A number ofW?1 researches W?2 aim to explore the biological significance of putative non-canonical structures in mammalian and other genomes (Zhao et al., 2010). Some studies have revealed the role of non-canonical DNAs in the milieu of gene regulation, both in prokaryotes (Hatfield & Benham, 2002) and eukaryotes (Bacolla & Wells, 2004; Rich & Zhang, 2003). Findings of these studies proposed that conformational domains in secondary structure, rather than the underlying sequence symmetry are associated with majorW?3 biological functions such as replication, transcription, maintenance of telomere ends and immune response (Ha et al., 2008; Neidle & Parkinson, 2003; Rich & Zhang, 2003). Most of the time those interactions with non-canonical DNA direct gene translocations, insertions, deletions and duplications and thus leading to genetic instability (Bacolla et al., 2004; Bacolla & Wells, 2004; G. Wang & Vasquez, 2004, 2006). Many evidences confirmed that non-canonical configurations of DNAs are related to the onset of genomic rearrangements which trigger human genetic diseases such as Fabry disease (Kornreich et al., 1990), mental retardation (Bonaglia et al., 2009; Rooms et al., 2007), ornithine transcarbamylase deficiency (Quental et al., 2009), uniparental disomy (Bena et al., 2010) and spermatogenic failure (Repping et al., 2002). Most types of cancers are caused by genomic instability (Forbes et al., 2015). Genomic rearrangements induced by non-canonical DNA redefines genomes by creating de novo fusion genes with oncogenic potential (Aparicio et al., 2014; Mertens et al., 2015; Shortt & Johnstone, 2012; Tsai et al., 2008). The reported events of gene fusion, resulting in cancer, are in follicular lymphoma, myxoid liposarcoma (Xiang et al., 2008), breast cancer (Banerji et al., 2012), low-grade astrocytomas (Lawson et al., 2011), and Burkitt lymphoma (Dalla-Favera et al., 1982).
W?1Many (too wordy)