A methylation is a common process which covalently modifies
es and adds a methyl group to the cytosine or adenine DNA bases.
en widely studied in many species including bacteria, plants, and
an cells [Capuano, et al., 2014]. Though methylation can occur
CpG and non-CpG islands, most studies have focused on the
ons at CpG islands in the promoter regions and the gene bodies
d Liang, 2009; de Carvalho, et al., 2010; Lou, et al., 2014]. The
methylation modification can be inherited across generations has
d investigations into various cellular functions and disease
ment [Law and Jacobsem, 2010; Boyko, et al., 2011; Iqbal, et al.,
dar and Bergman, 2012; Wagner, et al., 2014; Meng, et al., 2015].
on-reversible property of methylation has led to the studies of
hylation influences disease development [Jones and Liang, 2009;
al., 2011; Chambaz and Neuvial, 2016]. The methylation strength
red by the beta value which is defined as the ratio of methylated
ver total methylated and non-methylated signals [Chari, et al.,
he methylation strength is classified as the hypo- or hyper-
on representing less or more methylation depending on the
e and the sign of differential methylation ratio for comparing an
nt sample against a control sample [Ehrlich, 2002; Chari, et al.,
he hypo-methylation has been found in relationships with tumour
Ehrlich, 2002], gene expression profiling [O’Neil, et al., 1998;
t al., 1998; Morgan, et al., 1999; Tao, et al., 2000]. The hyper-
on can also affect gene expression profiling, leading to some
[Network, 2011; Fujiwara-Igarashi, et al., 2014; Bryan, et al.,
ombined or integrative study of the epigenetic and the genetic
s can be used to discover more biological insight than using a
ression data set alone. For instance, several studies have found
nterplay between the epigenetic and the genetic signatures is one
ost important mechanisms leading to cancer development and
functions [Chang, et al., 2003; Chari, et al., 2010; Baylin and
11; Sandoval and Esteller, 2012; You and Jones, 2012].