Figure 1.
Receptor-type protein tyrosine phosphatase (PTPR) genetic alterations In cancer. Three genetic mechanisms were reported in the Cancer Genome Atlas (TCGA): mutation (green), deletion (blue), and amplification (red). Alterations of 20 PTPR family members are summarized across 25 human cancers studied to date (all TCGA, provisional), including skin cutaneous melanoma, lung adenocarcinoma, gastric adenocarcinoma, bladder urothelial carcinoma, lung squamous cell carcinoma, uterine corpus endometrial carcinoma, sarcoma, colorectal adenocarcinoma, ovarian serous cystadenocarcinoma, head and neck squamous cell carcinoma, prostate adenocarcinoma, uterine carcinosarcoma, breast invasive carcinoma, adrenocortical carcinoma, cervical squamous cell carcinoma and endocervical adenocarcinoma, glioblastoma multiforme, renal papillary cell carcinoma, lymphoid neoplasm diffuse large B-cell lymphoma, renal chromophobe, hepatocellular carcinoma, acute myeloid leukemia, pancreatic adenocarcinoma, brain lower grade glioma, renal clear cell carcinoma, and thyroid carcinoma. Ratios were generated using the number of cases altered by each mechanism divided by the total number of cases examined in each cancer that contain the specific alteration.