TP53 is the most commonly mutated gene in human cancers. The missense mutations in the DNA-binding domain of p53 can affect its transcription factor activity and dysregulate target gene expression. Although the chromatin immunoprecipitation followed by sequencing (ChIP-seq) assays have been used to identify the genomic regions bound by mutant p53 in cancer cell lines, the landscape of regulatory regions driven by mutant p53 in primary tumors remains elusive. Here, we leveraged the chromatin accessibility data generated in the primary tumors of TCGA cohorts (especially in breast and colon cancers) and identified differential chromatin accessible regions in gain-of-function mutant p53 tumors compared to wild-type p53 tumors. Overall, we identified 1587 lost and 984 gained chromatin accessibility peaks in breast carcinoma, and 1143 lost and 640 gained peaks in colorectal adenocarcinoma. In both cancer types, we found that only less than 50% of peaks (gained and lost combined) contain p53 response elements or overlap with mutant p53 binding sites (inferred from ChIP-seq). Whereas in the remaining, we found an enrichment of binding motifs for pioneering factors such as FOX family TFs and NF-kB in the lost peaks and SMAD and KLF TFs in gained peaks of breast carcinoma. However, in colon adenocarcinoma, CDX family TFs and HNF4A were enriched in the gained peaks and ATF3 and FOS/JUN TFs in the lost peaks. By integrating the gene expression data, we identified known and novel target genes regulated by the mutant p53. Taken together, these results suggest the tissue- and tumor-type specific role of GOF mutant p53 in the chromatin changes and gene regulation