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. 2021 Nov 26;13(23):5962. doi: 10.3390/cancers13235962

Figure 2.

Figure 2

Experimental workflow for whole-exome sequencing (WES) in primary dedifferentiated endometrial carcinoma, lung metastasis, and PDX-mLung. (A) Schematic overview of sample collection. (B) Venn diagram of driver gene mutations identified in primary dedifferentiated endometrial carcinoma, lung metastasis, and PDX-mLung. (C) Comparison of copy number variations (CNVs) according to the results of WES. (D) Analysis of CCNE2 CNVs (qPCR) in peripheral blood mononuclear cells, primary dedifferentiated endometrial carcinoma, lung metastasis, and PDX-mLung. (E) Results of immunohistochemistry for FGFR2 and CCNE2 expression in primary dedifferentiated endometrial carcinoma (left panel), lung metastasis (middle panel) and PDX-mLung (right panel). (F) Agarose gel electrophoresis of RT-PCR products (p16 and GAPDH genes). M: 100 bp DNA marker; the size of the nucleotide ladder is indicated on the left side (100 to 200 bp). GAPDH was used as internal control. (G) Protein expression of p16 in HeLa and PDX-mLung, respectively. β-actin served as control for normalization. The numbers below the data mean densitometry-derived values normalized to HeLal (set to 1). β-actin served as loading control for normalization (H) Results of immunohistochemistry for p16 in PDX (upper panel) and vulvar carcinoma. Vulvar carcinoma specimens expressing p16 were used as positive controls (lower panel; scale bar = 50 μm).