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. Author manuscript; available in PMC: 2024 May 1.
Published in final edited form as: Gynecol Oncol. 2023 Mar 21;172:54–64. doi: 10.1016/j.ygyno.2023.03.010

Figure 1.

Figure 1.

Landscape of somatic chromatin remodeling gene (CRG) alterations in endometrial carcinomas. (A) Oncoprint depicting the most recurrent CRG alterations in endometrial carcinomas. Each column represents a tumor with the bar graphs at the top depicting the number/distribution of alterations per sample and the fraction of genome alterations per sample. The Oncoprint rows show alterations in each gene. The lower part of the graph shows the summary of molecular subtype of endometrial carcinoma and histologic type 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) Box-plot showing the distribution of fraction of genome altered (FGA) among molecular subtypes of endometrial carcinoma. (C) Box-plot showing the distribution of tumor mutation burden (TMB) among molecular subtypes of endometrial carcinoma. (D) Alluvial graphs showing the distribution of alterations in CRG categories among the four major molecular subtypes of endometrial carcinoma (18).

POLE, POLE exonuclease domain mutated carcinoma; MMR-deficient, DNA mismatch repair deficient carcinoma; NSMP, TP53 wild-type non-hypermutant endometrial carcinomas; p53 Altered, TP53 altered non-hypermutant endometrial carcinomas.

SWI/SNF, SWI/SNF complex; HLMT, Histone lysine methyltransferases; HDAC, Histone deacetylases; HAT, Histone acetyltransferases; HDM, Histone demethylases; PAMT, Protein arginine methyltransferases; OCRG, Other chromatin gene alterations.