Abstract
Malignant transformation and cancer progression are complex processes caused by dysfunction of genetic programs. It is well established that aberrant posttranscriptional regulation of messenger RNA contributes the pathogenesis of many types of tumors initiation, progression and treatment evasion (1). One such mechanism is the IFN-γ pathway activation of the ADAR1-p150 isoform in chronic myeloid leukemia (CML) progenitors. This pathway was shown to lead to activation of expression of self-renewal genes (2).
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.
