CEFYBO   02669
CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Unidad Ejecutora - UE
artículos
Título:
Antibodies against muscarinic receptors in breast cancer: agonizing tumor growth.
Autor/es:
FISZMAN GABRIEL; SALES MARIA ELENA
Revista:
Current Immunology Reviews
Editorial:
Benthan Science Publishers
Referencias:
Lugar: Bussum, The Netherlands; Año: 2008 vol. 4
ISSN:
1573-3955
Resumen:
Abstract: 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 first 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. This article will review recent results
concerning to the ability of muscarinic acetylcholine receptors (mAChR) expressed in transformed 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 in mAChR functions.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 first 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. This article will review recent results
concerning to the ability of muscarinic acetylcholine receptors (mAChR) expressed in transformed 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 in mAChR functions.