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. Author manuscript; available in PMC: 2022 Oct 1.
Published in final edited form as: Mod Pathol. 2022 Apr 1;35(9):1269–1278. doi: 10.1038/s41379-022-01066-y

Figure 2. Recurrent somatic genetic alterations in NSMP endometrial carcinomas.

Figure 2.

(A) Oncoprint depicting the most recurrent genomic alterations in uterine endometrioid carcinomas of no special molecular profile (NSMP-UEC). Each column represents a tumor with the bar graph at the top depicting the number/distribution of alterations per sample, and the Oncoprint rows showing alterations for each gene. The bottom part of the graph shows the summary of histopathologic and clinical information for each case. The bar graph on the right of the panel shows the number and distribution of alterations for each gene. Mutation types and clinicopathologic features are color-coded according to the legend. (B) Oncoprint depicting the most recurrent molecular alterations in NSMP-EEC focusing on alterations activating the PI3K/AKT/mTOR pathway in addition to CTNNB1 alterations. The bottom part of the graph shows the summary of molecular cluster information for each case. Note that majority of tumors harbor a combination of PIK3CA/PIK3R1 and PTEN mutations while AKT1 mutations occur in absence of upstream alterations. KRAS, ERBB2 and FGFR2 alterations are mutually exclusive. Mutation types and other features are color-coded according to the legend. C1, Cluster 1; C2, Cluster 2; C3, Cluster 3.