TONSILLAR ONCOGENESIS: CHRONIC TONSILLITIS AS AN INITIATOR AND COFACTOR OF OROPHARYNGEAL CANCER

Europäische Wissenschaftliche Gesellschaft Home About the Journal Peer Review Editorial Board For Authors Reviewer Recognition Archive Contact Impressum EWG e.V. Elektronische Zeitschriftbibliotek Logo Bielefeld Academic Search Engine Logo Erfolgreich durch internationale Zusammenarbeit Oncology and immunology Cite as: Archiv EuroMedica. 2026. 16; 1. DOI 10.35630/2026/16/Iss.1.017 Received 8 December 2025; Accepted 17 February 2026; Published 25 February 2026 TONSILLAR ONCOGENESIS: CHRONIC TONSILLITIS AS AN INITIATOR AND COFACTOR OF OROPHARYNGEAL CANCER Viktor Paramonov¹ email orcid id logo, Lev Vysotskiy¹ orcid id logo, Pavel Shchennikov¹ orcid id logo, Georgiy Potemkin¹ orcid id logo, Aleksey Dugin¹ orcid id logo, Andrey Tantsyrev¹ orcid id logo, Elena Subbotina¹ orcid id logo, Yuliya Mikhaylova¹ orcid id logo, Andrey Kharzov² orcid id logo, Yuriy Emelyanov¹ orcid id logo, Kristina Murzaeva¹ orcid id logo ¹ JSC Doctor Paramonov Clinic, Saratov, Russia ² Independent Clinical Neurologist, Saratov, Russia download article (pdf) info@dr-paramonov.ru ABSTRACT Background Oropharyngeal cancer represents a growing global public health problem and is predominantly characterized by a bimodal etiology associated either with exposure to tobacco and alcohol or with infection by human papillomavirus. At the same time, 15 to 25 percent of cases remain etiologically unexplained, indicating the presence of an additional pathogenetic mechanism. Chronic tonsillitis has traditionally been regarded as a background inflammatory condition without direct oncological significance; however, population based studies demonstrate a several fold increase in the risk of tonsillar cancer in such patients. Aims The aim of this work is a conceptual analysis of the role of chronic tonsillitis in oropharyngeal oncogenesis and the formulation of an integrative pathogenetic hypothesis explaining the contribution of chronic inflammation, microbial dysbiosis, and viral synergism to the development of both HPV positive and HPV negative cancer. Methods This study was conducted as a narrative review with a conceptual and analytical synthesis of epidemiological, experimental, and molecular literature relevant to chronic tonsillitis and oropharyngeal carcinogenesis. Literature selection involved a thematic and hypothesis driven selection of publications focusing on inflammation associated carcinogenesis, tonsillar microenvironmental alterations, microbial dysbiosis, immune evasion mechanisms, and interactions between bacterial inflammation and human papillomavirus. A formal systematic search protocol and quantitative data synthesis were not applied, as the primary objective was the development of an integrative pathogenetic model rather than estimation of effect sizes or prevalence. Results Based on analysis of the literature, a three stage model of tonsillar oncogenesis is proposed. It includes initiation of malignant transformation driven by chronic inflammation, crypt hypoxia, and genotoxic stress; promotion of tumor growth through microbial dysbiosis involving Fusobacterium nucleatum and bacterially mediated immune evasion via the Fap2 TIGIT axis; and acceleration of oncogenesis through activation of viral oncogene transcription E6 and E7 via the NF kappa B pathway. Conclusions Chronic tonsillitis may be regarded as a potentially significant factor in the formation of an oncogenic microenvironment of the oropharynx and as a common pathogenetic element for both HPV positive and HPV negative forms of cancer. The proposed model provides a biological explanation for the epidemiological association between chronic tonsillitis and tonsillar cancer and for the observed reduction in tonsillar cancer risk after tonsillectomy, and it underscores the need for further experimental and clinical studies.