%0 Journal Article
%T Potential Role of Meiosis Proteins in Melanoma Chromosomal Instability
%A Scott F. Lindsey
%A Diana M. Byrnes
%A Mark S. Eller
%A Ashley M. Rosa
%A Nitika Dabas
%A Julia Escandon
%A James M. Grichnik
%J Journal of Skin Cancer
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/190109
%X Melanomas demonstrate chromosomal instability (CIN). In fact, CIN can be used to differentiate melanoma from benign nevi. The exact molecular mechanisms that drive CIN in melanoma have yet to be fully elucidated. Cancer/testis antigens are a unique group of germ cell proteins that are found to be primarily expressed in melanoma as compared to benign nevi. The abnormal expression of these germ cell proteins, normally expected only in the testis and ovaries, in somatic cells may lead to interference with normal cellular pathways. Germ cell proteins that may be particularly critical in CIN are meiosis proteins. Here, we review pathways unique to meiosis with a focus on how the aberrant expression of meiosis proteins in normal mitotic cells ˇ°meiomitosisˇ± could impact chromosomal instability in melanoma and other cancers. 1. Introduction Melanomas exhibit chromosomal instability (CIN). In fact, CIN is one of the most useful molecular markers to differentiate melanomas from benign nevi [1, 2]. Bastian et al. found that 96.2% of melanomas demonstrated chromosomal aberrations while only 13.0% of benign nevi showed these same abnormalities, of which all were Spitz nevi with stable 11p duplications [1]. Melanomas generally exhibit an increased number of overall chromosomes with frequent large translocations [1]. The fact that melanomas have such unstable genomes comes as no surprise, as genomic instability is widely regarded as the hallmark of cancer [3¨C7]. While genomic instability decreases the viability of most cells, it may also permit a subpopulation of cells to acquire genetic changes that lead them to escape normal growth control mechanisms. In addition, genomic instability allows established cancers to evolve and evade immunologic and pharmacologic destruction [8]. The extent to which different mechanisms play a role in genomic instability is controversial [4]; however three pathways are generally most accepted. These are defective DNA repair, telomere crisis, and mitotic spindle malfunction [3, 9¨C12]. An underappreciated but potentially important research area is the abnormal expression of germ cell proteins. Expression of germ cell proteins has long been observed in cancer cells [13]. Cancer/testis antigens (CTAs) are a family of germ cell proteins expressed in a multitude of different histological tumor types [13, 14]. These proteins have been noted to have both diagnostic and prognostic value [2]. Studies have shown that expression of specific CTAs in melanoma can be used to predict tumor thickness, the presence of ulceration, and likelihood to
%U http://www.hindawi.com/journals/jsc/2013/190109/