From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
Chromosome
By Yasuhiko
Kaneko,
Translocations
Childhood
T-Cell
Nobuo
Maseki,
In
a
chromsome
lymphoma.
(q35;ql
) in
1
Southern
studies
both
study
we
found
one
patient,
blotting
and
in one
alleles
(TCRB)
were
involved
and
with
T-cell
1q35
chromsome
that
juxtaposition
tcl-2
located
of
the
I 1
of
A
TRANSLOCATION
chain
band
gene
14q32,
T-cell
be
with
antigen
receptor
a-subunit
genes
respectively,
a translocation
gene
T-cell
with
1q35
partner
Southern
techniques
was
blotting
and
to leukemic
that both TCRB
alleles
allele
had relocated
abnormal
chromosome
These
findings
that
the
T-cell
by
1q35
or
5 translocation-
breakpoint
or
of
14q32.
By
the
translocation.
oncogene
in
tcl-2
Japan.
Submitted
November
in part
16, 1987; accepted
March
by a Grant-in-Aidfrom
29, 1988.
the Ministry
of Health
and Welfarefor
Comprehensive
10-Year Strategy
for Cancer Control, Japan. and by Grants-in-Aid
for Cancer
Research
from
the
Ministry
ofEducation,
Science and Culture of Japan.
Address
reprint requests
to Yasuhiko
Kaneko,
MD. Department
ofLaboratory
Medicine.
Saitama
Saitama
362. Japan.
The publication
costs ofthis
charge payment.
This article
“advertisement”
in accordance
indicate this fact.
© 1988
by Grune
& Stratton.
0006-4971/88/7202-0050$3.OO/O
534
Cancer
article
must
with
Inc.
Center,
818
Komuro,
Ina.
were defrayed
in part by page
therefore
be hereby marked
18 U.S.C.
and
tcl-2.
with
may
breakpoints
ie.
7q35
a-subunit
Takaaki
cases
gene
that
TCRA.
activate
us
the
or IGH
to
a mechanism
with
these
& Stratton.
Inc.
14q1
(TCRA).
and
(IGH).
the
5 for
14q32
Thus,
expand
the
the
above
of TCRB
chromsomal
for
for
1 for
lpl
(TCRG).
juxtaposition
through
sites
TCRB,
gene
allow
propose
were
for
gene
a-subunit
heavy-chain
these
TCRG
by Grune
1988
11p13”
may
tion with TCRB.
report
suggest
important
‘y
and
From the Departments
of Laboratory
Medicine
and Cancer
Chemotherapy.
Saitama
Cancer Center. Ina; Department
of Virology,
Research
Institute,
Naitonal
Children’s
Hospital,
Setagaya.
Tokyo; Department
of Pediatrics.
Hokkaido
University.
Sapporo;
Department
of Pediatrics,
Aichi Medical
University.
Nagakute;
Department
ofPediatrics.
Osaka Medical
College.
Takatsuki;
and
Department
ofHematology,
Kagawa Children’s
Hospital.
Zentsuji.
Supported
receptor
receptor
hypothesis
Takeda,
genesis
chromosome
or
transof T-cell
transloca-
and
also
The
that
be activated
chromosome
the juxtaposition
through
the
translocations
of either
one of tcl-2,
TCRA,
and
step toward
genesis
of T-cell
juxtaposithat
TCRB
we
or
IGH
may
be
leukemia/lympho-
an
ma.
and
in
14q11,
putative
in
TCRG
or
were rearranged,
and that
to the fusion
point
of the
1 1 formed
indicate
all
genes,
immunoglobulin
band
in situ chromosomal
hybridcells with t(7;1 l)(q35;p13),
we proved
one TCRB
antigen
Takeo
resides.26
The
I lp13,
antigen
T-cell
S
also
(TCRB)-
or lpl
leukemia/lymphoma.
translocation
applying
ization
ofdata
(TCRA)
receptor
/3
been
mapped
antigen
have
7p15 are scarce.9”#{176}
We report
four patients
the
amount
translocations,
T-cell
in
tions.
the
in chromosome
with a translocation
14q1 I where
the
Mizutani,
function
location
toward
In
two
or 7pI5
Shimokawa
leukemia/lymphoma
reports
on T-cell
leukemia/lymphoma
or inversion
having
a break
in 7q35
,7.8
associated
suggest
oncogene
step
a break
A growing
the T-cell
findings
putative
a critical
had
for the immunoglobulin
heavy
involved
in the development
of
inversion
(TCRG)-subunit
allele
other
findings
p1 3 of the
leukemia/lymphoma.
leukemia/lymphoma
having
a break
in band
lpl
with
the
on T-cell
Although
TCRB
in band
These
).
with
leukemia/lymphoma.’
exist
one
gene
7q35
Shuki
and Tatsuo
for
that
$-subunit
Sakurai,
Yaoi,
lymphocyte
in 1 patient.
) demonstrated
point
(1 1 p-
the site
is directly
(IGH),
that
I
t(7;14)
hybridization
receptor
1 1 p1 3 may
this
1
Masaharu
Ko-ichi
leukemia
5;q32)
t(7;1
fusion
TCRB
in band
development
B-cell
the
and
to
T-ceII
chromosomal
antigen
Homma,
Fujimoto,
in 2 patients.
t(7;14)(pl
situ
rearranged.
from
childhood
1 )(q35;p13)
in
patient
of the
relocated
in
t(7;1
Chieko
Takeo
Shikano,
Involving
Band
Leukemia/Lymphoma
section
I 734 solely
to
MATERIALS
AND
METHODS
Patients.
lymphoma
University
Chromosomes
from 25 children
with T-cell leukemia/
were studied
at Saitama
Cancer
Center
or Hokkaido
Hospital between May 1982 and May 1987. Four of these
patients
were the subjects
of this report.
Detailed
clinical
and
cytogenetic
data on patient
1 have been reported
elsewhere.’2
Patients
I and 4 were diagnosed
as having lymphoblastic
lymphoma by tonsil or lymph node (LN) biopsy on the basis of the
Working
Formulation.’3
Patients
2 and 3 were diagnosed
as having
acute lymphoblastic
leukemia
(ALL)-Ll
by bone marrow
(BM)
smear
on the basis of French-American-British
(FAB)
classification.’
Cytogenetic
studies.
Samples
for chromosome
studies
were
obtained
from BM, peripheral
blood (PB), or LN before chemotherapy. Cells were cultured
for 24 hours without stimulation.
Chromosomes
were analyzed
with regular Giemsa staining
and Q-banding
methods.
Karyotypes
were described
according
to ISCN (l985).’
Clonality
was defined by using the criteria
of the First International
Workshop
on Chromosomes
in Leukemia
(1977)16
Immunophenotyping.
Immunophenotypes
of malignant
cells
obtained
from PB, BM, or LN of the four patients
were evaluated
before chemotherapy.
The cells were examined
by a direct immunofluorescence
method
for surface
immunoglobulin
and by rosette
formation
for sheep erythrocyte
receptor.
Cell surface antigens
were
examined
by an indirect immunofluorescence
method
using several
monoclonal
antibodies:
T6(CD1),
TI 1(CD2), T3/Leu-4(CD3),
T4/
Leu-3(CD4),
Tl /Leu- 1 (CD5),
and
T8/Leu-2(CD8)
for T-cell
markers,
B4(CD19)
and B1(CD2O)
for B-cell markers;
J5(CDIO)
for common
ALL antigen (CALLA);
and 12 for HLA-DR
(Coulter
Immunology,
Hialeah,
FL, and Becton Dickinson,
Mountain
View,
CA).
Southern
blot analysis.
Total genomic
DNA
was extracted
from peripheral
leukemia
cells of patient
2. Purified
DNA
was
digested with various
restriction
enzymes,
including
BamHI,
EcoRI,
and HindIII,
size-fractionated
by electrophoresis
through
0.5% to
0.9% agarose
gels, and transferred
onto nitrocellulose
filters. Analyses ofTCRB
and TCRG were carried out by using a constant
region
(BgIII-StuII
fragment)
cDNA probe isolated from the leukemic
cell
line Jurkat’7 and a 0.7-kilobase
(kb) Jrl (HindIII-EcoRI
fragment)
Blood,
Vol 72, No 2 (August),
1988:
pp 534-538
From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
1Q35
AND
715
ABNORMALITIES
IN
535
T-MALIGNANCIES
probe isolated from a genomic
library (pH6O), respectively.’8
Rearrangements
of immunoglobulin
gene were analyzed
with a JH region
(BamHI-HindIII
fragment)
probe.’9 All probes were oligolabeled
using 3P-dCTP
(Amersham,
Tokyo).
In situ
chromosomal
hybridization.
In situ chromosomal
hybridization
was performed
on leukemia
cells of patient
2 as
described
previously.#{176}The entire plasmid
containing
the human
C$l probe, a 3.5-kb EcoRI-HindIII
constant
region fragment2’
was
nicktranslated
with 3H-dATP
and 3H-dl’TP
(Amersham).
A specific activity
of I to 9 x l0 cpm/tg
DNA was obtained
after
separation
of the labeled DNA from the free nucleotides
by spindialysis using Sepharose
CL-6B. After hybridization,
the slides were
coated with Kodak NTB-2 emulsion,
and kept in darkness
at 4#{176}C
for
7 days. After development,
chromosomes
were stained with Wright’s
solution
and photographed.
Then the metaphase
cells were destained,
Q-banded,
and photographed
again. The locations
of the
grains were determined
by using two photographs
thus prepared
for
each cell.
and
laboratory
laboratory
data
ranging
telangiectasia.
Two
had hepatosplenomegaly.
of neoplastic
infiltration
at the
marrow
but
They
was
of
lymphoblastic
lymphoma.
and
CNS
relapsed
in
Patients
relapsed
BM
and
3 and 4 entered
and died. Patient
and
Table
the
died
2 months
1 . Clinical
and
He
with
complete
2 had
had
Data
Thus,
at Diagnosis
after
Patients
with
of Cells
1
Normal
Diploid
Total
BM
31
Abnormal
Karyotype
(No. of Cells)
Clonal
10
21
46,XY,t(7;11)(q35;p13)
(1 5)/46,XY,t(7;
1 1),
t(9;22)(q34;ql
2
PB
18
0
18
1)(6)
46,XY,del(5)(q31q35),
t(7;1 1)(q35;p13),del(9)
(p22)(1
3
BM
13
6
7
4
LN
30
10
20
8)
46,XY,t(7;14)(q35;qll)
(7)
46,XX,t(6;12)(q21;p13),
t(7;
now
alive
(November
1, 1987),
of
only
patient
for
Four
3
4 is
5;q32)(20)
14)(pl
23 months
after
the
2 shows
cytogenetic
of patient
and
1 had
14q11
(Fig
a 9;22
translocation,’2
del(5)(q31q35)
and
a 7;14 translocation
2),
and
data.
patients.
formed
and reacted
E rosettes
Neoplastic
cells
immunoglobulins
CD19,
CD2O,
T-cell
Patient
bands
and
lplS
and
Table
Malignant
with
Leukem
1 shows
cells
T1/Leu-1
antibodies.
reactive
with T4/Leu-3
of patients
2 and 4 were
and
HLA-DR
ia/ Lymphoma
2
antibodies.
and
Patient 3
14/M
+
-
1q35
or 7pl
Accordingly,
5 Translocation
Patient 4
10/F
-
3
0
Liver(cm)
0
4
7
0
10.9
10.4
(x
109/L)
12.7
34.5
67t
79
294.1
92
37.0
180.Ot
Immunophenotype
7.0
2.4
0
289.0
(% cells)
Erosettes
26
92
CD1(T6)
42t
ND
4
80
0
CD2(T11)
ND
46
98
90
ND
6
0
8
5
63
16
72
CD3(T3/Leu-4)
92
CD4(T4/Leu-3)
40f
CD5(T1/Leu-1)
80t
93
98
CD8(T8/Leu-2)
Sot
11
92
0
7
CR-R
NR
CR-R
CR
14
2
12
23
CD1O(J5)
Response
Survival
complete
BeIow
13.7t
72.8t
to therapy
(mo)
remission;
the costal
tData
on
jAfter
survival:
the
R, relapse;
NR,
no response,
ND,
not
0
done.
margin.
eighth
patient
hospital
is still
day when
alive.
the patient
developed
leukemic
transformation
of lymphoblastic
lymphoma.
and
not.
no surface
anti-CD
13,
10
BlastsinPB(%)
14q32,
immunophenoof all patients
0
1O9/L)
all cells
a del(9)(p22).
involving
bands
of all patients
examined
showed
and
negative
reactions
to
13/M
+
(g/dL)
on all
involving
Spleen(cm)
Platelets
diag-
data
2 had a 7;! 1 translocation
Immunophenotypic
typic
data
for all
Patie nts With
1
Table
1 and
Cells of patients
I and 3 were
T8/Leu-2
antibodies.
but those
disease.
but patient
to chemother-
data.
Patients
cells
1q35
7/M
Hemoglobin
T-Cell
or 7p1 5 Translocation
respectively.
diag-
5 months
Patient
mass
Leukocytes(x
CR.
No.
of patient
2 had
a
Patients
3 and 4 had
patient
progressive
(yr)/Sex
Mediastinal
Sotrce
some
He subsequently
Factor
Age
in Four
and 1q35
bands 1q35 and Ilpl3 (Fig 1). In addition to the t(7;11),
ages
and two
(CNS)
in any
remission,
no response
diagnosis.
Laboratory
Findings
No. of Cells Examined
Patient
patients.
of ataxia
8 days
involvement.
died
after
with
mass,
system
proved
transformation
developed
one girl
and
1 had normocellular
bone
at the time of diagnosis,
remission
apy
not
clinical
no signs
had mediastinal
Central
nervous
cells
leukemic
and
had
time of diagnosis.
Patient
with normal
differentials
developed
nosis
patients
! shows
3 boys
14 years.
Chromosome
Cytogenetic
Table
data.
for all patients,
7 to
from
2.
Leukemia/Lymphoma
nosis.
RESULTS
Clinical
Table
3
0
From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
KANEKO
536
grains
were
on the normal
on the
1 ip-
chromosomes.
The
(P
would
other
shown
3 were classified
the common
or
were
in different
Southern
I and
2 had
stages
leukemia/
stage,
and
of
TCRB,
TCRG,
and
One
line
and
with
on
145
was confirmed
BamHI
and
metaphase
of
C$1
probe
rearranged
the
13-kb
Germ-
JH
probe
DNA.
over
all
of the
1q35
arm
a
No
on chromsomes
7 or the
short
were
chromosomes.
observed
in band
testing
if there
I 1p
is
relocated
to
had
of the
chromo-
-
chromosome
the 1 IpI Ip-
chromo-
the translocation.
the
In contrast
cells
ing a break
increasing
with
ities
involving
the
3
t(7;1
I )(q35;pl
have
with
1q35
sented
the
chromosomal
this and the
of reports
3),
been
structural
in
our
I ),
studies
demonstrated
that
of the rearranged
relocation
of
hybridization.
other
alleles
TCRB,
and
on
none
T-cell
ie,
5;q32),
leukemia/
leukemic
evidenced
Whether
the
were functional
of
report,
t(7;14)(pl
both TCRB
alleles
may
as
hayon T-cell
abnormal-
this
with
transcripts
is not known.
Rearrangement
alleles
was
recently
reported
in two
lymphoma
cell lines
with
t(7;9)(q36;q34),
DOO
reports
knowledge,
in
association
hybridization
few
chromosome
To
t(7;14)(q35;qI
on T-cell
or inversions
described
reported
t(7;1 l)(q35;p13)
rearranged.
One
have
or ‘lpl
translocations
been
number
translocations
in I 4q 1 1 ,3.6 there
leukemia/lymphoma
in leukemic
grains
were
of patient
to the
leukemia/lymphoma
HindIII.
analysis
of TCRB
gene
Two
hundred
fifty-eight
leukemic
and
combination
A
between
of IGH
enzymes
they
differentiation.
analysis
band of TCRG
was observed
at 16.5 kb,
and 20-kb germline
bands,
in BamHI-digested
counted
portion
through
TCRB
normal
arm of
by chi-square
chromosome
in Fig 3. Thus,
lymphoma.
Southern
in the early
neoplastic
7;1 1 translocation,
JH genes in leukemic
cells with :(7;1 1).
restriction
enzymes
EcoRI
and HindIII,
showed
both Jfl2 alleles
to be rearranged.
In situ hybridization
cells
with
t(7;1 1).
on the
the short
be expected
were
1 1 , I 7 were
the other
DISCUSSION
as having
T-cell
mid-thymocyte
the same
of T-cell
hybridization
configuration
the restriction
.001)
<
grains
of grains
normal
11
patients
2 and 4 as having
leukemia/lymphoma
or immature
thymocyte
stage.22
Thus,
although
of patients
the
the terminal
Fig 1 .
G-banded
partial karyotypes
from 2 PB cells of patient
2
showing
normal
7 and 7q + chromosomes
on the left, and normal
11 and lipchromsomes
on the right.
The 7q+
and llqchromosomes
are the products
of the reciprocal
translocation.
t(7;l l)(q35;p13).
Arrows
point to breakpoints
in the translocation.
cells
of
grains
and
on the 7q+
on
some. The location
of each grain on the normal
7, the 7q+,
the normal
chromosome
11, and
7
I and
in
that
clustering
than
some
patients
lymphoma
number
distribution
significant
chromosome
205 were
clustering
of the
chromosome,
relative
to the
7, 3 were
normal
and
chromosome
7, the 1 lpthe 1 ipwas significant
random
c(-f’
chromosome
5 were on the
chromosome,
chromosome,
ET AL
cells
with
alleles
were
have repreby
in
rearrangements
and productive
in
T-cell
situ
of
of
both
TCRB
leukemia/
SUP-Tl,
and
U
0000000
0
2; 28
0
00
-
0
00
U
30
0
I
0
I
U
0
0
00
00
0
000
00
000
0000000
000000
7
14
Fig 2.
G-banded
partial
karyotype
from a BM cell of patient
3
showing
normal
7 and 7q + chromosomes
on the left, and normal
14 and 14qchromosomes
on the right.
The 7q+
and 14qchromosomes
are the products
of the reciprocal
translocation,
t(7;14)(q35;ql
1 ). Arrows
point
to breakpoints
in the translocation.
7
0
U
7q
11
11p
Fig 3.
Distribution
of grains on normal
chromosomes
7 and 1 1.
and abnormal
chromosomes
7 (7q + ) and 1 1 (1 1 p - ) resulting
from
t(7;i I )(q35;pl
3) in leukemic
cells of patient
2. Arrows
show fusion
points in the rearranged
chromosomes.
Clustering
of the grains on
the normal
chromosome
7. the 1 1 p - chromosome,
and the short
arm of the 1 1 p - was significant
(P < .001 ) by chi-square
testing.
From www.bloodjournal.org by guest on June 18, 2017. For personal use only.
7035
AND
715
ABNORMALITIES
SUPT-3.23’24
TCRB
to the
fusion
point
juxtaposed
cells
with
from
a DNA
sequence
and
the breakpoint
was isolated
that
suggested
somal
was found
to have relocated
of the involved
chromosome
SUPT-l
rounding
transcripts
537
IN T-MALIGNANCIES
SUPT-3.24
locus
and
also
9,23
of the
Moreover,
in 9q34.3
and
and designated
the TCRB
translocation,
in 9q34
from
neoplastic
a gene
productive
involved
sur-
in the chromo-
malignant
process,
of T
in situ
chromosomal
with
leukemia/lymphoma
and
constant
regions
11p13,
and
t(l
were
1),
shown
to the breakpoints
respectively.”
l;l4)(pl3;ql
with the
studies
1;14)(p13;qI
of TCRA
and were localized
I lp+
chromosomes,
cells with t(l
was juxtaposed
hybridization
the juxtaposition
was
region
tcl-2
believed
activated
through
Two
other
t(7;14)(pI
patients
small
juxtaposition
proposed,
but
not
with
regions
variable
the
variable
separated
translocations,
T-lymphocyte
patients
with
of TCRA
within
band
critical
functional
genes
the lymphocyte
other
on
in the
TCRA
1)
individuals
An
and
inverted
of TCRA
and
and
may
The
such translocations
individuals.
mechanisms
and
at the terminal
junction
constant
regions
regions
14q.283#{176}
The
may
t(1;l4)(q35;ql
operate
I)
or
may have
4, respectively.
portion
of IGH
at
fusion
cell
and
of the
of TCRA
resultant
in
the
T cells
to be a large
neoplastic
neoplastic
t(1;14)(pl5;q32),
fused to TCRA
The findings
t(7;14)(pls;q32)
suggest
that
in T
ataxia
In addition,
homology
to
As a result,
In conclusion,
tion
chromosome
gene
with
chromosomal
genesis
chromo-
also been
reported
and patients
with
that undergo
rearrangement.
functional
genes
have certain
sequence.
which
and
T-cells
of our two
T lymphocytes
or in
in neoplastic
T cells.34
T lymphocytes
fragile
at the chromosome
sites of the
DNA
l4q32
had
the
14q,
joined
proximal
genes
in both
points
of the inversion
I 4 produce
novel transcripts
may be involved
in T Cell oncogenesis.28#{176} Similar
fusion
TCRG
as
1, or
individuals.2527
and
ofthe
ofcells
cells
TCRB
IGH in our
t(7;14)(q35;ql
in the neoplastic
T cells
with these translocations
clone
T
and
ofour
may
through
with
and
patients
3
1) and
two patients
proliferate
a still
unknown
mechanism.
normal
telangiectasia.25’26
inv(14)(ql
1q32),
has
of normal
individuals
telangiectasia,27
and
may be particularly
with
t(7;14)(q35;ql
clones
ataxia
only
l4ql
these
translocations
may
have
a selective
chromosomally
normal
cells in patients
with
of the
portion
TCRB.
5;q32),
seen in the neoplastic
have been reported
in single
some
14,
lymphocytes
each
also
1q35,
of normal
In SUPT-l
with inv(14)(ql
1q32),
a T-cell
leukemia
line, the variable
region
of IGH had joined
the junction
variable
step
in the pathogenesis
of this T-cell
neoplasm.”
Our
findings
in the case with t(7;1 l)(q35;p13)
raise the possibility that the putative
oncogene
tcl-2
in band
I IpI3
may be
already
cells
carrying
advantage
over
the
to be the
1p15,
T lymphocytes
and
on the 14q - and the
Thus,
in the neoplastic
1), the constant
DNA
sequence
involving
the
in
constant
the
to have
occur
in T-cell
lymphocytes.
In
translocations
ataxia
telangiectasia,
in whom
cells with
were seen more frequently
than in normal
of multiple
These
works
tcl-3.24
was
in the
1q36
and
of 1-cell
the
juxtaposition
another
translocation
such
gene
may
of one
lymphocyte
or
oncogene
an
be an important
functhrough
step
toward
leukemia/lymphoma.
ACKNOWLEDGMENT
We are grateful
to Dr M. Kikuchi of Fukuoka
University
and Dr
Frizzera
of University
of Minnesota
for histologic
diagnosis
of
patients
I and 4, respectively.
We also thank Dr T. Mak of Ontario
Cancer
Institute
for providing
probe TCRB,
Dr T.H. Rabbitts
of
Medical
Research
Council for providing
probe TCRG,
Dr P. Leder
of Harvard
Medical
School for providing
probe IGH, and Dr 1.
Honjo of Kyoto University
for providing
probe TCRB.
G.
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1988 72: 534-538
Chromosome translocations involving band 7q35 or 7p15 in childhood Tcell leukemia/lymphoma
Y Kaneko, N Maseki, C Homma, M Sakurai, S Mizutani, T Takeda, T Shikano, T Fujimoto, K Yaoi and T
Shimokawa
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