Fig. 6: DeepMVP prediction of PTM-altering somatic mutations across 33 cancer types.
a, Distribution of the predicted PTM-altering somatic mutations across 33 cancer types. SKCM, skin cutaneous melanoma; LUSC, lung squamous cell carcinoma; LUAD, lung adenocarcinoma; UCEC, uterine corpus endometrial carcinoma; BLCA, bladder urothelial carcinoma; HNSC, head and neck squamous cell carcinoma; STAD, stomach adenocarcinoma; BRCA, breast invasive carcinoma; LIHC, liver hepatocellular carcinoma; OV, ovarian serous cystadenocarcinoma; CESC, cervical squamous cell carcinoma and endocervical adenocarcinoma; COAD, colon adenocarcinoma; ESCA, esophageal carcinoma; KIRC, kidney renal clear cell carcinoma; GBM, glioblastoma multiforme; KIRP, kidney renal papillary cell carcinoma; LGG, brain lower grade glioma; PRAD, prostate adenocarcinoma; SARC, sarcoma; READ, rectum adenocarcinoma; PAAD, pancreatic adenocarcinoma; THCA, htyroid carcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; ACC, adrenocortical carcinoma; LAML, acute myeloid leukemia; UCS, uterine carcinosarcoma; MESO, mesothelioma; TGCT, testicular germ cell tumors; PCPG, pheochromocytoma and paraganglioma; THYM, thymoma; KICH, kidney chromophobe; UVM, uveal melanoma; CHOL, cholangiocarcinoma. SNV, single-nucleotide variant. b,c, Predicted impact and existing knowledge of the substitutions p.E17K on AKT1 (b) and p.G266R on TP53 (c). d, Shapley value (SHAP) distribution of flanking amino acids for predicting phosphorylation site S269 on p53, with and without p.G266R. e, Predicted impact and existing knowledge of the substitution p.L169P on VHL. f, Shapley value distribution of flanking amino acids for predicting S168 phosphorylation on VHL, with and without p.L169P. g, Identification of pS269 in p53 and the corresponding unmodified peptide in cell lines expressing TP53 WT or TP53-G266R, as well as pS168 in VHL and the corresponding unmodified peptide in cell lines expression VHL WT or VHL-L169P.
