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CHCHD2 and EGFR protein expression in NSCLC

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Presentation on theme: "CHCHD2 and EGFR protein expression in NSCLC"— Presentation transcript:

1 CHCHD2 and EGFR protein expression in NSCLC
CHCHD2 and EGFR protein expression in NSCLC. A, amplification of EGFR and CHCHD2 genes in NSCLC subtypes. CHCHD2 and EGFR protein expression in NSCLC. A, amplification of EGFR and CHCHD2 genes in NSCLC subtypes. Shown are OncoPrint outputs (cBioPortal for Cancer Genomics; where each bar represents a tumor that was found to contain a DNA alteration (amplification, deletion, mutation, as indicated) in EGFR and CHCHD2 in the indicated NSCLC subtypes; note that aligned bars represent the same tumor. Data for LADC and LSCC are from TCGA resource, obtained through cBioPortal. For LADC, 40 of 230 cases (17%) contained a DNA alteration in the EGFR gene, while the incidence for CHCHD2 was 7%. In 13 of 15 cases, the genes were coamplified; odds ratio = 101.8, indicating a strong tendency toward cooccurrence of EGFR and CHCHD2 amplification. For LSCC 16 of 178 cases (9%) contained EGFR amplification or mutation, and an equal number of cases (13) contained amplification of both EGFR and CHCHD2. Odds ratio = infinite, indicating a strong tendency toward cooccurrence of EGFR and CHCHD2 amplification. EGFR as expected, but not CHCHD2, is in some instances mutated in addition to being amplified, as indicated by the green features. B, LC/MS-MS analysis of 11 human tumor-derived NSCLC xenografts (as indicated; A, adenocarcinoma; S, squamous cell carcinoma). C, EGFR and CHCHD2 expression were highly correlated as indicated by correlation of determination analysis (R2), as indicated. After removing sample S3 that was the only sample with a cytogenetically defined amplification of EGFR/7p11.2, the two proteins remained moderately correlated in their expression level (R2 = 0.35). D, Western blot analysis of CHCHD2 and EGFR expression in HEK293 cells (control), or this cell type stably expressing ectopic EGFR (EGFR). Transferrin receptor (TfR) was detected as an input control. Yuhong Wei et al. Mol Cancer Res 2015;13: ©2015 by American Association for Cancer Research


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