increased initially, then decreased.
is more common in northern European countries than in southern European ones.
is the leading cause of cancer-related mortality.
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 entirely genetic in origin.
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.
both studies clearly show no benefit to PSA screening for prostate cancer.
contamination of the control arm with PSA screening is a criticism of the PLCO cancer screening trial.
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.
5 times higher.
2 to 3 times higher.
1.5 times higher.
deficient in DNA repair.
histologically similar to sporadic prostate cancer.
inherited in an autosomal-recessive fashion.
inherited in X-linked fashion.
caused by defects in the BRCA2 gene.
control of the inflammatory response.
all of the above.
DNA repair mechanisms.
genes involved in susceptibility to infection.
the TMPRSS2 gene is expressed in malignant but not benign prostatic epithelium.
TRMPSS-related gene fusions are not specific for the presence of prostate cancer.
TMPRSS2 expression has been shown to be induced by estrogens.
the most common fusion in screen-detected prostate cancer involves TMPRSS2 fused to ETV1.
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.
stromal estrogen receptor (ER) α expression is silenced in early prostate cancers and re-emerges with disease progression.
aromatase-knockout mice all develop prostate cancer in their lifetime.
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.
estrogen’s treatment effect is partly through a direct inhibitory effect of estrogens on prostate epithelial cell growth.
reduced intraprostatic inflammation.
lower body mass index.
lower serum testosterone levels.
higher serum PSA levels.
higher risk of developing prostate cancer.
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.
vitamin D levels are higher in older men.
a calcium-poor diet predisposes men to prostate cancer.
men living in areas with less ultraviolet (UV) exposure have lower prostate cancer mortality rates.
lower free IGF-1.
better cancer-specific survival after radical prostatectomy.
protection against oxidative stress.
higher circulating androgens.
lower serum PSA levels.
hormonal response genes (ERα, ERβ, and RARβ).
genes controlling the cell cycle (CyclinD2 and 14-3-3σ).
DNA repair genes (GSTP1, GPX3, and GSTM1).
tumor suppressor genes (APC, RASSF1α, DKK3, TP16INK4α, E-cadherin, and TP57WAF1).
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.
Mutations of proto-oncogenes are usually associated with advanced disease.
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.
cost associated with treatment.
disease incidence and morbidity.
disease-promoting lifestyle habits.
the placebo effect.
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