In developed countries, cancer has replaced infectious diseases as a major cause of death. Currently, efforts in
the immunoprevention of cancer are beginning to resemble those presented by the prevention of infectious diseases by
immunization a century ago. Breast cancer is the most frequent type of tumor in women and is the second leading cause of
death by this illness, among them. Moreover, cancer incidence will grow during next years. Some findings in autoimmunity
related to breast cancer in animal models have been important to clarify mechanisms that potentiate tumor growth.
Clinical and experimental data now clearly indicate that chronic inflammation significantly contributes to cancer development.
Emerging out of these studies is an appreciation that persistent humoral immune responses exacerbate recruitment
and activation of innate immune cells in the neoplastic microenvironment where they regulate tissue remodeling,
pro-angiogenic and pro-survival pathways that together potentiate cancer development. Generally, antigens involved in
autoimmune response in breast cancer are modified self-proteins or over-expressed normal proteins that induce autoantibodies
(autoAbs) formation, which exhibit tumor promoting actions. Very frequently muscarinic acetylcholine receptors
(mAChR) are up-regulated in different types of tumors appearing in different animal species. mAChR have the ability to
act as autoantigens for tumor bearers. This article will review recent results concerning to the ability of mAChR expressed
in transformed breast cells to trigger autoAbs formation either in experimental models or in breast cancer patients. We
will also discuss the action of these antibodies as agonists of mAChR.
Keywords: Autoantibodies, autoantigens, cells proliferation, inositol monophosphate, MCF-7 T1N0Mx breast tumors, muscarinic
receptors, nitric oxide synthase, phospholipase Cβ2, protein kinase C, tumor progression
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