Abstract
Structure-dependent μ-opioid receptor (MOR) activity is an important element in cancer opioid analgesic effectiveness. It is widely accepted that guanine (G) substitution for adenine (A) at OPRM1 gene sequence position 118 changes receptor glycosylation pattern. This is associated with decreased binding ability in both exogenous and endogenous opioids, resulting in increased human pain resistance. The endogenous opioid system’s function in body homeostasis maintenance is considered mainly regulatory, so its participation in breast tumor formation and progression is identified herein. We examine the association of the most frequent MOR (A118G) gene polymorphism on breast cancer risk in a Northeastern Polish population by PCR-RFLP comparison of A and G allele frequency at OPRM1 gene A118G polymorphic site in breast cancer-diagnosed patients with healthy control group frequencies. Our results highlight a strong association between G allele presence at μ-opioid receptor A118G and increased breast cancer incidence (OR = 3.3, 95 % CI 2.2–5.0, p < 0.0001) and female gender (OR = 2.0, 95 % CI 1.4–2.9, p = 0.0004). Consequently, OPRM1 G allele presence at that site is a highly significant risk factor in breast cancer development.
Highlights
The GLOBOCAN 2012 International Agency for Research on Cancer database shows breast cancer (BC) is the most common cancer in females worldwide, at approximately 25 % of all female cancers, and the second most commonly occurring malignancy
The endogenous opioid system’s precise role in tumor initiation and development remains undetermined, a relationship with cancer is anticipated because it plays a regulatory function in organism homeostasis, and opioid peptides and receptors are present in cancer cells [14, 17, 18]
We investigated the association between A118G OPRM1 gene polymorphism and breast cancer risk
Summary
The GLOBOCAN 2012 International Agency for Research on Cancer database shows breast cancer (BC) is the most common cancer in females worldwide, at approximately 25 % of all female cancers, and the second most commonly occurring malignancy. It is currently believed that tumor development in the majority of cases is associated with a genetic background, and this includes sporadic tumors [2]. This resulted from increased focus on natural gene population variability as a determinant of cancer susceptibility. The previously untested μ-opioid receptor gene (OPRM1) is examined as the newest candidate in this regard
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