Expression data from transgenic mice with conditional deletion of CDKN2A/p16 in esophageal glandular cells

The tumor suppressor CDKN2A Exon 1a (coding for p16) was removed in esophageal and squmous-columnar junction (SCJ) epithelial cells when tamoxifen was injected in experimental mice. Sections of the SCJ were subjected to laser capture microdissection to retain only the glandular mucosal layer. RNA was extracted and analyzed by Affymetrix Clariom D Pico assay, mouse (Thermo Fisher, Waltham, MA). We used microarrays to identify transcriptomic changes associated with p16 knockout. We used 4 control mice (P16WT) and 4 experimental mice (p16KO) with p16 knocout in the SCJ. All mice express human IL1-beta in the esophagus and were treated with bile acids to induce Barrett's-like lesions. P16 conditional knockout results from CRE recombinase (modified with estrogen receptor moieties) expressed from the LGR5 promoter, upon activation by tamoxifen injection. LGR5 derived cells include most SCJ glandular epithelial cells, therefore P16 knockout is restricted to those cells. We microdissected the