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The Prostate 31:74–75 (1997)
pression of p185erbB-2. (Reprinted with
permission of Wiley-Liss, Inc., a division of
John Wiley & Son, Inc.)
Elevated Serum Levels of p105erbB-2
in Patients with Advanced-Stage
Prostatic Adenocarcinoma
Russell B. Myers, David Brown,
Denise K. Oelschlager, John W. Waterbor, M. Ernest Marshall, Sudhir Srivastava, Cecil R. Stockard, Donald A. Urban, and William E. Grizzle
From the Departments of Pathology [R.B.M., D.K.O., C.R.S., W.E.G.],
Epidemiology [D.B., J.W.W.], Medicine
[M.E.M.], and Surgery [D.A.U.], University of Alabama at Birmingham, Birmingham, AL; National Cancer Institute, Bethesda, MD, USA, [S.S.].
Int J Cancer 69:398–402, 1996.
Expression of a truncated or extracellular form (p105erbB-2) of p185erbB-2
has been demonstrated in the sera of
breast cancer patients. We examined
the levels of p105erbB-2 in the sera of
patients with various stages of prostatic adenocarcinoma, in patients with benign prostatic hyperplasia (BPH) and
in a series of control male patients hospitalized for illness unrelated to the
prostate. p105erbB-2 levels did not differ
between the controls and BPH patients
or between these groups and patients
with stage A, B or C adenocarcinomas.
In contrast, serum p105erbB-2 levels of
patients with stage D adenocarcinomas
were significantly elevated when compared with either control or BPH patients. There was no correlation between PSA and p105erbB-2 levels among
controls, patients with BPH or patients
with prostate cancer. Patients with
poorly differentiated tumors (combined Gleason score >7) or moderately
differentiated tumors (combined Gleason score 5–7) had higher p105erbB-2
levels as compared to patients with
well-differentiated tumors (combined
Gleason score <5), though this difference was not statistically significant.
There was no correlation between serum p105erbB-2 levels and p185erbB-2 expression in malignant tissue, as determined by immunohistochemistry.
However, patients with moderate to
strong expression of p185erbB-2 within
the adenocarcinomas were approximately 4 times more likely to demonstrate elevated serum p105erbB-2 levels
as compared with patients with low ex-
Soluble forms of CD44 and CD54
(ICAM-1) Cellular Adhesion
Molecules Are Released by Human
Prostatic Cancer Cell Lines
Oskar W. Rokhlin, Michael B. Cohen
From the Department of Pathology 118 ML, University of Iowa and
Veterans Affairs Medical Center, Iowa
City, IA 52242, USA [O.W.R., M.B.C.],
Department of Urology, University of
Iowa and Veterans Affairs Medical
Center, Iowa City, IA 52242, USA
Cancer Lett 107:29–35, 1996.
We have identified that human
prostatic cancer cell lines DU145, PC3,
ND1, ALVA31 and JCA1 released
soluble CD44 molecules and DU145,
PC3 and ND1 released soluble CD54.
Both soluble and surface CD44 were
not found in LNCaP, and both forms of
CD54 were not expressed in LNCaP
and JCA1. CD54 was found to be
highly expressed on cell surface in
ALVA31, but these cells did not release
soluble CD54. Expression of both cell
surface and soluble forms were examined after treatment of cells with IFN-g,
TGF-b1, or culturing in serum-free media. The concentration of soluble CD54
in supernatants changed to small extent after treatment with TGF-b1 and
increased after treatment with IFN-g or
in serum-free media. Cell surface expression of CD54 however, changed
only minimally after treatment. The
levels of cell surface and soluble CD44
also changed minimally after treatment
with IFN-g and TGF-b1 but decreased
in serum-free media and this was accompanied by marked elevation of
soluble CD44 in supernatants. These
data indicate that soluble CD44 might
be released from cell surface by shedding whereas alternative splicing is the
most likely mechanism of soluble
CD54 release. (Reproduced with permission of Elsevier Science Inc.)
Stromal Cells from Human Benign
Prostate Hyperplasia Produce a
Growth-Inhibitory Factor for
LNCaP Prostate Cancer Cells,
Identified As Interleukin-6
Armelle Degeorges, Roger Tatoud,
Françoise Fauvel-Lafeve, Marie-Pierre
Podgorniak, Guy Millot, Patricia de
Cremoux, and Fabien Calvo
From the Laboratoire de Pharmacologie, Institut de Génétique Moléculaire, Hôpital Saint-Louis [A.D., R.T.,
M-P.P., G.M., P.d.C., F.C.], and Unité
353 INSERM, Institut Universitaire
d’Hématologie, Paris, France [F.F-L.].
Int J Cancer 68:207–214, 1996.
To understand specific interactions between stromal cells and epithelial cells in benign prostatic hyperplasia (BPH) and prostatic adenocarcinoma, we developed stromal-cell
cultures from normal human prostate
(PNX) and BPH (BH101), composed of
fibroblasts and myofibroblasts. Their
role in epithelial-cell growth was studied using the established cancer cell
lines LNCaP, PC3 and DU145 and an
SV40 large T-immortalized normal epithelial-cell line, PNTIA, in doublediffusion co-culture chambers. PNTIA
was stimulated by PNX (× 1.6) and
more strongly by BH101 stromal cells
(× 2.7). Conversely, LNCaP growth decreased by 50% in the presence of
BH101 stromal cells (stromal/epithelial
ratio: 10). A BH101-conditioned medium (CM), obtained in serum-free
conditions, induced 90% inhibition of
[ 3 H]thymidine incorporation of the
LNCaP androgen-sensitive cell line.
Two other androgen-independent
prostate cancer cell lines were either insensitive to BH101 CM (PC3) or
slightly inhibited (40% for DU145).
BH101 produced large amounts of IL1b, IL-6 and IL-8. HPLC gel filtration
enabled separation of an inhibitory
fraction which contained IL-6. IL-6 was
demonstrated to be responsible for the
strong inhibitory effect since an IL-6neutralizing antibody abolished this
inhibition, which was reproduced by
human recombinant IL-6. Recombinant
IL-6 growth inhibition was observed
only on LNCaP prostate cancer androgen-sensitive cells. (Reprinted by permission of Wiley-Liss, Inc., a division of John
Wiley & Sons, Inc.)
Pretherapeutic Erythrocyte
Polyamine Spermine Levels
Discriminate High Risk Relapsing
Patients with M1 Prostate
Bernard G. Cipolla, Jean Ziade,
Jean-Yves Bansard, Jacques-Philippe
Moulinoux, Frédéric Staerman, Véro-
nique Quemener, Bernard Lobel, François Guillé
From the Department of Urology,
Institut de Recherche Contre le Cancer,
Centre Hospitalier Régional et Universitaire de Rennes, Université de
Rennes, Rennes Cedex, France [B.G.C.,
J.Z., F.S., B.L., F.G.], Groupe de Recherche en Thérapeutique Anti-cancereuse
(URA CNRS 1529), Institut de Recherche Contre le Cancer, Centre Hospitalier Régional et Universitaire de
Rennes, Université de Rennes, Rennes
Cedex, France [B.G.C., J-Y.B., J-P.M.,
V.Q., F.G.], Public Health (INSERM),
Institut de Recherche Contre le Cancer,
Centre Hospitalier Régional et Universitaire de Rennes, Université de
Rennes, Rennes Cedex, France [J-Y.B.]
Cancer 78:1055–1065, 1996.
Background. Androgen deprivation is currently the standard treatment
for patients with metastatic prostate
carcinoma. Few reliable prognostic
markers are able to select, at diagnosis,
patients who will respond favorably
and durably to hormone ablation. Circulating polyamines, markers of cell
proliferation that are elevated in prostate carcinoma, have been evaluated as
a prognostic tool.
Methods. Eighty-eight patients
with untreated, M1 classified prostate
carcinoma who received endocrine
therapy between 1988 and 1993 were
included in this study. Performance
status, hemoglobin, alkaline phosphatases, prostate specific antigen. Gleason
tumor grade, extent of disease by bone
scan, and circulating erythrocyte spermidine and spermine were correlated
with observed progression free and
cause-specific survivals. Multiple correspondence analysis and ascending
hierarchical classification were performed to determine significant pretreatment prognostic factors.
Results. Pretreatment performance status, alkaline phosphatase, hemoglobin, and erythrocyte spermine
levels were correlated with progression, with hemoglobin and erythrocyte
spermine level being the most significant independent variables (P <
0.00001 and P < 0.0001, respectively).
With regard to cause specific survival,
only hemoglobin and spermine erythrocyte levels were significant independent variables (P < 0.0001 and P <
0.0005, respectively). Patients with
spermine levels of less than 9 nmol/8–
109 had a statistically better outcome
than patients with 9 nmol/8–109 or
more erythrocytes. Erythrocyte spermine was the best sole determinant of
progression. A test combining spermine with performance status or hemoglobin improved each variable’s predictive values.
Conclusions. Circulating erythrocyte spermine levels, extracted from a
blood sample, can discriminate, at diagnosis, patients with hormone-refractory
from those with hormone-responsive
metastatic prostate carcinoma. (Reprinted
by permission of Wiley-Liss, Inc., a subsidiary
of John Wiley & Sons, Inc.)
Regulation of Apoptosis Induced by
Transforming Growth Factor-b1 in
Nontumorigenic and Tumorigenic
Rat Prostatic Epithelial Cell Lines
Andrew Y. Hsing, Kenji Kadomatsu, Michael J. Bonham, and David
From the Laboratory of Chemoprevention [A.Y.H., K.K., M.J.B., D.D.],
National Cancer Institute, Bethesda,
Maryland 20892.
Cancer Res 56:5146–5149, 1996.
Transforming growth factor-b1
(TGF-b1), which is induced in the prostate following castration, has been
speculated to mediate apoptosis of epithelial cells during prostatic involution. Here, we report the first evidence
of a direct effect of TGF-b on induction
of apoptosis in prostatic epithelial cells
in vitro, using NRP-152 nontumorigenic and NRP-154 tumorigenic rat
prostatic epithelial cell lines. TGF-b1
induces apoptosis of both cell lines
within 24 h, as shown by a decrease in
cell viability, in situ DNA nick-end labeling, and internucleosomal DNA
fragmentation. Moreover, the ability of
TGF-b to induce apoptosis of NRP-152
is strictly dependent on culture conditions, because dexamethasone enhances while insulin and insulin-like
growth factor-1 specifically block apoptosis induced by TGF-b. We suggest
that TGF-bs are direct physiological
regulators of apoptosis of prostatic epithelial cells. (Reproduced with permission of the American Association for Cancer Research, Inc.)
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