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. 2019 May 14;18(1):822–829. doi: 10.3892/ol.2019.10356

Figure 5.

Figure 5.

A higher frequency of Amp and Gain of IGF1R is present in ER-negative breast tumors compared with ER-positive breast tumors. (A) Genomic alteration of IGF1R and ER status of breast invasive carcinoma cases of TCGA cohort. Gray represents individual tumors without an IGF1R alteration. (B) The frequency of IGF1R alteration in differential subtypes of tumors was analyzed in TCGA (cell, 2015) cohort. (C) The frequency of IGF1R alteration in differential subtypes of tumors was analyzed in TCGA (Nature, 2012) cohort. (D) Overexpressed proteins associated with genomic alterations of IGF1R in the Cell 2015 TCGA cohort were identified. (E) Pathway analysis was performed with the significantly overexpressed genes using the ToppGene online tool. The x-axis indicates the significance of the enrichment of the pathway. The y-axis presents the pathway term. TCGA, The Cancer Genome Atlas; ER, estrogen receptor; IGF1R, insulin-like growth factor 1 receptor; IHC, immunohistochemistry; Gain, copy number gain; Amp, amplification; LumA/B, Luminal A/B-like A/B; EGFR, epidermal growth factor receptor; E2F, E2 factor; FOXM1, forkhead box M1; IRS, insulin receptor substrate; MAPK, mitogen-activated protein kinase pathway; mTOR, mammalian target of rapamycin; PI3K, phosphatidylinositol 3-kinase.