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. 2019 Dec;9(12):a036293. doi: 10.1101/cshperspect.a036293

Figure 1.

Figure 1.

PTEN gene and protein alterations in human tumors. (A) Frequency of PTEN gene deletion in human tumors and PTEN mutations causing loss of PTEN protein (premature termination codon [PTC] mutations and frameshift small deletions or insertions). (B) Frequency of PTEN messenger RNA (mRNA) down- or up-regulation in human tumors (z-score threshold ±2). In both cases, the alteration frequencies are indicated for 16 different human cancers from data generated by the TCGA Research Network and using the cBioPortal database (cBioPortal for Cancer Genomics; Cerami et al. 2012; Gao et al. 2013). Cancer types are as follows: endometrial, uterine corpus endometrial carcinoma; gliobastoma, glioblastoma multiforme; prostate, prostate adenocarcinoma; lung, lung squamous cell carcinoma; melanoma, skin cutaneous melanoma; gastric, stomach adenocarcinoma; cervical, cervical squamous cell carcinoma; soft tissue, sarcoma; breast, breast invasive carcinoma; ovarian, ovarian serous cystadenocarcinoma; liver, liver hepatocellular carcinoma; colorectal, colorectal adenocarcinoma; bladder, bladder urothelial carcinoma; kidney, kidney renal clear cell carcinoma; thyroid, thyroid carcinoma; pancreas, pancreatic adenocarcinoma. (C) Boxplot of the frequency of PTEN protein loss in human tumors as detected by immunohistochemistry (IHC). Whiskers represent the minimum and maximum of all of the data; boxes represent the values between quartiles 1 and 3, and bands inside the boxes represent the median. Data are compilations from Tables 2–4. Note that the cancer categories in C have a wider coverage of cancer subtypes than the categories in A and B.