Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2012
Human papillomavirus DNA is rarely detected in colorectal carcinomas and not associated with microsatellite instability: the Seattle colon cancer family registry.
Сравнительное исследованиеСтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Burnett-Hartman Andrea N, Feng Qinghua, Popov Viorica, Kalidindi Anisha, Newcomb Polly A
Аннотация
BACKGROUND: Persistent infection with oncogenic human papillomavirus (HPV) types-16 and -18 is an established cause of cervical and other cancers. Some studies report detection of oncogenic HPV DNA in colorectal carcinomas, with prevalence estimates as high as 84%. However, other studies report detecting no HPV DNA in colorectal tumors.
METHODS: To evaluate the prevalence of HPV in colorectal cancer subsets, we conducted a case-case comparison study. This study included 555 cases of incident colorectal cancer from the Seattle Colon Cancer Family Registry (CCFR), ages 20 to 74 years and diagnosed between 1998 and 2002. Standardized interviews were used to elicit demographics and risk factor data. Tumor DNA was assayed for HPV-16 and -18 DNA using real-time PCR. Microsatellite instability (MSI) status was assessed using a standard 10-marker panel and confirmed with immunohistochemical staining. Prevalence estimates were calculated for the overall sample, and stratified by patient and tumor characteristics. Fisher exact test was used to compare prevalence between strata.
RESULTS: HPV-16 DNA was detected in 2% of colorectal tumors, but no HPV-18 DNA was detected. HPV-16 prevalence did not vary between cases according to sex, age, race, smoking-status, or MSI-status (P > 0.05). HPV-16 prevalence in rectal carcinomas was 5% compared with 1% in colon carcinomas (P = 0.03).
CONCLUSIONS: Among a large sample of colorectal carcinomas, prevalence of HPV-16 and -18 was very low. Prior studies detecting high HPV prevalence in colorectal carcinomas are likely the result of contamination from the anal canal or clinical processing.
IMPACT: HPV is unlikely to play a large role in colorectal carcinogenesis.
METHODS: To evaluate the prevalence of HPV in colorectal cancer subsets, we conducted a case-case comparison study. This study included 555 cases of incident colorectal cancer from the Seattle Colon Cancer Family Registry (CCFR), ages 20 to 74 years and diagnosed between 1998 and 2002. Standardized interviews were used to elicit demographics and risk factor data. Tumor DNA was assayed for HPV-16 and -18 DNA using real-time PCR. Microsatellite instability (MSI) status was assessed using a standard 10-marker panel and confirmed with immunohistochemical staining. Prevalence estimates were calculated for the overall sample, and stratified by patient and tumor characteristics. Fisher exact test was used to compare prevalence between strata.
RESULTS: HPV-16 DNA was detected in 2% of colorectal tumors, but no HPV-18 DNA was detected. HPV-16 prevalence did not vary between cases according to sex, age, race, smoking-status, or MSI-status (P > 0.05). HPV-16 prevalence in rectal carcinomas was 5% compared with 1% in colon carcinomas (P = 0.03).
CONCLUSIONS: Among a large sample of colorectal carcinomas, prevalence of HPV-16 and -18 was very low. Prior studies detecting high HPV prevalence in colorectal carcinomas are likely the result of contamination from the anal canal or clinical processing.
IMPACT: HPV is unlikely to play a large role in colorectal carcinogenesis.