Abstract
Induction of cell differentiation and genomic stability in cancer, by an “multi epimutation-targeted therapy”, or MTET
Highlights
Recent research has opened scientists’ eyes to look deeper into biology of cancer cell and describe epigenetic networks, which drive tumor cells
One of the main therapeutic challenges in identifying actionable targets to treat in cancer is the tumor genomic instability in concert with its stem cell plasticity and epigenomic instability
IDH1, (Tet2 mutations), are epigenetic mutations in the case of CpG island mutated phenotype (CIMP), and inactivating Set Domain Containing 2 (SETD2) mutations are reported in the case of microsatellite instabilities (MSI) [1,2,3,4,5,6,7,8,9,10,11]
Summary
Recent research has opened scientists’ eyes to look deeper into biology of cancer cell and describe epigenetic networks, which drive tumor cells. In the presence of a genetic lesion, downregulation of SETD2 contributes to both initiation and progression during leukemia development by promoting the selfrenewal potential of leukemia stem cells [10] This target is of key interest, as our investigation allowed us to correlate this as the most likely genomic mutational event in relation to carcinogenesis through this epigenetic pathway. Inactivation of VHL can cause changes in micro RNAs. Since VHL plays such a key regulator in inducing a panepigenomic and genomic effect, through HIF-1, we believe that a targeted therapy that inhibits the methylation of this target, would significantly reduce the presence of genomic instability, stem cell plasticity and heterogeneity in cancer
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
