Cytogenet Cell Genet 88:145152 (2000)

Spectral karyotyping of the human colon

cancer cell lines SW480 and SW620
R. Melcher,a C. Steinlein,a W. Feichtinger,a C.R. Mller,a T. Menzel,b
H. Lhrs,b W. Scheppach,b and M. Schmida
a Institute

of Human Genetics, University of Wrzburg, and b Department of Gastroenterology, University Hospital, Wrzburg
(Germany)

Abstract. The cell lines SW480 and SW620, derived from

different stages of colon carcinoma in the same patient, have
been used for a number of biochemical, immunological, and
genetic studies on colon cancer. A comparative analysis of their
karyotypes may identify chromosomal aberrations that might
represent markers for metastatic spread. In the present study
spectral karyotyping (SKY) was applied to these two colon cancer cell lines. Compared to previously reported G-banded
karyotypes, 9 (SW480) and 7 (SW620) markers were identical,
3 (SW480) and 3 (SW620) markers could be redefined, 5
(SW480) and 8 (SW620) markers were newly identified, and 4
(SW480) and 5 (SW620) of the previous described markers
could not be confirmed. The redefined aberrations include very
complex rearrangements, such as a der(16) t(3;16;1;16;8;16;

1;16;10) and a der(18)t(18;15;17)(q12; p11p13;??) in SW620

and a der(19)t(19;8;19;5) in SW480, that have not been identified by conventional banding techniques. The resulting chromosome gains (5q11 5q15, 7pter q22, 11, 13q14 qter,
20pter p12, X) and losses (8pter p2, 18q12 qter, Y)
found in both SW480 and SW620 were in good agreement with
those frequently described in colorectal tumors as primary
changes in the stem cell. Abnormalities found exclusively in
SW620 cells only (gains of 5pter 5q11, 12q12 q23,
15p13 p11, and 16q21 q24 and losses of 2pter 2p24,
4q28 qter, and 6q25 qter) can be viewed as changes that
occurred in a putative metastatic founder cell.

Despite progress in cancer treatment, colorectal cancer is

still one of the major causes of death from malignant diseases.
The incidence of cancer of the colon is, at present, exceeded
only by that of breast and lung cancer. The biochemical and
clinical aspects of colorectal cancer, as well as the genetic alterations at the molecular level, have been well recognized (Fearon
and Vogelstein, 1990), whereas the pattern of cytogenetic
abnormalities is less clear. Previous cytogenetic studies indicate that the development of most solid malignancies involves
deletions and amplifications of multiple chromosome segments
(Mertens et al., 1997). In addition, complex chromosome rearrangements, homogenously staining regions (HSRs), and double minute chromosomes (dmins) are commonly seen in tumor
cells at metaphase.

As identification of such complex rearrangements is close to

impossible by banding techniques, a large number of marker
chromosomes often remain unclassified. Fluorescence in situ
hybridization (FISH) alleviates these shortcomings to some
degree, facilitating the confirmation of suspected chromosomal
aberrations with high sensitivity and specificity (Gray et al.,
1994). However, FISH is restricted to a targeted chromosomal
subregion and cannot serve as an a priori screening test for
chromosome rearrangements (LeBeau, 1993). Spectral karyotyping (SKY; Schrck et al., 1996) is a novel approach that
combines the sensitivity and specificity of FISH with the power
of conventional cytogenetic methods, i.e. the screening of entire
metaphases for chromosomal aberrations in a single experiment. SKY has been used to define chromosomal alterations in
hematological malignancies (Veldman et al., 1997), characterize tumor cell lines (Padilla-Nash et al., 1999; HeLa cells: Macville et al., 1999) and clarify chromosome alterations in solid
tumors (Zitzelsberger et al., 1999).
In the present study SKY was applied to two colon cancer
cell lines (SW480 and SW620). These cell lines were derived

Received 18 October 1999; revision accepted 17 December 1999.

Request reprints from Dr. Michael Schmid, Institut fr Humangenetik,
Am Hubland, D97074 Wrzburg (Germany); telephone: +49-931-888-4077;
fax: +49-931-888-4069; e-mail: m.schmid@biozentrum.uni-wuerzburg.de.

ABC

Fax + 41 61 306 12 34
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Copyright 2000 S. Karger AG, Basel

Accessible online at:

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from different stages of tumor progression in the same patient

(Leibovitz et al., 1976). The SW480 cell line originated from a
surgical specimen of a primary tumor of a moderately differentiated colon adenocarcinoma (grade 4, Duke class B). The
SW620 cell line was established from a biopsy of a metastatic
spread to the abdominal wall of the same patient. Both of these
cell lines have been used for a number of biochemical, immunological, and genetic studies on colon cancer (e.g., Goyette et
al., 1992; Ellis et al., 1996; Kubens et al., 1998; Flohr et al.,
1999). The genetic, especially cytogenetic, basis of colorectal
cancer metastasis remains poorly understood. Therefore, a
comparison of the SW480 and SW620 karyotypes may identify
cytogenetic markers that occur during metastatic dissemination. Gagos et al. (1995) previously karyotyped these cell lines
using standard chromosome banding techniques. They identified several chromosome aberrations, but due to the complexity of the rearrangements, some remained unclear and others were not detected at all. In the present study, SW480 and
SW620 were analyzed using SKY to clarify the numerous complex translocations and to uncover additional unrecognized
aberrations.

Materials and methods

Cells and culture conditions
The human colon cancer cell lines SW480 and SW620 (passages 95 and
104) were obtained from the American Type Culture Collection (ATCC
CCL-228 and ATCC CCL-227, respectively). SW480 cells were grown in
RPMI (Life Technologies) supplemented with 10 % (v/v) fetal bovine serum
(Sigma). SW620 were grown in DMEM (Life Technologies) supplemented
with 10 % (v/v) fetal bovine serum (Sigma), penicillin (100 U/ml), and streptomycin (100 g/ml). Cells were subcultured every 4 d using trypsin-EDTA
detachment. For each subculture 1/10 of the volume of the parental cell suspension was transferred to a new flask. To each new flask 9/10 volumes of
fresh medium was added.
Chromosome preparation
Freshly fed and nearly confluent cell cultures from these two cell lines
were incubated with Colcemid for 3 h at 37 C. Cells were dislodged with
trypsin-EDTA solution, transferred to centrifuge tubes, and centrifuged at
1,400 rpm for 8 min, after which the supernatant was discarded. Hypotonic
solution (0.075 M KCl, prewarmed to 37 C) was added to the cell pellet,
gently mixed by pipetting, incubated for 12 min at 37 C, and centrifuged at
1,400 rpm for 8 min. The supernatant was discarded, and 12 ml of modified
Carnoys fixative (3:1 methanol:acetic acid) was slowly added. Chromosome
preparations were made by dropping the cell suspension onto wet slides.
Pepsin treatment and chromosome denaturation
A pepsin solution (0.001 % pepsin, 0.01 M HCl) was applied onto the
chromosome slides and incubated for 3 min at 37 C. After the pepsin digest,
the slides were placed in denaturation solution (70 % formamide, 2 SSC)
for 1 min, immediately passed through a cold alcohol series (70 %, 80 %,
90 %, and 100 %), and air dried.
SKY
Optimally aged slides (315 d at room temperature) were hybridized
with a SKY probe mixture supplied by Applied Spectral Imaging, Inc. The
probe mixture contains 57 uniquely labeled chromosome-specific probes,
which are combinatorially labeled with three fluorochromes and two haptens
(Spectrum Green, Spectrum Orange, and Texas Red for direct labeling, as
well as biotin-16-dUTP and digoxigenin-11-dUTP for indirect labeling)
(Macville et al., 1999). After hybridization, biotin was detected with avidinF
Cy5, and digoxigenin with mouse anti-digoxigenin, followed by sheep antimouse custom-conjugated to Cy5.5. Metaphase preparations were counterstained with 4),6-diamidino-2-phenylindole (DAPI; 150 ng/ml) in 2 SSC

146

Cytogenet Cell Genet 88:145152 (2000)

and covered with antifade solution (Vectashield mounting medium; Vector

Laboratories). Image acquisition was achieved with the SpectraCube system
(Applied Spectral Imaging, Inc.) and analyzed with SKYview imaging software (Garini et al., 1996).
Chromosome banding analysis
Constitutive heterochromatin in the chromosomes was localized using
the CBG-banding technique (Sumner, 1972). Active nucleolus organizer
regions were detected using silver staining (Howell and Black, 1980). Distamycin A/DAPI bands were induced in the chromosomes as described by
Schweizer et al. (1978). For bright-field microscopy, Zeiss Axiophot microscopes were used. Distamycin A/DAPI fluorescence was analyzed with Zeiss
Axiophot microscopes equipped with HBO 50-W AC mercury lamps and
incident illumination by exciting with UV light in the 360400 nm range
(filter combination G 365/FT 395/LP 420). All photographic exposures were
taken with ORT 25 films (Macophot).

Results
SW480 karyotype
The SKY results are based on an analysis of 10 metaphase
spreads and generated a complete karyotype, leaving no markers of unknown origin. The average number of chromosomes
was 56 (range, 5258). Seventeen aberrant chromosomes were
detected. Karyotype details and marker analysis are shown in
Fig. 1 and Tables 1 and 2.
Chromosome breakpoints were found at 1q12, 2q24, 3p21,
3q11, 5q11, 5q15, 7q22, 8p11, 8q??, 9q11, 10p13, 12q13,
13q14, 14q22, 18q12, 19q13, and 20p12. Amplified chromosome segments involved 2pter q24, 3pter p21, 3pter
q11, 5q11 qter, 7pter q22, 8q, 9q11 qter, 11, 13q14
qter, 13, 14q22 qter, 17, 18pter q12, 21, X, and unidentified segments of chromosomes 5, 8, and 20. Deleted chromosomal segments were 8pter p11, 10pter p13, 18q12 qter,
19q13 qter, and 20pter 20p12.
A Y chromosome was not identified in any of these cells;
however, two normal copies of the X chromosome were present
in all metaphase spreads, even though these cells were derived
from a male patient.
Further analysis of SW480 marker chromosomes
The two translocations, t(1;9)(q12;q11) and der(8)t(8;9)
(p11;q11) (Fig. 1D), revealed a distinctive pattern of constitutive heterochromatin. In the long arm of the t(1;9)(q12;q11)
two C-bands and two Distamycin A/DAPI bands were detected
(Fig. 2AE). The C-band at the pericentromeric region corresponded to 1qh, whereas the C-band located approximately in
the middle of the long arm was contributed by 9qh. In the short
arm of the der(8)t(8;9)(p11;q11), a single, prominent Distamycin A/DAPI-positive heterochromatic band, corresponding to
9qh, was seen (Fig. 2FK).
SW620 karyotype
The SKY results are based on the analysis of 10 metaphase
cells and generated a complete karyotype, leaving no markers
of unknown origin. The average number of chromosomes was
48 (range, 4652). Eighteen marker chromosomes were detected. Karyotype details and marker analysis are shown in
Fig. 1 and Tables 1 and 2. A second clone (SW620/2) of SW620

Table 1. Marker chromosomes in the colon

carcinoma cell lines SW480 and SW620a

Table 2. Number of normal and rearranged

chromosomes in SW480 and SW620a

could be identified in 6 of 10 metaphase spreads having the

same alterations described for SW620/1 (Fig. 3 and Tables 1
and 2), with the exception of one der(X)t(X;6) marker chromosome (marker not shown in Fig. 3) and one normal copy of the
X chromosome, two normal copies of chromosome 13, and
three normal copies of chromosome 11. The chromosome
breakpoints detected were 2p24, 3p21, 4q28, 5q11, 5q15,
6q25, 7q22, 8p2, 10q24, 12q12; 12q23, 13q14, 13q22, 15p11,
15p13, 16q21, 16q24, 18q12, and 20p12. Amplified chromo-

somal segments identified were 5q15 q11, 5pter 5q11,

7pter 7q22, 11 (in SW620/2), 12q12 q23, 13q14 qter,
13q22 qter, 15p13 p11, 16q21 q24, 20pter p12, X, Xp
(in SW620/2), and unidentified segments of chromosomes 1, 8,
and 17. Deleted chromosome segments were 2pter 2p24,
4q28 qter, 6q25 qter, 8pter p2, and 18q12 qter. Analogous to the findings in SW480, no Y chromosome was identified in any of these cells, even though they were derived from a
male patient.

Cytogenet Cell Genet 88:145152 (2000)

147

Fig. 1. Spectral karyotyping analysis of the human colon cancer cell line SW480. (A) Inverse-DAPI stained metaphase cell.
(B) RGB image after hybridization with SKY probes and spectral karyotyping. (C) Pseudocolor image of the same metaphase
spread shown in A and B following per-pixel classification of the spectral data. (D) Karyotype of the pseudocolored chromosomes
of the metaphase spread shown in C.

Fig. 2. Selected translocation chromosomes, t(1;9)(q12;q11)

(AE) and der(8)t(8;9)(p11;q11) (FK), and marker chromosome
der(19;8;19;5) (LN) after SKY analysis (AC, FH, LN), CBG
banding (D, I), and distamycin A/DAPI counterstaining (E, K). In
D and E the primary constriction of t(1;9)(q12;q11) is marked by
the upper horizontal dash; the lower dash indicates the interstitial
heterochromatic 9qh band.

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Cytogenet Cell Genet 88:145152 (2000)

Fig. 3. Spectral karyotyping analysis of the human colon cancer cell line
SW620 (clone 2). (A) Inverse-DAPI
stained metaphase cell. (B) RGB image
after hybridization with SKY probes
and SKY. (C) Pseudocolor image of the
same metaphase spread shown in A
and B following per-pixel classification
of the spectral data. (D) Karyotype of
the pseudocolored chromosomes of the
metaphase spread shown in C.

Fig. 4. Selected complex derivative

chromosomes der(16)(t(3;16;1;16;8;16;
1;16;10) and der(18)t(18;15;17) after
SKY analysis (AC), GI)), conventional Giemsa staining (D, K), CBG banding (E, L), distamycin A/DAPI counterstaining (F, N), and AgNO3 staining
(M). Note in D the single primary (centromeric) constrictions connected by
horizontal dashes. In E and F the upper
horizontal dashes indicate the centromeric constriction of the derivative
chromosome and the lower dashes the
interstitially located 16qh bands. In K
M the horizontal dashes mark the location of the interstitial nucleolus organizer region, which is distinctly labeled
by AgNO3 staining (M).

Cytogenet Cell Genet 88:145152 (2000)

149

Further analysis of the SW620 marker chromosomes

The two complex derivative chromosomes, der(16)t(3;16;1;
16;8;16;1;16;10) and der(18)t(18;15;17) (Fig. 3D), were examined by additional cytogenetic techniques. The extremely large
der(16)t(3;16;1;16;8;16;1;16;10) marker was derived from five
different chromosomes (Fig. 4AC). Conventional Giemsa
staining showed this marker chromosome to be monocentric,
with a single primary constriction located in the upper third of
the chromosome (Fig. 4D). In none of the metaphase cells
examined, a further primary constriction (active centromere)
could be visualized along the chromatids of this multiple translocation product. CBG-banding (Fig. 4E), as well as Distamycin A/DAPI counterstaining (Fig. 4F) demonstrated that two
distinct bands of constitutive heterochromatin were present in
the long arm of the marker. Both of these bands are located
within the segments identified as derivatives of chromosome
16 (compare Fig. 4E, F and 4AC). One of the C-bands was
located adjacent to the primary constriction and the other one
at the distal quarter of the chromosome. Since both heterochromatic regions were brightly fluorescent after Distamycin A/
DAPI counterstaining (Fig. 4F), it can be concluded that they
represent the repetitive DNA sequences located originally in
the pericentromeric region of the long arm of two chromosomes
16, resulting in a duplication of the chromosome region
16q22 q24. The segment located between the two heterochromatic bands seems to be symmetrical, indicating an origin
by a single duplication event of a der(16)t(16;1;16;8) marker
chromosome resulting in a der(16)t(16;1;16;8;16;1;16) marker.
Only 16q is involved in this duplication. After this event, material of chromosomes 3 and 10 was translocated to the marker,
resulting in the der(16)t(3;16;1;16;8;16;1;16;10).
The derivative chromosome der(18)t(18;15;17) exhibited a
distinct secondary constriction in the middle of the long arm
after conventional Giemsa staining (Fig. 4K), CBG-banding
(Fig. 4L), and Distamycin A/DAPI counterstaining (Fig. 4N).
Following AgNO3-staining, this constriction was intensely labeled in all metaphase cells examined (Fig. 4M). This demonstrates that a nucleolus organizer region (NOR) containing
actively transcribed 18S and 28S ribosomal RNA genes must
be present within the secondary constriction. The latter finding
is in agreement with the SKY analyses, which identified the
corresponding der(18)t(18;15;17) marker as chromosome 15
material (Fig. 4GI). Therefore, the NOR inserted into the long
arm of the marker chromosome must have been derived from
the short-arm region of a chromosome 15 (bands 15p13
p11).
Chromosome alterations common to both cell lines
In both SW480 and SW620 the following common chromosome gains, losses, and breakpoints were found. Gains: 5q15
5q11, 7pter q22, 11 (in SW480 and SW620/2), 13q14 qter,
20pter 20p13, and X; losses: 8pter 8p2, 18q12 qter; and
Y; breakpoints : 5q11, 5q15, 7q22, 13q14, 18q12, and 20p12.
Chromosomal alterations specific to SW620
The chromosome segments 5pter 5q11, 12q12 q23,
15p13 p11, and 16q21 q24 were amplified, and the chro-

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Cytogenet Cell Genet 88:145152 (2000)

mosome regions 2pter p24, 4q28 qter, and 6q25 qter

were lost. Detected breakpoints were 2p24, 3p21, 4q28, 6q25,
8p2, 12q12, 12q23, 13q22, 15p11, 15p13, 16q21, and 16q24.
Comparison with previous G-banded karyotypes
Gagos et al. (1995) described 17 chromosome alterations in
SW480 and one marker chromosome of unknown origin. We
have observed and classified a total of 17 alterations. Common
aberrations identified in both studies were t(1;9)(q12;q11),
der(5)t(5;20)(q15;p12), der(7)t[inv(7);14][(q22;q36)(q22;q22)],
der(8)t(8;9)(p11;q11), 9, +11, der(18)del(18)(q12), +X, and
Y. Newly described markers in the present study were
der(3)del(3)(q11), der(5)t(5;20)(q11;??), der(7)t(7,13)(q22;q14),
der(8)t(8;19), and der(12)del(12)(q13). Refinements could be
made in der(19)t(19,?), which was identified as a der(19)t(19;
8;19;5) marker chromosome. The derivative chromosomes
der(2)t(2;3)(q24;p21) and der(10)t(10;12)(p13;q12) found by
Gagos et al. (1995) correspond to the markers der(2)t(2;12)
(q24;q13) and der(10)t(10;3)(p13;q21). We could not detect a
der(2)t(2;11)(p36;q22), der(2)dic(2;12)(q24;p13), der(5)del(5)
(q15), or 12 marker. In SW620, 14 altered chromosomes were
detected by Gagos et al. (1995), leaving one marker of unknown
origin. Our study detected 18 alterations. Confirmed were the
following changes: der(2)t(2;12)(p24;q12q23), der(4)del(4)
(q28), der(5)t(5;20)(q15;p12), der(7)del(7)(q22), +11, +X, and
Y. In addition we found the marker chromosomes der(3)
del(3)(p21), der(5)t(5;20)(q11;??), der(6)t(6;7)(q25;?), der(7)
del(7)(p;q), der(8)t(8;17)(p2;??), 13, der(18)t(18;15;17)
(q12;p11p13;??), and der(X)t(X,6). Refinements could be
made in der(8)t(8;13)(p11;q11), which was a der(8)t(8;13)(p2;
q14) marker; der(10)t(10,?), which was identified as a der(10)
t(10;13)(p13;p21) marker; and der(3;16)t(3;16)(p1;13)dup(16)
(q21q24)dic(16;16)(q24;p13), which was defined as the exceptional marker der(16)t(3;16;1;16;8;16;1;16;10). None of five
previously described alterations, der(3)del(3)(p21), der(5)
del(5)(q15), der(7)del(7)(p12), der(13)del(13)(q13), or der(18)
del(18)(q12), could be detected.

Discussion
Shared gains and losses in SW480 and SW620 may
represent chromosome alterations important for primary
colorectal tumors
The development of most colorectal carcinomas seems to be
dependent on deletions and amplifications of multiple chromosome segments (Mertens et al., 1997). We could identify common gains (5q15 5q11, 7pter q22, 11 [in SW480 and
SW620/2], 13q14 qter [in SW480 and SW620/2], 20pter
p12, and X) and losses (8pter p2, 18q12 qter, and Y) in
SW480 and SW620. Several studies using banding methods
(Bardi et al., 1995; Mertens et al., 1997), as well as comparative
genomic hybridization (CGH; Ried et al., 1996), identified
common amplifications and/or deletions in colorectal carcinomas. Frequently amplified chromosomal regions or chromosomes found in all studies were 1q, 7, 8q, 13q, and 20. Frequently lost were 1p, 5q, 8p, 17p, 18, and Y. Thus the altera-

tions in both SW480 and SW620 are in good agreement with

those frequently reported for other colorectal tumors and could
represent genetic alterations in primary tumor cells.
Gains and losses exclusively to SW620 may represent
genetic alterations important for metastatic growth
If the shared abnormalities between SW480 and SW620
represent the primary changes in a putative tumor stem cell,
then unique chromosome abnormalities limited to SW620 cells
could represent changes that occurred during the metastatic
spreading of the tumor. To date, only few data are available on
chromosomal abnormalities in metastases. CGH data of Korn
et al. (1999) indicate that colorectal metastases (27 examined)
show chromosome changes similar to those that have been
reported for primary tumors. Chromosome losses were seen at
higher frequency, particularly for chromosomes 14 and 15. AlMulla et al. (1999) examined 12 colorectal metastases by CGH
and found a reduced copy number of chromosome 17p. An
increased copy number of chromosomes 6p and 17q was associated with Dukes stage D and liver metastases. Comparison of
the primary tumor cell line SW480 with the metastatic cell line
SW620 showed gains of 5pter 5q11, 12q12 q23, 15p13
p11, and 16q21 q24 and losses of 2pter p24, 4q28 qter,
and 6q25 qter only in SW620.
Amplified chromosome regions in SW620 (5pter 5q11,
12q12 q23, 15p13 p11, and 16q21 q24) may point
to the location of oncogenes
Band 5p15.33 is known to harbor the telomerase reverse
transcriptase (TERT) gene (Meyerson et al., 1997). Kolquist et
al. (1998) studied TERT expression in normal colon epithelial
cells and in various stages of tumor progression and found that
the expression increased gradually during progression. Hahn et
al. (1999) reported that ectopic expression of TERT, in combination with two oncogenes (SV40-large T and HRAS), resulted
in tumorigenic conversion of normal epithelial cells. A putative
oncogene on chromosome 12 is the SAP2 gene, which was mapped to band 12q23 (Shipley et al., 1994). No information is yet
available on the role of SAP2 expression and metastasis, but
SAP1 (like SAP2, a transmembrane-type protein tyrosin phosphatase) is frequently overexpressed in human colorectal cancers (Seo et al., 1997). ERBB3 is an epidermal growth factor
receptor-related gene located at 12q13 (Plowman et al., 1990).
It is a transmembrane signaling molecule that has been implicated in cell transformation and tumor pathogenesis. Mauerer
et al. (1998) showed increased ERBB3-expression in 31/35
colonic cancers (81 %). To date, no oncogenes have been mapped to chromosome 15p13 p11. The MAF oncogene was
localized to 16q22 q23 (Yoshida et al., 1991). The amino
acid sequence of the gene product contains a leucine zipper
motif similar to that found in the FOS, JUN, or MYC oncogenes. Whether MAF plays a role in colorectal cancer or metastasis remains to be seen.

Deleted chromosome regions in SW620 (2pter p24,

4q28 qter, 6q25 qter) may point to the location of
tumor suppressor genes
Partial losses of chromosome 4q and 6q were found only in
SW620, but not in SW480. Ried et al. (1996) used CGH to
identify chromosome imbalances in colorectal adenomas and
adenocarcinomas. Chromosome 4 was frequently underrepresented. Mertens et al. (1997) found segments of chromosomes 4
and 6 frequently deleted. To date, no authenticated tumor suppressor genes or oncogenes have been mapped to either chromosome 4q or 6q, but it has been shown that chromosome 4 is
involved in cellular senescence in vitro (Ning et al., 1991). Loss
of the chromosome region 2pter p24 has not been a frequent
finding in either primary colorectal carcinomas or their corresponding metastases.
Conclusions
The application of SKY enabled a detailed analysis of marker chromosomes in two colorectal cancer cell lines. The results
clearly demonstrate the advantages of SKY over conventional
banding techniques. Several marker chromosomes previously
classified by G-banding analysis turned out to be more complex
alterations when analyzed by SKY: der(16)t(3;16;1;16;8;16;1;
16;10) in SW620 and der(19)t(19;8;19;5) in SW480. The (erroneously) classified marker chromosomes der(2)t(2;3)(q24;p21)
and der(10)t(10;12)(p13;q12), described by Gagos et al. (1995),
and several unidentified translocated fragments, e.g.,
der(5)t(5;20)(q15;p12) and der(8)t(8;17)(p2;q14), reflect the
difficulties in the identification of small translocated fragments
by conventional banding. Four oncogenes (TERT, SAP2,
ERBB3, and MAF) are located in chromosome segments that
were found to be amplified in SW620 but not in SW480. These
oncogenes could have been important for metastatic spread of
the specific tumor analyzed in this study. Further studies are
needed to clarify the general role of these oncogenes in the metastatic progression of colorectal cancer. The identification of
tumor-stage specific chromosome alterations could be important for prognosis and therapy planning.

Cytogenet Cell Genet 88:145152 (2000)

151

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