Cancer epidemiology · 2025
HPV-unrelated oropharyngeal cancer has elevated risk of synchronous hepatobiliary second primary malignancies compared to HPV-related oropharyngeal cancer: a population-based study from SEER.
СтатьяСравнительное исследованиеНазвание и аннотация: Перевод в очереди
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Cao Shaopan, Asad Ayoubi Mehran
Аннотация
BACKGROUND: Our aim was to compare risk of synchronous and metachronous hepatobiliary second primary malignancies (SPMs) in survivors of human papillomavirus (HPV)-related [i.e., p16(+)] and HPV-unrelated [i.e., p16(-)] oropharyngeal cancer (OPC).
METHODS: A retrospective study was conducted for cases with OPC diagnosis during years 2018-2021 who had known p16 status using data of USA from Surveillance, Epidemiology, and End Results (SEER) Program [Incidence - SEER Research Limited-Field Data, 22 Registries (excl IL and MA), Nov 2023 Sub (2000-2021)]. In the statistical analyses, death was considered as a competing event for the development of a hepatobiliary SPM. Bias due to unbalanced baseline characteristics was eliminated by adjustments using propensity score and inverse probability of treatment weighting (IPTW). Risk of development of a hepatobiliary SPM was assessed using propensity-score-adjusted time-varying Cox proportional hazard regression [adjusted hazard ratio (aHR) with 95 % confidence interval (95 % CI)].
RESULTS: Overall, 25759 cases with tumor status of p16(-) (6353) and p16(+) (19406) with median (interquartile range) follow-up times of 14 (6, 26) and 20 (9, 32) months, respectively, were included. From these, 48 had a hepatobiliary SPM. Compared to HPV-related OPC, HPV-unrelated OPC had significantly elevated risk of synchronous all hepatobiliary SPMs [aHR= 2.39 (95 % CI, 1.11-5.15); P = 0.026] and synchronous hepatocellular carcinoma (HCC) SPM [aHR= 2.86 (95 % CI, 1.18-6.92); P = 0.020], but not metachronous ones. Curves of cumulative incidence of a hepatobiliary (or HCC) SPM and cumulative survival probability for those with a hepatobiliary SPM, both stratified by p16 status and adjusted by IPTW, were generated. The median survival time among patients with a hepatobiliary SPM was shorter for HPV-unrelated OPC (0.8 years) compared to HPV-related OPC (2.6 years).
CONCLUSION: The observed elevated risk was likely due to heavy alcohol and tobacco use and the protective role of HPV infection against HCC development in carriers of hepatitis C virus.
METHODS: A retrospective study was conducted for cases with OPC diagnosis during years 2018-2021 who had known p16 status using data of USA from Surveillance, Epidemiology, and End Results (SEER) Program [Incidence - SEER Research Limited-Field Data, 22 Registries (excl IL and MA), Nov 2023 Sub (2000-2021)]. In the statistical analyses, death was considered as a competing event for the development of a hepatobiliary SPM. Bias due to unbalanced baseline characteristics was eliminated by adjustments using propensity score and inverse probability of treatment weighting (IPTW). Risk of development of a hepatobiliary SPM was assessed using propensity-score-adjusted time-varying Cox proportional hazard regression [adjusted hazard ratio (aHR) with 95 % confidence interval (95 % CI)].
RESULTS: Overall, 25759 cases with tumor status of p16(-) (6353) and p16(+) (19406) with median (interquartile range) follow-up times of 14 (6, 26) and 20 (9, 32) months, respectively, were included. From these, 48 had a hepatobiliary SPM. Compared to HPV-related OPC, HPV-unrelated OPC had significantly elevated risk of synchronous all hepatobiliary SPMs [aHR= 2.39 (95 % CI, 1.11-5.15); P = 0.026] and synchronous hepatocellular carcinoma (HCC) SPM [aHR= 2.86 (95 % CI, 1.18-6.92); P = 0.020], but not metachronous ones. Curves of cumulative incidence of a hepatobiliary (or HCC) SPM and cumulative survival probability for those with a hepatobiliary SPM, both stratified by p16 status and adjusted by IPTW, were generated. The median survival time among patients with a hepatobiliary SPM was shorter for HPV-unrelated OPC (0.8 years) compared to HPV-related OPC (2.6 years).
CONCLUSION: The observed elevated risk was likely due to heavy alcohol and tobacco use and the protective role of HPV infection against HCC development in carriers of hepatitis C virus.