q
sion,
six
of
in the
present
except present
case no. 11 where two copies oft(8;21)(pl2;qll) in addition to a normal no. 8 in a subclone.
the
increased
dosage
significance
in T-PLL
to
an
diagnosis
of
of the
T-CLL
localized
on
8q2427
has
The
high
incidence
by
benign
of
clinical
investigated
or tnisomy Tnisomy cases,
described
Zech
by
for a proliferation
morphology
and
large
ofT
et
than
laboratory
cases) series
al25
et al.25
to that
We
use
T ‘y cells)
lymphocytes
and
Six cases
the
of
term
with a
the more
not
have
inv(14)(qI
7q
was
observed
1q32)
partial
it is of interest
highly
disorders
T-PLL.
and
play
in thymic
trisomy
characteristic
ysis
of
that
for this
is a common
in
abnormality
four
ity
and
the
of
inv(14)(q1
cell
had
rear-
correlation was found
of chromosome
has
indicates
three
that
of to
cases
been
mapped c-myb
may
that, although T cell disorders
chrosuch
involving
I are
differentiation.33 revealed to other trisomy
for 8q are
immunologic, leukemias
classification confirming 1q32)
of
expres-
14q1
particularly
disease.
clinical, I
and
27
Tac
Four
in
translocations
1q32)
of this
A detailed objective
trisomy
7q,
with
expression
present, for
deletion
evidence
chromo-
Fisher exact test). quite common in T cell here
lymphocyte
as
inv(I4)(qI
At
4).
c-myb
studies on T-PLL have abnormalities common
6q-
with
antigen
(Table
observed
recent
to
a correlation
tested
interstitial
also
Our mosome present,
been
protooncogene
6q22-24,32
a role
or
was
The
showed
(P = .015, abnormality
is a deletion
6.#{176}’ This
no.
V-I-negative
those
stimulation.#{176}
positive
chromosome
aggres-
7q35
and two of l4qll. The of 7q35 and Tac expression
significant
Another
of T-CLL
for 8q. or
to be
in HTL
receptor)
have
were
an
chromosome affecting
that
7q35
mitogenic
which
with
with
T-CLL)
[IL-2]
malignancies
for Sq in case
is localized.8
SS,
factor
of
HTLV-I cases
we observed
rangements of 7q35 between abnormalities
no.
and i(8q) or reported under
is similar
(often
T-PLL.28 did
any
of morphological infora diagnosis of T-PLL in
Zech
cells
granular
evolution in our
;8q),
were Whether
to be seen.
T-CLL
cases
t(8p-
remains
our series of T-PLL. In the absence mation it is not possible to exclude some
or
of c-myc
of inv(14)(ql 1q32) (seven of eight t(8p-;8q) (five of eight cases) in the the
i(8q)
trisomy
gene
involving
cell growth cell
due
had
(I
four
rearrangements
(T-PLL,
abnormalities
T
also
five
had
study
disorders
these
were
T-CLL,
cell
or multisomy
with
the
j3 chain
In a previous I
Of
two
the TCR
in trisomy
associated
course.29
7 abnormalities,
was
Tnisomy
a disease
or
series
as
8q
series.
8 resulting
clinical
which
in six of I 2 chronic et
of chromosome
in ATLL,
DNA
yet to be investigated.
in nine
8q has
to the
involvement
partial
observed for
susceptible
abnormalities
of these the
and
T-PLL
and will
ultrastructural
be conducive
disorders,34
striking reported
with
association here.
analto a more
the possibilbetween
From bloodjournal.hematologylibrary.org by guest on July 10, 2011. For personal use only.
BAITO-BABAPULLE
930
Table
4.
Correlation
of Tac Expression
With
in 27 Cases No. With Abnormalities of 14q1 1 and 1q35
Disease SS
+
+
+
+
-
-
( 1) duplication(2)
-
+ +
+
-
+
+
+
-
-
+ / +
-
+
+
-
-
(3)
(4)
Inversion
(6)
(8)
Inversion/translocation
( 10)
+ +
-
-
Inversion/translocation
( 1 1)
+ / + +
-
-
+ +
-
-
+
-
+
lnversion(14)
+
-
-
Inversion
+
-
-
-
-
Translocation
(1 2)
(13)
Inversion
(5)
0/6 cases
with
an abnormality
abnormalities
of 14q1
of 7q35
were
1, and none
Tac
+
Translocation/inversion
All four
7q35
-
Inversion
had
14q1 1-12 -
Translocation
eight
of 14q1 1 and 1q35
Translocation
Translocation/inversion
Tac + , and
two
only
had abnormalities
of ten cases
AL
(HTLV-l-)
Translocation Inversion
1 2/ 1 5
T-CLL
Rearrangements
T Leukemia
Type of Rearrangement
2/6
T-PLL
Chromosome
of Chronic
ET
with
an abnormality
of 1 4q 1 1 were
Tac +
-
Of the 2 1 Tac-
.
cases,
of 7q35.
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