Page 38 - 20dynamics of cancer

AGE OF CANCER INCIDENCE 23

Figure 2.2 plots age-specific incidence for different cancers in the USA.
Solid lines show male incidences, and dashed lines show female inci-
dences. Figure 2.3 plots the age-specific accelerations. I find it useful
to look at both incidence and acceleration: incidence describes the fre-
quency of cancer at different ages; acceleration describes how rapidly
incidence changes with age at different times of life.
The acceleration plots in Figure 2.3 show nearly universal positive ac-
celeration for these adult cancers, which means that incidence increases
with age. Interestingly, the accelerations, although positive, often de-
cline late in life (Frank 2004b). I discuss possible explanations for the
late-life decline in acceleration in the following chapters.
Cancer incidence changes over time for people born in different years,
perhaps because they have different lifestyles or environmental expo-
sures (Greenlee et al. 2000). Cancer incidence also varies in different ge-
ographic locations (Parkin et al. 2002). To illustrate patterns in different
times and locations, The Appendix compares incidence and acceleration
of the common cancers in the USA in two time periods, 1973–1977 and
1993–1997, and in England, Sweden, and Japan in 1993–1997 (Figures
A.1–A.12).

2.3 Childhood Cancers

Inherited genetic defects sometimes cause tumors in very young chil-
dren (Ries et al. 1999). For example, bilateral retinoblastoma is inherited
in an autosomal dominant manner (Knudson 1971). Nearly all carriers
develop cancer. The early incidence and the decline in incidence with age
(Figure 2.4) occur because most cell divisions in the developing retina
happen in the first few years of life, and because incidence declines as
the onset of disease depletes the number of susceptible but previously
unaffected carriers. Unilateral retinoblastoma arises mainly in geneti-
cally normal individuals. The decline in incidence with age happens in
accord with the decline in cell division in the susceptible tissue.
In testicular cancer, the early cases up to age four appear similar
in pattern to the inherited early syndromes, whereas after puberty the
number of cases accelerates at ages during which cell division greatly
increases (Figure 2.4). Osteosarcomas increase in incidence during the
ages of rapid bone elongation; these cancers decline in frequency after
the teen years, with the decline in cellular division that accompanies