Tbilisi State Medical University, Tbilisi, Georgia.
Department of Physics, Biophysics, Biomechanics and Informative Technologies of Tbilisi State Medical University, Tbilisi, Georgia.
Asian Pac J Cancer Prev. 2024 Feb 1;25(2):465-472. doi: 10.31557/APJCP.2024.25.2.465.
We hypothesized that mutations in several genes disrupt oxidative metabolism, increasing the risk of developing tumors and their malignancy in patients with a family predisposition to cancer. The purpose of our study was to assess the characteristics of oxidative metabolism in patients with malignant and benign tumor with and without a family history of cancer and identify the marker predicting the likelihood of malignancy.
We conducted a study on patients with thyroid pathology (thyrotoxicosis, benign tumor pathology of the thyroid gland, and thyroid cancer) who underwent treatment at LLC "Oncology Scientific Research Center" in Tbilisi, Georgia between 2020-2021. In patients' blood the thyroid hormones content, the oxidative metabolism parameters (activity of nonenzymatic antioxidant system (TAA), malondialdehyde (MDA) content), geometrical and rheological (deformability index (EDI), membrane proteins content) characteristics of erythrocytes were determined.
in the patient's blood serum with benign tumor (47 patients) MDA exceeded (p<0.005) and TAA decreased (p<0.005) in comparison to the control level; in patients with thyroid cancer (35 patients), MDA also exceeded (p<0.005), while TAA increased (p<0.005) up to the control level. In patients with benign and malignant tumors, the size of erythrocytes increased compared to the control indicators (p<0.005); in patients with thyroid cancer and benign tumors with a family history of cancer (29 patients) EDI increased (p<0.005), content of GLUT1 in erythrocyte membranes decreased (p<0.005) compared to the control level.
Alterations in redox metabolism play a crucial role in tumor formation; an imbalance between anti-/pro-oxidant systems may contribute to tumor formation and support its progression into a more malignant state. Thyroid cancer is characterized by a reduction in erythrocyte deformability, related to TSH levels. These alterations are less detectable in patients with benign thyroid tumors with a family history of cancer.
我们假设几个基因的突变会破坏氧化代谢,增加有癌症家族易感性的患者发生肿瘤及其恶性肿瘤的风险。我们研究的目的是评估有和无癌症家族史的恶性和良性肿瘤患者的氧化代谢特征,并确定预测恶性程度的标志物。
我们对 2020 年至 2021 年期间在格鲁吉亚第比利斯 LLC“肿瘤科学研究中心”接受治疗的甲状腺病理患者(甲状腺毒症、甲状腺良性肿瘤和甲状腺癌)进行了研究。在患者的血液中,测定了甲状腺激素含量、氧化代谢参数(非酶抗氧化系统活性(TAA)、丙二醛(MDA)含量)、红细胞的几何和流变学(变形指数(EDI)、膜蛋白含量)特征。
在良性肿瘤患者(47 例)的血液血清中,MDA 升高(p<0.005),TAA 降低(p<0.005),与对照水平相比;在甲状腺癌患者(35 例)中,MDA 也升高(p<0.005),而 TAA 升高(p<0.005),达到对照水平。与对照指标相比,良性和恶性肿瘤患者的红细胞大小增加(p<0.005);在有甲状腺癌和有癌症家族史的良性肿瘤患者(29 例)中,EDI 升高(p<0.005),红细胞膜 GLUT1 含量降低(p<0.005),与对照水平相比。
氧化还原代谢的改变在肿瘤形成中起着关键作用;抗/促氧化剂系统之间的不平衡可能导致肿瘤的形成,并支持其向更恶性状态的发展。甲状腺癌的特征是红细胞变形能力降低,与 TSH 水平有关。这些改变在有癌症家族史的良性甲状腺肿瘤患者中不太明显。