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NCI CANCERLIT® Search: Prostate Cancer, Hereditary - October 2002
National Cancer Institute®
Last Modified: October 1, 2002
- Suicide gene therapy for urogenital cancer: current outcome and prospects.
- Tissue-specific promoters in gene therapy for the treatment of prostate cancer.
- Human hormone-refractory prostate cancers can harbor mutations in the O(2)-dependent degradation domain of hypoxia inducible factor-1alpha
- Genetic heterogeneity of single disseminated tumour cells in minimal residual cancer.
- CYP3A4 promoter variant is associated with prostate cancer risk in men with benign prostate hyperplasia.
- Alterations in gene expression profiles during prostate cancer progression: functional correlations to tumorigenicity and
- The role of vitamin D receptor gene polymorphisms in the susceptibility to prostate cancer of a southern European population.
- Metallothionein isoform 3 expression inhibits cell growth and increases drug resistance of PC-3 prostate cancer cells.
- Polymorphisms of the CYP1B1 gene have higher risk for prostate cancer.
- Identification of differentially expressed genes in organ-confined prostate cancer by gene expression array.
- Up-regulation of TRPM-2, MMP-7 and ID-1 during sex hormone-induced prostate carcinogenesis in the Noble rat.
- Maspin expression profile in human prostate cancer (CaP) and in vitro induction of Maspin expression by androgen ablation.
- Transition to androgen-independence in prostate cancer.
- Prostatic tissue in mature cystic teratomas of the ovary: a report of four cases, including one with features of prostatic adenocarcinoma, and
- Her2 expression in prostatic cancer: a comparison with mammary carcinoma.
- Modulation of cell proliferation and cell cycle regulators by vitamin E in human prostate carcinoma cell lines.
- Frequent hypermethylation of the RASSF1A gene in prostate cancer.
- The CAG trinucleotide repeat length in the androgen receptor does not predict the early onset of prostate cancer.
- A novel founder mutation in the RNASEL gene, 471delAAAG, is associated with prostate cancer in Ashkenazi Jews.
- Mapping of metastasis suppressor genes for prostate cancer by microcell-mediated chromosome transfer.
- KAI1/CD82 gene expression in benign prostatic hyperplasia and late-stage prostate cancer in Chinese.
- Bcl-2 antagonizes the combined apoptotic effect of transforming growth factor-beta and dihydrotestosterone in prostate cancer cells.
- Differential expression of 17beta-hydroxysteroid dehydrogenase isozyme genes in prostate cancer and noncancer tissues.
- Evaluation of HER-2/neu expression in prostatic adenocarcinoma: a requested for a standardized, organ specific methodology.
- Hereditary aspects of prostate cancer.
- The dilemma of hereditary prostate cancer.
- Hereditary prostate cancer.
- Transcription-targeted gene therapy for androgen-independent prostate cancer.
- Prostate cancer. Unlocking its DNA secrets.
Table of Contents
1
UI - 12006245
AU - Nasu Y; Kusaka N; Saika T; Tsushima T; Kumon H
TI -
Suicide gene therapy for urogenital cancer: current outcome and
prospects.
SO - Mol Urol 2000 Summer;4(2):67-71
AD - Department of Urology, Okayama University Medical School, Shikata,
Okayama, Japan. ynasu@med.okayama-u.ac.jp
Viral-mediated transfer of the herpes simplex virus thymidine kinase
(HSV-tk) gene has been demonstrated by several investigators to confer
sensitivity to nucleoside analogs such as ganciclovir (GCV) in a variety
of tumor cells including brain, prostate, bladder, kidney, ovary, head
and neck, lung, pancreas, and liver cancers. Fourteen suicide gene
clinical protocols using adenovirus vectors have been conducted,
including four in prostate cancer. Two additional protocols for prostate
cancer are in preparation in Japan and the Netherlands. A study
conducted at Baylor College of Medicine was the first to demonstrate the
safety of HSV-tk plus GCV therapy for human prostate cancer and the
anticancer activity of gene therapy in this disease. However, it is
still in the early stage of its development, with a number of problems
to be overcome. Systemic delivery, specific introduction, and specific
expression of the target gene are the major issues to be managed in
order to establish a clinically relevant treatment strategy.
2
UI - 12006246
AU - Shirakawa T; Gotoh A; Wada Y; Kamidono S; Ko SC; Kao C; Gardner TA;
TI -
Chung LW
Tissue-specific promoters in gene therapy for the treatment of prostate
cancer.
SO - Mol Urol 2000 Summer;4(2):73-82
AD - Department of Urology, Kobe University School of Medicine, Kobe, Japan.
toshiro@kobe-u.ac.jp
Delivery of therapeutic toxic genes to and their expression in tumor
cells through the use of tissue-specific promoters could decrease their
toxic effect on neighboring normal cells when virus-mediated gene
delivery results in their infection. We have demonstrated the utility of
two prostate cancer-specific promoters, long PSA and osteocalcin, for
tissue-specific toxic gene therapy for prostate cancer. The two
promoters were highly active in both androgen-dependent and
androgen-independent prostate cancer cells. We also introduce the Phase
I trial of osteocalcin promoter-based toxic gene therapy for bone
metastases of prostate cancer, which is in progress at the University of
Virginia.
3
UI - 12136249
AU - Anastasiadis AG; Ghafar MA; Salomon L; Vacherot F; Benedit P; Chen MW;
TI -
Shabsigh A; Burchardt M; Chopin DK; Shabsigh R; Buttyan R
Human hormone-refractory prostate cancers can harbor mutations in the
O(2)-dependent degradation domain of hypoxia inducible factor-1alpha
(HIF-1alpha).
SO - J Cancer Res Clin Oncol 2002 Jul;128(7):358-62
AD - The Department of Urology, College of Physicians and Surgeons, Columbia
University, Atchley Pavilion, 11th Floor, 161 Fort Washington Avenue,
New York, NY 10032, USA.
PURPOSE: Androgen ablation, the preferred therapy for advanced prostate
cancer, reduces blood flow and induces hypoxia in androgen-dependent
tissues. Given the transient effectiveness of this therapy, we must
consider whether a hypoxia-resistance mechanism might be involved in the
development of therapeutic resistance by prostate cancer cells. The
transcription factor protein, hypoxia-inducible factor 1alpha
(HIF-1alpha), helps increase the expression of gene products that enable
cells to survive conditions of hypoxic stress. Enhanced HIF-1alpha
expression during hypoxia results from a drastic reduction of its
degradation rate within a critical region of the protein referred to as
the "oxygen-dependent degradation (ODD) domain". We sequenced HIF-1alpha
cDNAs amplified from human prostate cancer cell lines and from hormone
resistant prostate cancer specimens to determine whether prostate cancer
cells might harbor mutations within the HIF-1alpha ODD domain. METHODS:
HIF-1alpha cDNAs were RT-PCR amplified from three prostate cancer cell
lines (LNCaP, PC-3, and DU145), from five different human
hormone-resistant prostate cancers and one normal prostate, all
microdissected, and were sequenced to determine whether the HIF-1alpha
gene products were wildtype or mutant. One specimen containing a
hormone-resistant prostate tumor that expressed a mutated HIF-1alpha
cDNA was further microdissected into benign and tumorous regions and
DNAs extracted from these regions were directly amplified by PCR and
sequenced to determine whether the HIF-1alpha mutation was specific to
the tumor. RESULTS: Although the HIF-1alpha cDNAs of all cell lines, the
normal prostate, and three of the tumors were found to have a wildtype
sequence, HIF-1alpha cDNAs amplified from two hormone-resistant tumors
had nucleic acid substitutions that resulted in significant amino acid
changes within the ODD domain of the HIF-1alpha protein. Analysis of the
DNA extracted from a benign or tumorous region of one of these specimens
showed that only the wildtype (nonmutated) form of the HIF-1alpha gene
was amplified from the normal DNA whereas only the mutated form of the
HIF-1alpha gene was amplified from the tumor. CONCLUSIONS: Some human
hormone-refractory prostate cancers have mutations in a critical
regulatory domain of the HIF-1alpha protein. We believe that these
mutations might enable expression of this protein under inappropriate
conditions and contribute to the development of therapeutic resistance
by the cancer cells. This hypothesis is currently being tested.
4
UI - 12241875
AU - Klein CA; Blankenstein TJ; Schmidt-Kittler O; Petronio M; Polzer B;
TI -
Stoecklein NH; Riethmuller G
Genetic heterogeneity of single disseminated tumour cells in minimal
residual cancer.
SO - Lancet 2002 Aug 31;360(9334):683-9
AD - Institut fur Immunologie, Ludwig-Maximilians-Universitat Munchen,
D-80336 Munchen, Germany. christoph.klein@ifi.med.uni-muenchen.de
BACKGROUND: Because cancer patients with small tumours often relapse
despite local and systemic treatment, we investigated the genetic
variation of the precursors of distant metastasis at the stage of
minimal residual disease. Disseminated tumour cells can be detected by
epithelial markers in mesenchymal tissues and represent targets for
adjuvant therapies. METHODS: We screened 525 bone-marrow, blood, and
lymph-node samples from 474 patients with breast, prostate, and
gastrointestinal cancers for single disseminated cancer cells by
immunocytochemistry with epithelial-specific markers. 71 (14%) of the
samples contained two or more tumour cells whose genomic organisation we
studied by single cell genomic hybridisation. In addition, we tested
whether TP53 was mutated. Hierarchical clustering algorithms were used
to determine the degree of clonal relatedness of sister cells that were
isolated from individual patients. FINDINGS: Irrespective of cancer
type, we saw an unexpectedly high genetic divergence in minimal residual
cancer, particularly at the level of chromosomal imbalances. Although
few disseminated cells harboured TP53 mutations at this stage of
disease, we also saw microheterogeneity of the TP53 genotype. The
genetic heterogeneity was strikingly reduced with the emergence of
clinically evident metastasis. INTERPRETATION: Although the
heterogeneity of primary tumours has long been known, we show here that
early disseminated cancer cells are genomically very unstable as well.
Selection of clonally expanding cells leading to metastasis seems to
occur after dissemination has taken place. Therefore, adjuvant therapies
are confronted with an extremely large reservoir of variant cells from
which resistant tumour cells can be selected.
5
UI - 11956645
AU - Tayeb MT; Clark C; Sharp L; Haites NE; Rooney PH; Murray GI; Payne SN;
TI -
McLeod HL
CYP3A4 promoter variant is associated with prostate cancer risk in men
with benign prostate hyperplasia.
SO - Oncol Rep 2002 May-Jun;9(3):653-5
AD - Department of Medicine and Therapeutics, University of Aberdeen,
Foresterhill, Aberdeen, UK.
Prostate cancer (PRCa) is one of the most common causes of cancer death
in men and determinants of PRCa risk remain largely unidentified. Benign
prostatic hyperplasia (BPH) is found in the majority of ageing men and
has been linked with PRCa. CYP3A4 may influence PRCa through its role in
testosterone metabolism. This nested case-control study assessed a
CYP3A4 single nucleotide polymorphism as a risk factor for developing
PRCa in patients with BPH. The CYP3A4 variant allele identified men with
BPH who are at increased risk of progressing to PRCa (odds ratio 6.3,
95% CI 2.3-17.3), providing a potential tool to assist prediction
strategies for this disease.
6
UI - 12235003
AU - Calvo A; Xiao N; Kang J; Best CJ; Leiva I; Emmert-Buck MR; Jorcyk C;
TI -
Green JE
Alterations in gene expression profiles during prostate cancer
progression: functional correlations to tumorigenicity and
down-regulation of selenoprotein-P in mouse and human tumors.
SO - Cancer Res 2002 Sep 15;62(18):5325-35
AD - Laboratory of Cell Regulation and Carcinogenesis, National Cancer
Institute/NIH, Building 41, Room C629, 41 Library Drive, Bethesda, MD
20892, USA.
To identify molecular changes that occur during prostate tumor
progression, we have characterized a series of prostate cancer cell
lines isolated at different stages of tumorigenesis from C3(1)/Tag
transgenic mice. Cell lines derived from low- and high-grade prostatic
intraepithelial neoplasia, invasive carcinoma, and a lung metastasis
exhibited significant differences in cell growth, tumorigenicity,
invasiveness, and angiogenesis. cDNA microarray analysis of 8700
features revealed correlations between the tumorigenicity of the
C3(1)/Tag-Pr cells and changes in the expression levels of genes
regulating cell growth, angiogenesis, and invasion. Many changes
observed in transcriptional regulation in this in vitro system are
similar to those reported for human prostate cancer, as well as other
types of human tumors. This analysis of expression patterns has also
identified novel genes that may be involved in mechanisms of prostate
oncogenesis or serve as potential biomarkers or therapeutic targets for
prostate cancer. Examples include the L1-cell adhesion molecule,
metastasis-associated gene (MTA-2), Rab-25, tumor-associated signal
transducer-2 (Trop-2), and Selenoprotein-P, a gene that binds selenium
and prevents oxidative stress. Many genes identified in the Pr-cell line
model have been shown to be altered in human prostate cancer. The
comprehensive microarray data provides a rational basis for using this
model system for studies where alterations of specific genes or pathways
are of particular interest. Quantitative real-time reverse
transcription-PCR for Selenoprotein-P demonstrated a similar
down-regulation of the transcript of this gene in a subset of human
prostate tumors, mouse tumors, and prostate carcinoma cell lines. This
work demonstrates that expression profiling in animal models may lead to
the identification of novel genes involved in human prostate cancer
biology.
7
UI - 12181642
AU - Medeiros R; Morais A; Vasconcelos A; Costa S; Pinto D; Oliveira J; Lopes
TI -
C
The role of vitamin D receptor gene polymorphisms in the susceptibility
to prostate cancer of a southern European population.
SO - J Hum Genet 2002;47(8):413-8
AD - Molecular Oncology Unit and Department of Urology, Laboratorios-PISO 4,
Instituto Portugues de Oncologia, R. Dr. Ant. Bernardino Almeida
4200-072 Porto, Portugal. mop06210@mail.telepac.pt
Epidemiological data indicate a relationship between ultraviolet
radiation, vitamin D, and prostate cancer risk. Antiproliferative
effects of vitamin D require the expression of the nuclear vitamin D
receptor (VDR). A three-fold increase in prostate cancer risk associated
with the less active vitamin D receptor allele (the T allele from VDR
TaqI polymorphism at codon 352) was reported. The role of VDR genotypes
in the susceptibility to prostate cancer has not yet been studied in
populations of southern Europe. In the present study, we determined VDR
TaqI genotypes in Portuguese prostate cancer cases ( n = 163) and
controls ( n = 211), a southern European population. When cases were
compared with controls, we found an association of VDR T allele with
prostate cancer risk (odds ratio [OR] = 1.87, 95% confidence interval
[CI] 1.02-3.37; P = 0.035). This association was confirmed using
logistic regression analysis (OR = 2.11, 95% CI 1.15-3.88; P = 0.015)
and in particular associated to risk of prostate cancer onset in men
over the age of 66 years (OR = 2.36, 95% CI 1.05-5.29; P = 0.036). Fifty
percent of cases older than 66 years could be attributed to the
influence of this risk factor. Our results indicate that the
contribution of VDR genotypes to prostate cancer susceptibility might
depend on the population studied and its geographic localization, and
that VDR genotypes are important in the definition of the genetic risk
profile of populations of southern Europe.
8
UI - 12111700
AU - Dutta R; Sens DA; Somji S; Sens MA; Garrett SH
TI -
Metallothionein isoform 3 expression inhibits cell growth and increases
drug resistance of PC-3 prostate cancer cells.
SO - Prostate 2002 Jul 1;52(2):89-97
AD - Program in Genetics and Developmental Biology, West Virginia University,
Morgantown, West Virginia 26506-9251, USA.
BACKGROUND: The third isoform of metallothionein (MT-3) is overexpressed
in prostate cancers and PIN lesions. The expression of MT-3 is highly
variable but appears to correlate to Gleason score. The goal of the
present study was to determine the effect of MT-3 overexpression on the
growth of the PC-3 prostate cancer cell line. METHODS: PC-3 cells were
stably transfected with either the MT-3 or MT-1E gene. Cell growth was
determined by counting DAPI-stained nuclei, drug resistance by the
colony formation assay, MT mRNA expression by reverse
transcriptase-polymerase chain reaction, and MT protein by immunoblot.
RESULTS: PC-3 cells that overexpress the MT-3 gene are growth inhibited
compared with either untransfected cells, cells with blank vector, or
cells with similar overexpression of the MT-1E gene. Furthermore,
increased chemotherapeutic drug resistance occurred in PC-3 clones
derived from MT-3- and MT-1E-transfected cells. CONCLUSION: The
overexpression of MT-3 can influence the growth and chemotherapeutic
drug resistance of the PC-3 prostate cancer cell line. Copyright 2002
Wiley-Liss, Inc.
9
UI - 12200121
AU - Tanaka Y; Sasaki M; Kaneuchi M; Shiina H; Igawa M; Dahiya R
TI -
Polymorphisms of the CYP1B1 gene have higher risk for prostate cancer.
SO - Biochem Biophys Res Commun 2002 Aug 30;296(4):820-6
AD - Department of Urology, University of California at San Francisco, 4150
Clement Street, San Francisco, CA 94121, USA.
Various carcinogenic factors including estrogen metabolites play a role
in malignant transformation. These metabolites are formed in part, as a
result of the hydroxylation activity of cytochrome P450 (CYP) 1B1.
Variant forms of this enzyme have been shown to enhance its activity,
and thus, we hypothesize that single nucleotide polymorphisms of the
CYP1B1 gene can be a risk factor for prostate cancer. To test this
hypothesis, the genetic distribution of six different CYP1B1
polymorphisms at intron 1 (C-->T), codon 48 (C-->G), codon 119 (G-->T),
codon 432 (C-->G), codon 449 (C-->T), and codon 453 (A-->G) was analyzed
in 117 prostate cancer samples and 200 healthy normal subjects from a
Japanese population. Results of these experiments demonstrate that the
genotype at codon 119 is significantly different between prostate cancer
patients and controls (P<0.001). The odds ratio of genotype T/T compared
to G/G (reference) was calculated as 4.02 with a 95% confidence interval
of 1.73-9.38. All other codons, except 453, showed polymorphisms but
were not significantly different between cancer patients and controls.
No association was found between stage and grade of cancer with any of
the polymorphic sites. This is the first report that demonstrates the
polymorphism at codon 119 of CYP1B1 to be associated with prostatic
carcinogenesis. These results are important in understanding the role of
CYP1B1 polymorphisms in the pathogenesis of prostate cancer.
10
UI - 11340636
AU - Chetcuti A; Margan S; Mann S; Russell P; Handelsman D; Rogers J; Dong Q
TI -
Identification of differentially expressed genes in organ-confined
prostate cancer by gene expression array.
SO - Prostate 2001 May 1;47(2):132-40
AD - Department of Medicine, University of Sydney, Sydney, NSW, Australia.
BACKGROUND: To understand the molecular mechanisms underlying prostate
cancer, we have utilized the gene expression array to search for genes
whose expression is altered in this disease. METHODS: RNA quality from
manual microdissected tissue was compared with that from microselected
tissue by electrophoresis. For array analysis, malignant and normal
prostate epithelium was enriched using microselection technique from
prostate cancer and the peripheral zone of a normal prostate. Identical
array membrane was hybridized to labeled cancer and normal cDNA,
respectively. The differentially expressed gene was further evaluated by
RT-PCR. RESULTS: Microdissection, but not microselection, causes visible
degradation to RNA. Of the 588 genes on the membrane, 87 genes yielded
significant signals. Based on a three fold difference relative to normal
prostate tissue, 1 gene was overexpressed and 12 genes underexpressed in
prostate cancer. Of them, five showed statistically significant
reduction in mRNA levels in six prostate cancer specimens compared with
seven normal prostate specimens. These five genes are glutathione
S-transferase M1 (GSTM1), monocyte chemotactic protein-1 (MCP-1), tumor
necrosis factor-alpha receptor-1 (TNFR-1), transforming growth factor
beta3 (TGF-beta3), and inhibitor of DNA binding-1 (ID-1). CONCLUSIONS:
GST-based metabolism, cytokine MCP-1 and TNFR-1, and TGF-beta3 signaling
pathways, and some helix-loop-helix nuclear proteins could be
potentially important in organ-confined prostate cancer and deserve
further investigation. Copyright 2001 Wiley-Liss, Inc.
11
UI - 11375906
AU - Ouyang XS; Wang X; Lee DT; Tsao SW; Wong YC
TI -
Up-regulation of TRPM-2, MMP-7 and ID-1 during sex hormone-induced
prostate carcinogenesis in the Noble rat.
SO - Carcinogenesis 2001 Jun;22(6):965-73
AD - Department of Anatomy, Faculty of Medicine, Li Shu Fan Building, 5
Sassoon Road, University of Hong Kong, Hong Kong, SAR, China.
Prostate cancer is the most frequently diagnosed malignancy in the
Western world and changes in the ratio of testosterone and estrogens
with advancing age is one of the potential risk factors in the
development of this disease. However, the molecular mechanisms
associated with hormone imbalance in prostate carcinogenesis are poorly
understood. In this study we induced a high incidence of prostate
hyperplasia, dysplasia and adenocarcinoma in the Noble rat using a
combination of testosterone and estradiol-17beta. Using this animal
model, we studied the gene expression profile during sex hormone-induced
prostate carcinogenesis using a cDNA array technique; the results were
further confirmed by RT-PCR, western blotting and immunohistochemical
analyses. We found up-regulation of TRPM-2 (testosterone-repressed
prostatic message-2), MMP-7 (matrix metalloproteinase-7) and Id-1
(inhibitor of differentiation or DNA binding) during development of sex
hormone-induced prostate cancer. Increased expression of TRPM-2 and
MMP-7 was observed in both premalignant and malignant tissues after sex
hormone treatment, indicating their role in the early stages of hormone
response and prostate cancer development. In contrast, Id-1 was
expressed at relatively low levels in all premalignant samples but
increased in malignant cells, suggesting its potential roles as a
biomarker for prostate cancer cells. Furthermore, expression of Id-1
appeared to be stronger in poorly differentiated lesions than in
well-differentiated carcinomas, suggesting that the levels of Id-1
expression may be correlated with the malignancy of tumors. Our results
provide the first evidence of up-regulation of TRPM-2, MMP-7 and Id-1
during sex hormone-induced prostate carcinogenesis and strongly suggest
their association with the development of prostate cancer.
12
UI - 12006534
AU - Zou Z; Zhang W; Young D; Gleave MG; Rennie P; Connell T; Connelly R;
TI -
Moul J; Srivastava S; Sesterhenn I
Maspin expression profile in human prostate cancer (CaP) and in vitro
induction of Maspin expression by androgen ablation.
SO - Clin Cancer Res 2002 May;8(5):1172-7
AD - Center for Prostate Disease Research, Department of Surgery, Uniformed
Services University of the Health Sciences, Rockville, Maryland 20852,
USA.
PURPOSE: Expression of tumor suppressor gene, MASPIN, is associated with
inhibition of tumor cell invasion and metastasis. Loss of or decreased
expression of Maspin is found frequently in breast and prostate cancer
cells. The objective of this study is to investigate Maspin expression
in prostate tumor specimens and explore the mechanisms of hormonal
regulation of Maspin expression in prostate tumors. EXPERIMENTAL DESIGN:
Immunohistochemical staining of Maspin expression was performed on
surgical whole-mounted prostate specimens. The expression of Maspin was
scored on individual tumors. Correlation of Maspin expression with
clinicopathological features was analyzed for statistical significance.
Androgen ablation-induced Maspin expression was analyzed by Maspin
promoter luciferase reporter assay and quantitative reverse
transcription-PCR analysis of endogenous Maspin expression in LNCaP
cells in vitro and in animal model. RESULTS: Comprehensive evaluation of
Maspin expression profile in multiple tumor foci from whole mounted
prostate specimens of prostate cancer patients revealed absence of
Maspin expression in a significant fraction (63%). However, Maspin
expression is significantly higher in tumor specimens (92%) of patients
treated with neoadjuvant androgen ablation therapy before radical
prostatectomy. LNCaP cells cultured in androgen-depleted medium show
induction of Maspin promoter activity in a promoter luciferase reporter
assay. In addition, Maspin expression is increased after castration in
LNCaP prostate cancer cells derived tumors in nude mice. CONCLUSIONS:
Maspin expression is frequently absent in primary prostate cancers.
Up-regulation of MASPIN in response to androgen ablation strongly
suggests a physiological role of Maspin in growth inhibition and/or
apoptosis of prostate cancer cells during androgen ablation.
13
UI - 12163131
AU - Navarro D; Luzardo OP; Fernandez L; Chesa N; Diaz-Chico BN
TI -
Transition to androgen-independence in prostate cancer.
SO - J Steroid Biochem Mol Biol 2002 Jul;81(3):191-201
AD - Department of Biochemistry, Instituto Canario de Investigacion del
Cancer (ICIC), P.O. Box 550, 35080 Las Palmas de Gran Canaria, Canary
Islands, Spain.
Prostate carcinoma is the most frequently diagnosed malignancy and the
second leading cause of death as a result of cancer in men in the
western countries. Withdrawal of androgens or the peripheral blockage of
androgen action remain the critical therapeutic options for the
treatment of advanced prostate cancer. However, after initial
regression, most of the prostate cancers become androgen-independent and
progress further, with eventual fatal outcome. Understanding the
mechanisms of transition to androgen independence and tumor progression
in prostate cancer is critical to finding new ways to treat aged
patients that are ineligible for conventional chemotherapy. A large
number of different molecular mechanisms might be responsible for the
transition to androgen-independence. Many of these involve the androgen
receptor (AR) and its signalling pathways, but they might also include
genetic changes that affect several genes, which results in the
activation of oncogenes or the inactivation of tumor suppressor genes.
Here, we discuss the most recent and relevant findings on androgen
resistance in prostate cancer in order provide a comprehensive
interpretation of the clinical behaviour of tumors at molecular levels.
14
UI - 12068172
AU - Halabi M; Oliva E; Mazal PR; Breitenecker G; Young RH
TI -
Prostatic tissue in mature cystic teratomas of the ovary: a report of
four cases, including one with features of prostatic adenocarcinoma, and
cytogenetic studies.
SO - Int J Gynecol Pathol 2002 Jul;21(3):261-7
AD - Department of Pathology, General Hospital of Ried, Austria.
Four cases of mature cystic teratoma that contained prostatic tissue are
reported. The ovarian tumors occurred in patients from 17 to 38 (mean
31) years of age and had no unusual clinical or gross aspects. The
microscopic findings for the most part were typical of a mature cystic
teratoma, but they also contained foci of prostatic tissue that ranged
from 0.2 to 1.9 cm in greatest dimension. In these areas there was a
lobular arrangement of medium-sized acini lined by cuboidal to columnar
cells with pale cytoplasm and round nuclei with inconspicuous nucleoli
except focally in one case as noted below. Basal cells were seen
focally. The prostatic acini lay in a paucicellular fibromuscular
stroma. In two cases thick layers of disorganized smooth muscle covered
by transitional-like pseudostratified epithelium, resulting in an
appearance resembling fetal bladder wall, were present next to the
prostatic glands. One tumor also contained prostatic-type acini, which
haphazardly infiltrated the stroma over an area approximately 5 mm in
maximal dimension. The acini, a few of which contained intraluminal
flocculent eosinophilic material, were lined by cells with eosinophilic
to amphophilic focally granular cytoplasm and had nuclei that were
enlarged compared with the benign-appearing, prostatic-type acini in the
four cases and had focally prominent nucleoli. Basal cells were not
identified in these infiltrating glands. Grading this focus according to
the approach in the prostate, the morphology was that of a Gleason grade
3 of 5 adenocarcinoma. Immunohistochemical stains of the putative
prostatic epithelial cells confirmed their nature by showing
immunoreactivity for prostatic-specific antigen in the lining epithelial
cells in all four cases and for prostatic-specific acid phosphatase in
the one case tested. The high molecular cytokeratin stain, 34betaE12,
highlighted basal cells to a variable extent in the three cases
containing only benign prostatic tissue. Material was not available to
immunostain for basal cells in the case with carcinoma. Cytogenetic
studies were performed in two cases and showed that the great majority
of the nuclei of the nonprostatic and prostatic tissue had an XX
karyotype but from 3% to 5% of the nuclei displayed trisomy for the X
chromosome. A small number of cases of prostatic tissue in ovarian
teratomas have previously been documented but none had morphologic
features of carcinoma.
15
UI - 12352406
AU - Jorda M; Morales A; Ghorab Z; Fernandez G; Nadji M; Block N
TI -
Her2 expression in prostatic cancer: a comparison with mammary
carcinoma.
SO - J Urol 2002 Oct;168(4 Pt 1):1412-4
AD - Department ofpathology, University of Miami-Jackson Memorial Medical
Center, Miami, Florida, USA.
PURPOSE: There is growing interest in HER2 and its downstream signaling
pathway molecules as treatment targets in human malignancies, including
prostatic carcinoma. We used a standard Food and Drug Administration
approved HER2 immunohistochemical kit to study HER2 expression in
prostate cancer. We compared the results with those reported for mammary
carcinoma. MATERIALS AND METHODS: For this study we selected 216
specimens obtained from patients who underwent radical prostatectomy for
primary untreated prostatic carcinoma. Immunohistochemical staining was
performed using the HercepTest kit (Dako Corp., Carpinteria, California)
in strict fashion according to the technical and analytical protocols
outlined in the kit. RESULTS: Of the tumors 33 (15%) were positive for
HER2, including 31 (94%) that were only weakly positive (2+). Of the
HER2 positive tumors 97% were Gleason grade 7 or higher. Of the 33
positive cases 22 (67%) showed only a focal positive reaction for HER2
in discrete tumor areas. CONCLUSIONS: HER2 is expressed in a minority of
untreated primary prostatic carcinomas. Unlike in mammary carcinoma,
HER2 positivity in prostatic cancer is usually weak in intensity and
focal in distribution. While the former casts doubt on the usefulness of
HER2 as a potential treatment target for most primary untreated
prostatic cancer, the latter phenomenon may lead to false-negative
results if the test is performed in small biopsies. Furthermore, HER2
staining of prostatic carcinoma can be technically and analytically
reproducible provided that there is strict adherence to the outlined
methodologies and interpretation.
16
UI - 12352461
AU - Venkateswaran V; Fleshner NE; Klotz LH
TI -
Modulation of cell proliferation and cell cycle regulators by vitamin E
in human prostate carcinoma cell lines.
SO - J Urol 2002 Oct;168(4 Pt 1):1578-82
AD - Division of Urology, Sunnybrook and Women's College Health Science
Centre, Toronto, Ontario, Canada.
PURPOSE: Vitamin E has been identified as a candidate agent for the
prevention of prostate cancer. We hypothesize that the mechanism for
this effect is in part a result of cell cycle inhibition rather than
only due to a reduction in reactive oxygen species. We tested whether
vitamin E induces cell cycle arrest in prostate carcinoma, mediated by
alterations in cell cycle regulatory proteins, including cyclin E, cdk2
and p27. MATERIALS AND METHODS: Cells were incubated with and without
vitamin E (alpha-tocopherol succinate, 20 microg./ml.), fixed and
stained with propidium iodide for flow cytometry analysis. In parallel
experiments total protein was extracted, immunoprecipitated with cyclin
E antibody and analyzed by Western blot for the expression of cell cycle
markers. RESULTS: Flow cytometry analysis revealed a dramatic reduction
in the S phase percent of LNCaP and PC3 cells in response to vitamin E
(69% and 95%, respectively). It was accompanied by over expression of
p27 (3-fold increase) with vitamin E treatment. CONCLUSIONS: This study
demonstrates that at physiological concentrations vitamin E induced
profound cell cycle arrest mediated by up-regulation of p27. This
observation provides a theoretical basis for the putative
chemopreventive effect of vitamin E.
17
UI - 12360410
AU - Liu L; Yoon JH; Dammann R; Pfeifer GP
TI -
Frequent hypermethylation of the RASSF1A gene in prostate cancer.
SO - Oncogene 2002 Oct 3;21(44):6835-40
AD - Department of Biology, Beckman Research Institute, City of Hope Cancer
Center, Duarte, California, CA 91010, USA.
Recently, we have cloned and characterized the Ras association domain
family 1A gene (RASSF1A) at 3p21.3, from which loss of genetic material
is one of the most frequent events in several types of human solid
tumors. The CpG island promoter region of this gene is highly methylated
in several human cancers, most notably in small cell lung cancer, breast
cancer, and renal cell carcinoma. In this study, we have analysed the
methylation status of RASSF1A in primary prostate tumors and in the
prostate cancer cell line LNCaP. In total, 37 out of 52 tumors (71%)
were methylated at the promoter region of RASSF1A. The relative
frequency of methylation was higher in more aggressive tumors compared
with less malignant tumors. For instance, tumors with a Gleason score of
7-10 (25 out of 30, 83%) were significantly more methylated compared
with Gleason 4-6 tumors (11 out of 20, 55%, P=0.032, Fisher's exact
test). Coincident with a hypermethylated promoter, transcripts of
RASSF1A were missing in LNCaP cells. Expression of RASSF1A was restored
with 5-aza-2'-deoxycytidine, a DNA methylation inhibitor. In conclusion,
our data suggest that epigenetic inactivation of RASSF1A by methylation
is a very common event in prostate cancer and might be involved in the
progression of the disease. Testing for RASSF1A methylation should
become useful in prostate cancer early detection and diagnosis and might
aid prognosis by gauging the potential status of progression.
18
UI - 12230620
AU - Mir K; Edwards J; Paterson PJ; Hehir M; Underwood MA; Bartlett JM
TI -
The CAG trinucleotide repeat length in the androgen receptor does not
predict the early onset of prostate cancer.
SO - BJU Int 2002 Oct;90(6):573-8
AD - Department of Surgery, Glasgow Royal Infirmary, UK.
OBJECTIVE: To relate the repeat length of the androgen-receptor CAG
trinucleotide to the age of onset of prostate cancer, stage and grade of
disease. PATIENTS AND METHODS: After obtaining ethical approval, 265
patients with locally confined or locally advanced/metastatic prostate
cancer were identified and evaluated for age at diagnosis (< 65 years
and > 75 years). DNA was extracted from peripheral blood lymphocytes and
1 micro g aliquots subjected to polymerase chain reaction using
fluorescently labelled primers. Samples were then run on an ABI 377 gene
scan analysis gel with an internal molecular weight marker. The length
of the CAG repeat was determined by comparing the gene scan product size
to samples where the CAG repeat length had been quantified using direct
sequencing. The Kruskal-Wallis, Mann-Whitney and Wilcoxon two sample
tests were used to analyse the data. RESULTS: The mean (range) length of
the CAG repeat in the androgen receptor was 22.2 (10-31) in the younger
and 22.5 (16-32) in the older group, and was not statistically
different. There was no significant association between the CAG repeat
length and the age of onset of prostate cancer (P = 0.568) or with stage
(P = 0.577) and grade (P = 0.891) of prostate cancer. CONCLUSION: These
results suggest that there is no correlation between the androgen
receptor CAG repeat length and the age of onset, stage and grade of
prostate cancer, confirming recent doubts from other similar studies of
a suggested correlation between shorter androgen receptor CAG repeat and
early onset and aggressiveness of prostate cancer.
19
UI - 12145743
AU - Rennert H; Bercovich D; Hubert A; Abeliovich D; Rozovsky U; Bar-Shira A;
TI -
Soloviov S; Schreiber L; Matzkin H; Rennert G; Kadouri L; Peretz T;
Yaron Y; Orr-Urtreger A
A novel founder mutation in the RNASEL gene, 471delAAAG, is associated
with prostate cancer in Ashkenazi Jews.
SO - Am J Hum Genet 2002 Oct;71(4):981-4
AD - Genetic Institute, Tel Aviv Sourasky Medical Center, Israel.
HPC1/RNASEL was recently identified as a candidate gene for hereditary
prostate cancer. We identified a novel founder frameshift mutation in
RNASEL, 471delAAAG, in Ashkenazi Jews. The mutation frequency in the
Ashkenazi population, estimated on the basis of the frequency in 150
healthy young women, was 4% (95% confidence interval [CI] 1.9%-8.4%).
Among Ashkenazi Jews, the mutation frequency was higher in patients with
prostate cancer (PRCA) than in elderly male control individuals (6.9%
vs. 2.4%; odds ratio = 3.0; 95% CI 0.6-15.3; P=.17). 471delAAAG was not
detected in the 134 non-Ashkenazi patients with PRCA and control
individuals tested. The median age at PRCA diagnosis did not differ
significantly between the Ashkenazi carriers and noncarriers included in
our study. However, carriers received diagnoses at a significantly
earlier age, compared with patients with PRCA who were registered in the
Israeli National Cancer Registry (65 vs. 74.4 years, respectively;
P<.001). When we examined two brothers with PRCA, we found a
heterozygous 471delAAAG mutation in one and a homozygous mutation in the
other. Loss of heterozygosity was demonstrated in the tumor of the
heterozygous sib. Taken together, these data suggest that the 471delAAAG
null mutation is associated with PRCA in Ashkenazi men. However,
additional studies are required to determine whether this mutation
confers increased risk for PRCA in this population.
20
UI - 11225974
AU - Ichikawa T; Hosoki S; Suzuki H; Akakura K; Igarashi T; Furuya Y;
TI -
Oshimura M; Rinker-Schaeffer CW; Nihei N; Barrett JC; Isaacs JT; Ito H
Mapping of metastasis suppressor genes for prostate cancer by
microcell-mediated chromosome transfer.
SO - Asian J Androl 2000 Sep;2(3):167-71
AD - Department of Urology, Chiba University School of Medicine, Japan.
ichikawa@urology1.m.chiba-u.ac.jp
AIM: To identify the metastasis suppressor genes for prostate cancer.
METHODS: A copy of human chromosomes was introduced into the highly
metastatic Dunning R-3327 rat prostate cancer cells by the use of
microcell-mediated chromosome transfer. Relationships between the size
of human chromosomes introduced into microcell hybrid clones and the
number of lung metastases produced by the clones were analyzed to
determine which part of human chromosomes contained the metastasis
suppressor gene(s) for prostate cancer. To determine portions of human
chromosomes introduced, G-banding chromosomal analysis, fluorescence in
situ hybridization analysis, and polymerase chain reaction analysis were
performed. RESULTS: Each of microcell hybrid clones containing human
chromosomes 7, 8, 10, 11, 12, or 17 showed decreased ability to
metastasize to the lung without any loss of tumorigenicity. This
demonstrates that these human chromosomes contain metastasis suppressor
genes for prostate cancer. Spontaneous deletion of portions of human
chromosomes was observed in the human chromosome 7, 10, 11, 12, and 17
studies. In the human chromosome 8 study, irradiated microcell-mediated
chromosome transfer was performed to enrich chromosomal arm deletions of
human chromosome 8. Molecular and cytogenetic analyses of microcell
hybrid clones demonstrated that metastasis suppressor genes on human
chromosomes were located on 7q21-22, 7q31.2-32, 8p21-12, 10q11-22,
11p13-11.2, 12p11-q13, 12q24-ter, and 17pter-q23. KAI1 and MKK4/SEKI
were identified as metastasis suppressor genes from 11p11.2 and 17p12,
respectively. CONCLUSION: This assay system is useful to identify
metastasis suppressor gene (s) for prostate cancer.
21
UI - 11225981
AU - Hu WL; Li YQ; He HX; Li QR; Tian Y; Lai RQ; Mei H
TI -
KAI1/CD82 gene expression in benign prostatic hyperplasia and late-stage
prostate cancer in Chinese.
SO - Asian J Androl 2000 Sep;2(3):221-4
AD - Department of Urology, The General Hospital of Guangzhou Military Area,
Chinese People's Liberation Army. weiliehu@hotmail.com
AIM: To evaluate KAI1/CD82 expression in Chinese patients with benign
prostatic hyperplasia (BPH) and late-stage carcinoma of prostate (CaP).
METHODS: Thirty Chinese patients with benign prostatic hyperplasia and
34 with CaP (adenocarcinoma clinical stage C and D) were analyzed by
means of immunohistochemical methods. RESULTS: The KAI1/CD82 expression
in BPH tissue was all positive, which was uniformly located on the
glandular cell membrane at the cell-to-cell borders, but KAI1/CD82
expression in metastasis CaP tissues was either significantly lower than
that of BPH or negative, and the immunostaining pattern was not
continuous. In late-stage CaP KAI1/CD82 expression was correlated
inversely to the pathological grade ( P < 0.05), but not to clinical
stage ( P > 0.05). CONCLUSION: The authors believe that decreased and
negative KAI1/CD82 expression in late-stage CaP may be related to tumor
progression and metastasis, and appears to be a prognostic marker.
22
UI - 12242728
AU - Bruckheimer EM; Kyprianou N
TI -
Bcl-2 antagonizes the combined apoptotic effect of transforming growth
factor-beta and dihydrotestosterone in prostate cancer cells.
SO - Prostate 2002 Oct 1;53(2):133-42
AD - Division of Urology, Department of Surgery, University of Maryland
School of Medicine, Baltimore, USA.
BACKGROUND: We previously demonstrated that dihydrotestosterone (DHT)
enhances transforming growth factor-beta (TGF-beta) -induced apoptosis
in human prostate cancer cells (Endocrinology 2001;142:2419-2426).
METHODS: In this study, the ability of the apoptosis suppressor bcl-2 to
directly antagonize the combined apoptotic effect of TGF-beta and DHT in
the androgen-sensitive LNCaP TbetaRII prostate cancer cells was
examined. The previously cloned TGF-RbetaII receptor LNCaP cells,
responsive to both TGF-beta and androgens, were engineered to
overexpress the bcl-2 oncoprotein and the profile of apoptosis induction
was analyzed in response to TGF-beta alone (5.0 ng/ml) or in combination
with DHT (1 nM). RESULTS: Biological characterization of cloned LNCaP
TbetaRII hygromycin/bcl-2 transfectants demonstrated that bcl-2
overexpression resulted in a significant inhibition of the combined
TGF-beta and DHT apoptotic effect in prostate cancer cells (P < 0.01).
Furthermore, molecular analysis indicated that this antagonistic effect
of bcl-2 on apoptosis was due to partial suppression of TGF-beta and
DHT-mediated induction of caspase-1 expression and activation in LNCaP
TbetaRII-hygro/bcl-2 transfectants. These results support a potential
bcl-2 interference with the TGF-beta and androgen apoptotic signaling in
prostate cancer cells by means of an antagonistic effect on caspase-1
activation. CONCLUSION: This evidence may have mechanistic significance
in understanding the contribution of bcl-2 overexpression in the
development of androgen-independent prostate cancer by means of
conferring resistance to TGF-beta-mediated apoptosis. Copyright 2002
Wiley-Liss, Inc.
23
UI - 12242730
AU - Koh E; Noda T; Kanaya J; Namiki M
TI -
Differential expression of 17beta-hydroxysteroid dehydrogenase isozyme
genes in prostate cancer and noncancer tissues.
SO - Prostate 2002 Oct 1;53(2):154-9
AD - Department of Urology, School of Medicine, Kanazawa University,
Ishikawa, Japan. kohei@med.kanazawa-u.ac.jp
BACKGROUND: The adrenal steroids dehydroepiandrosterone and
androstenediones are converted into active androgen testosterone in
prostatic tissues. Different 17beta-hydroxysteroid dehydrogenase
(17betaHSD) isozymes are characterized by either oxidation or reduction
reactions. These redox reactions represent an important step in both
biosynthesis and metabolism of androgens. This study presents the
differential expression of 17betaHSD isozyme genes in cancerous and
noncancerous prostate tissues of in vivo samples. METHODS: Thirty-four
fresh specimens of transrectal prostatic needle biopsy were obtained; 11
were pathologically diagnosed as adenocarcinoma and 23 as without
malignancy. The gene expression levels of five isozymes (type 1-5) of
17betaHSD were evaluated. The quantification of gene expression was
assessed by means of the real-time polymerase chain reaction. RESULTS:
The expression levels of the type 3 17betaHSD gene with malignancy were
significantly higher than those in prostatic tissues without malignancy,
and those of type 2 17betaHSD with malignancy were significantly lower
than those in nonmalignant tissues. There were no significant
differences in 17betaHSD type 1, type 4, and type 5 gene expression in
cancerous and noncancerous tissues. CONCLUSION: Our results suggest that
17betaHSD type 2 and type 3 play an important role in the conversion of
adrenal steroids into potential androgens in prostate cancer tissue.
Copyright 2002 Wiley-Liss, Inc.
24
UI - 12365012
AU - Sanchez KM; Sweeney CJ; Mass R; Koch MO; Eckert GJ; Geary WA; Baldridge
TI -
LA; Zhang S; Eble JN; Cheng L
Evaluation of HER-2/neu expression in prostatic adenocarcinoma: a
requested for a standardized, organ specific methodology.
SO - Cancer 2002 Oct 15;95(8):1650-5
AD - Department of Pathology and Laboratory Medicine, Indiana University
School of Medicine, Indianapolis, Indiana, USA.
BACKGROUND: Some evidence suggests a role for HER-2/neu overexpression
in prostate carcinoma progression. Reported rates of HER-2/neu
overexpression in patients with prostate carcinoma vary greatly.
METHODS: The authors studied radical prostatectomy specimens from 38
patients who had biochemical failure after undergoing radical
prostatectomy for prostate carcinoma. Immunohistochemistry for HER-2/neu
overexpression using the HercepTest kit (Dako Corporation, Carpenteria,
CA) was employed. Two different antigen-retrieval techniques were used:
1) the standard U.S. Food and Drug Administration (FDA)-approved
HercepTest assay and 2) a modified HercepTest, which employed an
alkaline citrate buffer, pH 9.0, for antigen retrieval and a 1-hour
primary antibody incubation time. The level of HER-2/neu expression was
evaluated on a scale from 0 (no staining) to 3+ according to the
published guidelines. Fluorescent in situ hybridization for gene
amplification was performed on all specimens. RESULTS: With the standard
technique, only one specimen had 2+ staining, and no specimens had 3+
staining. With the modified technique, 10 specimens (26%) had 2+
staining, and 9 specimens (24%) had 3+ staining. There was a significant
association between the level of HER-2/neu expression shown with the
modified technique and tumor stage (P = 0.03) as well as Gleason grade
(P = 0.01). None of the specimens had HER-2/neu gene amplification.
CONCLUSIONS: The authors report a simple modification of the HercepTest
that resulted in an increased rate of HER-2/neu expression, which was
correlated with poor-risk pathologic findings. The findings suggest that
adenocarcinoma of the prostate should be evaluated for HER-2/neu
expression with a prostate specific immunohistochemical procedure that
differs from the FDA-approved standard procedure. Copyright 2002
American Cancer Society.
25
UI - 7553490
AU - McLellan DL; Norman RW
TI -
Hereditary aspects of prostate cancer.
SO - CMAJ 1995 Oct 1;153(7):895-900
AD - Dalhousie University, Halifax, NS.
OBJECTIVE: To review current literature on the hereditary aspects of
prostate cancer and to evaluate the importance of family history in
history taking and screening for prostate cancer. DATA SOURCES: MEDLINE
was searched for articles in English or French published between Jan. 1,
1956, and Oct. 31, 1994, with the use of MeSH headings "prostatic
neoplasms," "genetics" and "chromosomes." Additional references were
selected from the bibliographies of articles found during the search.
STUDY SELECTION: Case-control studies involving the incidence of
prostate cancer and relative risk (RR) of such cancer in the families of
men with this disease, compared with a control group, were included.
Only studies in which prostate cancer was diagnosed on the basis of
histologic tests were included. Animal investigations were excluded.
DATA EXTRACTION: Ten case-control studies were evaluated critically in
terms of design, case and control groups, the size of the samples and
statistical results. The incidence of prostate cancer in the families of
cases, compared with that in the families of controls, and differences
in RR were reviewed. DATA SYNTHESIS: The lifetime risk of prostate
cancer is 9.5% and of death from prostate cancer is 2.9% for a man 50
years of age. For first-degree male relatives of men with prostate
cancer, the calculated RR ranges from 1.7 to 8.73. "Hereditary" prostate
cancer is a term applied to a specific subset of patients with prostate
cancer. This form of prostate cancer is transmitted by a rare,
autosomal, dominant allele with high penetrance; it accounts for an
estimated 43% of early-onset disease (affecting men less than 55 years
of age) but only 9% of all prostate cancer in men up to 85 years of age.
A greater number of affected family members and early onset among family
members are the most significant predictors of risk. CONCLUSIONS: Recent
confirmation of the familial clustering and Mendelian inheritance
patterns of some prostate cancer has important implications. It
increases the potential for directed research into the causes of
prostate cancer and for refinements in the current screening practices
to detect this common disease. Manoeuvres to detect prostate cancer
should be started earlier among men with one or more first-degree
relatives with the disease than among other men.
26
UI - 7553496
AU - Nickel JC
TI -
The dilemma of hereditary prostate cancer.
SO - CMAJ 1995 Oct 1;153(7):935-8
The observation that a family history of prostate cancer significantly
increases a man's risk of the disease (see pages 895 to 900 of this
issue) highlights many of the ethical, emotional and pragmatic
controversies in medical circles concerning the management of this
common form of cancer. This editorial describes a patient's personal
dilemma when he learns that his brother
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