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ADNP encoding a transcription factor interacting with BAF complexes exhibits frameshift mutations in gastric and colorectal cancers

Somatic mutations of genes for gene components for chromatin remodeling machineries are frequent targets in human cancers, for example, ARID1A gene [1] that is a component of BAF complex involved in chromatin remodeling. ADNP, a zinc finger protein with transcription factor activity, interacts with the BAF complex.[2] De novo ADNP inactivating mutations that hamper BAF complex recruitment cause an autism syndrome.[3] As for cancers, however, somatic mutations of ADNP have not been studied well. In the COSMIC database of cancers (http://cancer.sanger.ac.uk/cosmic), there are 174 nonsilent mutations of ADNP that include 56 frameshift (32.2%) and 13 (7.5%) nonsense mutations, which are believed to be typical loss-of-function mutations. Such a high incidence of loss-of-function mutations may suggest that ADNP inactivation by the mutations could possibly related to cancer development. However, somatic frameshift mutation status of ADNP gene remains undetermined in gastric (GCs) and colorectal (CRCs) cancers. There is a mononucleotide repeat (A8) in the coding sequence of ADNP that could be a target for frameshift mutation in cancers with microsatellite instability (MSI) such as GC and CRC.[4] To see whether ADNP gene harbored frameshift mutations within the repeat in GC and CRC, we analyzed the A8 repeat in exon 4 of ADNP in 34 GCs with high MSI (MSIH), 45 GCs with microsatellite stable/low MSI (MSS/MSI-L), 79 CRCs with MSI-H, and 45 CRCs with MSS/MSI-L by polymerase