Legends to tables and figures:
Table 1. Race/ethnicity-specific epidemiology of new cancer
cases [SEER 12 (2015-2019) + NPCR age-adjusted
participantsa] and cytomegalovirus seroprevalence
[NHANES III] (accessible data are selected for comparative
purposes).
Table 2. Age-standardized, delay-adjusted incidence
ratesa for the most common cancersb(all anatomical sites combined, both genders, all ages) among the
racial/ethnic groupsc (2012-2016)din the United States compared to their CMV seropositivity (%).
Table 3. Correlation between worldwide incidence rate (100,000
population/year) of individual malignant tumors across 73 countries
[WHO’s GLOBOCAN database (51)] and the country specific prevalence
of CMV seropositivity rates (28).
Figure 1. New cancer (all invasive types combined, all
sites)/105 country specific population plotted against
CMV seropositivity rates [28]. Inverse relationship over 73
countries [51] (Spearman’s ρ = -0.732;p <0.001), signals a globally pervasive protection
against tumorigenesis driven by CMV.
Figure 2. Malignant melanoma/105 populationvs. country specific prevalence of CMV seropositivity [28]
correlate strongly inversely (Spearman’s ρ = -0.763;p <0.001) across 73 countries [51].
Figure 3. Kidney cancer/105 population and
the country specific CMV seroprevalence [28] are strongly and
inversely connected across 73 countries [51] (Spearman’s ρ =
-0.754; p <0.001).
Figure 4. Incidence of breast cancer/105population and the country specific CMV seropositivity rate [28]
spanning 73 continent-wide countries [51]. An inverse (protective)
association is suggested by Spearman’s ρ = -0.719;p <0.001.
Figure 5. Incidence of Kaposi’s sarcoma (mostly in HIV+
people)/105 population and the specific country-level
rate of CMV seropositivity [28] covering 73 countries [51] are
not correlated (Spearman’s ρ = -0.007; p =0.953).