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As in a prior study on malignant lymphomas, 3 and 6 areas of Uganda showing low and high malarial endemicity, respectively, were selected for analysis and the data retrieved from the Kampala Cancer Registry, which in the 1960s and 1970s collected cases of cancer through a widely used free biopsy service from the whole country. Overall incidence rates were derived from 924 cases from the 12-year period 1964-1975. For reasons of economy, grade of tumour was determined only in cases pertaining to the 6-year period 1968-1973. Of 457 cases, 304 could be reviewed histologically. Only the group of squamous cell carcinomas (84.9%, 258 cases) was large enough for subsequent geographic analysis. High incidence rates of CC were found in areas with high malarial endemicity, whereas low incidence rates occurred where malaria was either frequent or rare. A correlate to malarial infection was the proportion of high-grade carcinomas irrespective of the overall incidence of CC. With high prevalence of malaria and high CPRs of 35-74%, the relative share of high-grade cancer amounted to 50-67%. Where malaria was rare with low CPRs of 8-11%, these values were lower and varied only from 25-39% with a similar range of 14%. Geographic agreement between malarial endemicity and the PI of high-grade cancer was high in the 9 study areas and only slightly lower than for BL, for which the association with malaria is beyond doubt. Compared to areas with little malaria, the RR for the incidence of high-grade carcinomas in areas with severe malaria was increased. The value was 2.04 with a 95% confidence interval of 1.37-3.04. Attributable to secondary immunodeficiency, lifelong exposure to malaria may result in excess frequency of high-grade malignant tumours not only in the group of malignant lymphomas but also in CC., (Copyright 2002 Wiley-Liss, Inc.)

The presence of several infections was determined in tissue and serum samples from 34 cases and 23 controls seen in 1984-85 at Mulago Hospital in Kampala, Uganda. When assessing single infections, association with cervical cancer could be shown for 5 agents, namely by Southern blot assay for human papillomavirus types 16 and 18 (HPV), and by serological tests at varying levels of antibody titres, for herpes simplex virus type I and/or 2 (HSV), cytomegalovirus (CMV), Epstein-Barr virus, viral capsid antigen (EBV-VCA), and Chlamydia trachomatis (CLT). Due to interaction, HSV and CMV were associated with cervical cancer only when infection by both of these agents was demonstrable. In the assessment of the simultaneous presence of these 5 infections, moderately high antibody titres were taken as the cut-off point for infection by HSV, CMV, EBV-VCA, and CLT. This showed that 3 and 4 infections at a time were seen in the majority of the cases in contrast to the controls with essentially no more than 2 such infections. A linear trend in the rise of risk for cervical cancer was noted with increasing number of infections.