[CANCER RESEARCH 48, 4307-4311, August 1, 1988]
Indistinguishable Patterns of Protooncogene Expression in Two Distinct but Closely
Related Tumors: Ewing's Sarcoma and Neuroepithelioma
Catherine McKeon, Carol J. Thiele, Robert A. Ross, Michael Kwan, Timothy J. Triche, James S. Miser, and
Mark A. Israel1
Pediatrie Branch, Division of Cancer Treatment [C.M., C.J.T., M.K., J.S.M., MA.l.J; the Laboratory of Pathology, Division of Cancer Biology and Diagnosis, [T.J.TJ
National Cancer Institute, NIH, Bethesda, Maryland 20892; and the Department of Biology, Fordham University, New York, New York 10023[Rjl.R.]
ABSTRACT
Genetic characterization of human tumors promises new insights of
biological importance and clinical relevance. We have found that two
solid tumors, peripheral neuroepithelioma and Ewing's sarcoma of bone,
which share a common cytogenetic rearrangement, are characterized by
an indistinguishable and highly reproducible pattern of protooncogene
expression, c-myc, N-myc, c-myb, and c-mll/raf-1 are all expressed at
similar levels in these tumors, c-fes and c-sis expression was not detected
in any specimens of either tumor. In contrast, the protooncogene ort.v-1,
located near the breakpoint of the chromosomal translocation in these
tumors, is variable in its expression. We also detected high levels of
choline acetyltransferase in these tumors, which suggests a common
neural origin. Since it is likely that the clinical behavior and therapeutic
responsiveness of tumors relate closely to their biological and genetic
features, the pattern of protooncogene expression of individual tumors
may provide a novel basis for their characterization.
INTRODUCTION
The practice of medicine is anchored in the classification of
disease into homogeneous disorders that make possible individ
ualized approaches to therapeutic intervention and prognosti
cation. It is ironic that while cancer is perhaps the most heter
ogeneous of diseases, we can rarely discern homogeneous bio
logical entities among the various solid tumors. Furthermore,
current tumor nosologies are based almost exclusively on the
appearance of tumor tissues and the cytological features of
tumor cells. Such an approach to classification greatly limits
the possibility of recognizing tumors that may be biologically
and even pathologically closely related if they cannot be recog
nized as arising in the same organ or in closely related tissues.
We investigated the possibility that patterns of protoonco
gene expression may identify genetically and biologically related
malignancies. Protooncogenes are the cellular homologues of
viral transforming genes and are differentially expressed in a
highly restricted manner during normal growth and develop
ment (for review, see Refs. 1 and 2). The expression of a
protooncogene in a specific tissue seems to be determined by a
number of cellular characteristics, such as tissue lineage, mat
urational stage, and growth rate (1, 3, 4). Since these same
features are important in determining the behavior of malignant
tumors, the pattern of protooncogene expression in individual
tumors might reflect clinically important features and identify
biologically homogeneous tumor groups.
In pursuit of this idea, we investigated the pattern of pro
tooncogene expression in two histopathologically distinct ma
lignancies, Ewing's sarcoma and neuroepithelioma, that are
both characterized by the cytogenetic rearrangement t(ll;22)
(q24;ql2). Ewing's sarcoma is the second most common child-
Received11/4/87;revised3/11/88;accepted4/26/88.
The costs of publication of this article were defrayed in part by the payment
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1To whom requests for reprints should be addressed, at Building 10, Room
13N240, Pediatrie Branch, Division of Cancer Treatment, National Cancer
Institute, Bethesda, MD 20892.
hood tumor of bone. Since the first description of a chromo
somal rearrangement in this tumor in 1983, this translocation
or a complex variant has been recognized as a consistent cyto
genetic finding in Ewing's sarcoma tumors (5-9). Neuroepithe
lioma is a rare tumor of the peripheral nervous system (S). A
t(l 1;22) (q24;ql2) chromosomal translocation is also found in
this tumor (9, 10). Despite intensive cytogenetic and molecular
analyses of the chromosomal rearrangement in these two tu
mors, it has not been possible to distinguish them from one
another (11-14). In contrast, histológica!, ultrastructural, and
immunohistochemical studies reveal many markers of neural
differentiation in neuroepithelioma but not in Ewing's sarcoma
(15-17). Indeed, the cell of origin of Ewing's sarcoma has been
a topic of considerable speculation largely because of the ab
sence of recognizable markers of tissue-specific differentiation
in this tumor.
Despite their histológica! and cytological differences, we
found that the pattern of protooncogene expression in Ewing's
sarcoma and neuroepithelioma are highly predictable and in
distinguishable. We also found that these two tumors share at
least one common neuron-specific marker, namely high levels
of choline acetyltransferase activity. These similarities suggest
that Ewing's sarcoma and neuroepithelioma arise from cells of
a common lineage and that the determination of patterns of
protooncogene expression may be a useful approach to the
characterization and classification of tumors.
MATERIALS AND METHODS
Tissues and Cell Lines. Tissue samples were obtained either during
surgery or at autopsy from tumors diagnosed as either ES2 of bone or
NE on the basis of standard clinical and pathological evaluation. Only
tumor samples with a classic ES or NE pathology were used for this
study. Extraosseous ES tumors were excluded from this analysis, since
they do not show a t(ll;22) and may represent a separate entity (9).
Most specimens were frozen in liquid nitrogen and stored at — 70°C
before isolation of RNA. Specimens of normal human brain were
obtained in the same manner and were studied to determine protoon
cogene patterns in a normal neuronal tissue. Most tumor samples were
karyotyped by examination of material cultured overnight. All tumor
specimens that could be evaluated had demonstrable t(ll;22) marker
chromosomes (see Table 1). Tissue culture lines were started from
tumor specimens by dispersing cells in 0.02% trypsin and culturing in
RPMI 1640 medium supplemented with 15% fetal calf serum. (The
NE lines N1000, N1008, N1016, N1043, N1046, and TC32 and the
ES lines N1001, N1002, N1050, TC71, TC106, 5838,6647, and A4573
are continuous cell lines established at NIH; CHP100 was obtained
from Children's Hospital, Philadelphia, PA and SK-N-MC from Dr.
June Biedler, Sloan-Kettering Memorial Hospital, New York, NY.)
We used all the ES and NE tissue culture lines available to us which
had been karyotyped (9)3 (see Table 1). In addition, fibroblasts and a
lymphocyte (IM-9) cell line were studied for mRNA expression.
Neurotransmitter Enzyme Assays. Tissue culture cells were grown in
2 The abbreviations used are: ES, Ewing's sarcoma; NE, neuroepithelioma;
TH, tyrosine hydroxylase; CAT, choline acetyltransferase; DBH, dopamine ,¡
hydroxylase; poly(A)*, polyadenylated; kb, kilobase.
3J. Whang-Peng and M. A. Israel, unpublished results.
4307
Research.
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