ICANCER RESEARCH 53, 1670-1675, April I, 1993]
Chromosome 12 Breakpoints Are Cytogenetically Different in Benign and Malignant
Lipogenic Tumors: Localization of Breakpoints in Lipoma to 12ql5 and in Myxoid
Liposarcoma to 12Q13.31
Krzysztof Mrózek,2 Constantino P. Karakousis, and Clara D. Bloomfield
C\tof>enetics Research Laboraron' ¡K. M.]. Department of Medicine ¡C. D. B.. K. M.}. and Department of Surgical Oncologv [C. P. K.J. Roswell Park Cancer Institute.
Buffalo. New York 14263
ABSTRACT
able to achieve high resolution banding patterns, indicating that the
chromosome 12 breakpoints differed between benign and malignant
lesions.
Cytogenetic study of short-term cultures from 10 adipose tissue tumors
(eight lipomas, one myxoid liposarcoma, and one mixed liposarcoma) have
revealed clonal chromosome abnormalities in seven cases. In both malig
nant tumors, translocation (12;16) was the sole aberration, and in the
mixed liposarcoma, the breakpoints could be sublocalized to bands
12ql3.3 and Idpi 1.2, thus confirming findings of Eneroth et al., Cancer
Genet. Cytogenet., 48: 101-107, 1990. Three lipomas displayed predomi
nantly normal karyotypes; in a fourth case, the karyotype 44,XX,-6,der
(7)t(6;7)(p21.3-22;p22)ins(7)(p22qll.2q22),-13
was found. Four remain
MATERIALS
ing lipomas were characterized by structural rearrangements of chromo
some 12. We were able to achieve high resolution banding patterns in two
tumors with translocations (3;12)(q28;ql5) and (I;2;12)(p36.;ql3;ql5).
In
both of these cases, the chromosome 12 breakpoint could be unequivocally
assigned to band ql5. Similarly, band 12ql5 was also rearranged in two
other lipomas with translocations (12;14)(ql5;q32) and (12;20)(ql5;ql3.
1). Our results support the hypothesis that the chromosome 12 breakpoint
in lipomas is located more distally than the breakpoint in myxoid liposarcomas and some other soft-tissue malignant neoplasms and that it is
cytogenetically identical with breakpoints detected in such benign tumors
as uterine leiomyoma and pleomorphic adenoma of the salivary gland.
Cytogenetic studies of lipomas, benign tumors of adipose tissue,
have shown that clonal chromosome aberrations are present in about
50% of >250 cases analyzed to date. The most consistent finding has
been recombination of the region 12ql3-15 with various chromo
somes, particularly often with chromosome 3 as t(3;12)(q27-28;ql314) (1-3). Nonrandom involvement of the long arm of chromosome
12. in the form of a translocation (12;16)(ql3;pl 1), is also character
istic for some types of malignant lipogenic neoplasms, namely, myx
oid and mixed liposarcoma (4). However, since the original descrip
tion of 12ql3-14 rearrangements in lipoma (5, 6) and myxoid
liposarcoma (7, 8), the question of whether the exact breakpoints in
benign and malignant tumors are the same or different remains un
answered. Whereas the chromosome 12 breakpoint in myxoid liposar
coma has been consistently mapped to 12ql3, in lipoma breakpoints
have been described as 12ql3, 12ql4, or 12ql5 (l^t). Recently,
Eneroth et al. (9) sublocalized the myxoid liposarcoma breakpoints to
subbands 12ql3.3 and 16pll.2. To our knowledge, analogous sublocalization of breakpoints in lipomas with 12ql3-ql5 changes has not
been accomplished to date.
We present results of Cytogenetic studies performed on 10 adipose
tissue tumors. Rearrangements of chromosome 12 were detected in
two liposarcomas and four lipomas; in three of these cases, we were
NIH.
2 Permanent address: Department of Biology and Genetics, Medical Academy. Gdansk,
Poland. To whom requests for reprints should be addressed, at Cytogenetics Research
Laboratory. Department of Medicine, Carlton House. Room A 420, Roswell Park Cancer
Institute, Elm and Carlton Streets, Buffalo, NY 14263.
Ten tumors, eight benign and two malignant, were studied. Basic clinical
and pathological data are summarized in Table 1.
The tumors of patients 1 and 2 were diagnosed histopathologically as mixed
(myxoid with round cell areas) and myxoid liposarcomas. respectively, and
cases 3-10 were lipomas.
All lipomas were located subcutaneously. and all, with the exception of case
8, were solitary.
Nine tumor samples were obtained immediately after surgery; the specimen
from case 2 was delivered to the Cytogenetic laboratory after having been
stored in transporting medium (RPMI 1640 with antibiotics) in a refrigerator at
4°Cfor 4 days (approximately 90 h). The specimens were processed for
Cytogenetic analysis as described by Limon et al. ( 10). In brief, the tissue was
minced with scissors and disaggregated in collagenase (200 units/ml) overnight
and cultured in RPMI 1640 medium with 4-(2-hydroxyethyl)-l-piperazineethanesulfonic acid buffer supplemented with 15% fetal bovine serum,
L-glutamine, and antibiotics. After 4-10 days, the cultures were exposed to
colcemid. hypotonie solution, and three changes of fixative. The chromosomes
were G-banded with trypsin and Wright's stain; in case IO, a method of
INTRODUCTION
Received 11/17/92; accepted 1/27/93.
The costs of publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked advertisement in accordance with
18 U.S.C. Section 1734 solely to indicate this fac!.
1 Financial support: Coleman Leukemia Research Fund and Grant CA-16056 from
AND METHODS
simultaneous G- and C-banding was also applied ( 11). At least 15 cells were
analyzed per case. Chromosome aberrations were described as recommended
by the International System for Human Cytogenetic Nomenclature ( 1991 ) ( 12).
The translocation breakpoints were specified by careful comparison of the
morphology of derivative chromosomes to the schematic chromosome repre
sentations corresponding to 550 (cases 1, 5, and 9) and 400 bands (cases 2, 6,
7. and 10), published in the International System for Human Cytogenetic
Nomenclature (1985) (13).
RESULTS
Detailed Cytogenetic data concerning the 10 tumors analyzed are
presented in Table 1. Both in the mixed and myxoid liposarcoma
(cases 1 and 2), the t(12;16) was a sole abnormality; in case 1, it was
possible to localize the breakpoints at the subband level to 12ql3.3
and 16pll.2 (Fig. 1).
Three lipomas (cases 3, 4, and 8) displayed predominantly normal
karyotypes. However, in all three cases, nonclonal changes, mainly
losses of various chromosomes, were present. In tumor 8, one
metaphase with a sole structural aberration, t(l;l l)(p32;q24-25), was
found.
Clonal chromosome aberrations were detected in five lipomas. In
case 6, in addition to monosomy 13, a derivative chromosome 7
originating from insertion of material from 7q to band 7p22 and
subsequent translocation with chromosome 6 followed by loss of
der(6) was observed (Fig. 2). Alternatively, the sequence of events
may have been reversed with the translocation (6;7)(p21.3-22;p22)
occurring first, followed by an insertion of a segment 7ql 1.2-q22 into
the vicinity of the translocation breakpoint.
The remaining four benign tumors were characterized by reciprocal
translocations between chromosome 12 and various autosomes,
namely, 3, 14, and 20 and chromosomes 1 and 2 in a complex trans-
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LOCALIZATION OF LIPOMA AND LIPOSARCOMA BREAKPOINTS
Table 1 Clinicopathological
CaseNo.1T34567
(yr)M/73M/43M/28F/37M/55F/48F/53
and cytogenetic data concerning 10 cases of adipose tissue tumors
of cells
(cm)11x9x620 analyzed22152520241619
15x77x6x312
x
10x512x8x510
x
I5pter->cen->15qll.2::3q25.1->3qter).der(20)t(8;20)(8qter->8q21.3::20pl3-»cen-»20qter)[cp3]''37-14.XX,-6.der(7
15)t(3:15)(
x
backAbdomen 10x49x8x2
15x9x43x2x17x4x3No.
46.XY[23]/92.XXYY[2r46.XX,t(l:2;12Kp36.1:ql3;ql5)[32]/46,idem,inv(8)(pll.2q21.2||cp2]/92.idemx212]/46,XX[4]
M/57F/32M/50Diagnosis"MxLSMLSLLLLL
ThighCalfShoulderSize
264041Karyotype46.XY.t(12;16)(ql3.3:pll.2)[21|''46,XY,t(12;16)(ql3;pll)[15]46.XY124]*46.XX[20]46.XY.t(3;12)(q28;ql5U(3;1
LLLLocationKneeThighNeckButtockHipUpper
8910Sex/age
Y,t(12;20)(q15;q13.1)[cp3]/42-45.XY,idem,dic(6;l3)(q11;ql 2)[cp26]/46,XY[12]
" MxLS, mixed liposarcoma;MLS, myxoid liposarcoma;L, lipoma.
''The presence of a single cell with abnormalities not described in the karyotype.
Fig. I. Partial karyotypes of three cells (A. B,
and C) from the mixed liposarcoma (case 1) with
t(12;16)(ql3.3;pl 1.2) ileft) and corresponding dia
grammatic representation (right). Arrows, break
points.
B
M'
V
12
16
location (l ;2; 12). The morphology of both derivative chromosomes of
the t(3;l2) found in case 5 (Fig. 3) clearly indicated that breakpoints
in this translocation were 3q28 and I2ql5. The dark segment present
at the distal end of the long arm of the der( 12) was composed of two
dark bands: an apparently intact 12ql4 and located distally to this
band 3q28. In case 9 with the t(l:2:12) and case 10 with the t(12;20),
breaks in chromosomes 1 and 20 occurred within lightly stained bands
Ip36.1 and 20ql3.1, respectively, allowing for unambiguous assign
ment of the chromosome 12 breakpoint to ql5 (Figs. 4 and 5). More
difficult was mapping of breakpoints in the translocation (12; 14)
present in case 7 because of lower banding quality than in the other
tumors and some similarities of the banding patterns between the
regions of chromosomes 12 and 14 involved in this rearrangement.
Although all of the following pairs of breakpoints: 12ql3 and 14q24,
12ql4 and 14q31. and 12ql5 and 14q32, would give rise to similar
derivative chromosomes, our interpretation favored breakpoints in
volving 12ql5 and 14q32 as those most closely reflecting the mor
phology of the derivative chromosomes (Fig. 6).
DISCUSSION
Cytogenetic analyses of lipoma have led to identification of at least
six karyotypically distinct subgroups, characterized by the presence of
a normal diploid chromosome complement, structural changes involv-
12
16
ing I2ql3-l5,
supernumerary ring chromosomes, del(13)(ql2q22).
aberrations involving Ilql3, and rearrangements of 6p21-23 (\-4).
Sometimes overlapping of cytogenetic subtypes has been noted, with
two or even more recurrent abnormalities occurring in the same tumor
(3). Our case 6 may serve as an example of such a situation, because
both monosomy 13 and a nonreciprocal translocation involving
6p21-22 were found in this tumor. Similarly, in a sideline of case 10.
in addition to t(12;20), loss of 13q material due to dic(6;13)(qll;ql2)
was observed. It is of interest that rearrangements of a region 6p21-23
have also been described in uterine leiomyomas (14), in pleomorphic
adenomas of the salivary gland (15), in endometrial polyps (16-18),
and in pulmonary chondroid hamartomas (19, 20), suggesting that this
region harbors a gene or genes of importance in the development of a
wide spectrum of benign lesions.
Four of five karyotypically abnormal lipomas in our series were
characterized by translocations between chromosome 12 and other
autosomes, confirming previous observations that abnormalities of
12q are the most frequently encountered cytogenetic changes in li
poma. Several chromosomes have been described as 12q translocation
partners, but t(12;14) and t(12;20) observed in our cases 7 and 10,
respectively, hitherto have not been reported. Thus, the addition of
these cases means that only chromosomes 13, 16. 18, 22, and Y have
not yet been seen to be involved in translocations with chromosome
12 in lipoma (2, 3).
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LOCALIZATION
OF LIPOMA
AND LIPOSARCOMA
BREAKPOINTS
ft.
\»
B
f
ÃŽ
Fig. 2. Partial karyotypes of three cells (A, B, and CI from the lipoma of case 6 demonstrating der(7)t(6;7)(p2l J-22;p22)ins(7)(p22ql
representation (right). Arrows, breakpoints.
1.2q22) (leftl and corresponding
schematic
l
12
12
15
Fig. 3. Partial karyotypes of three cells (A. B. and C) representative
corresponding diagrammatic representation (right). Arrows, breakpoints.
for the stemline in the lipoma of case 5 illustrating t(3;l2)(q28:ql5)
15
and t(3:lS)(q2S.I:ql
1.2) tlefn and
1672
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LOCALIZATION
OF LIPOMA
AND LIPOSARCOMA
BREAKPOINTS
'
L
isi
\'*
1
-.n
2
12
8l l
1
2
Fig. 4. Partial karyotypes of three cells (A, B. and C) from the lipoma of case 9 showing complex t( I;2;l2)(p36.I;ql3;ql5)
(lefi) and corresponding ideogram (righi). The segment
of chromosome 1 distal to 1p36.1 has been translocated onto chromosome 2 at 2q 13. the segment of chromosome 2 distal to 2q 13 has been translocated onto chromosome 12 at 12q 15.
and the segment of chromosome 12 distal to 12ql5 has been translocated onto chromosome 1 at Ip36.1. Arrows, breakpoints. Loss of chromosome 2 in the cell A is random.
The morphology of derivative chromosomes in all cases with 12q
rearrangements studied by us clearly demonstrates that the chromo
some 12 breakpoint in lipoma is in 12ql5. The exact mapping of
breakpoints in reciprocal translocations can be cytogenetically diffi
cult, especially when regions which share similar banding features, as
in t(3;12)(q27-28;ql3-15),
are juxtaposed. Thus, inconsistencies in
12q breakpoint assignments in the literature may not reflect true
heterogeneity of breakpoints but rather interpretation differences be
tween examiners. Although the possibility that in some lipomas struc
tural aberrations involve 12ql4 or 12ql3 cannot be ruled out (3, 21),
our results indicate that the proportion of lipomas with 12ql5 changes
is higher than was previously estimated.
Structural aberrations of the long arm of chromosome 12 have also
been repeatedly found in such benign tumors as uterine leiomyoma
S 9
i
Fig. 5. Partial karyotypes of two cells M and B )
from the lipoma of case 10 showing t(12;20)
(ql5;ql3.1 ) (left) and corresponding diagrammatic
representation (righi). Arrow.1,,breakpoints.
B
Ì'
12
ti
20
12
20
1673
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LOCALIZATION
A
Fig. 6. Partial karyolypes of two cells (A and B)
from the lipoma of case 7 demonstrating t(12;14)
(ql5;ql2) (left) and corresponding schematic rep
resentation (right). Armws. breakpoints.
OF LIPOMA AND LIPOSARCOMA
t t
i|
B
12
14
and pleomorphic adenoma of the salivary gland. In both of these
entities, 12q breakpoints have been predominantly mapped to ql4 or
ql5 (14, 15, 22, 23). A recent high resolution cytogenetic study
performed by Pandis et al. (24) showed that the 12q breakpoint in
t(12;14), the translocation typical for uterine leiomyoma, is in 12ql5.
Thus, it is quite possible that the same locus at 12ql5 is affected by
chromosomal rearrangements in all three benign tumors: lipoma, uter
ine leiomyoma, and pleomorphic adenoma of the salivary gland.
In myxoid and mixed liposarcomas, however, the chromosome 12
breakpoint has been consistently assigned to 12ql3 and never to
12ql5 or 12ql4. Both liposarcomas studied by us, as well as about 20
tumors reported in the literature (2, 4), displayed the t(12;16)
(ql3;pll). We were able to sublocalize liposarcoma breakpoints to
12ql3.3 and 16pll.2 in one mixed liposarcoma, thus corroborating
findings of Eneroth et al. (9). Interestingly, the chromosome 12 break
point in another nonrandom aberration, the t(12;22)(ql3;ql2),
that is
specific for clear cell sarcoma of tendons and aponeuroses also has
been mapped to 12ql3 (25-27). Moreover, this band has been rear
ranged in a leiomyosarcoma with the t(12;13)(ql3;q22) (28), in an
alveolar and four embryonal rhabdomyosarcomas (29, 30), in two
malignant hemangiopericytomas (31), and in four chondrosarcomas
(32-34). On the other hand, a benign chondroma studied by Mandahl
et al. (33) had a complex four-way translocation (X;12;8;13) with the
chromosome 12 breakpoint at ql5.
Hence, our results support the hypothesis that the chromosome 12
breakpoint in lipomas is located more distally than the breakpoint in
myxoid liposarcomas and some other soft-tissue malignant neoplasms
and that it is cytogenetically identical with breakpoints detected in
uterine leiomyoma and pleomorphic adenoma of the salivary gland.
ACKNOWLEDGMENTS
The authors wish to thank Drs. C. Perez-Mesa
BREAKPOINTS
and U. N. M. Rao for
histológica! interpretation of tumor tissue, and Prof. S. Heim for critical read
ing of the manuscript.
ADDENDUM
After submission of our article. Aman et al. (35) described rearrangements
of the CHOP gene, which maps to 12ql3, in all nine myxoid liposarcomas
studied and in none of the seven lipomas with cytogenetic changes of the
region 12ql3-15. These findings support our conclusion that chromosome 12
breakpoints in myxoid liposarcoma and lipoma are different.
12
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Chromosome 12 Breakpoints Are Cytogenetically Different in
Benign and Malignant Lipogenic Tumors: Localization of
Breakpoints in Lipoma to 12q15 and in Myxoid Liposarcoma to
12q13.3
Krzysztof Mrózek, Constantine P. Karakousis and Clara D. Bloomfield
Cancer Res 1993;53:1670-1675.
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