Tumor growth is stimulated by muscarinic receptors agonism. Role of autoantibodies from breast cancer patients

SALES MARIA ELENA

Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry

Bentham Science Publishers

Año: 2012 vol. 12

1871-5222

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 that 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 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 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 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 auto-Abs formation either in experimental models or in breast cancer patients. We will also discuss the action of these antibodies as agonists of mAChR.