Vol. 1, 129-136, January 1995 Clinical Cancer Research 129
3 L. M. Wakefield, unpublished data.
Transforming Growth Factor- 31 Circulates in Normal Human
Plasma and Is Unchanged in Advanced Metastatic
Breast Cancer
Lalage M. Wakefield,1 John J. Letterlo,
Theresa Chen, David Danielpour,
Robin S. H. Allison, Lee H. Pai,
Andrea M. Denicoff, Marianne H. Noone,
Kenneth H. Cowan, Joyce A. O’Shaughnessy,
and Michael B. Sporn
Laboratory of Chemoprevention [L. M. W., J. J. L., T. C., D. D.,
R. S. H. A., M. B. S.] and Medicine Branch [L H. P., A. M. D.,
M. H. N., K. H. C., J. A. 0’S.], National Cancer Institute, Bethesda,
Maryland 20892-5055
ABSTRACT
A method has been developed to determine true plasma
transforming growth factor 1 (TGF- 3) levels by using the
platelet a granule-specific marker, platelet factor 4, to cor-
rect for the TGF- 3 contributed by platelets degranulated ex
vivo. TGF-f3 levels were measured on acid-ethanol extracts
of human plasma using isoform-specific sandwich enzyme-
linked immunosorbent assays. Normal human subjects had
41 ± 2.0 ng/ml TGF- 31 (range, 2.0-12.0; n 42), <0.2
ng/ml TGF- 32, and <0.1 ng/ml TGF- 3 in their plasma.
There were no significant changes with age or with hor-
monal status, but any given individual showed fluctuations
of up to 3-fold in measured plasma TGF-f levels due to
unknown factors. Of 28 patients with advanced metastatic
breast cancer, 2 had greatly elevated TGF- 31 levels, while
the rest were in the normal range. The presence of physio-
logically significant levels of TGF- 31 in the plasmas of
normal human subjects may indicate previously unsus-
pected endocrine roles for this peptide, while TGF- 2 and
TGF- 33 appear to act only in a local autocrine/paracrine
fashion.
INTRODUCTION
The TGF- 3s2 are multifunctional cytokines whose proper-
ties include being highly potent inhibitors of epithelial cell
growth (1). The presence of one or more isoforms in essentially
every epithelial tissue probably reflects a critical role in regu-
lating normal epithelial homeostasis. TGF431 null mice show
hyperproliferation in the basal layer of the epidermis (2), and
Received 7/19/94; accepted 9/2/94.
1 To whom requests for reprints should be addressed, at Laboratory
of Chemoprevention, National Cancer Institute, Building 41, Room
Bi 11 1, 41 LIBRARY DR MSC 5055, Bethesda, MD 20892-5055.
2 The abbreviations used are: TGF- 3, transforming growth factor 3;
PF4, platelet factor 4; 3Th, 3-thmombogIobulin; SELISA, sandwich
enzyme-linked immunosombent assay.
epidermal tumors derived from TGF- 31 null keratinocytes show
more rapid malignant progression than their wild-type counter-
parts, suggesting that dysregulation of TGF- 31 function may
enhance the carcinogenic process (3). Similarly, colon carci-
noma cells transfected with antisense TGF- 31 show a more
aggressive phenotype when grown in nude mice than do their
untransfected counterparts (4). The observation that the anti-
estrogen tamoxifen increases TGF- 3 isoform expression in
breast cancer cells in vitro and locally in vivo in human breast
tumors is also consistent with a potential role for TGF- 3s in
preventing tumor progression (5, 6).
In later phases of tumor progression, TGF- 3 overexpmes-
sion may actually enhance tumorigenesis through paracnine
stimulation of the tumor stroma and inhibition of the immune
surveillance system. Transfection of a rat prostatic carcinoma
cell line with TGF- 3i resulted in larger, more metastatic tumors
(7). Furthermore, three immunohistochemical studies (8-10)
have shown a correlation between increased staining for
TGF- 31 in human mammary carcinomas and disease progres-
sion, although it is not clear whether this is causally related
to progression or represents a failed homeostatic response.
Clearly, changes in local TGF- 3 levels may be important during
carcinogenesis in a number of organ systems, with potentially
different effects at different stages in the process. We therefore
wished to develop a method for accurate determination of cir-
culating TGF43 levels to evaluate their potential usefulness as
prognostic indicators, as disease markers, or as intermediate
biomarkers of chemopreventive or chemotherapeutic efficacy.
Human platelets contain large amounts of TGF- 31 in the a
granules (- 2500 molecules/platelet (1 i). Thus measurements
of circulating TGF- 3 levels must be made on plasma, not serum.
Since it is extremely difficult to prepare plasma without any
platelet degranulation, it is not clear whether previously deter-
mined levels of TGF- 3 in the plasma of normal subjects might
not have been derived from platelets degranulated ex vivo in the
course of sample handling (12-14). To circumvent this problem,
we have developed a method to correct for the platelet contri-
bution by measuring levels of the specific platelet a granule
protein, PF4. We now present our results for normal controls
and for patients with advanced metastatic breast cancer.
MATERIALS AND METHODS
Collection of Blood and Preparation of Plasma
Plasma TGF43 levels were determined in 42 apparently
healthy subjects, ranging in age from 20 to 60 years, and
included 17 males, 14 premenopausal females, 6 pregnant fe-
Research.
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