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Plasmonic Nanoparticles for Cancer Bioimaging, Diagnostics and Therapy
Published in Klaus D. Sattler, st Century Nanoscience – A Handbook, 2020
Bridget Crawford, Tuan Vo-Dinh
Regulation of the expression of genes that are involved in cancer-related pathways is the goal of various experimental cancer treatment approaches. In the 1990s, a novel method of controlling gene expression was discovered where a short double-stranded RNA was used to specifically and selectively suppress the expression of the target gene [170]. This phenomenon was called RNAi or RNA interference and the double-stranded RNA was termed small interfering RNA, or siRNA. Due to the short in vivo half-life of naked siRNA, siRNA-based cancer gene therapy is often degraded by nucleases in biological fluids [171]. Naked siRNA cannot penetrate endothelial cells and tissues due to its size (∽15 kDa) and is further prevented from diffusing efficiently into the cellular membrane by the extracellular matrix. In addition to these biological barriers, siRNA’s negative charge prevents it from penetrating through negatively charged cell membranes and even if entry into the cell is successful, the siRNA encounters the harsh environment produced by endosomes, which often results in clearing of siRNA through endosomal pathways.
Modelling combined virotherapy and immunotherapy: strengthening the antitumour immune response mediated by IL-12 and GM-CSF expression
Published in Letters in Biomathematics, 2018
Adrianne L. Jenner, Chae-Ok Yun, Arum Yoon, Adelle C. F. Coster, Peter S. Kim
Controlling the CTL induced apoptosis rates k could be achieved through the introduction of an experimental cancer treatment known as CTLA-4 blockades (Henson, Macaulay, Kiani-Alikhan, & Akbar, 2008; Parry et al., 2005). CTLA-4 is a well-known T cell inhibitory B7-receptor that is expressed by activated T cells. Using the CTLA-4 blockade, researchers have shown that this treatment can enhance T cell cytotoxic responses and induce the differentiation of cytotoxic CD4 T cells Leach et al. (1996). Therefore, one possible way to investigate whether perturbations in the CTL induced apoptosis rates k would result in the outcomes presented in Figure 3(e), would be to look at combining CTLA-4 blockades with oncolytic virus expressing IL-12 and GM-CSF.