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• Castro-Vega, I
• Redondo, M
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• Castro-Vega, I
• Redondo, M
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• Serrano, A
• Castro-Vega, I
• Redondo, M

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

Article

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

Alfonso Serrano ¹ , Isabel Castro-Vega ¹  and Maximino Redondo ^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; in revised form: 9 March 2011 / Accepted: 24 March 2011 / Published: 29 March 2011

(This article belongs to the Special Issue Epigenetics of Cancer Progression)

Download PDF Full-Text [188 KB, uploaded 29 March 2011 09:45 CEST]

Abstract: 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

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