Familial cancer risk in family members and spouses of patients with early‐onset head and neck cancer

Abstract

Background Reported patterns of familial aggregation of head and neck cancer (HNC) vary greatly, with many studies hampered by the limited number of subjects. Methods Altogether 923 early‐onset (≤40 years old) HNC probands, their first‐degree relatives, spouses, and siblings' offspring were ascertained. Cumulative risk and standardized incidence ratios (SIRs) were estimated. Results Of all early‐onset HNC families, only 21 (2.3%) had familial HNC cancers at any age and less than five familial early onset HNC cancers among first‐degree relatives. The cumulative risk of HNC for siblings by age 60 (0.52%) was at population level (0.33%). No increased familial risk of early‐onset HNC could be discerned in family members (SIR 2.68, 95% CI 0.32‐9.68 for first‐degree relatives). Conclusions Our study indicates that the cumulative and relative familial risk of early‐onset HNC is modest in the Finnish population and, at most, only a minor proportion of early‐onset HNCs are due solely to inherited genetic mutations.

Incidence and survival in oral and pharyngeal cancers in Finland and Sweden through half century

“…According to the Swedish and Danish Cancer Registries the case ranking follows the frequency order—oral, oropharyngeal, hypopharyngeal and nasopharyngeal cancers, with male cases outnumbering female cases [ 2 , 3 ]. The main risk factors for these cancers in Western countries are tobacco, alcohol and their interactions and infection with human papillomavirus (HPV), but their contributions may vary by site [ 1 , 4 – 6 ]. According to the International Agency for Research on Cancer (IARC), nasopharyngeal cancer may be less responsive to tobacco carcinogenesis than other pharyngeal or oral cavity cancers [ 4 ].…”

Survival in oral and pharyngeal cancers is catching up with laryngeal cancer in the NORDIC countries through a half century

“…While the overall risk of smoking may be somewhat lower for these cancers than it is for lung cancer, the positive influence of quitting smoking appears to be faster than that for lung cancer, and after 10 years of quitting the excess risk may have disappeared 2 . The main risk factor for oropharyngeal cancers in industrialized countries is infection with human papillomavirus (HPV), in addition to tobacco and alcohol 2,3,5,6 . The increasing incidence and male prominence in oropharyngeal cancer have been attributed to an increasing burden of HPV infections through oral sex 7–10 ; it is assumed that over 90% of oral HPV infections are sexually transmitted 11,12 .…”

“…2 The main risk factor for oropharyngeal cancers in industrialized countries is infection with human papillomavirus (HPV), in addition to tobacco and alcohol. 2 , 3 , 5 , 6 The increasing incidence and male prominence in oropharyngeal cancer have been attributed to an increasing burden of HPV infections through oral sex 7 , 8 , 9 , 10 ; it is assumed that over 90% of oral HPV infections are sexually transmitted. 11 , 12 HPV‐positivity varied in over 2000 European oropharyngeal cancer patients assessed from publications between 2014 and 2018 from 18% to 65%.…”

Family History of Head and Neck Cancers

“…The incidence of HNC varies globally depending on risk factors; the incidence is increasing in many regions, whereby the estimated annual number of new diagnoses is reaching one million [1]. In Western countries, alcohol and tobacco and their interactions are the main risk factors, but chronic viral infections with human papillomavirus (HPV) and Epstein Barr virus (EBV) also contribute to the risk of HNC [3][4][5]. According to the International Agency for Research on Cancer (IARC), cancers of the pharynx and larynx are the most responsive sites, and those of the nasopharyx and nasal cavities are the least responsive sites for tobacco carcinogenesis [3].…”

“…Molecular control of HPV-positive HNCs is steered by the integrated HPV genome, which often leads to inactivation of p53 and other proteins controlling the cell cycle, while in HPV-negative cases, mutations of TP53 are common; survival is better in HPV-positive cases. Familial risks for HNC have been considered in several case-control and a few cohort studies, as discussed [5]. Large studies have been able to describe risks at individual sites, reporting clear effects of smoking, weaker effects of alcohol, but strong joint effects of both [14][15][16][17][18][19][20].…”