Future therapeutic implications of new molecular mechanism of colorectal cancer

Figure 2 Analysis of ataxia-telangiectasia mutated gene, anoctamin 5, adenomatous polyposis coli, and tumor protein 53 expression in normal and pan-cancer samples. A: Expression profiles of ataxia-telangiectasia mutated (ATM), anoctamin 5 (ANO5), adenomatous polyposis coli (APC), and tumor protein 53 (TP53) in normal human organs or tissues; B: Heatmap of log2[fragments per kilobase of exon per million mapped fragments (FPKM) + 1] expression status of ATM, ANO5, APC, and TP53 between cancer and cancer-adjacent samples. Red and blue represent upregulation and downregulation of gene expression, respectively; C: Log2(FPKM + 1) expression status of ATM, ANO5, APC, and TP53 between cancer and cancer-adjacent samples; D: Rectal adenocarcinoma (READ) and normal samples; E: Colon adenocarcinoma (COAD) and normal samples; F: READ-COAD and normal samples. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. KICH: Kidney chromophobe; KIRC: Kidney renal clear cell carcinoma; COAD: Colon adenocarcinoma; READ: Rectal adenocarcinoma; LIHC: Liver hepatocellular carcinoma; BRCA: Breast invasive carcinoma; UCEC: Uterine corpus endometrial carcinoma; HNSC: Head and neck squamous cell carcinoma; LUSC: Lung squamous cell carcinoma; PRAD: Prostate adenocarcinoma; BLCA: Breast invasive carcinoma; THCA: Thyroid carcinoma; KIRP: Kidney renal papillary cell carcinoma; LUAD: Lung adenocarcinoma; ESCA: Esophageal carcinoma; STAD: Stomach adenocarcinoma; CHOL: Cholangiocarcinoma; GBM: Glioblatoma; APC: Adenomatous polyposis coli; ANO5: Anoctamin 5; ATM: Ataxia-telangiectasia mutation; TP: Tumor protein.