107

Epidemiology, Etiology, and

Prevention of Prostate Cancer

Eric A. Klein; Andrew J. Stephenson

Questions

1.Following the prostate-specific antigen (PSA) "cull effect," the incidence of prostate cancer in the United States:

a.is decreasing.

b.is stable.

c.is increasing.

d.increased initially, then decreased.

e.is fluctuating.

2.In the United States, the highest prostate cancer incidence rates are seen in:

a.whites.

b.African Americans.

c.Hispanic/Latinos.

d.Asian Americans

e.Native Americans.

3.Worldwide, prostate cancer:

a.is the leading cancer diagnosis in men.

b.is the leading cause of cancer-related mortality.

c.incidence is highest in countries with the highest rates of screening.

d.is entirely genetic in origin.

e.has the lowest age-adjusted mortality rates per 100,000 men in North America.

4.With respect to two large randomized trials assessing the effect of PSA screening on prostate cancer mortality:

a.overall incidence rates were higher in the European Randomized Study of Screening for Prostate Cancer (ERSPC) but overall mortality rates

were higher in the Prostate, Lung, Colorectal, and Ovarian (PLCO) trial.

b.the ERSPC showed no significant difference in survival between screened and unscreened men.

c.the PLCO cancer screening trial demonstrated a 20% risk reduction in prostate cancer mortality in screened men compared to unscreened men.

d.contamination of the control arm with PSA screening is a limitation of the PLCO cancer screening trial.

e.both studies clearly show no benefit to PSA screening for prostate cancer.

5.Compared with a man with no family history of prostate cancer, the risk of developing prostate cancer in a man with one affected first-degree relative is:

a.unchanged.

b.1.5 times higher.

c.2 to 3 times higher.

d.5 times higher.

e.100%.

6.Biologic functions of known prostate cancer susceptibility genes include:

a.control of the inflammatory response.

b.homeobox genes.

c.DNA repair mechanisms.

d.susceptibility to infection.

e.all of the above.

7.Which of the following statements regarding gene fusions in prostate cancer are correct?

a.The most frequent fusions are between the TMPRSS2 serine protease to members of the ETS family of oncogenic transcription factors.

b.The TMPRSS2-ERG fusion gene is present in prostate stem cells.

c.TMPRSS2 expression has been shown to be induced by androgens.

d.TRMPSS2-related gene fusions are highly specific for the presence of prostate cancer.

e.All of the above.

8.All of the following statements regarding estrogens and prostate cancer are correct, EXCEPT:

a.Estrogen's treatment effect is primarily related to a negative feedback on the hypothalamo-pituitary-gonadal axis.

b.Estrogen's treatment effect is partly through a direct inhibitory effect of estrogens on prostate epithelial cell growth.

c.Aromatase-knockout mice all develop prostate cancer in their lifetime.

d.Stromal estrogen receptor (ER)α expression is silenced in early prostate cancers, and re-emerges with disease progression.

e.Prostate epithelial ERβ may play an important role in initiation of prostate cancer.

9.Elevated serum levels of insulin-like growth factor (IGF) 1 have been associated with:

a.higher serum PSA levels.

b.lower body mass index.

c.reduced intraprostatic inflammation.

d.higher risk of developing prostate cancer.

e.lower serum testosterone levels.

.Evidence suggesting that vitamin D affects the risk of prostate cancer includes the fact that:

a.men living in areas with less ultraviolet exposure have lower prostate cancer mortality rates.

b.vitamin D levels are higher in older men.

c.a calcium-poor diet predisposes men to prostate cancer.

d.native Japanese, whose diet is rich in vitamin D derived from fish, have a high incidence of prostate cancer.

e.polymorphisms conferring lower vitamin D receptor activity are associated with increased risk for prostate cancer.

.High body mass index is associated with:

a.protection against oxidative stress.

b.higher circulating androgens.

c.lower serum PSA levels.

d.better cancer-specific survival after radical prostatectomy.

e.lower free IGF-1.

.Hypermethylation of the following genes may play a role in prostate cancer etiology:

a.DNA repair genes (GSTpi, GPX3, and GSTM1).

b.hormonal response genes (ERαA, ERβ, and RARβ).

c.genes controlling the cell cycle (CyclinD2 and 14-3-3σ).

d.tumor suppressor genes (APC, RASSF1α, DKK3, p16INK4?−α, E- cadherin, and p57WAF1).

e. all of the above.

.The existence of multiple prostate cancer susceptibility genes and chromosomal loci suggests:

a.dominant inheritance pattern.

b.common clinical features associated with all identified genes.

c.genetic heterogeneity in the cause of prostate cancer.

d.need for yearly screening in those with a family history.

e.multifocal tumors in affected individuals.

.Epigenetic mechanisms active in prostate cancer include:

a.chromatin remodeling

b.promoter hypomethylation and hypermethylation

c.microRNAs that lead to gene silencing

d.long noncoding RNAs

e.all of the above.

.Findings of the Selenium and Vitamin E Cancer Prevention Trial (SELECT) include:

a.a significant reduction in the incidence of prostate cancer in the combination arm.

b.a significant effect of selenium and vitamin E on reducing the risk of cardiovascular disease and nonprostate malignancies.

c.a significant increased incidence of diabetes mellitus in the selenium arm.

d.a reduction in prostate-cancer specific mortality.

e.an increased risk of prostate cancer in those taking vitamin E alone.

.The protective effect of lycopene against prostate cancer may best be achieved by consuming:

a.cooked foods.

b.pure form as oral capsules.

c.pure form with other antioxidants.

d.raw vegetables.

e.fresh fruit.

.In the Prostate Cancer Prevention Trial (PCPT), compared with placebo, finasteride use was associated with a higher incidence of:

a.prostatitis.

b.urinary tract infection.

c.surgical intervention for lower urinary tract symptoms.

d.sexual dysfunction.