1.
Treatment of Aggressive Thyroid Cancer.
Huang, J, Harris, EJ, Lorch, JH
Surgical pathology clinics. 2019;(4):943-950
Abstract
Although thyroid cancer generally has a good prognosis, there is a subset of patients for whom standard care (ie, treatment limited to surgery or surgery plus radioactive iodine) is either not appropriate because of the aggressive nature of their disease or not sufficient because of disease progression through standard treatment. Most of these tumors are in 3 groups: radioactive iodine-refractory differentiated thyroid carcinoma including poorly differentiated thyroid carcinoma anaplastic thyroid carcinoma, and progressive medullary thyroid carcinoma. Major classes of treatments in clinical development for these aggressive thyroid tumors include tyrosine kinase inhibitors, mammalian target of rapamycin inhibitors, and mitogen-activated protein kinase kinase inhibitors.
2.
The Possible Mechanisms of HSV-TK/Hyperthermia Combined with 131I-antiAFPMcAb-GCV Nanospheres to Treat Hepatoma.
Lin, M, Zhou, C, Huang, J, Tian, W, Yu, H, Jiang, X, Ye, J, Guo, T, Shi, Y, Xiao, Y, et al
Analytical cellular pathology (Amsterdam). 2018;:8941908
Abstract
Our previous findings showed a good therapeutic effect of the combination of suicide gene HSV-TK, nuclide 131I, and magnetic fluid hyperthermia (MFH) on hepatoma by using magnetic nanoparticles as linkers, far better than any monotherapy involved, with no adverse effects. This combination therapy might be an eligible strategy to treat hepatic cancer. However, it is not clear how the combination regimen took the therapeutic effects. In the current study, to explore the possible mechanisms of radionuclide-gene therapy combined with MFH to treat hepatoma at tissue, cellular, and molecular levels and to provide theoretical and experimental data for its clinical application, we examined the apoptosis induction of the combination therapy and investigated the expression of the proteins related to apoptosis such as survivin, livin, bcl-2, p53, and nucleus protein Ki67 involved in cell proliferation, detected VEGF, and MVD involved in angiogenesis of tumor tissues and analyzed the pathologic changes after treatment. The results showed that the combination therapy significantly induced the hepatoma cell apoptosis. The expression of survivin, VEGF, bcl-2, p53, livin, Ki67, and VEGF proteins and microvascular density (MVD) were all decreased after treatment. The therapeutic mechanisms may be involved in the downregulation of Ki67 expression leading to tumor cell proliferation repression and inhibition of survivin, bcl-2, p53, and livin protein expression inducing tumor cell apoptosis, negatively regulating VEGF protein expression, and reducing vascular endothelial cells, which results in tumor angiogenesis inhibition and microvascular density decrease and tumor cell necrosis. These findings offer another basic data support and theoretical foundation for the clinical application of the combination therapy.