- Cancer Types
Information about risk, prevention, screening, symptoms, diagnosis, treatment, and support for all cancers Cancer A to Z - Cancer Treatment
Cancer Treatment
Information about cancer treatment, including surgery, chemotherapy, radiation therapy, clinical trials, proton therapy, complementary medicine, and cutting edge technologies.
- Risk and Prevention
- Cancer Drugs
- Support
Support
Ways for cancer patients and caregivers to cope with cancer, side effects, nutrition, general cancer support issues, grief/end of life issues, and shared survivor's experiences.
- Healthcare Professionals
- Clinical Trials
My Patient Treatment Binder
OncoLink Blogs
What's My Cancer Risk?
OncoPilot: Navigating Your Cancer Journey
Community Events Calendar
OncoLink eNews
Abramson Cancer CenterNCI CANCERLIT® Search: Prostate Cancer, Hereditary - September 2002
National Cancer Institute®
Last Modified: September 1, 2002
- A breast cancer family from Spain with germline mutations in both the BRCA1 and BRCA2 genes.
- The effect of a single BRCA2 mutation on cancer in Iceland.
- Nuclear/Nucleolar morphometry and DNA image cytometry as a combined diagnostic tool in pathology of prostatic carcinoma.
- A polymorphism in the CYP17 gene and risk of prostate cancer.
- Selective detection of membrane proteins without antibodies: a mass spectrometric version of the Western blot.
- Application of microfluidic devices to proteomics research: identification of trace-level protein digests and affinity capture of
- Association studies of serum prostate-specific antigen levels and the genetic polymorphisms at the androgen receptor and prostate-specific
- Bicalutamide functions as an androgen receptor antagonist by assembly of a transcriptionally inactive receptor.
- Visualization of advanced human prostate cancer lesions in living mice by a targeted gene transfer vector and optical imaging.
- Estrogens affect endothelin-1 mRNA expression in LNCaP human prostate carcinoma cells.
- Cten, a COOH-terminal tensin-like protein with prostate restricted expression, is down-regulated in prostate cancer.
- Meta-analysis of microarrays: interstudy validation of gene expression profiles reveals pathway dysregulation in prostate cancer.
- Comprehensive gene expression analysis of prostate cancer reveals distinct transcriptional programs associated with metastatic disease.
- Methylation state of the prostate specific membrane antigen (PSMA) CpG island in prostate cancer cell lines.
- A simple analysis of gene expression and variability in gene arrays based on repeated observations.
- [Prostate cancer, generalized screening soon?]
- Polymorphisms in the androgen receptor and type II 5 alpha-reductase genes and prostate cancer prognosis.
- Postatrophic hyperplasia of the prostate in Japan: histologic and immunohistochemical features and p53 gene mutation analysis.
- Mutational analysis of ETV6 in prostate carcinoma.
- Loss of heterozygosity at 7q31.1 and 12p13-12 in advanced prostate cancer.
- Association of the G289S single nucleotide polymorphism in the HSD17B3 gene with prostate cancer in Italian men.
- Linkage between polymorphisms in the prostate specific antigen ARE1 gene region, prostate cancer risk, and circulating tumor cells.
- DNA mismatch repair enzyme activity and gene expression in prostate cancer.
- Transcriptional regulation of bcl-2 by nuclear factor kappa B and its significance in prostate cancer.
- Hereditary prostate cancer: clinical aspects.
- Size of the androgen receptor CAG repeat and prostate cancer: does it matter?
- Racial variation in CAG repeat lengths within the androgen receptor gene among prostate cancer patients of lower socioeconomic status.
- Repression of androgen receptor mediated transcription by the ErbB-3 binding protein, Ebp1.
- Transcriptional programs activated by exposure of human prostate cancer cells to androgen.
- Bcl-2-dependent modulation of Ca(2+) homeostasis and store-operated channels in prostate cancer cells.
- Metallothionein isoform 3 expression inhibits cell growth and increases drug resistance of PC-3 prostate cancer cells.
- Huntingtin-interacting protein 1 is overexpressed in prostate and colon cancer and is critical for cellular survival.
- Single-nucleotide polymorphism in the E-cadherin gene promoter modifies the risk of prostate cancer.
- Few FH mutations in sporadic counterparts of tumor types observed in hereditary leiomyomatosis and renal cell cancer families.
- Prostatic intraepithelial neoplasia in mice with conditional disruption of the retinoid X receptor alpha allele in the prostate epithelium.
- The program of androgen-responsive genes in neoplastic prostate epithelium.
- alpha-Methylacyl-CoA racemase: expression levels of this novel cancer biomarker depend on tumor differentiation.
- Inhibition of prostate tumor cell hyaluronan synthesis impairs subcutaneous growth and vascularization in immunocompromised mice.
- Age specific and attributable risks of familial prostate carcinoma from the family-cancer database.
- Diet and the prevention of cancer.
- Lack of referral bias in genetic studies of prostate cancer.
- Endothelial nitric oxide synthase gene polymorphisms and genetic susceptibility to prostate cancer.
- A multistate model for the genetic analysis of the ageing process.
- Phase I study of replication-competent adenovirus-mediated double suicide gene therapy for the treatment of locally recurrent prostate
- Fibroblast growth factor 8 isoform B overexpression in prostate epithelium: a new mouse model for prostatic intraepithelial neoplasia.
Table of Contents
1
UI - 12161611
AU - Caldes T; de la Hoya M; Tosar A; Sulleiro S; Godino J; Ibanez D; Martin
TI -
M; Perez-Segura P; Diaz-Rubio E
A breast cancer family from Spain with germline mutations in both the
BRCA1 and BRCA2 genes.
SO - J Med Genet 2002 Aug;39(8):e44
2
UI - 12114473
AU - Tulinius H; Olafsdottir GH; Sigvaldason H; Arason A; Barkardottir RB;
TI -
Egilsson V; Ogmundsdottir HM; Tryggvadottir L; Gudlaugsdottir S; Eyfjord
JE
The effect of a single BRCA2 mutation on cancer in Iceland.
SO - J Med Genet 2002 Jul;39(7):457-62
AD - Icelandic Cancer Society, Reykjavik, Iceland University of Iceland,
Reykjavik, Iceland. hrafnt@krabb.is
OBJECTIVE: To estimate the risk of malignant diseases in families of
probands with the same mutation in the BRCA2 gene. DESIGN: A cohort
study using record linkage of a breast cancer family resource and the
Icelandic Cancer Registry. SETTING: Iceland. SUBJECTS: Families of 995
breast cancer patients, from which 887 were tested for a single founder
999del5 mutation; 90 had the mutation and 797 did not. RESULTS:
Relatives of probands with the mutation had significantly increased
relative risk (RR) of breast cancer. For first degree relatives, the RR
was 7.55 (95% CI 6.04 to 9.03) but was 1.72 (95% CI 1.49 to 1.96) in
first degree relatives of probands without the mutation. For prostate
and ovarian cancer, the first and second degree relatives of probands
with the mutation had a significantly increased RR, but in families of
probands without the mutation no significant familial risk was found.
CONCLUSIONS: The 999del5 mutation in the BRCA2 gene explains a
substantial proportion of familial risk of breast cancer in Iceland, but
significant familial risk remains in relatives of probands without the
mutation. For prostate and ovarian cancer, the mutation accounts for
most of the familiality observed in families of breast cancer patients.
3
UI - 11876548
AU - Kavantzas N; Agapitos E; Lazans AC; Pavlopoulos PM; Sofikitis N; Davaris
TI -
P
Nuclear/Nucleolar morphometry and DNA image cytometry as a combined
diagnostic tool in pathology of prostatic carcinoma.
SO - J Exp Clin Cancer Res 2001 Dec;20(4):537-42
AD - Dept. of Pathology, Medical School, National University of Athens,
Greece. nkavan@cc.uoa.gr
Paraffin tissue sections from 50 patients with prostate adenocarcinoma
were used to study nuclear and nucleolar morphometric features by image
analysis. The results were compared to DNA ploidy and Gleason grade. In
the examined histological samples nuclear and nucleolar areas were
positively interrelated. It was also noticed that the higher the
percentage of nucleolated nuclei, the bigger the nuclear and nucleolar
areas. The morphometric characteristics did not differ significantly
among the four grades of the examined specimens. In well-differentiated
carcinomas the DNA index was lower than in the rest at a statistically
significant level. Hypodiploid carcinomas were found to possess
significantly bigger nuclear areas than any other DNA index group.
Morphonuclear evidence of anaplasia and DNA aneuploidy may be used as
diagnostic tools in prostate cancer in addition to Gleason grade.
4
UI - 11895872
AU - Stanford JL; Noonan EA; Iwasaki L; Kolb S; Chadwick RB; Feng Z;
TI -
Ostrander EA
A polymorphism in the CYP17 gene and risk of prostate cancer.
SO - Cancer Epidemiol Biomarkers Prev 2002 Mar;11(3):243-7
AD - Division of Public Health Sciences, Fred Hutchinson Cancer Research
Center, Seattle 98109, USA. jstanfor@fhcrc.org
Steroid hormones are important in the etiology and progression of
prostate cancer, and expression of genes involved in hormone production
may alter susceptibility. One such gene is CYP17, which encodes the
cytochrome P450c17a enzyme responsible for the biosynthesis of
testosterone. A T to C transition (A2 allele) in the 5' promoter region
of the gene is hypothesized to increase the rate of gene transcription,
increase androgen production, and thereby increase risk of prostate
cancer. To test this hypothesis, germ-line DNA samples from a large
population-based study of incident prostate cancer cases (n = 590) and
controls (n = 538) of similar age without the disease were genotyped.
The frequency of the A2 allele was similar in cases and controls.
Compared with men with the A1/A1 genotype, the adjusted odds ratio was
0.81 for the A1/A2 and 0.87 for the A2/A2 genotype. Risk estimates did
not vary substantially by age or race. However, stratification by family
history of prostate cancer revealed that among white men with an
affected first-degree relative, homozygotes for the A2 allele had a
significant elevation in risk (odds ratio = 19.2; 95% confidence
interval, 2.2-157.4) compared with men who were homozygous for the A1
allele (interaction P = 0.0005). These results suggest that the CYP17
A2/A2 genotype predicts susceptibility to prostate cancer in white men
with a family history of the disease. It is also possible that CYP17
interacts with other genes that influence risk of familial prostate
cancer.
5
UI - 12096133
AU - Arnott D; Kishiyama A; Luis EA; Ludlum SG; Marsters JC Jr; Stults JT
TI -
Selective detection of membrane proteins without antibodies: a mass
spectrometric version of the Western blot.
SO - Mol Cell Proteomics 2002 Feb;1(2):148-56
AD - Department of Protein Chemistry, Genentech, Inc., South San Francisco,
California 94080, USA. arnott@gene.com
A method has been developed, called the mass western experiment in
analogy to the Western blot, to detect the presence of specific proteins
in complex mixtures without the need for antibodies. Proteins are
identified with high sensitivity and selectivity, and their abundances
are compared between samples. Membrane protein extracts were labeled
with custom isotope-coded affinity tag reagents and digested, and the
labeled peptides were analyzed by liquid chromatography-tandem mass
spectrometry. Ions corresponding to anticipated tryptic peptides from
the proteins of interest were continuously subjected to
collision-induced dissociation in an ion trap mass spectrometer; heavy
and light isotope-coded affinity tag-labeled peptides were
simultaneously trapped and fragmented accomplishing identification and
quantitation in a single mass spectrum. This application of ion trap
selective reaction monitoring maximizes sensitivity, enabling analysis
of peptides that would otherwise go undetected. The cell surface
proteins prostate stem cell antigen (PSCA) and ErbB2 were detected in
prostate and breast tumor cell lines in which they are expressed in
known abundances spanning orders of magnitude.
6
UI - 12096134
AU - Li J; LeRiche T; Tremblay TL; Wang C; Bonneil E; Harrison DJ; Thibault P
TI -
Application of microfluidic devices to proteomics research:
identification of trace-level protein digests and affinity capture of
target peptides.
SO - Mol Cell Proteomics 2002 Feb;1(2):157-68
AD - Institute for Biological Sciences, 100 Sussex Dr., Ottawa, Ontario K1A
0R6, Canada.
This report describes an integrated and modular microsystem providing
rapid analyses of trace-level tryptic digests for proteomics
applications. This microsystem includes an autosampler, a
microfabricated device comprising a large channel (2.4 microl total
volume), an array of separation channels, together with a low dead
volume enabling the interface to nanoelectrospray mass spectrometry. The
large channel of this microfluidic device provides a convenient platform
to integrate C(18) reverse phase packing or other type of affinity media
such as immobilized antibodies or immobilized metal affinity
chromatography beads thus enabling affinity selection of target peptides
prior to electrophoretic separation and mass spectrometry analyses on a
quadrupole/time-of-flight instrument. Sequential injection,
preconcentration, and separation of peptide standards and tryptic
digests are achieved with a throughput of up to 12 samples/per h and a
concentration detection limit of approximately 5 nM (25 fmol on chip).
Replicate injections of peptide mixtures indicated that reproducibility
of migration time was 1.2-1.8%, whereas relative standard deviation
ranging from 9.2 to 11.8% are observed on peak heights. The application
of this device for trace-level protein identification is demonstrated
for two-dimensional gel spots obtained from extracts of human prostatic
cancer cells (LNCap) using both peptide mass-fingerprint data base
searching and on-line tandem mass spectrometry. Enrichment of target
peptides prior to mass spectral analyses is achieved using
c-myc-specific antibodies immobilized on protein G-Sepharose beads and
facilitates the identification of antigenic peptides spiked at a level
of 20 ng/ml in human plasma. Affinity selection is also demonstrated for
gel-isolated protein bands where tryptic phosphopeptides are captured on
immobilized metal affinity chromatography beads and subsequently
separated and characterized on this microfluidic system.
7
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
UI - 12101115
AU - Xu J; Meyers DA; Sterling DA; Zheng SL; Catalona WJ; Cramer SD; Bleecker
TI -
ER; Ohar J
Association studies of serum prostate-specific antigen levels and the
genetic polymorphisms at the androgen receptor and prostate-specific
antigen genes.
SO - Cancer Epidemiol Biomarkers Prev 2002 Jul;11(7):664-9
AD - Center for Human Genomics, Wake Forest University School of Medicine,
Winston-Salem, North Carolina 27157, USA.
Testing for serum prostate-specific antigen (PSA) levels has been widely
used to screen for prostate cancer. However, PSA testing has low
specificity and sensitivity because PSA is not prostate cancer-specific.
PSA is encoded by the APS gene, and the expression of this gene is
regulated by androgens. W. Xue et al. Cancer Res., 60: 839-841, 2000
reported recently that serum PSA levels are associated with a G/A
polymorphism at androgen responsive element 1 (ARE1) of APS and/or the
CAG repeats in exon 1 of the androgen receptor (AR) gene. This result,
if confirmed, may significantly increase the specificity and sensitivity
of PSA testing by incorporating genotype-specific thresholds. In this
study, we tested for the association between serum PSA levels and these
single nucleotide polymorphisms (SNPs) in a large sample of 518 men. For
the AR gene, we observed slightly (but not statistically significant)
higher mean serum PSA levels in men with shorter CAG repeats (
UI - 12015321
AU - Masiello D; Cheng S; Bubley GJ; Lu ML; Balk SP
TI -
Bicalutamide functions as an androgen receptor antagonist by assembly of
a transcriptionally inactive receptor.
SO - J Biol Chem 2002 Jul 19;277(29):26321-6
AD - Cancer Biology Program, Hematology-Oncology Division, Department of
Medicine, Beth Israel Deaconess Medical Center and Harvard Medical
School, Boston, Massachusetts 02215, USA.
Prostate cancers (PCa) that relapse after androgen deprivation therapy
invariably express high levels of androgen receptor (AR) and
AR-regulated genes. Most do not respond to secondary hormonal therapies,
including AR antagonists, and the mechanisms of AR activation in these
clinically androgen-independent tumors are unclear. Bicalutamide, the
most widely used AR antagonist, is a competitive antagonist shown
previously to stabilize AR association with cytosolic heat shock protein
complexes. This study found nuclear AR expression in
bicalutamide-treated androgen-independent PCa and found that
bicalutamide could stimulate AR nuclear translocation. Moreover,
specific DNA binding by the bicalutamide-liganded AR was demonstrated in
vivo using a VP16-AR fusion protein and was confirmed by chromatin
immunoprecipitation showing binding to the prostate-specific antigen
enhancer in LNCaP PCa cells. Nonetheless, bicalutamide could not
stimulate interactions between the AR N and C termini or recruitment of
steroid receptor coactivator proteins (SRC-1 or -2), although SRC
transfection augmented AR activity in the presence of
dihydrotestosterone and inhibitory concentrations of bicalutamide. These
results demonstrate that bicalutamide stimulates the assembly of a
transcriptionally inactive AR on DNA and support altered coactivator (or
corepressor) expression as a mechanism of bicalutamide-resistant
androgen-independent PCa.
UI - 12134144
AU - Adams JY; Johnson M; Sato M; Berger F; Gambhir SS; Carey M;
TI -
Iruela-Arispe ML; Wu L
Visualization of advanced human prostate cancer lesions in living mice
by a targeted gene transfer vector and optical imaging.
SO - Nat Med 2002 Aug;8(8):891-7
AD - Department of Urology, David Geffen School of Medicine at UCLA, Los
Angeles California 90095, USA.
Non-invasive imaging and transcriptional targeting can improve the
safety of therapeutic approaches in cancer. Here we demonstrate the
ability to identify metastases in a human-prostate cancer model,
employing a prostate-specific adenovirus vector (AdPSE-BC-luc) and a
charge-coupled device-imaging system. AdPSE-BC-luc, which expresses
firefly luciferase from an enhanced prostate-specific antigen promoter,
restricted expression in the liver but produced robust signals in
prostate tumors. In fact, expression was higher in advanced,
androgen-independent tumors than in androgen-dependent lesions.
Repetitive imaging over a three-week period after AdPSE-BC-luc injection
into tumor-bearing mice revealed that the virus could locate and
illuminate metastases in the lung and spine. Systemic injection of low
doses of AdPSE-BC-luc illuminated lung metastasis. These results
demonstrate the potential use of a non-invasive imaging modality in
therapeutic and diagnostic strategies to manage prostate cancer.
UI - 12074801
AU - Grande M; Carlstrom K; Stege R; Pousette A; Faxen M
TI -
Estrogens affect endothelin-1 mRNA expression in LNCaP human prostate
carcinoma cells.
SO - Eur Urol 2002 May;41(5):568-72; discussion 573-4
AD - Department of Women and Child Health, Research Laboratory for
Reproductive Health, Karolinska Institute, C4:U1 Karolinska Hospital,
S-171 77, Stockholm, Sweden. mirtha.grande@kbh.ki.se
OBJECTIVE: To study effects of estrogens on endothelin-1 (ET-1) mRNA
expression in the androgen-sensitive LNCaP-FGC cell line and its
androgen-resistant derivative LNCaP-r. Further, if effects of estrone
sulfate (E1S) are mediated via conversion to estradiol-17beta (E2).
Estrogens have been shown to down-regulate ET-1, a mediator of the
osteoblastic response of bone to metastatic prostate cancer.METHODS:
Cells were grown in steroid-depleted medium and incubated for 2-4 and 48
hours with 0, 1, 10, and 100 nM of either E1S or E2. mRNA levels were
measured with an RT-PCR technique. Estrogen metabolism by LNCaP-FGC
cells was studied by incubation with estrone (E1) and E1S at the same
conditions, followed by determination of E1 and E2.RESULTS: ET-1 mRNA
expression in LNCaP-FGC cells was significantly suppressed by E2 and E1S
following incubation for 2-4h but after 48 h only by E2 at 1 and 10nM
and in LNCaP-r cells only by E2 at 100 nM following 2-4h of incubation.
ET-1 mRNA expression was significantly higher in untreated LNCaP-r than
in untreated LNCaP-FGC cells. E1 was efficiently transformed into E2 by
LNCaP-FGC cells but very little to E1 and no E2 was formed from
E1S.CONCLUSION: ET-1 mRNA expression in LNCaP-FGC can be inhibited by
E2, but also by its prehormone E1S. The lack of formation of E2 from E1S
suggests a mode of action not related to classical steroid receptors.
The higher level of ET-1 mRNA expression found in LNCaP-r cells may
reflect the capability of a hormone refractory tumor to maintain
activity on its own, independently of known regulatory mechanisms such
as sex steroids.
UI - 12154022
AU - Lo SH; Lo TB
TI -
Cten, a COOH-terminal tensin-like protein with prostate restricted
expression, is down-regulated in prostate cancer.
SO - Cancer Res 2002 Aug 1;62(15):4217-21
AD - Center for Tissue Regeneration and Repair, Department of Orthopaedic
Surgery, The University of California-Davis, Sacramento, California
95817, USA. shlo@ucdavis.edu
Tensin is a signaling molecule that binds to actin filaments and
localizes to focal adhesions. Recently, we have discovered that tensin
represents a new gene family with related members that are expressed in
a variety of tissues. In this study, we report the identification and
characterization of a new COOH-terminal tensin-like molecule, cten.
Human cten cDNA encodes a 715 amino acid sequence containing the Src
homology 2 and phosphotyrosine-binding domains that are similar to the
COOH termini of tensin molecules. Although cten is shorter and does not
have the actin-binding domain found in other tensins, analysis of the
genomic structure has suggested that cten is related to the tensin gene
family. In addition, cten also localizes to focal adhesions. In contrast
to other tensin members, cten expression is restricted to prostate and
placenta by Northern blot analysis. Furthermore, examination of cten
expression in prostate cancer/cell lines has revealed its
down-regulation in tumor samples. Our studies have suggested that during
evolution, cten has preserved its role in mediating signal transduction
at focal adhesions through the Src homology 2 and
phosphotyrosine-binding domains but has lost its function in binding to
actin filaments. The evolutionary divergence has produced the first
focal adhesion protein specifically expressed in the prostate and the
placenta, which may be involved in preventing prostate tumor formation.
UI - 12154050
AU - Rhodes DR; Barrette TR; Rubin MA; Ghosh D; Chinnaiyan AM
TI -
Meta-analysis of microarrays: interstudy validation of gene expression
profiles reveals pathway dysregulation in prostate cancer.
SO - Cancer Res 2002 Aug 1;62(15):4427-33
AD - Department of Pathology, University of Michigan Medical School, Ann
Arbor, Michigan 48109, USA.
The increasing availability and maturity of DNA microarray technology
has led to an explosion of cancer profiling studies. To extract maximum
value from the accumulating mass of publicly available cancer gene
expression data, methods are needed to evaluate, integrate, and
intervalidate multiple datasets. Here we demonstrate a statistical model
for performing meta-analysis of independent microarray datasets.
Implementation of this model revealed that four prostate cancer gene
expression datasets shared significantly similar results, independent of
the method and technology used (i.e., spotted cDNA versus
oligonucleotide). This interstudy cross-validation approach generated a
cohort of genes that were consistently and significantly dysregulated in
prostate cancer. Bioinformatic investigation of these genes revealed a
synchronous network of transcriptional regulation in the polyamine and
purine biosynthesis pathways. Beyond the specific implications for
prostate cancer, this work establishes a much-needed model for the
evaluation, cross-validation, and comparison of multiple cancer
profiling studies.
UI - 12154061
AU - LaTulippe E; Satagopan J; Smith A; Scher H; Scardino P; Reuter V; Gerald
TI -
WL
Comprehensive gene expression analysis of prostate cancer reveals
distinct transcriptional programs associated with metastatic disease.
SO - Cancer Res 2002 Aug 1;62(15):4499-506
AD - Department of Pathology, Memorial Sloan-Kettering Cancer Center, New
York, New York 10021, USA.
The identification of genes that contribute to the biological basis for
clinical heterogeneity and progression of prostate cancer is critical to
accurate classification and appropriate therapy. We performed a
comprehensive gene expression analysis of prostate cancer using
oligonucleotide arrays with 63,175 probe sets to identify genes and
expressed sequences with strong and uniform differential expression
between nonrecurrent primary prostate cancers and metastatic prostate
cancers. The mean expression value for >3,000 tumor-intrinsic genes
differed by at least 3-fold between the two groups. This includes many
novel ESTs not previously implicated in prostate cancer progression.
Many differentially expressed genes participate in biological processes
that may contribute to the clinical phenotype. One example was a strong
correlation between high proliferation rates in metastatic cancers and
overexpression of genes that participate in cell cycle regulation, DNA
replication, and DNA repair. Other functional categories of
differentially expressed genes included transcriptional regulation,
signaling, signal transduction, cell structure, and motility. These
differentially expressed genes reflect critical cellular activities that
contribute to clinical heterogeneity and provide diagnostic and
therapeutic targets.
UI - 12168830
AU - Noss KR; Singal R; Grimes SR
TI -
Methylation state of the prostate specific membrane antigen (PSMA) CpG
island in prostate cancer cell lines.
SO - Anticancer Res 2002 May-Jun;22(3):1505-11
AD - Research Service, Overton Brooks Veterans Affairs Medical Center,
Shreveport, Louisiana 71101-4295, USA.
BACKGROUND: PSMA expression varies among prostate cell lines. We
examined the role of CpG methylation and histone deacetylation in PSMA
transcriptional repression in prostate cell lines. MATERIALS AND
METHODS: The methylation status of a PSMA CpG island was investigated in
LNCaP, DU145 and PC3 prostate cell lines. Cells were treated with a
demethylating agent and a histone deacetylase inhibitor to determine if
PSMA transcription could be activated in nonexpressing cells. A
transfection assay with methylated and unmethylated PSMA
promoter/enhancer-driven luciferase expression constructs was performed
to examine the effect of methylation on transcription. RESULTS: The PSMA
CpG island was only methylated in DU145 cells but transcription could
not be activated by demethylation or histone deacetylase inhibition.
Methylation repressed PSMA transcription in LNCaP cells. CONCLUSION:
Although promoter methylation represses PSMA transcription in LNCaP
cells, another method inhibits PSMA expression in DU145 and PC3 cells.
UI - 12174675
AU - Jovanovic BD; Huang S; Liu Y; Naguib KN; Bergan RC
TI -
A simple analysis of gene expression and variability in gene arrays
based on repeated observations.
SO - Am J Pharmacogenomics 2001;1(2):145-52
AD - Department of Preventive Medicine, General Clinical Research Center,
Robert H. Lurie Comprehensive Cancer Center of Northwestern University,
Chicago, Illinois, USA. borko@northwestern.edu
BACKGROUND AND AIM: At the present time there is an explosion of
research in the area of gene arrays, and their application for detection
of genes related to disease as well as its therapeutic manipulation.
However, as individual arrays are expensive, comparisons of gene
expression are often not repeated. In the current study, gene array
experiments were repeated multiple times in order to understand the
variability associated with measurements of gene expression. By focusing
upon the pharmacologically important target of prostate cancer cell
detachment, the current study employed multiple repeats of gene array
experiments. This was used as a model system to demonstrate the utility
of the experimental approach and statistical methods used. METHODS: To
identify genes involved in detachment of prostate cancer cells (a
prerequisite for metastases), we analyzed gene expression changes in
metastatic variant PC3-M cells undergoing spontaneous detachment in
culture. The data were interpreted using an elementary statistical
approach. The between-experiment and within-repeated-observations
variability in expression of 3582 genes possibly related to prostate
cancer was also evaluated. RESULTS: One important gene related to
prostate cell detachment was identified, based on the magnitude of its
change in expression, as measured by a ratio of the expression after
cell detachment and expression before detachment. On average, the
variation between experiments was greater by about 30 to 40% than the
variation between repeated observations. CONCLUSION: These findings have
implications relating to the use of gene arrays to detect variance of
gene expression, and should be taken into consideration in the
prospective design of array experiments.
UI - 12212509
AU - Girault V
TI -
[Prostate cancer, generalized screening soon?]
SO - Presse Med 2002 Aug 10;31(26):1205
UI - 12210487
AU - Shibata A; Garcia MI; Cheng I; Stamey TA; McNeal JE; Brooks JD;
TI -
Henderson S; Yemoto CE; Peehl DM
Polymorphisms in the androgen receptor and type II 5 alpha-reductase
genes and prostate cancer prognosis.
SO - Prostate 2002 Sep 1;52(4):269-78
AD - Department of Health Research and Policy, Stanford University School of
Medicine, Stanford, California 94305-5405, USA. ashibata@stanford.edu
BACKGROUND: Cytosine-adenine-guanine repeat length of the androgen
receptor gene and the A49T and V89L polymorphisms of the 5
alpha-reductase (SRD5A2) gene have been associated with prostate cancer.
METHODS: We investigated the relationship of the three genetic
polymorphisms to tumor grade among 211 men who had undergone radical
prostatectomy. Subjects had prostate cancer <3 cm(3) with a percentage
of cancer represented by Gleason grade 4 or 5 (% Gleason grade 4/5) of
either > or = 20% or < or = 5%. We also examined the association between
those genetic markers and prostate specific antigen (PSA) failure among
112 subjects with > or = 20% Gleason grade 4/5. RESULTS: In
cross-sectional analysis, none of the polymorphisms was a significant
predictor of % Gleason grade 4/5. In longitudinal analysis, the LL
genotype at the V89L site was associated with statistically significant
four- to sixfold increase in PSA failure risk after adjustment for
clinicopathologic variables. CONCLUSIONS: We observed poorer prognosis
among men with the LL genotype at codon 89 of the SRD5A2 gene. Lack of
consistency between studies must be resolved before clinical utility of
this marker is established. Copyright 2002 Wiley-Liss, Inc.
UI - 12210488
AU - Tsujimoto Y; Takayama H; Nonomura N; Okuyama A; Aozasa K
TI -
Postatrophic hyperplasia of the prostate in Japan: histologic and
immunohistochemical features and p53 gene mutation analysis.
SO - Prostate 2002 Sep 1;52(4):279-87
AD - Department of Pathology, Osaka University Medical School, Suita, Osaka,
Japan.
BACKGROUND: Postatrophic hyperplasia (PAH) is one of the patterns of
prostatic atrophy but has been regarded as a precursor of prostatic
cancer (PCA) because of its possible increase in proliferative activity
compared with simple atrophy and morphologic mimicry of PCA. METHODS:
Radical prostatectomy specimens obtained from 28 patients with PCA were
analyzed by histologic and immunohistochemical methods by using 34 beta
E12 and Ki-67 as primary antibodies. Tissue from PAH, PCA, high-grade
prostatic intraepithelial neoplasia (HGPIN), a possible precursor of
PCA, and benign hyperplasia were microdissected and p53 gene mutations
were examined by the polymerase chain reaction-single strand
conformation polymorphism method followed by direct sequencing. RESULTS:
Histologically, PAH consists of compactly arranged small acini with
irregular atrophic-appearing contours, mimicking PCA. PAH lesions were
detected in 7 (25%) of 28 cases with PCA: multifocal in 6 of 7 (85.7%)
cases, maximum size of lesions ranged from 0.3 to 2.3 mm. Mild nuclear
enlargement and small nucleoli were observed in all cases. Capsular or
perineural invasion, crystalloids, and mitotic figures were not found in
any case. Inflammatory changes and fibrosis near PAH were found in 100%
and 71% of cases, respectively. PAH involved non-transition zone in all
cases and occasionally involved transition zone. Forty-three percent of
PAH lesions were in proximity (<2 mm) to PCA. None of the clinical and
pathologic factors examined were correlated with the presence of PAH.
Immunohistochemical analysis by using 34 beta E12 revealed intact basal
cells. Proliferative activity defined by positive rate for labeling with
MIB-1 antibody was intermediate between benign prostatic hyperplasia and
HGPIN. The frequency of p53 mutations in PAH lesions was 5.3%, which was
similar to that in HGPIN lesions (4.2%). Benign glands never showed
mutations. CONCLUSION: These findings suggested that PAH might be a
precursor for PCA. Copyright 2002 Wiley-Liss, Inc.
UI - 12210491
AU - Kibel AS; Faith DA; Bova GS; Isaacs WB
TI -
Mutational analysis of ETV6 in prostate carcinoma.
SO - Prostate 2002 Sep 1;52(4):305-10
AD - Division of Urologic Surgery, Washington University School of Medicine,
St. Louis, Missouri 63110, USA. kibela@msnotes.wustl.edu
BACKGROUND: In an effort to better understand the molecular events
responsible for progression of prostate carcinoma to metastatic disease,
we have recently identified a homozygous deletion at 12p12-13 involving
ETV6 (tel). Although mutational analysis of ETV6 has not been examined
previously in prostate carcinoma, it is an attractive candidate prostate
cancer tumor suppressor gene since as it previously has been implicated
in malignancy. Therefore, we decided to analyze 43 prostate cell lines,
xenografts, and metastatic foci for inactivating mutations. METHODS: DNA
was isolated from 7 cell lines, 18 xenografts, and 18 metastatic
deposits. Single-strand conformational polymorphism (SSCP) analysis of
ETV6, was performed by polymerase chain reaction (PCR) amplification of
each exon by using intron specific primers. PCR products were then
resolved by gel electrophoresis, and aberrantly migrating PCR products
were then sequenced. RESULTS: Two previously described polymorphisms and
four novel sequence changes were identified. Polymorphisms at nucleotide
258 (G --> A, Thr --> Thr) and 602 (T --> C, Leu --> Pro) were
identified in eight and one specimen(s), respectively. Analysis of
noncancerous DNA confirmed the presence of the polymorphisms in the
germ-line. Four possible mutations were identified at nucleotides 24 (T
--> G, Cys --> Trp), 380 (G --> A, Arg --> Glu), 776 (G --> T, Arg -->
Leu), and 876 (C --> T, Leu --> Leu). Three were in xenografts or cell
lines. Because normal DNA was not available, these could represent rare
polymorphisms. The sole mutation in a clinical specimen, at nucleotide
876, did not result in an amino acid change. CONCLUSION: Our data
suggest that mutational inactivation ETV6 may occur in prostate
carcinoma. The functional significance of these potential inactivating
mutations remains to be determined. Copyright 2002 Wiley-Liss, Inc.
UI - 12210480
AU - Kawana Y; Ichikawa T; Suzuki H; Ueda T; Komiya A; Ichikawa Y; Furuya Y;
TI -
Akakura K; Igarashi T; Ito H
Loss of heterozygosity at 7q31.1 and 12p13-12 in advanced prostate
cancer.
SO - Prostate 2002 Sep 15;53(1):60-4
AD - Department of Urology, Graduate School of Medicine, Chiba University,
Chiba, Japan.
BACKGROUND: Allelic losses on chromosome arms 2q, 3p, 5q, 6q, 7q, 8p,
9p, 10p, 10q, 11p, 11q, 12p, 13q, 16q, 17p, 17q, 18q, and 21q are
reportedly associated with progression and/or initiation of prostate
cancer. In the present study, we performed a polymerase chain reaction
(PCR) analysis of polymorphic microsatellite loci on the human
chromosomes 7 and 12p13-12 in prostate cancer tissue to investigate the
extent of involvement of these regions, which may contain putative tumor
suppressor genes. METHODS: Tissue samples were obtained at autopsy from
17 men who died of hormone-refractory prostate cancer at Chiba
University, Japan, and affiliated hospitals between June of 1992 and
June of 1995. DNA from normal tumor or metastatic tissue was used as the
template for PCR amplification of a set of 16 polymorphic microsatellite
loci on human chromosome 7 and 6 loci on the human chromosome region
12p13-12. RESULTS: The frequencies of cases with loss of heterozygosity
(LOH) at 7q31.1 were 8% in primary tumor tissue and 11% in metastatic
tissue. The frequencies of cases with LOH at 12p13-12 were 12% in
primary tumor tissue and 25% in metastatic tumor tissue. CONCLUSIONS: In
the present study, the frequencies of LOH at 7q31.1 were lower than in
Western patients, suggesting that LOH in this region is not related to
progression of prostate cancer in Japanese patients. The frequency of
LOH at 12p13-12 was similar to that reported in Western countries,
indicating that 12p13-12 may contain a tumor suppressor gene of prostate
cancer. Copyright 2002 Wiley-Liss, Inc.
UI - 12210481
AU - Margiotti K; Kim E; Pearce CL; Spera E; Novelli G; Reichardt JK
TI -
Association of the G289S single nucleotide polymorphism in the HSD17B3
gene with prostate cancer in Italian men.
SO - Prostate 2002 Sep 15;53(1):65-8
AD - Institute for Genetic Medicine, USC Keck School of Medicine, Los
Angeles, California 90089-9075, USA.
BACKGROUND: Prostate cancer is a significant public health problem in
this country. Substantial data support a plausible role for androgens in
the etiology of this disease. The human HSD17B3 gene encodes the
testicular (or type III) 17 beta-hydroxysteroid dehydrogenase enzyme,
which catalyzes testosterone biosynthesis in men. METHODS: We have
investigated the G289S (glycine at codon 289 replaced by serine)
polymorphism at the HSD17B3 locus as a candidate single nucleotide
polymorphism (SNP) for prostate cancer risk in constitutional DNA from
103 Italian prostate cancer patients and 109 Italian disease-free
centenarians to assess the role of this SNP in susceptibility to
prostate cancer. RESULTS: The G289S polymorphism confers a significant
increase in risk for prostate cancer (odds ratio = 2.5; 95% confidence
interval, 1.03-6.07) in our study population. CONCLUSION: Our data are
consistent with a plausible role of the G289S SNP in prostate cancer
susceptibility. Therefore, the HSD17B3 gene may be a plausible candidate
gene for prostate cancer risk. Copyright 2002 Wiley-Liss, Inc.
UI - 12210484
AU - Medeiros R; Morais A; Vasconcelos A; Costa S; Pinto D; Oliveira J;
TI -
Carvalho R; Lopes C
Linkage between polymorphisms in the prostate specific antigen ARE1 gene
region, prostate cancer risk, and circulating tumor cells.
SO - Prostate 2002 Sep 15;53(1):88-94
AD - Molecular Oncology Unit, Instituto Portugues de Oncologia, Porto,
Portugal. mop06210@mail.telepac.pt
BACKGROUND: The prostate specific antigen (PSA) gene has a polymorphic
androgen response element (ARE) sequence with two alleles, A and G. PSA
A-allele carriers have higher serum PSA levels in healthy men (HM).
METHODS: We analysed DNA samples from 278 (556 alleles) unrelated
individuals, 127 HM and 151 prostate cancer (PC) patients, for PSA ARE1
genotypes. RESULTS: The analysis of the frequencies from the 556 alleles
indicates a significant overrepresentation of A-allele in the PC group
under the age of 67 compared with the HM group (63.3% vs. 48.8%; P =
0.009). We found that men carrying two A-alleles have increased risk for
PC onset under the age of 67 (odds ratio [OR] = 2.92; 95% confidence
interval [CI], 1.10-7.86; P = 0.013). Multivariate logistic regression
analysis confirmed this association (OR = 1.82; 95% CI, 1.03-3.22; P =
0.037). Furthermore, the homozygosity for the A-allele was associated
with higher serum PSA levels (P = 0.027) and with the presence of
circulating tumor cells in the blood of PC patients (P = 0.018).
CONCLUSION: Our results indicate that polymorphism in the PSA gene
promoter may be an important biomarker for prostate cancer risk,
especially for an earlier onset of PC. Copyright 2002 Wiley-Liss, Inc.
UI - 11444857
AU - Yeh CC; Lee C; Dahiya R
TI -
DNA mismatch repair enzyme activity and gene expression in prostate
cancer.
SO - Biochem Biophys Res Commun 2001 Jul 13;285(2):409-13
AD - Department of Urology, Veterans Affairs Medical Center, 4150 Clement
Street, San Francisco, CA 94121, USA.
Microsatellite instability (MSI) of short repetitive sequences in human
chromosomal DNA can result from defective DNA mismatch repair function
in tumor cells. We hypothesize that DNA mismatch repair (MMR) activity
is down-regulated during prostatic carcinogenesis. To test this
hypothesis, MMR activities and mismatch repair-related genes were
analyzed in five different prostate cancer cell lines. Our results
demonstrate that MMR activities were decreased as compared to MMR
proficient HeLa cells. Interestingly, LNCaP, PC-3 and DU145 had much
lower MMR activities as compared to DUPro and TSUPr1. The MMR-related
genes (hMLH1, hPMS1, hPMS2, hMSH2, hMSH3, hMSH6) showed mRNA transcripts
in all prostate cancer cell lines. However, Western blotting showed
decreased or absent hMLH1 protein expression in PC-3, DU145, DUPro and
TSUPr1 cells. Similarly, the hMSH2 protein expression was low or absent
in DU145 and LNCaP cells. This is the first report that demonstrates
decreased MMR activities is associated with low expression of hMLH1,
hMSH2 and other MMR-related proteins in prostate cancer. Copyright 2001
Academic Press.
UI - 11704864
AU - Catz SD; Johnson JL
TI -
Transcriptional regulation of bcl-2 by nuclear factor kappa B and its
significance in prostate cancer.
SO - Oncogene 2001 Nov 1;20(50):7342-51
AD - Department of Molecular and Experimental Medicine, The Scripps Research
Institute, 10550 North Torrey Pines Road, La Jolla, California, CA
92037, USA.
This work presents direct evidence that the bcl-2 gene is
transcriptionally regulated by nuclear factor-kappa B (NF-kappa B) and
directly links the TNF-alpha/NF-kappa B signaling pathway with Bcl-2
expression and its pro-survival response in human prostate carcinoma
cells. DNase I footprinting, gel retardation and supershift analysis
identified a NF-kappa B site in the bcl-2 p2 promoter. In the context of
a minimal promoter, this bcl-2 p2 site 1 increased transcription 10-fold
in the presence of the p50/p65 expression vectors, comparable to the
increment observed with the consensus NF-kappa B site, while for the
full p2 promoter region transcriptional activity was increased sixfold
by over-expression of NF-kappa B, an effect eliminated by mutating the
bcl-2 p2 site 1. The expression of Bcl-2 has been linked to the
hormone-resistant phenotype of advanced prostate cancer. Here we show
that an increase in the level of expression of Bcl-2 in the human
prostate carcinoma cell line LNCaP observed in response to hormone
withdrawal is further augmented by TNF-alpha treatment, and this effect
is abated by inhibitors of NF-kappa B. Concomitantly, bcl-2 p2 promoter
studies in LNCaP cells show a 40-fold increase in promoter activity
after stimulation with TNF-alpha in the absence of hormone.
UI - 12187189
AU - Bratt O
TI -
Hereditary prostate cancer: clinical aspects.
SO - J Urol 2002 Sep;168(3):906-13
AD - Unit for Urology, Helsingborg Hospital, Sweden.
PURPOSE: We review the current epidemiological and genetic knowledge
regarding hereditary prostate cancer, and outline its clinical
implications. MATERIALS AND METHODS: Published articles on hereditary
prostate cancer were identified using the MEDLINE data base. RESULTS: A
risk of prostate cancer, particularly early onset disease, is strongly
affected by family history (number of relatives with prostate cancer and
their age at diagnosis). A family history of prostate cancer increases
the positive predictive value of prostate specific antigen testing and,
hence, heredity should always be assessed when deciding whether to
perform biopsies in a man with a prostate specific antigen level of 3 to
10 ng./ml. Epidemiological studies indicate that dominantly inherited
susceptibility genes with high penetrance cause 5% to 10% of all
prostate cancer cases, and as much as 30% to 40% of early onset disease.
More than a half dozen chromosome loci that may comprise such genes have
of major importance had been cloned. Most likely, environmental factors
and comparatively common variants of several other genes affect prostate
cancer risk in families with or without multiple cases of the disease.
On average, hereditary prostate cancer is diagnosed 6 to 7 years earlier
than sporadic prostate cancer, but does not otherwise differ clinically
from the sporadic form. As a consequence of the earlier onset, a greater
proportion of men with hereditary prostate cancer die of the disease
than those with nonhereditary prostate cancer. At present, the only
clinically applicable measure to reduce prostate cancer mortality in
families with hereditary disease is screening, with the aim of
diagnosing the disease when it is still in a curable stage. CONCLUSIONS:
Hereditary susceptibility is now considered the strongest risk factor
for prostate cancer and has profound clinical importance. The genetic
mechanism behind such susceptibility has turned out to be more complex
than initially thought, and will probably not be completely understood
for many years to come.
UI - 12202654
AU - Coetzee G; Irvine R
TI -
Size of the androgen receptor CAG repeat and prostate cancer: does it
matter?
SO - J Clin Oncol 2002 Sep 1;20(17):3572-3
UI - 12202660
AU - Bennett CL; Price DK; Kim S; Liu D; Jovanovic BD; Nathan D; Johnson ME;
TI -
Montgomery JS; Cude K; Brockbank JC; Sartor O; Figg WD
Racial variation in CAG repeat lengths within the androgen receptor gene
among prostate cancer patients of lower socioeconomic status.
SO - J Clin Oncol 2002 Sep 1;20(17):3599-604
AD - Mid-West Center for Health Services Research and Development, Department
of Veterans Affairs Medical Center, Chicago, IL 60611, USA.
cbenne@northwestern.edu
PURPOSE: To evaluate (1) whether there were racial differences in the
androgen receptor gene CAG repeat length and in clinical or laboratory
attributes of prostate cancer at the time of diagnosis; (2) whether
there were differences in race, Gleason score, prostate-specific antigen
(PSA) level, and stage at diagnosis by androgen receptor gene CAG repeat
length; and (3) whether sociodemographic, clinical, and laboratory based
factors might be associated with advanced-stage prostate cancer. To our
knowledge, our study is the first to report on CAG repeat lengths in a
cohort of prostate cancer patients, which includes large numbers of
African-American men. METHODS: CAG repeat lengths on the androgen
receptor gene were evaluated for 151 African-American and 168 white
veterans with prostate cancer. The chi(2) test, t test, and logistic
regression analyses were used to evaluate the associations between CAG
repeat lengths and race, stage, histologic grade, and PSA levels at
diagnosis. RESULTS: The mean age of the cohort at the time of diagnosis
was 68.7 years. At presentation, 42.0% had stage D prostate cancer,
26.5% had Gleason scores of 8 to 10, and 53.0% had PSA levels >/= 10
ng/dL. Mean androgen receptor gene CAG repeat length for white veterans
was 21.9 (SD, 3.5) versus 19.8 (SD, 3.2) for African-American veterans
(P =.001). Men with shorter CAG repeats were more likely to have stage D
prostate cancer (P =.09) but were not more likely to have a higher PSA
concentration or Gleason score. CONCLUSION: In this cohort of men with
prostate cancer, short CAG repeat length on the androgen receptor gene
was associated with African-American race and possibly with higher stage
but not with other clinical or pathologic findings.
UI - 12165860
AU - Zhang Y; Fondell JD; Wang Q; Xia X; Cheng A; Lu ML; Hamburger AW
TI -
Repression of androgen receptor mediated transcription by the ErbB-3
binding protein, Ebp1.
SO - Oncogene 2002 Aug 15;21(36):5609-18
AD - Greenebaum Cancer Center, University of Maryland, Baltimore, Maryland,
MD 21201, USA.
Members of the ErbB family of receptors have been implicated in
regulation of androgen receptor (AR) activity. Ebp1, an ErbB-3 binding
protein recently cloned in our laboratory, possesses an LXXLL motif
important in mediating interactions with nuclear hormone receptors.
Therefore, we sought to determine if Ebp1 could bind AR and influence AR
transcriptional activation potential. We demonstrate in this study that
Ebp1 bound to AR in vitro and in vivo, and that this binding was
increased by androgen treatment. The C terminal 79 amino acids of Ebp1
were sufficient to bind AR. The N terminal domain of AR was responsible
for binding Ebp1. Ligand-mediated transcriptional activation of both
artificial and natural AR regulated promoters was inhibited by ectopic
expression of ebp1 in transient transfection systems. Ebp1 deletion
mutants that either lacked the C terminal AR binding region or had a
mutated LXXLL motif failed to inhibit AR activated transcription. PSA
expression from its endogenous promoter was also decreased in LNCaP
prostate cancer cells overexpressing Ebp1. The growth of AR positive
LNCaP cells was inhibited by ectopic expression of ebp1, but mutants
that failed to repress transcription did not inhibit cell growth. These
studies suggest that Ebp1 may play a role in the function of the AR and
provide a link between ErbB receptors and the AR.
UI - 12184806
AU - DePrimo SE; Diehn M; Nelson JB; Reiter RE; Matese J; Fero M; Tibshirani
TI -
R; Brown PO; Brooks JD
Transcriptional programs activated by exposure of human prostate cancer
cell
Cancer Types
Bone Cancer
Brain Tumors
Breast Cancer
Carcinoid Tumors
Endocrine System Cancers
Gastrointestinal Cancers
Gynecologic Cancers
Head and Neck Cancers
Leukemia
Lung Cancers
Lymphomas
Myelomas
Pediatric Cancers
Penile Cancer
Prostate Cancer
Sarcomas
Skin Cancers
Testicular Cancer
Thyroid Cancer
Urinary Tract Cancers
OncoLink Vet
Cancer Treatment
Biologic Therapy
Bone Marrow Transplants
Chemotherapy
Clinical Trials
Complementary Medicine
Gene Therapy
General Treatment Concerns
Hormone Therapy
PDT Center
Proton Therapy
Radiation Oncology
Surgical Oncology
Targeted Therapies
Vaccine Therapies
Cancer Support
Caregivers
Hospice Care and Bereavement
Nutrition and Cancer
Sexuality & Fertility
Side Effects
Support
Survivorship
Exercise and Cancer
Cancer Resources
Cancer News
OncoLink University
Nurses' Notes
Conferences
Newly Diagnosed Patients
Causes and Prevention
Legal and Financial Information for Patients
LGBT Resources
NCI Resources
Global Resources
Cancer Resource List
Resources for Young Adults
OncoLink Media Library
OncoLink TV
Book, Music and Video Reviews
Ask the Experts
Brown Bag Chat
Tracy's Corner
About OncoLink
About OncoLink
Giving to OncoLink
Contact Information
Usage Policy
Editorial Board
How to Partner with OncoLink
Link to OncoLink
Mission Statement
