[CANCER RESEARCH 28, 481-490,March 1988]
Chromosome
C. P. Miles, F. O'Neill,
University
Patterns
of Human Leukocyte
Established
Cell Lines1-2
D. Armstrong, B. Clarkson, and J. Keane
oj Utah School of Medicine, Salt Lake City, Utah 84112, and Sloan-Kettering
Institute,
New York City, New York 10021
SUMMARY
MATERIALS AND METHODS
Of 14 lines of human leukocytes, designated LK1D, LK57,
LK60, LK63, LK87A, LK91, SK-L1, SK-L3, SK-L4, SK-L5,
SK-L6, SK-L7, RPMI 7216, and RPMI 7466, all were classi
cally diploid or very near-diploid when first examined.
All but one showed occasional No. 10 chromosomes with the
near terminal secondary constriction seen in Burkitt lymphoma
cells in vitro. Nine lines showed accentuation of secondary con
strictions at the usual sites on Chromosomes No. 1 and/or
No. 16. Exchanges often occurred at these sites. Some cells
in various lines showed multiple secondary constrictions or
fragmentation (pulverization), but these and other chromo
some abnormalities were in lower incidence than in Burkitt
lymphoma strains. Many of the abnormalities in these lines
may reflect underlying abnormalities of nucleoli or of nucleolarassociated heterochromatin.
For chromosome work, technics for cell culture have been
similar to those used with Burkitt lymphoma lines (22), ex
cept that milk dilution bottles are used. Although cells do not
grow spread out on the glass, the greater surface area afforded
by these bottles seems to permit more rapid growth.
In general, the conditions of culture do not permit highly
accurate estimates of the age of a line in passages or genera
tions. Assuming a generation time of 30-40 hours, one obtains
a figure of about 18-20 generations per month of active multi
plication. For fuller details the reader should consult the perti
nent references (1, 5, 23).
Cells are harvested for chromosome analysis 24 hours after
a change of medium. The cultures are incubated for 1.75
hours with colchicine at a final concentration of 0.5 microgram
per ml. Chromosome preparations were made as previously
described (22).
INTRODUCTION
It has only recently been shown that human leukocytes, ma
lignant or benign, can be continuously grown in cell culture
(1, 5, 9, 15, 23, 24). Reports or brief mention have appeared
on chromosome patterns in some of these lines (5, 18, 23, 24).
The present paper concerns 6 established lines (the LK lines)
plus further details on 8 lines on which some cytogenetic data
have appeared (5, 23). Recently zur Hausen (36) has published
details on 3 of the LK and 2 of the SK lines. The precise
origin of the various lines is described in the appropriate
references (1, 5, 23). Briefly, all the SK and LK lines were
derived from patients with leukemia. The 2 RPMI lines stem
from individuals without neoplastic disease. Details, other than
cytogenetic, on LK63, LK87A, and LK91, will be reported at a
later date by one of us (D. A.). (LK87A and LK91 stem from
patients with chronic myeloid leukemia and LK63 from a pa
tient with acute lymphoblastic leukemia.)
Thus far all human leukocyte strains in vitro have been
diploid or very near diploid (4, 5, 16-18, 22, 24, 28, 32, 34)
except for one substrain of EB2 (6). In this respect these
strains have tended to show less deviation from the normal
karyotype than do acute leukemia cells from direct prepara
tions or short term culture (26, 29).
1 Supported
by Damon Runyon
Memorial
Fund, Grant
DRG798, and by NCI CA08748.
2 A portion of this work has been reported to the American
Association for Cancer Research, Chicago, April, 1967 (Proc. Am.
Assoc. Cancer Res., 8: 181, 1967).
Received July 17, 1967; accepted November 5, 1967.
MARCH
RESULTS
Table 1 lists the cell lines studied. The majority of these
lines were classically diploid when first examined. One, LK87A,
was hypodiploid with a possible marker in lieu of a 4-5 chromo
some (stemline at 45) (Figs. 1, 2), while another, SK-L3, ap
parently had two stemlines at 46 and 47 (Fig. 3). Although
LK87A and LK91 derive from patients with chronic myeloid
Table 1
DesignationLK1DLK57LK60LK63LK87ALK91SK-L1SK-L3SK-L4SK-L5SK-L6SK-L7RPMI
sexXXXXXXXX?XXXXXYXYXXXXXXXYXYStemline
No.4646464645464646-47"46464646«4646Class
diploidYesYesYesYesNoYesYe
7216RPMI
7466Chromosomal
Status of lines when first examined.
a Sublines of SK-L3 and SK-L7 are now near-tetraploid.
The
lines in general tend to show a high incidence of polyploidy.
1968
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481
C. P. Miles, F. O'Neill, D. Armstrong, B. Clarkson, and J. Keane
leukemia, we have not found convincing examples of the Ph 1
chromosome in either. Recently two substrains in continuous
passage, LK63 and LK1D, have developed probable markers.
(The word "marker" will be used here in the broad sense of
any clearly abnormal chromosome).
The LK63 strain has a
chromosome in the 6-12 group with an abnormally short short
arm (Figs. 4-6). The LK1D strain lacks a 21-22 chromosome
and has an extra chromosome with about the configuration of
a 4-5 chromosome. This chromosome often has a distinctive
secondary constriction
(Fig. 7), and may have been formed
by fusion of a short acrocentric with the long arm of Chromo
some No. 1 (see below), i.e., 46, XX, G—,t(lq+G)+
to use the
Chicago Conference nomenclature
(3).
Although often classically diploid, these cell lines show a
higher incidence of variant karyotypes than do fibroblast cul
tures or short-term lymphocyte cultures (Table 2). However,
the variation is not so marked as that in some of the Burkitt
lymphoma strains (22). Another feature common with the
Burkitt strains is the occasional presence of a near-terminal
secondary constriction on the long arm of Chromosome No. 10
(Table 3; Figs. 8, 9).
A number of the lines have tended to show a high incidence
of near-tetraploidy,
and a few substrains have become pre
dominantly
subtetraploid.
However, we have observed with
some lines that there are more tetraploids
among the cells
which tend to adhere loosely to the glass. Conversely, with
such lines, if cells in suspension are carefully decanted off,
there are fewer tetraploids.
While this observation
is as yet
tentative, it seems worth recording, since it suggests that the
incidence of tetraploidy may sometimes depend in part on the
precise manner in which chromosome preparations
are made.
The most distinctive feature of a majority of the lines (9 of
14) is the high incidence of prominent secondary constrictions
on Chromosomes No. 1 and No. 16 (Table 3, Fig. 10). Both
the incidence and the degree of attenuation are often markedly
increased. In addition, there are frequent associations between
the constrictions
on these chromosomes. In some cases where
constrictions are associated together, chromatid exchanges have
occurred (Fig. 10).
The marker [t (lq,G)] mentioned in line LK1D frequently
assumed variant forms or was accompanied by other elements.
In a few cells, what is plausibly the long arm of a No. 1 ap
peared as an acentric fragment (Fig. 12). However, this cell
is somewhat ambiguous, since what is probably the marker
cannot be distinguished from an extra 4-5 chromosome). An
other cell (Fig. 11) contained two such fragments as well as
the marker. One cell (Fig. 13) contained a marker which ap
pears to represent a long acrocentric fused to the long arm
of a No. 1, i.e., 46, D—, t(lqD). Appropriately,
this cell lacks
a long acrocentric but has a full complement of short acrocentrics (in contrast with the stemline karyotype
which has
only 3). In at least 4 cells the fusion appeared to have occurred
between the No. 1 long arm and (presumably)
the telomere of
the short arm of a C-group chromosome (Fig. 14). In a few
cells, the chromosome number or group of the element fused
to the No. 1 long arm was uncertain.
Since secondary constrictions
(8, 30) and acrocentric asso
ciations (8, 27, 30) have been postulated
to be related, the
types of acrocentric association were also scored in Table 3.
In some of the cell lines (especially LK63) there was a high
sporadic incidence of dicentric chromosomes.
Twenty-three
metaphase figures with dicentrics were analyzed in an attempt
to determine which chromosomes had fused (the assumption
being that the two missing homologs formed the dicentric). The
types of dicentrics and their incidence are shown in Table 4.
The data cannot definitely be said to be nonrandom as regards
the original formation of dicentrics, since an occasional dicen
tric may persist through more than one cell division. However,
in 19 of 23 cells there appeared to be no gain or loss of chro
mosome material (Figs. 4-6, 15). In two cells, the dicentric
Table 2
atLineLK1DLK57LK60LK63SK-L1SK-L3SK-L4SK-L5SK-L6SK-L7RPMI
Cell with counts
4n232212148814000Variants,
etc.1
markers,
502
cell at
markers3
cells with
markers1
cells with
482
cell each at 43 &
markers1
cells with
5/666/21/663/
492
cell each at 42, 43,
cells1
pulverized
511
cell at
7/676/22/666/16/666/15/6612/20/6612/24/6644311000211003104573563155456211463740363839925322942394348474703522
481
cell at
431
cell at
marker1
cell with
marker2
cell with
7216RPMI
fragments1
cells with
7466367«366»Date3/24/663/22/663/24/663/10/667/
431
cell at
pulverized cell
Chromosome counts: variants, 50 cells.
•
Peripheral lymphocyte cultures.
482
CANCER
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Chromosomes of Leukocyte Lines
Table 3
of secondary
of
constriction on
acrocori rie association
types6D-G18152319211935321540333119161834244947462813173515586025D
by
No.10802540150313002131201021163100010230261512071440610720600131200101162100260140148030037050000120011090
Chromosome
prepara
DescriptionLK1DLK57LK60LK63LK87ALK91SK-L1SK-L3SK-L4SK-L5SK-L6SK-L7RPMI
tion3-24-664-13-673-22-662-24-673-24-661-13-673-10-663-14-6712-13-664-14-677(months)11241021717416611172615213115616277101131Incidence
of
oftine
5-664-13-676-21-6612-29-667-
5-6637-676-22-666-16-664-18-676-15-6612-20-6612-20-663-
7216RPMI
7466EB2366«367«WI38<*Date
7-674-13-6512-13-661-26-66Age«
Incidence of secondary constrictions and acrocentric association in 100 cells for each prep
aration.
»
LK1D was frozen from 12-66 to 1-67; SK-L1 was frozen from 12-66 to 2-67.
6 More than two acrocentrics associated together were scored as D-G unless all 3, 4, or
more were of the same type. Acrocentrics were scored as associated if the short arms pointed
toward one another and were less than a chromosome thickness apart.
" Peripheral lymphocyte cultures.
d See Reference 10.
appeared to have gained material. Two cells could not be
analyzed, one because one of the components of the dicentric
was of uncertain origin and the other because it contained
multiple dicentrics (Fig. 6).
DISCUSSION
The cell lines described are similar to Burkitt cell lines in
tending to be diploid or near-diploid, although near-tetraploid
substrains have occasionally emerged. Sporadic markers which
may occasionally become fixed in the stemline are also common
to both Burkitt and peripheral leukocyte lines. It would ap
pear that, in order to maintain a particular stemline karyotype
in leukocyte cell lines, one must monitor and occasionally dis
card deviant substrains, or grow out frozen aliquots from the
original line.
The presumed No. 10 chromosome with a near terminal
secondary constriction might conceivably be a feature of any
permanent cell line of leukocytes, whether originally malignant
or benign. Note that it occurs also in RPMI 7466, although
this line stems from an individual without neoplastic disease.
On the other hand, the line RPMI 7466 may represent a case
of in vitro "transformation" or "alteration." This latter process
might be a form of oncogenic transformation. The No. 10 con
striction has thus far apparently never been seen in direct
chromosome preparations of neoplastic cells. However, there
MARCH 1968
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483
C. P. Miles, F. O'Neill, D. Armstrong, B. Clarkson, and J. Keane
Table 4
Chromosome
or involvedc
group
No.
c2+
C4/5
+
C3 +
C1+21
+
4/52
+
162+
+
?16
C17/18
+
C21/22+
C21/22+
16MultipleNo.
+
telomeres of other chromosomes, suggest a similar process. More
specifically,
it appears to be the secondary constriction in
ofinstances7421111111111
Chromosome No. 1 which is involved, just as with the chroma
tid exchanges with the No. l homolog or with Chromosome
No. 16 (Fig. 10). When the long arm of No. 1 appears alone
it closely resembles the marker labeled Del-1 in SV40 trans
formed cells (25). Whether the short arm of the No. 1 has
simply been lost in the course of cell division or has been frag
mented as described by zur Hausen (36) cannot be determined.
Two of us (C. M. and F. O'N.) have also observed the G2
Origin of dicentric chromosomes in 23 cells.
is a recent report of its occurrence in normal leukocytes after
growth with irradiated Burkitt cells (12). In this connection,
it is of interest that RPMI 7466 is reported (23) to contain
herpes-like virus similar to that seen in Burkitt cell lines.
The high incidence and degree of attenuation of the second
ary constriction on Chromosomes No. 1 and No. 16 are promi
nent features of some of the peripheral leukocyte cell lines. As
with the constriction on Chromosome No. 10, it is also seen
in RPMI 7466; therefore, it is not restricted to cells stemming
from leukemia cases. Moreover, there is a strong tendency for
the No. 1 and No. 16 attenuated constrictions to appear first,
or at least in higher incidence, in later passages. In addition,
one of the Burkitt line (Ogun) substrains now shows a high
incidence of secondary constriction on Chromosome No. 1
(Fig. 10), as does a cell line of malignant melanoma (kindly
furnished us by Dr. Alice Moore of the Sloan-Kettering In
stitute). Thus, this feature is not necessarily restricted to
peripheral leukocyte cultures.
The No. 1 and No. 16 chromosomes tended to associate to
gether at their constrictions and, occasionally, to exchange
chromatid arms at these sites. As seen in Table 3, there does
not appear to be any definite correlation, direct or inverse,
between the incidence of attentuated constrictions and the in
cidence of acrocentrie associations. (Perhaps one should better
compare secondary constrictions and satellite length, but this
is technically very difficult.) It may be of interest that, in 18
preparations of 28, the types of acrocentrie association were
ranked as follows: 13-21 more than 13-13 more than 21-21.
In 25 preparations of the 28, there were more 13-21 than 13-13
instances of association. These frequencies do not constitute a
distinctive feature of leukocyte cell lines since they are similar
to those found by Ferguson-Smith and Handmaker (7) in
benign lymphocytes. (They found lower incidences of associa
tion, probably because they specified that satellites had to be
touching.)
The tendency for dicentric chromosomes to be formed with
little or no apparent loss of chromosome material suggests
that they may arise by some process akin to centric fusion
and secondary to telomeric association.
The various markers in LK1D, probably involving the long
arm of a No. 1 with the short arms of acrocentrics and the
484
labeling of fragments, as pointed out by zur Hausen, as well
as, more generally, the G2 labeling of all spontaneously pulver
ized chromosomes.
Since most of the LK1D cells contain only 3 small acrocen
trics (the 4th presumably being fused to the marker), it is
possible that cells with 4 small acrocentrics and other forms
of the marker are arising de novo as a result of a break at the
point of union of the two elements forming the marker. This
would lead to the reappearance of the 4th small acrocentrie
in the karyotype and might thus suggest that centric fusion is
potentially reversible.
The recent work of Hsu et al. (13) and of Heneen and
Nichols (11) suggests that nucleoli may be associated not only
with acrocentrics, but also with telomeres and with areas of
secondary constriction. The observations that acrocentrics (30)
may associate with the secondary constriction on Chromosome
No. 1 or on other chromosomes (8) bolsters the latter part of
this suggestion. The tendency for homologs with secondary
constrictions to associate together may make them liable to
nondisjoin.
The appearance of accentuated secondary constrictions in
cancer cells (21), or in cells transformed in vitro, abnormalities
such as tririadials (19, 20), which often appear to be formed
at the sites of secondary constrictions (14, 31) markers arising
through centric fusion (2, 20, 33, 35; C. P. Miles, G. Moldavannu, and D. G. Miller. Chromosome Studies of Canine Lymphosarcomas, in preparation), as well as dicentrics and nondisjunction, probably secondary to chromosome association, all
suggest the possibility that many cytogenetic abnormalities
may be consequences of some more fundamental derangement
of nucleoli, or perhaps of nucleolar-associated heterochromatin.
ACKNOWLEDGMENTS
We are grateful to Dr. G. E. Moore for providing us with sam
ples of RPMI 7216 and 7466. We thank Miss Lynn Steger for
technical assistance.
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485
C. P. Miles, F. O'Neill, D. Armstrong, B. Clarkson, and J. Keane
Figs. 1, 2. Two apparently identical karyotypes with 45 chromosomes in LK87A. The last chromosome in the first row is probably a
marker being in general larger than the 4-5 chromosomes. (However, a familial polymorphism cannot be ruled out.) This marker was
probably present in all cells, but, in occasional cells, could not be clearly distinguished from a 4-5 chromosome.
Fig. 3. A karyotype of SK-L3 with 47 chromosomes, trisomy No. 3. Note secondary constrictions on Nos. 1 and 16. Other SK-L3 cells
had 46 chromosomes and appeared classically diploid.
Figs. 4, 5. LK63 karyotypes with dicentrics. The last chromosome in the C group (second row) is a marker which always occurred in
stemline karyotypes. In Fig. 4 the dicentric appears to have been formed by a No. 2 and a C group chromosome, in Fig. 5 by two C
group chromosomes.
Fig. 6. LK63; 3 dicentrics of uncertain origin, 2 possibly of common origin and involving a long acrocentric.
Fig. 7. LK1D. The marker may result from fusion of a short acrocentric chromosome with the long arm of a No. 1 broken at the
secondary constriction. (This, of course, assumes trisomy for the No. 1 long arm.)
Fig. 8. LK63. Karyotype showing near terminal secondary constrictions on Chromosome No. 10.
Fig. 9. No. 10 chromosomes from various cell lines.
Fig. 10. Associations and chromatid exchanges, Chromosome Nos. 1 and 16. The last examples in the first and second rows are from
the Burkitt line, Ogun. The last row shows associations of 16's with the centromere of Chromosome No. 2.
Fig. 11. LK1D. A No. 1 is missing and replaced by two fragments (or telocentrics?) possibly representing the arms of the missing No.
1. A long acrocentric is also missing, presumably having fused with the long arms of the marker and, perhaps, having displaced the
short acrocentric which is now restored to its original place in the karyotype.
Fig. 12. LK1D. Acentric fragment—long arm of No. 1? Since a short acrocentric is missing, the usual marker is probably here but
cannot be distinguished from a No. 4-5 in this cell.
Fig. 13. LK1D. Presumed long arm of No. 1 fused with short arm of a long acrocentric.
Fig. 14. LK1D. Marker formed apparently by a 6-12 chromosome fused to a No. 1 long arm.
Fig. 15. LK63. Dicentric formed by apparent fusion of a No. 16 with a 6-12 chromosome.
486
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VOL. 28
Chromosomes of Leukocyte Lines
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Chromosome Patterns of Human Leukocyte Established Cell
Lines
C. P. Miles, F. O'Neill, D. Armstrong, et al.
Cancer Res 1968;28:481-490.
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