increased initially, then decreased.
has higher 5-year rates in Denmark, Poland, and Algeria compared with the United States, Canada, and Australia.
is the leading cancer diagnosis in men.
is the leading cause of cancer-related mortality.
is more common in northern European countries than in southern European ones.
is entirely genetic in origin.
both studies clearly show no benefit to PSA screening for prostate cancer.
the European Randomized Study of Screening for Prostate Cancer (ERSPC) had a shorter median follow-up than the Prostate, Lung, Colorectal, and Ovarian (PLCO) cancer screening trial.
contamination of the control arm with PSA screening is a criticism of the PLCO cancer screening trial.
the ERSPC showed no significant difference in survival between screened and unscreened men.
the PLCO cancer screening trial demonstrated a 20% risk reduction in prostate cancer mortality in screened men compared with unscreened men.
5 times higher.
2 to 3 times higher.
1.5 times higher.
inherited in an autosomal-recessive fashion.
deficient in DNA repair.
histologically similar to sporadic prostate cancer.
caused by defects in the BRCA2 gene.
inherited in X-linked fashion.
genes involved in susceptibility to infection.
all of the above.
control of the inflammatory response.
DNA repair mechanisms.
it results from the fusion of the 5′ untranslated end of the TMPRSS2 serine protease gene to members of the ETS family of oncogenic transcription factors.
TMPRSS2 expression has been shown to be induced by estrogens.
the TMPRSS2 gene is expressed in malignant but not benign prostatic epithelium.
the most common fusion in screen-detected prostate cancer involves TMPRSS2 fused to ETV1.
TRMPSS-related gene fusions are not specific for the presence of prostate cancer.
aromatase-knockout mice all develop prostate cancer in their lifetime.
estrogen’s treatment effect is partly through a direct inhibitory effect of estrogens on prostate epithelial cell growth.
stromal estrogen receptor (ER) α expression is silenced in early prostate cancers and re-emerges with disease progression.
estrogen’s treatment effect is primarily related to a negative feedback on the hypothalamo-pituitary-gonadal axis.
prostate epithelial ERβ may play an important role in initiation of prostate cancer.
lower body mass index.
higher risk of developing prostate cancer.
lower serum testosterone levels.
reduced intraprostatic inflammation.
higher serum PSA levels.
native Japanese, whose diet is rich in vitamin D derived from fish, have a high incidence of prostate cancer.
polymorphisms conferring lower vitamin D receptor activity are associated with increased risk for prostate cancer.
a calcium-poor diet predisposes men to prostate cancer.
vitamin D levels are higher in older men.
men living in areas with less ultraviolet (UV) exposure have lower prostate cancer mortality rates.
better cancer-specific survival after radical prostatectomy.
lower free IGF-1.
protection against oxidative stress.
lower serum PSA levels.
higher circulating androgens.
tumor suppressor genes (APC, RASSF1α, DKK3, TP16INK4α, E-cadherin, and TP57WAF1).
DNA repair genes (GSTP1, GPX3, and GSTM1).
genes controlling the cell cycle (CyclinD2 and 14-3-3σ).
hormonal response genes (ERα, ERβ, and RARβ).
Absent expression of prostate membrane-specific antigen (PSMA) is observed after androgen withdrawal and in hormone refractory disease.
The enzyme glutathione-S-transferase–1 (GST-1) is always active in prostate cancer.
There is evidence that telomere lengthening plays a role in prostate cancer.
Drugs that increase vascular endothelial growth factor (VEGF) activity are being investigated in the treatment of prostate cancer.
Mutations of proto-oncogenes are usually associated with advanced disease.
cost associated with treatment.
disease-promoting lifestyle habits.
disease incidence and morbidity.
the placebo effect.
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