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Abramson Cancer CenterNCI CANCERLIT® Search: Prostate Cancer, Hereditary - July 2002
National Cancer Institute®
Last Modified: July 1, 2002
- Liposome-mediated gene therapy using HSV-TK/ganciclovir under the control of human PSA promoter in prostate cancer cells.
- [Analysis of loss of heterozygosity on chromosome 6 in human prostate carcinoma and prostatic intraepithelial neoplasia]
- Expression and gene copy number analysis of ERBB2 oncogene in prostate cancer.
- Mouse models of prostate carcinogenesis.
- Identification and characterization of Bimgamma, a novel proapoptotic BH3-only splice variant of Bim.
- Molecular biology of the androgen receptor: from molecular understanding to the clinic.
- Decrease and gain of gene expression are equally discriminatory markers for prostate carcinoma: a gene expression analysis on total and
- Molecular biology of the androgen receptor.
- Nkx3.1 mutant mice recapitulate early stages of prostate carcinogenesis.
- Targets of c-Jun NH(2)-terminal kinase 2-mediated tumor growth regulation revealed by serial analysis of gene expression.
- Stromal cells promote angiogenesis and growth of human prostate tumors in a differential reactive stroma (DRS) xenograft model.
- Identification of differentially expressed genes in normal and malignant prostate by electronic profiling of expressed sequence tags.
- Influence of cytokine gene polymorphisms on the development of prostate cancer.
- The RASSF1A tumor suppressor gene is inactivated in prostate tumors and suppresses growth of prostate carcinoma cells.
- Mixture modelling of gene expression data from microarray experiments.
- Protamine-fragment peptides fused to an SV40 nuclear localization signal deliver oligonucleotides that produce antisense effects in prostate and
- A polymorphism in the UDP-Glucuronosyltransferase 2B15 gene (D85Y) is not associated with prostate cancer risk.
- The G gamma / T-15 transgenic mouse model of androgen-independent prostate cancer: target cells of carcinogenesis and the effect of the
- The Duffy antigen/receptor for chemokines (DARC) and prostate cancer. A role as clear as black and white?
- Response of cancer cells to molecular interruption of the CK2 signal.
- Androgen receptor mutations in carcinoma of the prostate: significance for endocrine therapy.
- Phase I clinical trial of interleukin 2 (IL-2) gene therapy for prostate cancer.
- Prostate cancer genomics.
- Gene therapy for prostate cancer.
- Analysis of the RNASEL gene in familial and sporadic prostate cancer.
- TMEFF2 is an androgen-regulated gene exhibiting antiproliferative effects in prostate cancer cells.
- HER-2 testing in prostate carcinoma.
- Detection of low level HER-2/neu gene amplification in prostate cancer by fluorescence in situ hybridization.
- Molecular engineering of a two-step transcription amplification (TSTA) system for transgene delivery in prostate cancer.
- Germline alterations of the RNASEL gene, a candidate HPC1 gene at 1q25, in patients and families with prostate cancer.
- p53 regulates Stat3 phosphorylation and DNA binding activity in human prostate cancer cells expressing constitutively active Stat3.
- CHC1-L, a candidate gene for prostate carcinogenesis at 13q14.2, is frequently affected by loss of heterozygosity and underexpressed in
- The role of p53 in radiation therapy outcomes for favorable-to-intermediate-risk prostate cancer.
- Broadened ligand responsiveness of androgen receptor mutants obtained by random amino acid substitution of H874 and mutation hot spot T877 in
Table of Contents
1
UI - 11598449
AU - Suzuki S; Tadakuma T; Kunitomi M; Takayama E; Sato M; Asano T; Nakamura
TI -
H; Hayakawa M
Liposome-mediated gene therapy using HSV-TK/ganciclovir under the
control of human PSA promoter in prostate cancer cells.
SO - Urol Int 2001;67(3):216-23
AD - Department of Urology, National Defense Medical College, 302 Namiki,
Tokorozawa, Saitama 359-8513, Japan. sushi@fa2.so-net.ne.jp
To more accurately determine the tissue-specific expression of the
target gene in prostate cancer cells, we introduced the enhancer element
(-4,777 to -3,934; PSAR) and the promoter region (PSAP) of the
prostate-specific antigen (PSA) gene. Furthermore, to elucidate the
advantages of using liposomes as a gene carrier, we screened more than
20 liposome preparations in this study. The 5' upstream region of PSA
gene (PSARPSAP) was conjugated to either the chloramphenicol
acetyltransferase (CAT) gene or herpes simplex virus thymidine kinase
(TK) gene, and the transfection of these plasmids was carried out using
cationic liposomes, DMRIE-C (Gibco) or LipoTAXI (Stratagene). The
expression of CAT activity was clearly observed when PSARPSAP-CAT
plasmid was transfected into PSA-positive LNCaP cells, whereas no CAT
activity was detected in PSA-negative DU145 cells or bladder carcinoma
T24 cells. The CAT activity increased after the addition of
testosterone. We then evaluated the therapeutic effect of the
PSARPSAP-TK plasmid in vitro. When PSARPSAP-TK plasmid was transfected
and ganciclovir was added to the medium, the growth of LNCaP cells was
inhibited, while no growth inhibition was observed in DU145 cells.
Furthermore, this inhibitory effect was observable even when the cells
were cultured in a medium supplemented with dialyzed fetal bovine serum.
These results suggest that the liposome-mediated transfection of
PSARPSAP-TK appears to be a potentially effective approach for selecting
the optimal treatment for tumor cells producing PSA even with the low
androgen levels seen in patients treated by anti-androgen therapy.
Copyright 2001 S. Karger AG, Basel
2
UI - 11866981
AU - Wang Z; Lai FM; Zhang J
TI -
[Analysis of loss of heterozygosity on chromosome 6 in human prostate
carcinoma and prostatic intraepithelial neoplasia]
SO - Zhonghua Bing Li Xue Za Zhi 2001 Dec;30(6):414-7
AD - Department of Pathology, Affiliated Zhongda Hospital of Southeast
University, Nanjing 210009, China. wangzhaoming@sina.com
OBJECTIVE: To detect the significance of loss of heterozygosity (LOH) on
chromosome 6 in prostate carcinoma and high grade prostatic
intraepithelial neoplasia (PIN). METHODS: Pure DNA was obtained from
prostate neoplasms and normal tissues after tissue microdissection. LOH
of chromosome 6 was detected by PCR based microsatellite polymorphism
analysis technique using 20 pairs of microsatellite primers in 10
prostate carcinoma cases and 10 high grade PIN cases. RESULTS: Allelic
loss at one or more loci was observed on chromosome 6 in 8 of 10
prostate carcinoma cases. 6q21-6q23 and 6q25-6q27 were two of LOH high
frequency regions. 5 high grade PIN cases had LOH detected on chromosome
6. CONCLUSIONS: Two high frequency LOH regions were detected on
chromosome 6 of prostate carcinoma. Cyclin C, IGF2R genes were two
candidate tumor suppressor genes located in these two regions, they may
be involved in the initiation and progression of prostate cancer.
3
UI - 11786427
AU - Savinainen KJ; Saramaki OR; Linja MJ; Bratt O; Tammela TL; Isola JJ;
TI -
Visakorpi T
Expression and gene copy number analysis of ERBB2 oncogene in prostate
cancer.
SO - Am J Pathol 2002 Jan;160(1):339-45
AD - Laboratory of Cancer Genetics, Institute of Medical Technology,
University of Tampere, Tampere, Finland.
An anti-ERBB2 antibody, trastuzumab, has been shown to be highly
efficient in the treatment of metastatic breast cancers overexpressing
the ERBB2 gene. It has been suggested that overexpression and even
amplification of ERBB2 may play a role in the development of prostate
cancer. Here, we have analyzed gene copy number and expression of the
ERBB2 gene in both androgen-dependent primary and metastatic tumors, as
well as recurrent hormone-refractory tumors. The expression levels were
compared to the expression of ERBB2 in breast cancers with or without
ERBB2 gene amplification. Of 126 prostate tumors, chromogenic in situ
hybridization (CISH) revealed only 1 case containing borderline (six to
eight copies) amplifications of ERBB2. This hormone-refractory tumor,
however, did not express ERBB2 protein. Immunohistochemical staining of
ERBB2 protein was negative (0 or 1+ intensity) in all prostate samples
(n = 124) analyzed. To quantitate the level of ERBB2 mRNA expression in
prostate tumors (n = 34) and cell lines (n = 3), as well as in breast
tumors (n = 30) and cell lines (n = 16), real-time reverse
transcriptase-polymerase chain reaction (LightCycler) methodology was
used. The expression level was similar in all prostate tumor types and
corresponded to the level of expression in breast carcinomas without
ERBB2 amplification. Breast tumors with ERBB2 amplification expressed,
on average, approximately 20 times (P < 0.001) higher mRNA levels than
prostate tumors or breast carcinomas without the gene amplification. In
conclusion, the expression of ERBB2 in prostate cancer is relatively
low, and is not altered during disease progression. Thus, it is unlikely
that treatment modalities relying on the overexpression of ERBB2 gene
will be useful in treating prostate cancer.
4
UI - 12047956
AU - Abate-Shen C; Shen MM
TI -
Mouse models of prostate carcinogenesis.
SO - Trends Genet 2002 May;18(5):S1-5
AD - Center for Advanced Biotechnology and Medicine, Department of
Neuroscience, UMDNJ-Robert Wood Johnson Medical School, 679 Hoes Lane,
Piscataway, NJ 08854, USA. abate@cabm.rutgers.edu
In recent years, numerous mouse models have been generated that
recapitulate salient features of prostate carcinogenesis in humans. Here
we review progress in the generation and validation of mouse models for
prostate cancer, discuss current limitations of these models, and
highlight directions of future research.
5
UI - 12019181
AU - Liu JW; Chandra D; Tang SH; Chopra D; Tang DG
TI -
Identification and characterization of Bimgamma, a novel proapoptotic
BH3-only splice variant of Bim.
SO - Cancer Res 2002 May 15;62(10):2976-81
AD - Department of Carcinogenesis, the University of Texas M. D. Anderson
Cancer Center, Science Park Research Division, Park Road 1C, Smithville,
TX 78957, USA.
BH3 (Bcl-2 homology 3)-only proteins of the Bcl-2 family play an
essential role in apoptosis. In this study, a novel human BH3-only
protein, Bcl-2-interacting mediator (Bim)gamma, was identified during
our study of regulation of prostate cancer cell death by Bcl-2 family
proteins. Bimgamma shares the highest amino acid sequence homology to
BimEL and BimL, two proapoptotic BH3-only Bcl-2 proteins derived from
alternative mRNA splicing. Genomic studies indicate that Bimgamma is a
novel splice variant of Bim and is generated as a result of the
retention of a 126-bp intron of the bim gene. Bimgamma mRNA displays a
tissue-specific expression pattern distinct from those of the other Bim
isoforms. Subcellular fractionation studies indicate that Bimgamma is
localized both in intracellular membranes and cytosol. Interestingly,
Bimgamma mRNA, similar to the BimEL protein, is up-regulated in the
majority of the prostate cancer cell lines studied, whereas several
other proapoptotic Bcl-2 proteins, including Bax, Bak, and Bad, are
down-regulated in prostate cancer cells. Functional studies indicate
that Bimgamma inhibits clonal growth in prostate cancer cells and
promotes apoptosis, which is inhibited by overexpressing Bcl-2. Because
both Bimgamma and BimEL are proapoptotic BH3-only proteins and both are
up-regulated in prostate cancer cells, they may play a unique role in
prostate cancer development.
6
UI - 11684838
AU - Eder IE; Culig Z; Putz T; Nessler-Menardi C; Bartsch G; Klocker H
TI -
Molecular biology of the androgen receptor: from molecular understanding
to the clinic.
SO - Eur Urol 2001 Sep;40(3):241-51
AD - Department of Urology, University of Innsbruck, Austria.
The androgen receptor (AR) is the key regulatory element of androgen
signaling in the cell. It mediates action of androgens and is therefore
essential for growth, function and differentiation of the human male
urogenital tract. Genetic alterations in the AR gene may cause impaired
development resulting in androgen insensitivity syndromes (AIS) or in
neurodegenerative diseases like Kennedy syndrome. Besides the crucial
role in the process of virilization during embryogenesis and puberty,
the AR also plays an important role in the adult man as the
intracellular mediator of androgen action. Androgen withdrawal and/or AR
blockade is the main choice of treatment of nonorgan-confined prostate
cancer. Unfortunately, this treatment is only palliative and a majority
of these tumors recur and progress to an androgen-independent and
therapy-resistant stage. Recent findings gave new insight into the
molecular structure and function of the AR and improved our
understanding about prostate cancer progression, consequently resulting
in the development of novel treatments. It has become evident that the
AR is a nuclear transcription factor that can be activated
ligand-dependently by androgens as well as ligand-independently by other
hormones and various growth factors, respectively. Moreover, it was
shown that the interaction of the AR with other proteins of the
intracellular signal transduction cascade may promote prostate tumor
growth. This review will summarize the most important findings about the
AR and the androgen signaling pathway to improve the understanding of
prostate diseases and novel treatment strategies that may be useful in
the clinic.
7
UI - 12057920
AU - Ernst T; Hergenhahn M; Kenzelmann M; Cohen CD; Bonrouhi M; Weninger A;
TI -
Klaren R; Grone EF; Wiesel M; Gudemann C; Kuster J; Schott W; Staehler
G; Kretzler M; Hollstein M; Grone HJ
Decrease and gain of gene expression are equally discriminatory markers
for prostate carcinoma: a gene expression analysis on total and
microdissected prostate tissue.
SO - Am J Pathol 2002 Jun;160(6):2169-80
AD - Department of Cellular and Molecular Pathology, Deutsches
Krebsforschungszentrum Heidelberg, Heidelberg, Germany.
Information on over- and underexpressed genes in prostate cancer in
comparison to adjacent normal tissue was sought by DNA microarray
analysis. Approximately 12,600 mRNA sequences were analyzed from a total
of 26 tissue samples (17 untreated prostate cancers, 9 normal adjacent
to prostate cancer tissues) obtained by prostatectomy. Hierarchical
clustering was performed. Expression levels of 63 genes were found
significantly (at least 2.5-fold) increased, whereas expression of 153
genes was decreased (at least 2.5-fold) in prostate cancer versus
adjacent normal tissue. In addition to previously described genes such
as hepsin, overexpression of several genes was found that has not drawn
attention before, such as the genes encoding the specific granule
protein (SGP28), alpha-methyl-acyl-CoA racemase, low density lipoprotein
(LDL)-phospholipase A2, and the anti-apoptotic gene PYCR1. The
radiosensitivity gene ATDC and the genes encoding the DNA-binding
protein inhibitor ID1 and the phospholipase inhibitor uteroglobin were
significantly down-regulated in the cancer samples. DNA microarray data
for eight genes were confirmed quantitatively in five normal and five
cancer tissues by real-time reverse transcriptase-polymerase chain
reaction with a high correlation between the two methods. Laser capture
microdissection of epithelial and stromal compartments from cancer and
histological normal specimens followed by an amplification protocol for
low levels of RNA (<0.1 microg) allowed us to distinguish between gene
expression profiles characteristic of epithelial cells and those typical
of stroma. Most of the genes identified in the nonmicrodissected tumor
material as up-regulated were indeed overexpressed in cancerous
epithelium rather than in the stromal compartment. We conclude that
development of prostate cancer is associated with down-regulation as
well as up-regulation of genes that show complex differential regulation
in epithelia and stroma. Some of the gene expression alterations
identified in this study may prove useful in the development of novel
diagnostic and therapeutic strategies.
8
UI - 12089231
AU - Gelmann EP
TI -
Molecular biology of the androgen receptor.
SO - J Clin Oncol 2002 Jul 1;20(13):3001-15
AD - Department of Oncology, Lombardi Cancer Center, Georgetown University
School of Medicine, 3800 Reservoir Rd NW, Washington, DC 20007-2197,
USA. gelmann@georgetown.edu
Androgen receptor (AR) is a member of the steroid hormone receptor
family of molecules. AR primarily is responsible for mediating the
physiologic effects of androgens by binding to specific DNA sequences
that influence transcription of androgen-responsive genes. The
three-dimensional structure of the AR ligand-binding domain has shown it
is similar to other steroid hormone receptors and that ligand binding
alters the protein conformation to allow binding of coactivator
molecules that amplify the hormone signal and mediate transcriptional
initiation. However, AR also undergoes intramolecular interactions that
regulate its interactions with coactivators and influence its activity.
A large number of naturally occurring mutations of the human AR gene
have provided important information about AR molecular structure and
intermolecular interactions. AR is also a critical mediator of prostate
cancer promotion, conferring growth signals to prostate cancer cells
throughout the natural history of the disease. Late-stage prostate
cancer, unresponsive to hormonal deprivation, sustains AR signaling
through a diverse array of molecular strategies. Variations in the AR
gene may also confer genetic predisposition to prostate cancer
development and severity. Further understanding of AR action and new
strategies to interfere with AR signaling hold promise for improving
prostate cancer therapy.
9
UI - 12036903
AU - Kim MJ; Bhatia-Gaur R; Banach-Petrosky WA; Desai N; Wang Y; Hayward SW;
TI -
Cunha GR; Cardiff RD; Shen MM; Abate-Shen C
Nkx3.1 mutant mice recapitulate early stages of prostate carcinogenesis.
SO - Cancer Res 2002 Jun 1;62(11):2999-3004
AD - Department of Neuroscience, Center for Advanced Biotechnology and
Medicine, 679 Hoes Lane, Piscataway, NJ 08854, USA.
Recent studies of human cancers and mutant mouse models have implicated
the Nkx3.1 homeobox gene as having a key role in prostate
carcinogenesis. Consistent with such a role, here we show that Nkx3.1
displays growth-suppressing activities in cell culture, and that aged
Nkx3.1 mutant mice display histopathological defects resembling
prostatic intraepithelial neoplasia (PIN), the presumed precursor of
human prostate cancer. Using a tissue recombination approach, we found
that PIN-like lesions from Nkx3.1 mutants can undergo progressively
severe histopathological alterations after serial transplantation in
nude mice. Our findings indicate that Nkx3.1 loss-of-function is a
critical event in prostate cancer initiation, and that Nkx3.1 mutant
mice accurately model early stages of prostate carcinogenesis. More
generally, our tissue recombination assay provides an empirical test to
examine the relationship of PIN to prostate carcinoma.
10
UI - 12036942
AU - Potapova O; Anisimov SV; Gorospe M; Dougherty RH; Gaarde WA; Boheler KR;
TI -
Holbrook NJ
Targets of c-Jun NH(2)-terminal kinase 2-mediated tumor growth
regulation revealed by serial analysis of gene expression.
SO - Cancer Res 2002 Jun 1;62(11):3257-63
AD - Cell Stress and Aging Section, Laboratory of Cellular and Molecular
Biology, Gerontology Research Center, National Institute on
Aging-IRP/NIH, Baltimore, MD 21224, USA.
Although the c-Jun NH(2)-terminal kinase (JNK) pathway has been
implicated in mediating cell growth and transformation, its downstream
effectors remain to be identified. Using JNK2 antisense oligonucleotides
(JNK2AS), we uncovered previously a role for JNK2 in regulating cell
cycle progression and survival of human PC3 prostate carcinoma cells.
Here, to identify genes involved in implementing JNK2-mediated effects,
we have analyzed global gene expression changes in JNK2-deprived PC3
cells using Serial Analysis of Gene Expression. More than 40,000 tags
each were generated from control and PC3-JNK2AS libraries, corresponding
to 15,999 and 20,698 unique transcripts, respectively. Transcripts
corresponding to transcription factors, stress-induced genes, and
apoptosis-related genes were up-regulated in the PC3-JNK2AS library,
revealing a significant stress response after the inhibition of JNK2
expression. Genes involved in DNA repair, mRNA turnover, and drug
resistance were found to be down-regulated by inhibition of JNK2
expression, further highlighting the importance of JNK2 signaling in
regulating cell homeostasis and tumor cell growth.
11
UI - 12036948
AU - Tuxhorn JA; McAlhany SJ; Dang TD; Ayala GE; Rowley DR
TI -
Stromal cells promote angiogenesis and growth of human prostate tumors
in a differential reactive stroma (DRS) xenograft model.
SO - Cancer Res 2002 Jun 1;62(11):3298-307
AD - Department of Molecular and Cellular Biology, Baylor College of
Medicine, Houston, TX 77030, USA.
Reactive stroma has been reported in many cancers, including breast,
colon,and prostate. Although changes in stromal cell phenotype and
extracellular matrix have been reported, specific mechanisms of how
reactive stroma affects tumor progression are not understood. To address
the role of stromal cells in differential regulation of tumor incidence,
growth rate, and angiogenesis, LNCaP xenograft tumors were constructed
in nude mice with five different human prostate stromal cell lines as
well as GeneSwitch-3T3 cells engineered to express lacZ under
mifepristone regulation. Alone, LNCaP prostate carcinoma cells were
essentially nontumorigenic, whereas combinations of LNCaP cells with
three different human prostate stromal cell lines (L/S tumors) resulted
in a tumor incidence (50-63%) similar to that of control LNCaP plus
Matrigel (L/M) tumors over a 9-week period. In contrast, LNCaP
combinations with two other human prostate stromal cell lines were
nontumorigenic, illustrating that stromal cell effects are differential.
L/S tumors exhibited well-developed blood vessels at 2 weeks, whereas
control L/M tumors were avascular at 2 weeks and exhibited blood lakes
in lieu of extensive vessels at later time points. Xenografts
constructed under three-way conditions (LNCaP, Matrigel, and stromal
cells; L/M/S tumors) exhibited a 100% tumor incidence and showed rapid
blood vessel formation as early as day 7 with mature vessels formed by
day 10. L/M/S tumors exhibited a 10.3-fold increase in microvessel
density, and the corresponding hemoglobin:tumor weight ratio was
increased 2-fold relative to L/M control tumors at day 10. L/M/S tumor
wet weight and volume increased by 1.6- and 2.4-fold, respectively, by
day 21, compared with control L/M tumors. L/M/S tumors made with LNCaP
cells plus GeneSwitch-3T3-pGene/lacZ stromal cells showed similar
results. Mifepristone-regulated gene expression was observed in stromal
cells immediately adjacent to clusters of carcinoma cells and in vessel
walls in a mural cell (pericyte) position. This study shows that
regulation of angiogenesis is one mechanism through which stromal cells
affect LNCaP tumor incidence and growth rate. This regulation may be
mediated through direct recruitment and interactions of stromal cells
with endothelial cells. Furthermore, this study describes for the first
time a model system with regulated transgene expression in the stromal
compartment of an experimental carcinoma. These findings point to the
stromal compartment as a potential source of new prognostic markers and
therapeutic targets and show the utility of the carcinoma-stromal
xenograft model system in dissecting specific mechanisms of reactive
stroma.
12
UI - 12036949
AU - Asmann YW; Kosari F; Wang K; Cheville JC; Vasmatzis G
TI -
Identification of differentially expressed genes in normal and malignant
prostate by electronic profiling of expressed sequence tags.
SO - Cancer Res 2002 Jun 1;62(11):3308-14
AD - Division of Experimental Pathology, Department of Laboratory Medicine
and Pathology, Mayo Clinic and Foundation, 200 First Street SW,
Rochester, MN 55905, USA.
Differentially expressed genes between corresponding normal and
cancertissue can advance our understanding of the molecular basis of
malignancy and potentially serve as biomarkers or prognostic markers of
malignancy. To identify differentially expressed genes in prostate
cancer, we used a procedure combining electronic expression profiling of
the prostate expressed sequence tag (EST) database and molecular biology
techniques. A novel electronic expression-profiling algorithm was
developed to search publicly available EST sequences for genes that show
significant differential expression in prostate cancer compared with
normal prostate tissue. Approximately 600 genes expressed in prostate
were identified through adequate EST counts of ESTs for electronic
profiling. Of these 600 genes, 9 showed statistically significant
differences in their EST counts between cancer and normal prostate and
were further analyzed. The predictions associated with electronic
profiling were experimentally verified for two genes, cysteine-rich
secretory protein 3 (CRISP-3) and deadenylating nuclease (DAN), using
real-time reverse transcription-PCR with total RNA extracted from cells
isolated by laser capture microdissection. In five of five Gleason score
6 cancer cases, CRISP-3 expression was increased >50 fold, whereas the
expression of DAN was reduced by >80%.
13
UI - 12067976
AU - McCarron SL; Edwards S; Evans PR; Gibbs R; Dearnaley DP; Dowe A;
TI -
Southgate C; Easton DF; Eeles RA; Howell WM
Influence of cytokine gene polymorphisms on the development of prostate
cancer.
SO - Cancer Res 2002 Jun 15;62(12):3369-72
AD - Department of Histocompatibility and Immunogenetics, Southampton
University Hospitals NHS Trust, SO16 6YD, United Kingdom.
Polymorphisms in the promoter regions of cytokine genes may influence
prostate cancer (PC) development via regulation of the antitumor immune
response and/or pathways of tumor angiogenesis. PC patients (247) and
263 controls were genotyped for interleukin (IL)-1beta-511, IL-8-251,
IL-10-1082, tumor necrosis factor-alpha-308, and vascular endothelial
growth factor (VEGF)-1154 single nucleotide polymorphisms. Patient
control comparisons revealed that IL-8 TT and VEGF AA genotypes were
decreased in patients compared with controls [23.9 versus 32.3%; P =
0.04, odds ratio (OR) = 0.66, 95% confidence interval (CI) 0.44-0.99 and
6.3 versus 12.9%; P = 0.01, OR = 0.45, 95% CI 0.24-0.86, respectively],
whereas the IL-10 AA genotype was significantly increased in patients
compared with controls (31.6 versus 20.6%; P = 0.01, OR = 1.78, 95% CI
1.14-2.77). Stratification according to prognostic indicators showed
association between IL-8 genotype and log prostate-specific antigen
level (P = 0.05). These results suggest that single nucleotide
polymorphisms associated with differential production of IL-8, IL-10,
and VEGF are risk factors for PC, possibly acting via their influence on
angiogenesis.
14
UI - 12067994
AU - Kuzmin I; Gillespie JW; Protopopov A; Geil L; Dreijerink K; Yang Y;
TI -
Vocke CD; Duh FM; Zabarovsky E; Minna JD; Rhim JS; Emmert-Buck MR;
Linehan WM; Lerman MI
The RASSF1A tumor suppressor gene is inactivated in prostate tumors and
suppresses growth of prostate carcinoma cells.
SO - Cancer Res 2002 Jun 15;62(12):3498-502
AD - Intramural Research Support Program, SAIC-Frederick, Inc., National
Cancer Institute Frederick, Maryland 21702, USA. kuzmin@mail.ncifcrf.gov
We analyzed expression status of the recently identified tumor
suppressor geneRASSF1A in primary prostate carcinomas and in prostate
cell lines. We found complete methylation of the RASSF1A promoter in 63%
of primary microdissected prostate carcinomas (7 of 11 samples). The
remaining 4 samples (37%) were partially methylated, possibly because of
contamination with normal cells. No promoter methylation was observed in
matching normal prostate tissues. High levels of RASSF1A transcript and
no methylation of RASSF1A promoter were found in explanted primary
normal prostate epithelial and stromal cells. Complete silencing and
methylation of RASSF1A promoter was observed in five widely used
prostate carcinoma cell lines, which acquired the ability to grow in
culture spontaneously, including LNCaP, PC-3, ND-1, DU-145, 22Rv1, and
one primary prostate carcinoma immortalized by overexpression of the
human telomerase catalytic subunit (RC-58T/hTERT). However, no silencing
of RASSF1A was found in four other prostate carcinoma cell lines, which
were adapted for cell culture after transformation with human
papillomaviral DNA. Suppression of cell growth in vitro was demonstrated
after the reintroduction of RASSF1A-expressing construct into LNCaP
prostate carcinoma cells. Our data implicate the RASSF1A gene in human
prostate tumorigenesis.
15
UI - 11847075
AU - Ghosh D; Chinnaiyan AM
TI -
Mixture modelling of gene expression data from microarray experiments.
SO - Bioinformatics 2002 Feb;18(2):275-86
AD - Department of Biostatistics, School of Public Health, University of
Michigan, 1420 Washington Heights, Room M4057, Ann Arbor, MI 48109-2029,
USA. ghoshd@umich.edu
MOTIVATION: Hierarchical clustering is one of the major analytical tools
for gene expression data from microarray experiments. A major problem in
the interpretation of the output from these procedures is assessing the
reliability of the clustering results. We address this issue by
developing a mixture model-based approach for the analysis of microarray
data. Within this framework, we present novel algorithms for clustering
genes and samples. One of the byproducts of our method is a
probabilistic measure for the number of true clusters in the data.
RESULTS: The proposed methods are illustrated by application to
microarray datasets from two cancer studies; one in which malignant
melanoma is profiled (Bittner et al., Nature, 406, 536-540, 2000), and
the other in which prostate cancer is profiled (Dhanasekaran et al.,
2001, submitted).
16
UI - 11906253
AU - Benimetskaya L; Guzzo-Pernell N; Liu ST; Lai JC; Miller P; Stein CA
TI -
Protamine-fragment peptides fused to an SV40 nuclear localization signal
deliver oligonucleotides that produce antisense effects in prostate and
bladder carcinoma cells.
SO - Bioconjug Chem 2002 Mar-Apr;13(2):177-87
AD - Howard Florey Institute of Experimental Physiology and Medicine,
University of Melbourne, Parkville, Victoria, 3052, Australia.
The development of antisense technology has focused on improving methods
for oligonucleotide delivery into cells. In the present work, we
describe a novel strategy for oligonucleotide delivery based on a
bifunctional peptide composed of a C-terminal protamine-fragment that
contains a DNA-binding domain and an N-terminal nuclear localization
signal sequence derived from the SV40 large-T antigen (The sequences of
two of the peptides are R6WGR6-PKKKRKV [s-protamine-NLS] and
R4SR6FGR6VWR4-PKKKRKV [l-protamine-NLS]). We demonstrated, by intrinsic
fluorescence quenching, that peptides of this class form complexes with
oligodeoxynucleotides. To evaluate delivery, we used a 20-mer
phosphorothioate oligomer (Isis 3521) targeted to the 3'-untranslated
region of the PKC-alpha mRNA and G3139, an 18-mer phosphorothioate
targeted to the first six codons of the human bcl-2 open reading frame,
and complexed them with either of two peptides (s- or l-protamine-NLS).
These peptides bind to and deliver antisense oligonucleotides to the
nucleus of T24 bladder and PC3 prostate cancer cells, as demonstrated by
confocal microscopy. Furthermore, as shown by Western and Northern
blotting, the peptide-oligonucleotide complexes produced excellent
downregulation of the expression of the complementary mRNAs, which in
turn resulted in downregulation of protein expression. However, under
certain circumstances (predominantly in PC3 cells), incubation of the
cells with chloroquine was required to produce antisense activity. Using
this strategy, PKC-alpha protein and mRNA expression in T24 and PC3
cells and bcl-2 expression in PC3 cells was reduced by approximately 75
+/- 10% at a minimum concentration of oligomer of 0.25 microM, in
combination with 12-15 microM peptide. On the basis of our results, we
conclude that arginine-rich peptides of this class may be potentially
useful delivery vehicles for the cellular delivery of antisense
oligonucleotides. This new strategy may have several advantages over
other methods of oligonucleotide delivery and may complement already
existing lipid-based technologies.
17
UI - 12010866
AU - Gsur A; Preyer M; Haidinger G; Schatzl G; Madersbacher S; Marberger M;
TI -
Vutuc C; Micksche M
A polymorphism in the UDP-Glucuronosyltransferase 2B15 gene (D85Y) is
not associated with prostate cancer risk.
SO - Cancer Epidemiol Biomarkers Prev 2002 May;11(5):497-8
AD - Division of Applied and Experimental Oncology, Institute of Cancer
Research, University of Vienna, Austria. andrea.gsur@univie.ac.at
18
UI - 12050097
AU - Perez-Stable CM; Schwartz GG; Farinas A; Finegold M; Binderup L; Howard
TI -
GA; Roos BA
The G gamma / T-15 transgenic mouse model of androgen-independent
prostate cancer: target cells of carcinogenesis and the effect of the
vitamin D analogue EB 1089.
SO - Cancer Epidemiol Biomarkers Prev 2002 Jun;11(6):555-63
AD - Geriatric Research, Education, and Clinical Center and Research Service,
Veterans Affairs Medical Center, Miami, Florida 33125, USA.
cperez@med.miami.edu
Transgenic mouse models of prostate cancer provide unique opportunities
to understand the molecular events in prostate carcinogenesis and for
the preclinical testing of new therapies. We studied the G gamma T-15
transgenic mouse line, which contains the human fetal globin promoter
linked to SV40 T antigen (Tag) and which develops androgen-independent
prostate cancer. Using the immunohistochemistry of normal mouse
prostates before tumor formation, we showed that the target cells of
carcinogenesis in G gamma T-15 mice are located in the basal epithelial
layer. We tested the efficacy of the 1,25(OH)(2)D(3) analogue, EB 1089,
to chemoprevent prostate cancer in these transgenic mice. Compared with
treatment with placebo, treatment with EB 1089 at three different time
points before the onset of prostate tumors in mice did not prevent or
delay tumor onset. However, EB 1089 significantly inhibited prostate
tumor growth. At the highest dose, EB 1089 inhibited prostate tumor
growth by 60% (P = 0.0003) and the growth in the number of metastases,
although this dose also caused significant hypercalcemia and weight
loss. We conducted several in vitro experiments to explore why EB 1089
did not prevent the occurrence of the primary tumors. EB 1089
significantly inhibited the growth of a Tag-expressing human prostate
epithelial cell line, BPH-1, and an androgen-insensitive subline of
LNCaP cells [which was not inhibited by 1,25(OH)(2)D(3)]. Thus, neither
Tag expression nor androgen insensitivity explain the absence of
chemopreventive effect. Conversely, neither 1,25(OH)(2)D(3) nor EB 1089
inhibited the growth of the normal rat prostate basal epithelial cell
line NRP-152. It is likely that EB 1089 was not effective in delaying
the growth of the primary tumor in G gamma T-15 transgenic mice because
the target cells of carcinogenesis in these mice are located in the
basal epithelial layer. We conclude that G gamma T-15 transgenic mice
are a useful model for testing vitamin D-based therapies in
androgen-insensitive prostate cancer but are not suitable for studies of
vitamin D-based chemoprevention. The superiority of EB 1089 over
1,25(OH)(2)D(3) in the growth suppression of androgen-insensitive
prostate cancer cells supports the use of EB 1089 in
androgen-insensitive prostate cancer.
19
UI - 12087071
AU - Lentsch AB
TI -
The Duffy antigen/receptor for chemokines (DARC) and prostate cancer. A
role as clear as black and white?
SO - FASEB J 2002 Jul;16(9):1093-5
AD - Department of Surgery, University of Cincinnati College of Medicine,
Cincinnati, Ohio 45267-0558, USA. alex.lentsch@uc.edu
Prostate cancer is the most commonly diagnosed cancer and the second
leading cause of cancer-related death among men in the United States.
African American men have a 60% greater incidence of prostate cancer and
a twofold higher mortality rate than Caucasian men. The Duffy
antigen/receptor for chemokines (DARC) is a receptor expressed on
erythrocytes and vascular endothelial cells that binds to and clears
angiogenic chemokines. The DARC also functions as the erythrocyte
receptor for invasion by malarial parasites. Approximately 70% of
African Americans lack erythrocyte expression of the DARC as a genetic
mechanism of protection against malaria infection. Given the importance
of angiogenic chemokines in the development of tumor vascular networks
and the chemokine binding properties of the DARC, the possibility that a
lack of DARC expression on erythrocytes may represent an epigenetic
factor that predisposes African American men to a greater incidence and
mortality of prostate cancer should be considered.
20
UI - 11827168
AU - Wang H; Davis A; Yu S; Ahmed K
TI -
Response of cancer cells to molecular interruption of the CK2 signal.
SO - Mol Cell Biochem 2001 Nov;227(1-2):167-74
AD - Department of Laboratory Medicine and Pathology and University of
Minnesota Cancer Center, University of Minnesota, Minneapolis, USA.
Protein kinase CK2 is one of the key cellular signals for cell survival,
growth, and proliferation. It is has been observed to be elevated in
various cancers that have been examined. Various observations suggest
that moderate dysregulation of CK2 may profoundly influence the cell
response. We have examined the effects of interfering with the CK2
signal in various cancer cell lines by employing antisense
oligodeoxynucleotides (ODN) against the alpha and beta subunits of CK2.
Our results demonstrate that antisense CK2-alpha and antisense CK2-beta
ODNs markedly influence cell viability of these cancer cells in a dose
and time-dependent manner. Antisense CK2-alpha was slightly more
effective than antisense CK2-beta in most of the cells tested. The
efficacy of the antisense ODN seemed to vary with the cell type;
however, in all cases potent induction of apoptosis was observed.
Significantly, the effects of the antisense ODN on the CK2 activity in
the nuclear matrix were relatively small compared to the much stronger
induction of apoptosis in cells. This suggests that modest
downregulation of CK2 can evoke a much greater apoptotic response in
cancer cells.
21
UI - 12083956
AU - Culig Z; Klocker H; Bartsch G; Hobisch A
TI -
Androgen receptor mutations in carcinoma of the prostate: significance
for endocrine therapy.
SO - Am J Pharmacogenomics 2001;1(4):241-9
AD - Department of Urology, University of Innsbruck, Innsbruck, Austria.
zoran.culig@uibk.ac.at
Endocrine therapy for advanced prostate cancer involves androgen
ablation (orchiectomy or application of luteinizing hormone releasing
hormone analogs) and/or blockade of the androgen receptor (AR) with
either steroidal (cyproterone acetate) or nonsteroidal
(hydroxyflutamide, bicalutamide and nilutamide) antiandrogens. These
antagonists prevent androgen-induced conformational change and
activation of the AR. During long term androgen ablation, the AR adapts
to an environment with low androgen concentrations and becomes
hypersensitive to low concentrations of androgens, either alone or in
combination with various cellular regulators. Bicalutamide can switch
from antagonist to agonist during long-term androgen withdrawal, as
shown in prostate cancer LNCaP cells. AR point mutations were detected
in metastatic lesions from human prostate cancer more frequently than in
primary tumors. Although functional characterization of only some mutant
AR detected in prostate cancer tissue has been performed, data available
suggest that they are activated by dihydrotestosterone, its precursors
and metabolites, synthetic androgens, estrogenic and progestagenic
steroids and hydroxyflutamide. A direct association between AR mutations
and endocrine withdrawal syndrome has been investigated in only one
study thus far. There is no evidence at present that activation of any
of the mutant AR genes detected in prostate cancer is enhanced in the
presence of a nonsteroidal AR stimulator. Coactivators of the AR are
proteins that associate with the receptor, possess histone acetylase
activity and facilitate AR activation. The coregulatory proteins ARA70
and ARA160 differentially affected the activity of the mutated AR
Glu(231)-->Gly, which was discovered in a mouse authochthonous prostate
tumor. ARA70 enhanced receptor activation by both androgen and
estradiol, whereas ARA160 augmented only androgen-induced AR activity.
Novel experimental therapies that down-regulate AR expression have been
developed; they include the application of ribozymes and antisense
oligonucleotides.
22
UI - 12084292
AU - Pantuck AJ; Belldegrun AS
TI -
Phase I clinical trial of interleukin 2 (IL-2) gene therapy for prostate
cancer.
SO - Curr Urol Rep 2001 Feb;2(1):33
23
UI - 12084298
AU - Li PE; Nelson PS
TI -
Prostate cancer genomics.
SO - Curr Urol Rep 2001 Feb;2(1):70-8
AD - Division of Human Biology, Fred Hutchinson Cancer Research Center, 1100
Fairview Avenue North, Mailstop D4-100, Seattle, WA 98109-1024, USA.
pli@u.washington.edu
The molecular processes contributing to cancer of the human prostate
gland are under intensive investigation. Methods used for discovering
genetic alterations involved in prostate neoplasia include family
studies designed to map hereditary disease loci, chromosomal studies to
identify aberrations that may locate oncogenes or tumor suppressor
genes, and comprehensive gene expression studies. These studies
determine how various molecular signaling pathways influence or reflect
the process of carcinogenesis. However, a comprehensive overview of the
cell is necessary to understand all of the dynamic interactions between
genes, their protein products, and the network of cellular processes
resulting in tumorigenesis. Unraveling the complexity of these systems
in a timely manner involves the integration of computers,
miniaturization, and automation into molecular biology. New
biotechnologies such as the development of automated DNA sequencing and
complementary DNA microarrays allow for a systematic, "discovery-driven"
approach. These and other technologies afford a comprehensive view of
biology and pathology that have the potential to fully characterize the
processes involved in neoplasia and therefore provide potential targets
for the therapy of prostate and other cancers.
24
UI - 12084265
AU - Gingrich JR; Chauhan RD; Steiner MS
TI -
Gene therapy for prostate cancer.
SO - Curr Urol Rep 2001 Jun;2(3):199-208
AD - Department of Urology, University of Tennessee Medical Center, 956 Court
Avenue, H216, Memphis, TN 38163, USA. Jgingrich@utmem.edu
Basic research continues to unravel the molecular complexity of normal
and abnormal biologic processes. The development of means to affect the
expression level of genes that promote or contribute to cellular
transformation, invasion, and metastasis has spawned the concept of gene
therapy. This relatively new field seeks to reverse or suspend the
pathologic progression of a variety of diseases including the malignant
transformation of prostatic epithelial cells. Initial clinical trials
for prostate cancer have thus far shown gene therapy to be relatively
safe, although definitive evidence of durable therapeutic efficacy
remains to be demonstrated. In this article, recent preclinical
research, current therapeutic strategies, and recent results of gene
therapy clinical trials for the treatment of prostate cancer are
reviewed.
25
UI - 12022038
AU - Wang L; McDonnell SK; Elkins DA; Slager SL; Christensen E; Marks AF;
TI -
Cunningham JM; Peterson BJ; Jacobsen SJ; Cerhan JR; Blute ML; Schaid DJ;
Thibodeau SN
Analysis of the RNASEL gene in familial and sporadic prostate cancer.
SO - Am J Hum Genet 2002 Jul;71(1):116-23
AD - Department of Laboratory Medicine, Mayo Clinic and Foundation,
Rochester, MN 55905, USA.
The RNASEL gene on chromosome 1q25 was recently identified as a
candidate gene for hereditary prostate cancer (PC). To confirm these
findings, we screened 326 patients from 163 families with familial PC
for potential germline mutations, by use of conformation-sensitive gel
electrophoresis, followed by direct sequence analysis. A total of six
variants were identified, including one intronic and five exonic changes
(three missense and two silent alterations). There were no unequivocal
pathogenic changes. To further test for potential associations between
genes and increased risk for disease, the three missense polymorphisms
(Ile97Leu, Arg462Gln, and Glu541Asp) were genotyped in 438 patients with
familial PC and in 510 population-based control subjects. Association
testing revealed no significant differences between patients and control
subjects for either the Leu97 variant (chi(2) trend test = 1.42; P=.23)
or the Asp541 variant (chi2=1.52; P=.22). However, significant
differences were detected for the Arg462Gln genotypes (chi2=5.20; P=.02;
odds ratio [OR] = 0.54; 95% confidence interval [CI] 0.32-0.91) when the
genotype Gln/Gln was compared with Arg/Arg. In subset analyses,
associations were also observed in the younger group (age at diagnosis
26
UI - 12101412
AU - Gery S; Sawyers CL; Agus DB; Said JW; Koeffler HP
TI -
TMEFF2 is an androgen-regulated gene exhibiting antiproliferative
effects in prostate cancer cells.
SO - Oncogene 2002 Jul 18;21(31):4739-46
AD - Division of Hematology/Oncology, Cedars-Sinai Medical Center, Los
Angeles, California, CA 90048, USA. gerys@schc.org
We have identified a gene that is highly expressed in the
androgen-dependent prostate cancer cell line, LNCaP. Sequence analysis
revealed that it was identical to a recently cloned gene designated
TMEFF2, which encodes a transmembrane protein containing an epidermal
growth factor (EGF)-like motif and two follistatin domains. This gene
was highly expressed only in primary samples of normal prostate and
prostate cancer as well as normal brain. Expression of the gene was
controlled by androgen as shown by dihydrotestosterone markedly
increasing TMEFF2 expression in LNCaP cells. Also, androgen-dependent
human prostate cancer xenografts (CWR22) expressed high levels of TMEFF2
and these levels markedly decreased by day 10 after castration of the
mice. Furthermore, a large number of androgen-dependent xenografts
(CWR22, LuCaP-35, LAPC-4AD, LAPC-9AD) exhibited higher levels of TMEFF2
mRNA than androgen-independent xenografts (CWR22R, LAPC-3AI, LAPC-4AI,
LAPC-9AI). Ectopic expression of TMEFF2 in DU145 and PC3 cells resulted
in their prominent inhibition of growth. Taken together, the results
demonstrate that TMEFF2 is a androgen-regulated gene, which can suppress
growth of prostate cancer cells and our xenograft data show that escape
of prostate cancer cells from androgen modulation causes them to
decrease their expression of this gene, which may result in their more
malignant behavior.
27
UI - 11693894
AU - Stern DF
TI -
HER-2 testing in prostate carcinoma.
SO - Cancer J 2001 Sep-Oct;7(5):372-4
AD - Department of Pathology, Yale University School of Medicine, New Haven,
Connecticut 06510, USA.
28
UI - 11693898
AU - Liu HL; Gandour-Edwards R; Lara PN Jr; de Vere White R; LaSalle JM
TI -
Detection of low level HER-2/neu gene amplification in prostate cancer
by fluorescence in situ hybridization.
SO - Cancer J 2001 Sep-Oct;7(5):395-403
AD - Department of Internal Medicine, University of California, San
Francisco, USA.
PURPOSE: Although expression of the HER-2/neu oncogene has been
correlated with tumor progression in prostate cancer, the biologic
significance of detecting HER-2/neu gene amplification by fluorescence
in situ hybridization (FISH) or evidence for protein overexpression by
immunohistochemistry (IHC) remains unclear. In this study, we directly
compared HER-2/neu FISH and IHC to determine which may be more
predictive of the response to trastuzumab. PATIENTS AND METHODS: Forty
patients with prostate cancer were analyzed for gene amplification by
FISH performed with HER-2/neu and chromosome 17 (CEP 17) DNA probes
(Vysis). Protein expression was examined by immunofluorescence and by
IHC using the DAKO HercepTest antibody protocol and a monoclonal
antibody to Her-2/neu on archival paraffin sections. The patients
included 30 men with primary tumors that were treated with radical
prostatectomy. Of these, 15 demonstrated subsequent disease progression
within 3 years. Five patients with prostatic intraepithelial neoplasia
were tested, as were five with metastatic disease whose samples were
obtained before androgen ablation therapy. RESULTS: None of the 30
primary prostate cancer specimens showed overexpression for HER-2/neu by
immunofluorescence or by IHC with the DAKO protocol. One sample showed
3+ membrane expression with the monoclonal antibody. In contrast, low
copy number gene amplifications (3-8 HER-2/neu signals/nucleus) were
detected in 16 of 30 samples (53%) by FISH. Most amplified cells were
diploid for CEP 17, demonstrating that amplification was not due to
total cell aneuploidy. FISH and IHC determined that prostatic
intraepithelial neoplasia samples were normal. Four of five (80%)
metastatic samples were amplified for HER-2/neu by FISH. Nearly 70% of
metastatic cancer cells among all five specimens demonstrated
aneuploidy. A single lymph node metastasis showed 3+ membrane stain
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