Young-Age Prostate Cancer
Young-Age Prostate Cancer
Autopsy studies have shown that in West-European and American men, the prevalence of prostate cancer at the age of 40–50 years is about 20%–30%. Most, but not all studies show that PSA-detected prostate cancers at age under 55 years are low grade. More aggressive early-onset prostate cancer is seen more frequently in African-American men than in Caucasian men. Young-age prostate cancer is associated with a considerably increased risk of prostate cancer in family members. The literature seems to suggest that high-grade early-onset prostate cancers have a clinically worse outcome than their elderly-onset counterparts. A feature distinguishing young-age from elderly-onset prostate cancer is the more frequent activation of the androgen–androgen receptor axis, as reflected by the increased frequency of the TMPRSS2–ERG fusion. Some modest progress on the involvement of susceptibility genes has been made in the past few years. This includes the identification of BRCA2-associated prostate cancers with intraductal carcinoma component as an aggressive early-onset category, whereas HOXB13 mutation-associated cancers often have a characteristic histological architecture and a more indolent behaviour. Recognition of unique genetic factors in men with early onset carcinoma and aggressive behaviour can help to target screening and therapy and thus reduce prostate-cancer-specific death among younger men.
Conclusions
Autopsy studies have shown that in West-European and American men, the prevalence of prostate cancer at the age of 40–50 years is about 20%–30%. Most, but not all studies show that PSA-detected prostate cancers at age under 55 years are low grade. More aggressive early-onset prostate cancer is seen more frequently in African-American men than in Caucasian men. Young-age prostate cancer is associated with a considerably increased risk of prostate cancer in family members. The literature seems to suggest that high-grade early-onset prostate cancers have a clinically worse outcome than their elderly-onset counterparts. A feature distinguishing young-age from elderly-onset prostate cancer is the more frequent activation of the androgen–androgen receptor axis, as reflected by the increased frequency of the TMPRSS2–ERG fusion. Some modest progress on the involvement of susceptibility genes has been made in the past few years. This includes the identification of BRCA2-associated prostate cancers with intraductal carcinoma component as an aggressive early-onset category, whereas HOXB13 mutation-associated cancers often have a characteristic histological architecture and a more indolent behaviour. Recognition of unique genetic factors in men with early onset carcinoma and aggressive behaviour can help to target screening and therapy and thus reduce prostate-cancer-specific death among younger men.