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S. J. Clark and J. Melki, “DNA Methylation and Gene Silencing in Cancer, Which Is the Guilty Party,” Oncogene, Vol. 21, No. 35, 2002, pp. 5380-5387. doi:10.1038/sj.onc.1205598

has been cited by the following article:

• TITLE: Cell Cycle Arrest Mediates Global DNA Methylation Patterns in Normal Human Keratinocytes, Epidermoid Carcinoma Cells and Murine Embryonic Fibroblasts

  AUTHORS: John J. Wille, Jong Y. Park

  KEYWORDS: Anoikis; Epitheliod Carcinoma Cells Cell Cycle; DNA Methylation; G1 Phase; Restriction Points

  JOURNAL NAME: Journal of Cancer Therapy, Vol.4 No.1, February 20, 2013

  ABSTRACT: The 5-methylationcytosine (5-MC) DNA content of murine embryonic fibroblasts arrested in G1 by four growth conditions (Gc, Gn, Gd, and Gs) were hypermethylated relative to rapidly growing (RG) fibroblasts. Normal human keratinocytes (NHK) arrested in G1 by suspension were hypermethylated relative to RG cultures. Four RG cultures of epidermoid carcinoma cells (ECC) were hypomethylated relative to RG NHK cultures, and two cultures (SCC25 and A431) were further hypomethylated by SUS-induced arrest. Linear regression analyses established a positive linear correlation between growth rate and 5-MC content for three murine fibroblasts lines, and a negative correlation for both NHK and ECC lines.