Meta-analysis of the impact of human papillomavirus (HPV) on cancer risk and overall survival in head and neck squamous cell carcinomas (HNSCC)

Abstract

BackgroundHPV is important in a subset of HNSCC. Our meta-analysis determined the clinical characteristics of HPV-related HNSCC.MethodPubmed search terms "HPV" and "HNSCC" were used to identify 34 studies since 1980. We obtained pooled adjusted odds ratio (OR) or hazard ratio (HR) using random or fixed-effects model and compared OS depicted in forest plot.ResultsA total of 5681 patients were included. The prevalence of HPV+ tumors was 22%, with 86.7% of HPV16+ genotype. The OR for HNSCC in HPV16+ patients was 4.44 (95% CI = 2.87-6.02). HPV status was associated with p16 expression (adj OR = 3.00; 0.90-9.70), and HPV+ tumors were less likely to harbor p53 mutations (adj OR = 0.21; 0.04-0.38). The HR for death in HPV+ patients was 0.42 (0.27-0.57). HPV+ HNSCC also had a better response to therapy.ConclusionHPV+ HNSCC are established as a separate biologic entity. Prospective trials are needed to establish the optimal therapy for HPV+ HNSCC.

Biology of Human Papillomavirus Infections in Head and Neck Carcinogenesis

“…Seven years later, in 1983, we published the first evidence suggesting that a subgroup (some 20 %) of oral cancers is associated with HPV, based on detection of HPV structural proteins in these lesions using an antibody prepared against pooled HPV types [39]. We subsequently identified HPV types 11, 16 and 18 in these samples [40][41][42][43][44][45][46][47][48][49]. This concept has now been well accepted, and a growing body of evidence is supporting that approximately 20 % of oral cancers and 60-80 % of oropharyngeal cancers are caused by HPV [41][42][43][44].…”

“…Importantly, HPV-positive HNSCCs differ remarkably from HPV-negative HNSCCs in their clinical response and molecular properties. HPV-positive HNSCCs have a better overall-survival than HPV-negative HNSCCs [46,47]. HPV-positive HNSCCs harbor the wild-type p53, while the classical smoking-and alcohol-induced cancers have mutated p53.…”

Systemic and local human papillomavirus 16‐specific T‐cell immunity in patients with head and neck cancer

“…In all cultures, both CD8þ and CD4þ T cells grew out (CD4/CD8 ratio median 2.45, average 5.1 and range 0. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19]. The composition of T cells was not clearly influenced by the culture conditions (Fig.…”

“…2 Patients with HPV-induced HNCSCC often present with advanced disease but their prognosis is better than HNCSCC associated with smoking and drinking. [3][4][5] Notably, the majority but not all patients with an HPVþ tumor display a strong gene signature for adaptive immune response in their tumor 6 as well as strong tumor infiltration by T cells 4 suggesting that the presence of HPV may be related to an enhanced local tumor-specific T-cell response.…”

Human Papilloma Virus Attributable Head and Neck Cancer in the Sudan Assessed by p16INK4AImmunostaining

“…High-risk HPV subtype 16 accounts for more than 85% of all HPV-positive (HPV+) tumors in HNSCC (Dayyani et al, 2010). Patients with HPV-positive HNSCC had a lower risk of dying, and a lower risk of recurrence than HPV-negative HNSCC patients (Fakhry et al, 2008).…”