[CANCER RESEARCH 40, 796-802, March 19801
0008-5472/80/0040-0000$02.00
Nonrandom Abnormalities in Chromosome 1 in Human Testicular Cancers1
Nancy Wang,2 Beth Trend, David L. Bronson, and Elwin E. Frabey
Departments of Laboratory Medicine and Pathology (N. W., B. T.] and Urologic Surgery ID. L. B., E. E. F.], University of Minnesota, College of Health Sciences,
Minneapolis, Minnesota 55455
ABSTRACT
Tyrpsin G banding was performed on metaphase chromo
somes from 14 cell lines derived from primary tumors or me
tastases of 11 patients with testicular cancer. Most of the cell
lines, 11 of 14, have a modal number between 51 and 61 . All
lines have numerical and structural changes involving chro
mosome 1 with tnisomy of the q arm being the common aber
ration. Break points in chromosome 1 were nonrandom, being
concentrated in the regions of p12, qi 2, p36, and p22, which
resulted in morphobogically identical marker chromosomes in
different cases. These changes probably are not artifacts of
cell culture. In one instance, three lines derived from the same
patient, one from tissue removed at operation, and two from
separate metastases removed at autopsy nearly 3 years later
after unsuccessful radiotherapy and chemotherapy had iden
ticabchromosome compositions. In another case, lines derived
from a primary tumor and a metastasis from the same patient
also had identical marker chromosomes. The consistent in
volvement of chromosome 1 in aberrations may be associated
with the highly malignant nature of testicular cancers.
INTRODUCTION
Few analyses have been made of the chromosomes of human
testicular tumors (2, 29). Atkin (2) found that the modal chro
mosome number generally is 50 or more, and in this, testicular
tumors are different from tumors at other sites. Martineau (29)
performed conventional karyotypic analyses on 25 testicular
tumors and reported that seminomas have higher modal chro
mosome numbers than do other histological types. She also
observed marker chromosomes in various kinds of testicular
tumors as determined by statistical analysis of total chromo
some length and arm ratios. However, it is impossible to identify
precisely the origin of these marker chromosomes by conven
tional analysis.
To obtain information detailing the chromosome constitution
of human testicular cancers and to determine whether specific
nonrandom chromosome abnormalities exist, we performed
trypsin G-banding studies on 14 cell lines derived from 11
patients with testicular cancer. Specific marker chromosomes
were identified, and nonnandom abnormalities of chromosome
1 were observed in all of the cell lines.
MATERIALS
AND METHODS
833K; 11560; 1218E; 1242B; 12550; 2044L; 2061H;
21O2EP; 21O2ER; Tera-1 ; and Tera-2. The origin of the cell
lines and the tissue types of the tumors from which they were
derived are summarized in Table 1. Tera-1 and Tera-2 were
established in Dr. JørgenFogh's laboratory (8) at the Sloan
Kettering Institute for Cancer Research. The rest of the cell
lines were established by Bronson et a!.3
The cell lines were maintained in Roswell Park Memorial
Institute Medium 1640 containing 10% fetal calf serum (Grand
Island Biological Co., Grand Island, N.Y.), 100 units penicillin
per ml, 100 sg streptomycin per ml, and 10 mt.i 4-(2-hydroxy
ethyl)-1-piperazineethanesulfonic acid buffer and subcultured
weekly. Cultures were harvested for chromosome studies when
40% confluent, treated with 0. 14 @g
Colcemid per ml for 2 hn,
and trypsinized to obtain a single-cell suspension. The cells
were then treated hypotonicalby with 0.075 M KCI on 0.7%
sodium citrate for 10 mm and fixed in methanob:glaciabacetic
acid (3:1 ; v/v). Slides were prepared by the air-dried method
and were treated to obtain trypsin G banding by the method of
Wang and Fedoroff (51 ). Briefly, slides were heated on a 70°
hot plate for 2 mm, treated with 0.0725% trypsin (in 0.9% NaCI
solution) for 20 to 45 sec, rinsed with 0.9% NaCI solution, and
stained with Giemsa for 2 to 5 mm. For each cell line, 25 to 30
metaphase figures were analyzed.
RESULTS
577ML, 577MF, and 577MR. These 3 lines were derived
from
lung,
from separate
I This
work
was
supported
by
American
Cancer
Society
Grant
Minn. Medical Foundation Grant SMF-245-79.
2 To
whom
requests
for
reprints
should
be
addressed.
Received October 29, 1979; accepted December 10, 1979.
796
In-i
3-R-26
and retropenitoneal
metastases,
nespec
metastases
removed
at autopsy
nearby 3 years
later after unsuccessful chemotherapy and radiotherapy. The
chromosome numbers range from 45 to 58 for 577ML, 50 to
56 for 577MF, and 50 to 54 for 577MR, and the modal
chromosome number is 55 for all 3 lines. One normal chmo
mosome 1 and 3 marker chromosomes (Ml , M2, and M3) (Fig.
1A) involving chromosome 1 were found in every cell of the 3
cell lines. As shown in Fig. 1A, chromosome Ml results from
the addition of a dark band of unknown origin to the distal end
of the p arm of chromosome 1. Chromosome M2 is a transbo
cation product of chromosome 18 and the q arm of chromo
some 1. Chromosome M3 is a normal chromosome 1 with
almost all of the p arm deleted.
11560.
Cytogenetic studies were performed on 14 testicular cancer
cell lines derived from 11 patients. The cell lines had been
given the following designations: 577ML; 577MF; 577MR;
forehead,
tiveby,from a single patient, and all were classified histologically
as tenatocarcinoma. 577MR was established from tissue me
moved at operation while 577MF and 577ML were established
This cell line was derived from a mixed primary
tumor. The chromosome number ranges from 46 to 58, and
the modal number is 53. As shown in Fig. 1B, themeis one
normal chromosome 1, and of the 11 marker chromosomes, 2
involve chromosome 1 (Fig. 2B). Chromosome Ml results from
and
3 D.
L. Bronson,
P. W.
Andrews,
D.
Solter,
J. Cervenka,
P.
H.
Lange,
and
E.
E. Fraley. A cell line derived from a metastasis of a human testicular germ cell
tumor, manuscript in preparation.
CANCERRESEARCHVOL. 40
Downloaded from cancerres.aacrjournals.org on June 18, 2017. © 1980 American Association for Cancer Research.
Chromosome Abnormalities in Human Testicular Cancers
linesPatient
Site of origin
Treatmenta
Pas
sages i@
culture
Retroperitoneum
Lung
Forehead
Abdomen
Primary
Primary
Primary
None
RT, CT
RT, CT
CT
None
None
None
7
13
15
29
13
27
13
9
11
7
10
10
15
EC(fast
3
Primary
Retroperitoneum
Lung
Primary
Retroperitoneal
TCnode
lymph
None
None
None
None
None
12
42
27
56
37
11
20
14
15
14
Lung
Lung
RT, CT
RT, CT
39
22
age
Cell
Diagnosis577MR
line
(yr)
TCC577ML 24
TC577MF
24
TC833K
24
T1
19
S11560
22
S1
218E
23
242B
23
growing)1
S2044L
2550
22
EC2061
24
TC21H
19
Y21
O2EP
23
O2ER
23
metastasisTera-i
TTera-2
47
ECa
22
Treatment
b Passages
C RT,
Table 1
Summary data on the testicular cell
before removal of tissue for culture.
and months in culture when cytogenetic
radiotherapy;
CT,
chemotherapy;
EC,
embryonal
analysis
carcinoma;
Mos. in
culture8
EC, CC, 5,
EC, CC,
EC,
TC,
TC,
8 yr
7 yr
was performed
CC,
for each cell line.
choriocarcinoma;
TC,
teratocar
cinoma; S. seminoma; T, teratoma; Y, yolk sac tumor.
the addition of a segment containing 3 bands from the distal
end of the q arm of chromosome 1 to the distal end of the p
arm of another chromosome 1. Chromosome M2, bike the
chromosome M3 in 577M, is a chromosome 1 with the p arm
deleted.
1242B. This cell line was derived from a primary embryonab
carcinoma. The chromosome number ranges from 68 to 95,
and the modal number is 86. As shown in Fig. 1C, the line is
trisomic for chromosome 1. Six marker chromosomes were
observed (Fig. 2C), 2 of which involve chromosome 1 and are
identical to the Ml and M2 markers in 1156Q (Fig. 1B).
However, the cell line differs from 1156Q in its modal chro
mosome number and its other marker chromosomes (Fig. 2, B
and C).
I 2550. Thislinewasderivedfroma primaryteratocarcinoma
with seminoma. The chromosome number ranges from 46 to
61 with a modal number of 51 . As shown in Figs. 1D and 2D,
themeis one normal chromosome 1, and among the 9 marker
chromosomes, 4 involve chromosome 1. Chromosome Ml
results from an inversion of the terminal segment of chromo
some 1 wIth the break point at the p2 region and the addition
of a segment involving 2 dark bands of unknown origin to the
distal end of chromosome 1 after the inversion. Chromosome
M2 results from the translocation of one 1q arm to the proximal
end of the p arm of another chromosome 1. Chromosome M3,
identical to the chromosome Ml in 1156Q and in 1242B,
results from the addition of a segment containing 3 bands from
the distal end of the q arm of chromosome 1 to the distal end
of another chromosome 1. Chromosome M4 is the remaining
part of chromosome 1 with the entire q arm deleted.
2102EP. This cell line was derived from a primary tumor
classified histologically as tematocancinomawith yolk sac tumor.
The chromosome number ranges from 48 to 61 with a modal
number of 56. Approximately 40% of the cells are tnisomic for
chromosome 1. Another 40% contain 2 normal No. 1 chno
mosomes and a marker chromosome Ml (Fig. 1E) which result
from the addition of 2 dark bands of unknown origin to the
distal end of the 1p arm. The remaining 20% of the cells
contain 2 normal No. 1 chromosomes and 2 identical Ml
markers. The Ml is the only marker chromosome found in this
MARCH
cell line (Fig. 2E).
2102ER. This cell line was derived from a retnopenitoneal
metastasis of the 21O2EP tumor and was classified histobogi
cably as teratocarcinoma. The chromosome number ranges
from
45 to 59 with a modal
number
of 56. The chromosome
composition of the cell line is similar to that of the 21O2EPcells
having 2 normal No. 1 chromosomes and 2 M1 marker chro
mosomes with each cell of this line containing 2 identical Ml
markers (Figs. 1F and 3).
833K. This cell line was derived from an abdominal metas
tasis classified histologically as embryonal carcinoma, chonio
carcinoma, seminoma, and teratoma. The chromosome number
ranges from 58 to 61 with a modal number of 58. Most (90%)
of the cells contain 3 copies of normal chromosome 1. The
others contain only 2 copies. In addition, 2 marker chromo
somes were found in every cell examined. As shown in Fig.
1G, chromosome Ml results from the transbocation of a seg
ment involving 4 dark bands from the distal end of the 1q arm
to the distal end of the p arm of a chromosome 2. Chromosome
M2 is identical to the M3 marker observed in cell line 12550
(Fig. lD).
1218E. This cell line was derived from a primary tumor
classified histologically as embryonal carcinoma and semi
noma. The chromosome number ranges from 95 to 117 with a
modal number of 115. As shown in Fig. 1H, the chromosome
content includes 2 normal No. 1 chromosomes and 3 marker
chromosomes, 2 Ml and one M2. Chromosome M2 results
from a chromosome
1 with 2 dark bands deleted
from the distal
end of the q arm. Chromosome Ml probably is derived from a
M2 marker by the addition of a chromosome segment identified
as 2p to the break point (Fig. 1H).
2044L. This cell line was derived from a retmopenitoneal
lymph node metastasis classified histologically as embryonal
carcinoma. The chromosome number ranges from 50 to 57
with a modal number of 53. Each cell contains 2 normal No. 1
chromosomes and a giant dicentnic marker chromosome re
suIting from the inversion and transbocation of the entire 1q arm
to the terminal end of the 1p arm of another chromosome 1
(Fig. 1!).
2061 H. This cell line was derived from a lung metastasisof
1980
Downloaded from cancerres.aacrjournals.org on June 18, 2017. © 1980 American Association for Cancer Research.
797
N. Wang
et a!.
a teratocarcinoma. The chromosome number ranges from 92
to 105 with a modal number of 98. Each cell contains 2 normal
No. 1 chromosomes and 4 marker chromosomes (Ml to M4)
involving chromosome 1 (Fig. 1J). Chromosome Ml is derived
from the breaking off of the short arm of a chromosome 1 at
the p22 region and its tmansbocationto the distal end of the p
arm of another chromosome
tion for all the cell lines studied (Fig. 1); (c) the break point of
chromosome 1 involved in different structural changes is non
random (occurring most frequently at the regions of p12, ql 2,
p22, and p36) with these nonmandomstructural changes me
suIting in morphobogically identical marker chromosomes in
different cases (Fig. 1); (d) with the exception of I 218E,
1242B, and 2061 H, the modal chromosome number of all the
cell lines is in the range of 51 to 61 , hypendipboidy(Table 2);
and (e) the chromosome compositions of the cell lines estab
bished independently from separate sites of the same patient
are identical (Fig. 2, A and E).
DISCUSSION
Nonrandom chromosome abnormalities have been found in
histologically related human cancers. The most convincing are
the presence of the Ph1 chromosome in chronic myelocytic
leukemia (43), the partial or total deletion of a No. 22 chro
mosome in meningioma (22, 23, 27, 28, 58), and the tmanslo
of chromosome
14 in Burkitt's
lymphoma (13, 21 , 24, 59). Also, through the analyses of the
peripheral blood cells, specific chromosome abnormalities
have been identified in the patients of certain cancer types.
These include the interstitial deletion of chromosome 13 in
netinobbastoma patients (9, 40, 41 , 49, 54, 57), the partial
4 Tera-i
and
Tera-2
cells
were
a
gift
from
Dr.
Institute for Cancer Research, New York, N. Y.
798
Jergen
Fogh,
Sloan-Kettering
analysis
For each cell line, 25 to 30 G-banded metaphases were analyzed. The
numerical
and strSummary
summarized.Cell
uctural changes involving chromosome 1 were
1. Chromosome M2 results from
a transbocation between a chromosome 12q and 1q. Chromo
some M3 is derived from a chromosome with the majority of
the p arm broken off at the p22 region. Chromosome M4 is
identical to the M3 marker found in line 12550 (Fig. 10) and
the M2 marker found in line 833K (Fig. 1G).
Tera-1 .@This cell line was derived from a lung metastasis
classified histologically as embryonal carcinoma. The chro
mosome number ranges from 56 to 67 with a modal number of
61 . Chromosome abnormalities include trisomy for chromo
some 1 and one isochnomosome derived from the centromenic
fusion of two 1q arms (Fig. 1K).
Tera-2.4 This cell line was derived from an embryonabcarci
noma metastasis to lung. The chromosome number ranges
from 59 to 67 with a modal number of 61 . The line is tnisomic
for chromosome 1 and has 2 markers involving chromosome
1. Chromosome M1 results from the centromenic fusion be
tween 1q and 2p with the addition of a segment of 2p1 5 to
2p25 to the distal end of the 2p arm (Fig. 1L). Chromosome
M2 is a chromosome 1 with the p22 to p36 region deleted (Fig.
1L).
In this study, through the G-banding chromosome analysis
of 14 testicular tumor lines, the following nonrandom chmomo
some abnormalities were observed: (a) chromosome 1 is in
volved in both numerical and structural changes in each of the
14 lines (Table 2); (b) a tnisomy state of the q arm of chromo
some 1 has been found as the common chromosomal abemra
cation with the involvement
Table 2
data on the cytogenetic
lineNo.
arm577ML
577MF
577MR
Chromosome
no. range
50—56
50-54
of
markers
No. of
Chromo- involving normal
some
chromo- chromomodal no. some 1 some 1
Total
copies
of the
q
55
3
1
4
55
55
3
3
1
1
4
4
11560
46-58
53
2
1
3
1242B
68-95
86
2
3
5
12550
2102EP
21O2ER
833K
i2i8E
2044L
46-61
48-61
45-59
58-61
95-117
50-57
51
56
56
58
115
53
4
1
2
2
3
1
1
2
2
3
2
2
4
3
4
4
5
4
206iH
Tera-i
Tera-245-58
92-105
56-67
59—67
98
61
61
4
1
2
2
3
3
5
4
5
deletion of the p arm of chromosome 11 in Wibms' tumor
patients (42), and the transbocation between chromosomes 3
and 8 in the hereditary renal cell carcinoma cases reported
recently (6, 18). The meaning of these nonnandom chmomo
some abnormalities observed among the tumors of histobogi
cabbyrebatedtissues onorgans is not yet clear. However, on the
basis of comprehensive cytogenetic studies of chemically and
virally induced tumors in rats (1, 20, 30) and mice (52), com
mon chromosome abnormalities may reflect a common etiology
of the tumors.
In this communication, nonrandom chromosomab aberration
for nonseminomatous testicular cancers is being added to the
aforementioned group of human cancers. Fourteen cell lines
derived from 11 patients were analyzed, and the consistent
involvement of chromosome 1 in both tnansbocationand partial
tnisomy was found in every case.
The nonmandomchromosome aberrations reported in this
study do not seem to be artifacts of in vitro cultivation. Evidence
for this is the identical chromosome
composition
observed in
3 different cell lines (577ML, 577MF, and 577MR) derived
from metastases at different locations in a single patient. It is
unlikely that artifact would produce 6 identical marker chro
mosomes (Fig. 2A) and identical modal chromosome numbers
(Table 2) in these 3 independent cell lines, one derived from
tissue removed at operation and 2 from separate metastases
removed at autopsy nearby 3 years later after unsuccessful
radiotherapy and chemotherapy. In addition, the primary and
metastasized cell lines 21O2EP and 21O2ER from another
patient again yield identical chromosome composition with the
exception of the appearance of one additional MI marker
chromosome in the metastasized line (Fig. 3).
Chromosome 1 abnormalities are not limited to testicular
cancers. They have been occasionally reported for a variety of
other human cancers affecting ovary (4, 14, 16), lung (14, 16,
39), bladder (47), breast (7, 15, 19, 36), brain (5), colon (39),
and cervix (3), and in bymphoma(21 , 24—26),malignant meba
noma (17), and hematobogicabcancers (10—1
2, 31 ‘-35,
37, 38,
44—46,50, 53, 55, 56, 60). However, a consistent involvement
of chromosome 1 in both structural and numerical changes
such as that observed in testis cancers has not been reported
in any of these tumors. The consistency of this association of
CANCERRESEARCHVOL. 40
Downloaded from cancerres.aacrjournals.org on June 18, 2017. © 1980 American Association for Cancer Research.
Chromosome Abnormalities in Human Testicular Cancers
chromosome I abnormalities with nonseminomatous testicular
cancers may reflect the highly malignant nature of the neo
plasms. It has been suggested by Atkin and Pickthalb (4) that
the involvement of chromosome 1 may be a relatively bate
concomitant of malignant transformation and that its presence
can serve as an indication of an unfavorable prognosis or high
degree of cancer.
Further cytogenetic studies on primary testicular tumors,
both seminomas and nonseminomatous
24.
25.
26.
27.
cancers, are required
to extend the observations reported herein. These studies, by
clarifying the role of chromosome 1 abnormalities in cancer
transformation, may be of clinical value in predicting the cancer
potential for seminomas. In addition, detailed analysis of the
sex chromosome composition of the various testicular cancers
may aid in determining the time of germ cell transformation
during spermatogenesis.
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CANCERRESEARCHVOL. 40
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Chromosome Abnormalities in Human Testicular Cancers
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CANCERRESEARCHVOL. 40
Downloaded from cancerres.aacrjournals.org on June 18, 2017. © 1980 American Association for Cancer Research.
Nonrandom Abnormalities in Chromosome 1 in Human
Testicular Cancers
Nancy Wang, Beth Trend, David L. Bronson, et al.
Cancer Res 1980;40:796-802.
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