Fig 1: The protein expression levels of GMNN in our ACC and normal tissues. GMNN was negative or weakly expressed in normal tissues (A), moderately expressed in non-metastatic ACC tissues (B), and highly expressed in metastatic ACC tissues (C). Red arrow: positively stained ACC cells; blue arrow: negatively stained ACC cells. ACC adrenocortical carcinoma
Fig 2: Identification of the most significant module and validation of GMNN in the TCGA cohort. (A) The most significant module and GMNN as a hub gene were recognized in the PPI network. B GMNN was differentially expressed. (C–E) GMNN was significantly related to poor OS, DSS, and PFI in TCGA ACC sample. (F, G) Univariate Cox regression and multivariate Cox regression analyses indicated that GMNN was independently related to OS of TCGA ACC patients. (H–J) The expression level of GMNN was associated with stage, T, and M in ACC. (K, L) GMNN was closely related to OS and PFI of ACC patients treated with mitotane. OS overall survival, DSS disease-specific survival, PFI progression-free interval, ACC adrenocortical carcinoma
Fig 3: A prognostic nomogram with clinical features, GMNN expression levels, and DEGs-based signature risk score was established for ACC. (A) The nomogram could superiorly predict 1-, 2-, and 3-, 5-year OS of ACC patients. (B–C) The calibration plots also demonstrate excellent agreement between prediction and observation for the 1- and 3-year OS probabilities of the TCGA ACC patients. DEG differentially expressed gene, ACC adrenocortical carcinoma, OS overall survival
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