Additional file 2 of PTEN loss correlates with T cell exclusion across human cancers

Additional file 2: Supplementary Figure 1. Association of PTEN genomic alteration with PTEN expression and key pathway activation. Difference of PTEN mRNA expression, PI3K-AKT-mTOR pathway activation(represented by p-AKT [phosphorylated at Thr308 or Ser473], p-mTOR [phosphorylated at Ser2448], and ssGSEA score of PI3K pathway) and STAT3 activation (p-STAT3 [phosphorylated at Tyr705] between tumors with genomic PTEN loss and tumors with genomic Intact PTEN for each tumor types. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns, not significant. Supplementary Figure 2. Gene set enrichment analysis (GSEA) of T-cell inflamed signature between tumors with PTEN loss and tumors with Intact PTEN. T-cell inflamed signature was highly enriched in tumors with intact PTEN for multiple cancer types; but for a few other cancer types, T-cell inflamed signature was highly enriched in tumors with PTEN loss. Supplementary Figure 3. Correlation of innate immune population with genomic alteration in PTEN, PIK3CA, PIK3CB. (a) Difference in the infiltration of innate immune cells, including dendritic cells (DC), macrophages and natural killer cells (NK) between tumor with PTEN loss and tumor with Intact PTEN; (b) Difference in the infiltration of innate immune cells (DC, macrophages and NK) between tumor with PIK3CA loss and tumor with wide-type PIK3CA; (c) Difference in the infiltration of innate immune cells (DC, macrophages and NK) between tumor with PIK3CB loss and tumor with wide-type PIK3CB. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns, not significant. Supplementary Figure 4. Association of PTEN genomic alteration with expression of immunosuppressive markers. Logarithmic transferred mRNA expression of immunosuppressive genes (FOXP3, IDO1, CCL2, CSF1 and IL6) that had been reported to be associated with PTEN were compared between tumors with genomic PTEN loss and tumors with genomic Intact PTEN for each tumor types. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ns, not significant. Supplementary Figure 5. Survival impact of PTEN in Pan-cancer. Kaplan-Meier plots of overall survival difference between tumors with PTEN loss and tumors with Intact PTEN for each tumor type

附加文件2：补充图1。PTEN基因组改变与PTEN表达及关键通路激活的关联。针对每种肿瘤类型，比较基因组PTEN缺失肿瘤与基因组PTEN完整肿瘤之间的PTEN mRNA表达、PI3K-AKT-mTOR通路激活（以p-AKT[苏氨酸308或丝氨酸473位点磷酸化]、p-mTOR[丝氨酸2448位点磷酸化]以及PI3K通路的单样本基因集富集分析（ssGSEA）评分表示）以及STAT3激活（p-STAT3[酪氨酸705位点磷酸化]）的差异。*p < 0.05；**p < 0.01；***p < 0.001；****p < 0.0001；ns，无统计学意义。
补充图2：PTEN缺失肿瘤与PTEN完整肿瘤之间T细胞炎症特征的基因集富集分析（GSEA）。在多种癌症类型中，T细胞炎症特征在PTEN完整肿瘤中显著富集；但在少数其他癌症类型中，T细胞炎症特征在PTEN缺失肿瘤中显著富集。
补充图3：先天免疫细胞群与PTEN、PIK3CA、PIK3CB基因组改变的相关性。(a) 比较PTEN缺失肿瘤与PTEN完整肿瘤的先天免疫细胞（包括树突状细胞[DC]、巨噬细胞和自然杀伤细胞[NK]）浸润差异；(b) 比较PIK3CA缺失肿瘤与PIK3CA野生型肿瘤的先天免疫细胞（DC、巨噬细胞和NK）浸润差异；(c) 比较PIK3CB缺失肿瘤与PIK3CB野生型肿瘤的先天免疫细胞（DC、巨噬细胞和NK）浸润差异。*p < 0.05；**p < 0.01；***p < 0.001；****p < 0.0001；ns，无统计学意义。
补充图4：PTEN基因组改变与免疫抑制标志物表达的关联。针对每种肿瘤类型，比较基因组PTEN缺失肿瘤与基因组PTEN完整肿瘤之间已报道与PTEN相关的免疫抑制基因（FOXP3、IDO1、CCL2、CSF1及IL6）的经对数转换的mRNA表达水平差异。*p < 0.05；**p < 0.01；***p < 0.001；****p < 0.0001；ns，无统计学意义。
补充图5：PTEN在泛癌中的生存影响。针对每种肿瘤类型，绘制PTEN缺失肿瘤与PTEN完整肿瘤之间总生存期差异的Kaplan-Meier曲线。