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).