A reason to be grateful for Springtime sneezes?

From the "it is what it is" department, here is an interesting recent article (abstract only):

https://www.ncbi.nlm.nih.gov/pubmed/30700443

Allergic conditions may prevent some cancers by promoting immune surveillance. We examined associations of allergic rhinitis, asthma, and eczema with cancer risk among elderly Americans. . . We used Surveillance, Epidemiology, and End Results (SEER)-Medicare linked data to perform a case-control study. Cases were individuals with first cancer diagnosed in SEER registries (1992-2013, ages 66-99; N=1,744,575). Cancer-free controls (N=100,000) were randomly selected from Medicare, matched on sex, age and selection year. Allergic conditions were identified using Medicare claims, and logistic regression was used to estimate adjusted odds ratios (aORs) with significance gauged with a Bonferroni p-value cutoff (p<0.00034). . . Allergic rhinitis, asthma, and eczema were present in 8.40%, 3.45%, and 0.78% of controls, respectively. For allergic rhinitis, strong inverse associations (aORs 0.66-0.79) were observed for cancers of the hypopharynx, esophagus (squamous cell), cervix, tonsil/oropharynx, and vagina/vulva. More modest but significant inverse associations were noted for cancers of the esophagus (adenocarcinoma), stomach, colon, rectosigmoid/rectum, liver, gallbladder, lung, uterus, bladder, and miscellaneous sites. Associations were stronger in analyses requiring a dispensed medication to confirm the presence of allergic rhinitis. Asthma was associated with reduced risk of liver cancer (aOR 0.82, 95%CI 0.75-0.91), while eczema was associated with elevated risk of T-cell lymphoma (aOR 4.12, 3.43-4.95). . . Inverse associations with allergic rhinitis are present for multiple cancers and require etiologic investigation. . . Understanding of mechanisms by which allergic conditions reduce cancer risk may advance cancer prevention and treatment.

There is always the possibility that allergy medications such as singulair could also be responsible for this result.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5535846/

Our previous cohort study showed that cysteinyl leukotriene receptor antagonists, mainly montelukast, decreased the lung cancer risk in asthma patients. In the current study, we conducted in vivo and in vitro experiments to demonstrate the inhibiting effect of montelukast on lung cancer and to investigate the underlying mechanisms. Using Lewis lung carcinoma-bearing mice, we showed that feeding montelukast significantly delayed the tumor growth in mice (p < 0.0001). Montelukast inhibited cell proliferation and colony formation and induced the cell death of lung cancer cells. Further investigation showed the down-regulation of B-cell lymphoma 2 (Bcl-2), up-regulation of Bcl-2 homologous antagonist/killer (Bak), and nuclear translocation of apoptosis-inducing factor (AIF) in montelukast-treated lung cancer cells. Montelukast also markedly decreased the phosphorylation of several proteins, such as with no lysine 1 (WNK1), protein kinase B (Akt), extracellular signal-regulated kinase 1/2 (Erk1/2), MAPK/Erk kinase (MEK), and proline-rich Akt substrate of 40-kDa (PRAS40), which might contribute to cell death. In conclusion, montelukast induced lung cancer cell death via the nuclear translocation of AIF. This study confirmed the chemo-preventive effect of montelukast shown in our previous cohort study. The utility of montelukast in cancer prevention and treatment thus deserves further studies.

See also, https://www.ncbi.nlm.nih.gov/pubmed/30144515