Skip to main content
Fig. 3 | Journal of Hematology & Oncology

Fig. 3

From: A WEE1 family business: regulation of mitosis, cancer progression, and therapeutic target

Fig. 3

WEE1 and PKMYT1 mutations and copy number alterations (CNAs) in cancer. a Frequency of patients with WEE1 or b PKMYT1 gene mutations across cancers from TCGA cohorts. c Distribution of mutations according to the WEE1 and d PKMYT1 amino acid (aa) sequence and protein domains (WEE1 transcript ENST00000450114, 646 aa; PKMYT1 transcript ENST00000262300, 499 aa). e Frequency of patients with copy number gain or loss in WEE1 or f PKMYT1 across cancers (https://portal.gdc.cancer.gov; ACC adrenocortical carcinoma, BLCA bladder urothelial carcinoma, BRCA breast invasive carcinoma, CESC cervical squamous cell carcinoma and endocervical adenocarcinoma, COAD colon adenocarcinoma, CHOL cholangiocarcinoma, DLBC diffuse large B cell lymphoma, ESCA esophageal carcinoma, GBM glioblastoma multiforme, HNSC head and neck squamous cell carcinoma, KICH kidney chromophobe, KIRK kidney renal clear cell carcinoma, KIRP kidney renal papillary cell carcinoma, LGG brain lower grade glioma, LIHC liver hepatocellular carcinoma, LUAD lung adenocarcinoma, LUSC lung squamous cell carcinoma, MESO mesothelioma, OV ovarian serous cystadenocarcinoma, PAAD pancreatic adenocarcinoma, PCPG pheochromocytoma and paraganglioma, PRAD prostate adenocarcinoma, READ rectum adenocarcinoma, SARC sarcoma, SKCM skin cutaneous melanoma, STAD stomach adenocarcinoma, TGCT testicular germ cell tumors, THYM thymoma, UCS uterine carcinosarcoma, UCEC uterine corpus endometrial carcinoma)

Back to article page