A 92) in all populations except Latinos and

A meta-analysis of 8 prospective and 8 case-control
studies published in 2009 found no association between Allergy, asthma, and
atopy and CRC risk (60). A study of
Taiwanese population reported an inverse relationship between allergic rhinitis
and rectum cancer. However, this association was not significant for colon
cancer (61). The Cancer
Prevention Study II (CPS-II) announced a non-significantly 10% reduction in CRC
incidence and a significantly 21% lower CRC mortality for individuals with both
hay fever and asthma, with weaker relationships for those with only one of
these conditions(9,
62). Additionally, the
Iowa Women’s Health study highlighted history of two or more atopic conditions correlated
with a 42% decrement in CRC risk (63). More recent
cohort study among multiethnic population explained that Allergy were a
protective effect against CRC among both men and women (RR = 0. 86, 95% CI: 0.8-0.
92) in all populations except Latinos and was significant in whites, African
Americans, Native Hawaiians, and Japanese Americans. Also, Allergy cases had a
20% fewer CRC-related mortality(64).

The biological mechanism for the correlation of Allergy
with CRC is not understood but could be as a result of antitumor functions of
type I Ig E-mediated immune activity. This effect leads to migration of immune
cells such as eosinophils and mast cells to intestinal mucosa. Allergens can
enter the body through respiratory system and the digestive system, where mast
cells and eosinophils are widespread (65). This can result
to type I Ig E-mediated hypersensitivity reactions, due to the high activation
of eosinophils and mast cells and over response of T-helper cell type II. Complexes
of Ig E and cancer cell can degranulate mast cells which release factors in
order to increase permeability and inflammation (66). Eosinophil
levels are speculated to have cytotoxic effects and antitumor activity on
precancerous cells that drive from high proliferating tissues, such as the gut
lining (63,
67, 68). Due to the high presence of
eosinophils and degranulation of mast cell in the respiratory mucosal lining of
asthmatic cases, leukocytes in the gut of subjects with atopic conditions is
more (69). Another theory,
termed the prophylaxis hypothesis proposed that immune responses and
inflammation in mucosal layer can cause to further rapid clearance of mutagenic
stimulators (10).

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Brain cancer

The hypothesis that Allergy may be related with a
lower risk of brain tumors was suggested in the early 1990s(59), and has been
explored in many case–control and a few cohort studies(70-74).

In a case–control study in Boston displayed an
inverse association of glioblastoma with medications for any kind of allergies (RR=
0.6, 95% CI: 0.4–1.0) (75). In 1999, a
German group published a multicenter international case–control research recruited
data from eight study including 1178 glioma patients(76-79). An inverse association was
observed in 7 study, of which 5 are statistically significant. Altogether,
history of allergy was a protective factor (OR=0.4, 95% CI:0.5–0. 7) for glioma.
This pattern also repeated for specific Allergy, such as asthma. Two case–control
studies carried out in the USA in 2002 highlighted the protective effect of Allergy
against glioma (Table1)(80,
81). Wiemels and
coworker pointed that history of any allergy such as pollen, dairy and nut
allergies presented protective effect (OR= 0.5, 95% CI: 0.3–0.7)(80). In mentioned
study, declining risk was correlated with elevating numbers of allergies, but
not associated to numbers of symptoms or intensity. In second case–control
study consisting 489 glioma patients demonstrated 30 % reduction risk (OR=0.7,
95% CI: 0.5–0.9) for previous allergic history and for having asthma (OR=0.6,
95% CI: 0.4–0.9) (81). Consistently,
3 cohorts sustained this finding (22). It has been
presented a lower risk of glioma among people with a history of allergy (OR=0.5;
95% CI: 0.2–1.0) in Swedish twins cohort and (HR=0.5; 95% CI: 0.1–1.9) for
high-grade glioma in hospital discharges cohort(22). A
meta-analysis published in 2009 disclosed that meningioma (a low-grade tumor)
did not display inverse relationship with Allergy in adults (71).

INTERPHONE is a large population based case–control
study performed among 13 country included 793 glioma, 394 acoustic neuroma, 832
meningioma, and 84 parotid gland cancer patients, as well as  2520 normal controls. Finding of this study
indicated an significant inverse association between a history of any allergy
and glioma (OR = 0.73, 95 % CI 0.60–0.88), acoustic neuroma (OR = 0.64, 95 %
CI:0.49–0.83) , and meningioma (OR = 0.77, 95 % CI: 0.63–0.93), but not parotid
gland tumors (OR = 1.21, 95 % CI: 0.73–2.02) (82). There
are few reports about acoustic neuroma. Brenner et al. in a US
case–control study of 96 cases and 799 controls reported a significant positive
association between a history of hay fever and acoustic neuroma (OR = 2.36, 95
% CI 1.38–4.03), which was stronger with an older age at diagnosis or shorter
disease duration(81). Combined
results from the UK and Nordic INTERPHONE studies indicated no association
between a history of allergy and acoustic neuroma overall or according to
disease duration (83). Moreover, two
studies in adults noted an inverse relationship between prediagnostic IgE
levels and glioma risk (74,
84).

Another population-based case–control study (CEFALO),
among children and adolescents was performed in Denmark, Norway, Sweden, and
Switzerland. There was no relationship between Allergy and all type of brain
tumor (OR=1.03; 95% CI: 0.70–1.34). The risk of atopic condition atopic at
present and in the past were 0.76 and 1.22 (95% CI 0.53–1.11; 95% CI 0.86–1.74)
respectively. Similarly, these results were repeated for glioma (85). In contrast,
results of two case–control studies among children with brain tumor was
compatible with the results of studies of adults (86,
87). They reported greater
declines risk for PNET/medulloblastoma than pilocytic astrocytoma or glioma (86,
87).The older
age-range of participants in
CEFALO
study (7–19 years) compared with 0–14 years in the two other reports might
explain some of controversies, as the distribution of brain cancer subtypes vary
between these studies. Moreover, the distribution of glioma subtypes greatly
differs from adults. The main type of adult glioma is stage 4, and the rest are
stage 3 or 2, but main gliomas in children are stage 1 (pilocytic astrocytoma).
This may explain the discrepancy between findings of studies with different age
range.

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