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.
 T. Mikeska, C. Bock, H. Do and A. Dobrovic, “DNA Methylation Biomarkers in Cancer: Progress towards Clinical Implementation,” Expert Review of Molecular Diagnostics, Vol. 12, No. 5, 2012, pp. 473-487. doi:10.1586/erm.12.45
 C. Stirzaker, J. Z. Song, B. Davidson and S. J. Clark, “Transcriptional Gene Silencing Promotes DNA Hypermethylation through a Sequential Change in Chromatin Modification in Cancer Cells,” Cancer Research, Vol. 64, No. 11, 2004, p. 3871. doi:10.1158/0008-5472.CAN-03-3690
 V. Mutskov and G. Felsenfeld, “Silencing of Transgene Transcription Precedes Methylation of Promoter DNA and Histone H3 Lysine 9,” The EMBO Journal, Vol. 23, No. 1, 2004, pp. 138-149. doi:10.1038/sj.emboj.7600013
 E. G. Tora?o, S. Petrus, A. F. Fernandez and M. F. Fraga, “Global DNA Hypomethylation in Cancer: Review of Validated Methods and Clinical Significance,” Clinical Chemistry and Laboratory Medicine, Vol. 50, No. 10, 2012, pp. 1733-1742. doi:10.1515/cclm-2011-0902
 F. Gaudet, J. G. Hodgson, A. Eden, L. Jackson-Grusby, J. Dausman, J. W. Gray, H. Leonhardt and R. Jaenisch, “Induction of Tumors in Mice by Genomic Hypomethylation,” Science, Vol. 300, No. 5618, 2003, pp. 489-492. doi:10.1126/science.1083558
 T. M. Holm, L. Jackson-Grusby, T. Brambrink, Y. Yamada, W. M. 3rd Rideout and R. Jaenisch, “Global Loss of Imprinting Leads to Widespread Tumorigenesis in Adult Mice,” Cancer Cell, Vol. 8, No. 4, 2005, pp. 275-285. doi:10.1016/j.ccr.2005.09.007
 H. Cui, M. Cruz-Correa, F. M. Giardiello, D. F. Hutcheson, D. R. Kafonek, S. Brandenburg, Y. Wu, X. He, N. R. Powe and A. P. Feinberg, “Loss of IGF2 Imprinting: A Potential Marker of Colorectal Cancer Risk,” Science, Vol. 299, No. 5613, 2003, pp. 1753-1755. doi:10.1126/science.1080902
 F. Tian, F. Z.Tang, G. Song, Y. Pan, B. He, Q. Bao and S. Wang, “Loss of Imprinting of IGF2 Correlates with Hypomethylation of the H19 Differentially Methylated Region in the Tumor Tissue of Colorectal Cancer Patients,” Vol. 5, No. 6, 2012, pp. 1536-1540.
 E. Daura-Oller, M. Cabre, M. Montero, J. L. Paternain, and A. Romeu, “Single Gene Hypomethylation and Cancer: New Insights into Coding Region Feature Trends,” Bioinformation, Vol. 3, No. 8, 2009, pp. 340-343. doi:10.6026/97320630003340
 R. Lister, M. Pelizzola, R. H. Dowen, R. D. Hawkins, G. Hon, J. Tonti-Filippini, J. R. Nery. L. Lee, Z. Ye, Q. M. Ngo, L. Edsall, J. Antosiewicz-Bourget, R. Stewart, V. Ruotti, A. H. Millar, J. A. Thomson, B. Ren, J. R. Ecker, “Human DNA Methylomes at Base Resolution Show Widespread Epigenetic Differences,” Nature, Vol. 462, No. 7271, 2009, pp. 315-322. doi:10.1038/nature08514
 A. Razin, C. Webb, M. Szyf, J. Yisraeli, A. Rosenthal, T. Naveh-Many, N. Sciaky-Gallili and H. Cedar, “Variations in DNA Methylation during Mouse Cell Differentiation in Vivo and in Vitro,” Proceedings of National Academy Sciences of the USA, Vol. 81, No. 8, 1984, pp. 2275-2279. doi:10.1073/pnas.81.8.2275
 M. R. Choi, Y. H. In, J. Park, T. Park, K. H. Jung, J. C. Chai, M. K. Chung, Y. S. Lee and Y. G. Chai, “Genome-Scale DNA Methylation Pattern Profiling of Human Bone Marrow Mesenchymal Stem Cells in Long-Term Culture,” Experimental & Molecular Medicine, Vol. 44, No. 8, 2012, pp. 503-512. doi:10.3858/emm.2012.44.8.057
 J. J. Wille and R. E. Scott, “Topography of the Predifferentiation GD Growth Arrest State Relative to Other Growth Arrest States in the G1 Phase of the Cell Cycle,” Journal of Cellular Physiology, Vol. 112, No. 1, 1982, pp. 115-122. doi:10.1002/jcp.1041120117
 R. E. Scott, D. L. Florine, J. J. Wille Jr. and K. Yun, “Coupling of Growth Arrest and Differentiation at a Distinct State in G1 Phase of the Cell Cycle, GD,” Proceedings of National Academy Sciences of the USA, Vol. 79, No. 3, 1982, pp. 845-849. doi:10.1073/pnas.79.3.845
 S. T. Boyce and R. G. Ham, “Calcium Regulated Differentiation of Normal Human Epidermal Keratinocytes in Chemically Defined Clonal Cultures and Serum-Free Serial Cultures.” Journal of Investigative Dermatology, Vol. 81, Suppl. 1, 1983, pp. 33-40. doi:10.1111/1523-1747.ep12540422
 M. R. Pittelkow, J.J. Wille Jr. and R. E. Scott, “Two Functionally Distinct Classes of Growth Arrest States in Human Prokeratinocytes that Regulate Clonogenic Potential,” Journal of Investigative Dermatology, Vol. 86, No. 4, 1986, pp. 410-417. doi:10.1111/1523-1747.ep12285684
 H. Wu, V. Coskin, J. Tao, W. Xie, W. Ge, K. Yoshikawa, K. E. Lee. Y. Zhang and Y. Sun, “Dnmt3a-dependent Non-Promoter Methylation Facilitates Transcription of Neurogenic Genes,” Science, Vol. 329, No. 5990, 2010, pp. 444-448. doi:10.1126/science.1190485
 G. D. Shipley, M. R. Pittelkow, J. J. Wille Jr., R. E. Scott, H. L. Moses, “Reversible Inhibition of Normal Human Prokeratinocytes by Type-Beta Transforming Growth Factor/Growth Inhibitor in Serum-Free Medium,” Cancer Research, Vol. 46, No. 4, 1986, pp. 2068-2071.
 D. Breitkreutz, H. J. Stark, P. Plein, M. Baur, N. E. Fusenig, “Differential Modulation of Epidermal Keratinization in Immortalized (HaCat) and Tumorigenic Human Skin Keratinocytes (Hacat-Ras) by Retinoic Acid and Extracellular Ca2+ Differentiation,” Vol. 54, No. 3, 1993, pp. 201-217. doi:10.1111/j.1432-0436.1993.tb01602.x
 I. Venza, M. Visalli, B. Tripoido, G. De Grazia, S. Loddo, D. Teti and M. Venza,“FOXE1 is a Target for Aberrant Methylation in Cutaneous Squamous Cell Carcinoma,” British Journal of Dermatology, Vol. 162, No. 5, 2009, pp. 1093-1097. doi:10.1111/j.1365-2133.2009.09560.x