1. Introduction
Numerous epidemiological studies have investigated associations between a history of allergic diseases and cancer risk or prognosis contributing to progress in the field of AllergoOncology.1-5 Notably, investigations have revealed findings of inverse associations between allergies and cancer risk, in particular for glioma.6 However, despite these findings, there remain outstanding questions and research gaps for IgE-mediated diseases and cancer, including glioma.7,8
Allergic diseases and cancer are both influenced by genetic and environmental factors, with potential impacts of allergic inflammation in cancer depending on the tumour subtype and its microenvironment. Several hypotheses have been proposed to define this complex interplay, with pro- and anti-tumoral outcomes integrated into the “combinatorial hypothesis”.8 In the cancer initiation phase, the “prophylaxis hypothesis” suggests that allergic symptoms may decrease tumour risk by expelling environmental carcinogens and stimulating behavioural avoidance. The “immunosurveillance hypothesis” defines atopy as general enhanced immune responsiveness. The “chronic inflammation hypothesis” proposes that allergic inflammation, oxidative damage, and subsequent gene mutations, increase neoplastic cell risk. Finally, the “Th2-skewing hypothesis” argues that type-2 (T2) immune response dominance in allergic disorders potentiates a pro-tumoral microenvironment over anti-tumoral Th1-immunity (Figure 1).8
Figure 1: Proposed hypotheses of associations between allergic disorders and cancer development and progression within the concept of immunosurveillance and immunoediting.