A characteristic feature of uterine pathologies is a specific change in cell metabolism, which predominantly manifests as a shift in the need for nutrients, thereby directing cells to engage in different angiogenic marker activities. Angiogenesis is one of the main signals supporting the survival and development of cells and tissues not only under physiological conditions. Therefore, it is necessary that we understand pathological hyperactivation in all uterine diseases, from endometriosis through ovarian endometrioid adenocarcinoma to malignant transformed cells of the uterine epithelium and body. This work presents the gene expression results of selected angiogenesis targets (VEGF-A, TGF-β1, ANG1/2, and HIF-1α), cell migration, and cell–cell interaction determined in vitro. Our results suggest that angiogenesis varies in the tested pathological conditions (ectopic endometriosis—12Z; ovarian endometrioid adenocarcinoma—A2780; tumors—SK-UT-1 and RL-95-2) compared to physiological angiogenesis (HME1). The differential expression of angiogenic factors may contribute (or is a contributing factor) to the observed differences to acknowledge an inherent variability in angiogenesis among cell lines. Determining the genomic phenomena responsible for processes associated with inadequate angiogenesis in the pelvic region could help us to develop individual treatment strategies and explain resistance to treatment.
子宫病理学的一个特征性表现是细胞代谢的特异性改变，这主要表现为对营养物质需求的转变，从而引导细胞参与不同的血管生成标记物活动。血管生成不仅是生理条件下支持细胞和组织存活与发育的主要信号之一。因此，我们必须理解从子宫内膜异位症到卵巢子宫内膜样腺癌，再到子宫上皮和体部恶性转化细胞等所有子宫疾病中的病理性过度激活。本研究展示了在体外测定的选定血管生成靶点（VEGF-A、TGF-β1、ANG1/2和HIF-1α）的基因表达结果、细胞迁移以及细胞间相互作用。我们的结果表明，与生理性血管生成（HME1）相比，测试的病理条件（异位子宫内膜异位症—12Z；卵巢子宫内膜异位样腺癌—A2780；肿瘤—SK-UT-1和RL-95-2）中的血管生成存在差异。血管生成因子的差异表达可能是（或作为一个促成因素）观察到的差异的原因，这承认了细胞系之间血管生成的内在变异性。确定与盆腔区域血管生成不足相关过程负责的基因组现象，可能有助于我们制定个体化治疗策略并解释治疗抵抗性。
肿瘤(癌症)患者之家