Deletion of RDINK4/ARF enhancer: a novel mutation to “inactivate” the INK4-ARF locus

Publication date: Available online 24 June 2017
Source:DNA Repair
Author(s): Ming J. Poi, Thomas J. Knobloch, Junan Li
The presence of an enhancer element, RD^INK4/ARF (RD), in the prominent INK4-ARF locus provides a novel en bloc mechanism to simultaneously regulate the transcription of the p15^INK4B (p15), p16^INK4A (p16), and p14^ARF tumor suppressor genes. While genetic inactivation of p15, p16, and p14^ARF in human cancers has been extensively studied, little is known about RD alteration and its potential contributions to cancer progression. In this review, we discuss recent developments in RD alteration and its association with p15, p16, and p14^ARF alterations in human cancers, and demonstrate that RD deletion may represent a novel mechanism to simultaneously down-regulate p15, p16, and p14^ARF, thus promoting carcinogenesis.



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