我们试图评估 KpB 小鼠的饮食和血管生成生物标志物之间的关联，以及这些标志物、体重指数 (BMI) 和高级别浆液性癌症 (HGSC) 中总生存期 (OS) 之间的关联。先前从 KpB 获得的肿瘤根据 CD-31 微血管密度 (MVD) 评估接受高脂肪饮食 (HFD, n = 10) 或低脂肪饮食 (LFD, n = 10) 的小鼠的血管生成情况。利用先前在 10 只小鼠中进行的微阵列分析（Agilent 244 K 阵列）获得的数据来评估饮食与血管生成生物标志物之间的关联。安捷伦（小鼠）和 Affymetrix 人类基因组 U133a 探针与 162 个血管生成相关基因连接。在 HGSC 内部数据库 (IDB) (n = 40) 中评估了生物标志物、BMI 和 OS 之间的关联。在 TCGA-OV 数据库 (n = 339) 中评估了未经调整 p < 0.05 的基因与 OS 的关联。CD-31 与小鼠饮食之间没有关联 (p = 0.66)。与 HFD 和 LFD 相关的 16 个血管生成相关基因通过了 p < 0.05 阈值。转化生长因子-α (TGFA) 在 HFD 小鼠中的表达量比 LFD 小鼠高 72% (p = 0.04)。与小鼠研究类似，在我们的 HGSC IDB 中，较高的 TGFA 表达与较高的 BMI (p = 0.01) 和较短的生存期 (p = 0.001) 相关。在 TCGA-OV 数据集中，BMI 数据不可用，并且 TGFA 和 OS 之间没有关联 (p = 0.48)。HFD 和肥胖可能通过 TGFA 的差异调节促进肿瘤进展。我们无法在 TCGA 数据集中确认这一发现。需要对 TGFA 进行进一步评估，以确定这是否是肥胖驱动的 HGSC 的独特靶点。版权所有 © 2023。由 Elsevier Inc. 出版。

We sought to evaluate the association between diet and angiogenic biomarkers in KpB mice, and the association between these markers, body mass index (BMI), and overall survival (OS) in high-grade serous cancers (HGSC).Tumors previously obtained from KpB mice subjected to high-fat diets (HFD, n = 10) or low-fat diets (LFD, n = 10) were evaluated for angiogenesis based on CD-31 microvessel density (MVD). Data from prior microarray analysis (Agilent 244 K arrays) conducted in 10 mice were utilized to assess associations between diet and angiogenetic biomarkers. Agilent (mouse) and Affymetrix Human Genome U133a probes were linked to 162 angiogenic-related genes. The associations between biomarkers, BMI, and OS were evaluated in an HGSC internal database (IDB) (n = 40). Genes with unadjusted p < 0.05 were evaluated for association with OS in the TCGA-OV database (n = 339).There was no association between CD-31 and diet in mice (p = 0.66). Sixteen angiogenic-related genes passed the p < 0.05 threshold for association with HFD vs. LFD. Transforming growth factor-alpha (TGFA) demonstrated 72% higher expression in HFD vs. LFD mice (p = 0.04). Similar to the mouse study, in our HGSC IDB, higher TGFA expression correlated with higher BMI (p = 0.01) and shorter survival (p = 0.001). In the TCGA-OV dataset, BMI data was not available and there was no association between TGFA and OS (p = 0.48).HFD and obesity may promote tumor progression via differential modulation of TGFA. We were unable to confirm this finding in the TCGA dataset. Further evaluation of TGFA is needed to determine if this is a target unique to obesity-driven HGSC.Copyright © 2023. Published by Elsevier Inc.