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Role of Gene Methylation in Antitumor Immune Response: Implication for Tumor Progression
AbstractCancer 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.
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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.View more citation formats
Serrano A, Castro-Vega I, Redondo M. Role of Gene Methylation in Antitumor Immune Response: Implication for Tumor Progression. Cancers. 2011; 3(2):1672-1690.Chicago/Turabian Style
Serrano, Alfonso; Castro-Vega, Isabel; Redondo, Maximino. 2011. "Role of Gene Methylation in Antitumor Immune Response: Implication for Tumor Progression." Cancers 3, no. 2: 1672-1690.