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Human herpesvirus 8 (HHV-8) is associated with endothelial and B-cell malignancies; however, its potential involvement in epithelial cancers, including breast and colorectal cancer, remains controversial. Therefore, in this study, we aimed to investigate the prevalence of HHV-8 DNA in malignant tissues of colorectal and breast cancers compared with non-malignant tissues in Shiraz, Iran. In this study, 210 specimens of colorectal paraffin-embedded tissue, including 70 normal mucosa, 70 adenomatous polyps, and 70 adenocarcinomas, as well as 287 paraffin-embedded breast specimens, including 144 malignant and 143 benign lesions, were included. After deparafinization, the DNA was extracted using a commercial kit. The quality of the extracted DNA was evaluated using PCR on the beta globin gene. Those samples that were positive for the beta globin gene were screened for HHV-8 DNA using real-time PCR. χ², or Fisher’s exact tests were used for statistical analysis. The mean age of colorectal patients was 52 ± 1.64 years, while the mean age was 45.0 ± 9.4 years in the malignant breast cancer group and 35.2 ± 12.1 years in the benign breast lesion group. In colorectal cancer, 112 cases (53.3%) were men. HHV-8 DNA was detected in 36/210 (17.1%) of colorectal samples, including 13/70 (18.6%) of normal mucosa, 12/70 (17.1%) of adenomas, and 11/70(15.7%) of adenocarcinomas, with no significant differences among groups ( p = 0.942). HHV-8 detection in colorectal tissues was not associated with sex, age strata, anatomic sub-site, or HPV co-infection (all p > 0.05). Moreover, the results of qPCR showed that in the breast tissues, HHV-8 DNA was identified in 31/144 (21.5%) malignant specimens and 28/143 (19.6%) benign specimens, which was not significantly different between the two groups ( p = 0.770). HHV-8 DNA was detected at low and comparable frequencies in normal, premalignant, and malignant colorectal tissues as well as in malignant versus benign breast specimens, providing no evidence for tumor-specific enrichment. These findings support an incidental/background carriage model rather than a direct oncogenic role in these epithelial cancers; tissue-localization and viral-load studies are warranted.
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Jazi et al. (2026) studied this question.
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