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Cancers 2011, 3(2), 1672-1690; doi:10.3390/cancers3021672

Role of Gene Methylation in Antitumor Immune Response: Implication for Tumor Progression

1, 1 and 2,*
1 Department of Immunology, Hospital Clinico Universitario, Campus Universitario Teatinos S/N, 29010 Malaga, Spain 2 Department of Biochemistry, CIBER ESP, Hospital Costa del Sol, Marbella, Málaga, Carretera de Cadiz km 187, 29603, Spain
* Author to whom correspondence should be addressed.
Received: 22 December 2010 / Revised: 9 March 2011 / Accepted: 24 March 2011 / Published: 29 March 2011
(This article belongs to the Special Issue Epigenetics of Cancer Progression)
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Cancer immunosurveillance theory has emphasized the role of escape mechanisms in tumor growth. In this respect, a very important factor is the molecular characterization of the mechanisms by which tumor cells evade immune recognition and destruction. Among the many escape mechanisms identified, alterations in classical and non-classical HLA (Human Leucocyte Antigens) class I and class II expression by tumor cells are of particular interest. In addition to the importance of HLA molecules, tumor-associated antigens and accessory/co-stimulatory molecules are also involved in immune recognition. The loss of HLA class I antigen expression and of co-stimulatory molecules can occur at genetic, transcriptional and post-transcriptional levels. Epigenetic defects are involved in at least some mechanisms that preclude mounting a successful host-antitumor response involving the HLA system, tumor-associated antigens, and accessory/co-stimulatory molecules. This review summarizes our current understanding of the role of methylation in the regulation of molecules involved in the tumor immune response.
Keywords: methylation; tumor; HLA; clusterin methylation; tumor; HLA; clusterin
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Serrano, A.; Castro-Vega, I.; Redondo, M. Role of Gene Methylation in Antitumor Immune Response: Implication for Tumor Progression. Cancers 2011, 3, 1672-1690.

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