Eble JN, Sauter G., Epstein JI, Sesterhenn IA - iarc
Eble JN, Sauter G., Epstein JI, Sesterhenn IA - iarc
Eble JN, Sauter G., Epstein JI, Sesterhenn IA - iarc
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contrast, mortality among migrants from<br />
East Africa, of predominantly Asian<br />
(Indian) ethnicity, are not high {966}.<br />
Migrants from low-risk countries to areas<br />
of higher risk show quite marked increases<br />
in incidence (for example, Japanese<br />
living in the United States). Some of this<br />
change reflects an elimination of the<br />
'diagnostic bias" influencing the international<br />
incidence rates. Localized prostate<br />
cancer forms a small proportion of cases<br />
in Japan (24%) compared with 66-70% in<br />
the U.S.A; incidence in Japan could be<br />
3-4 times that actually recorded if, for<br />
example, all transurethral prostatectomy<br />
(TURP) sections were carefully examined<br />
{2392}. However, rates in Japanese<br />
migrants remain well below those in the<br />
U.S. White populations, even in<br />
Japanese born in the United States,<br />
which suggests that genetic factors are<br />
responsible for at least some of the differences<br />
between ethnic groups.<br />
Fig. 3.02 International trends in age-standardized mortality rates of prostate cancer (world standard).<br />
Source: WHO/NCHS<br />
Age distribution<br />
The risk of prostate cancer rises very<br />
steeply with age. Incidence of clinical<br />
disease is low until after age 50, and then<br />
increases at approximately the 9-10th<br />
power of age, compared with the 5-6th<br />
power for other epithelial cancers {488}.<br />
Worldwide, about three-quarters of all<br />
cases occur in men aged 65 or more.<br />
Time trends<br />
Time trends in prostate cancer incidence<br />
and mortality have been greatly affected<br />
by the advent of screening for raised levels<br />
of serum Prostate-Specific Antigen<br />
(PSA), allowing increasing detection of<br />
preclinical (asymptomatic) disease<br />
{2100}. In the USA, prostate cancer incidence<br />
rates were increasing slowly up to<br />
the 1980’s, probably due to a genuine<br />
increase in risk, coupled with increasing<br />
diagnosis of latent, asymptomatic cancers<br />
in prostatectomy specimens, due to<br />
the increasing use of TURP {2099}.<br />
Fig. 3.03 Prostate cancer incidence: ASR (World) per 10 5 (1993-1997). 1 From D.M. Parkin et al. {2016}.<br />
Beginning in 1986, and accelerating<br />
after 1988, there was a rapid increase in<br />
incidence. The recorded incidence of<br />
prostate cancer doubled between 1984<br />
and 1992, with the increase being mainly<br />
in younger men (under 65) and confined<br />
to localized and regional disease.<br />
The incidence rates began to fall again in<br />
1992 (1993 in Black males), probably<br />
because most of the prevalent latent<br />
cancers in the subset of the population<br />
reached by screening had already been<br />
detected {1467}. With the introduction of<br />
PSA screening, there was also an<br />
increase in the rate of increase in mortality,<br />
but this was very much less marked<br />
than the change in incidence. More<br />
recently, (since 1992 in White men, 1994<br />
in Black men), mortality rates have<br />
decreased. The contribution that PSA<br />
screening and/or improved treatment<br />
has made to this decline has been the<br />
subject of considerable debate {728,<br />
763,1015}. The increased mortality was<br />
probably partly due to mis-certification of<br />
cause of death among the large number of<br />
men who had been diagnosed with latent<br />
prostate cancer in the late 80’s and early<br />
90’s. The later decline may be partly due to<br />
a reversal of this effect; it seems unlikely<br />
that screening was entirely responsible.<br />
International trends in mortality have<br />
been reviewed by Oliver et al. {1956},<br />
and in incidence and mortality by Hsing<br />
et al. {1130}. The largest increases in<br />
incidence, especially in younger men,<br />
Acinar adenocarcinoma<br />
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