Explore chapters and articles related to this topic
Nanomedicine Clinical and Preclinical Use
Published in Bertrand Henri Rihn, Biomedical Application of Nanoparticles, 2017
Roudayna Diab, Sanghoon Kim, Ileana-Alexandra Pavel, Nadia Canilho, Fernanda Bianca Haffner, Sijin Li, Alain Celzard, Mihayl Varbanov, Emmanuel Lamouroux, Andreea Pasc
An ideal therapeutic against autoimmune diseases counteracts the harmful inflammatory responses without impairing the immune homeostasis. Indeed, traditional treatment is based on immunosuppressive drugs that down-regulate the global immune response leading to increased susceptibility to infections and decreased tumor cell suppression. Besides, severe adverse effects inherent to treatment are also observed, for example, hematological toxicities, especially for antimetabolite agents, as well as difficulty in treatment management because of the narrow therapeutic range and low bioavailability, especially for calcineurin and mTOR inhibitors. In addition, mAb-based therapy may induce a life-threatening anaphylactic shock.
In Silico Approach to Cancer Therapy
Published in Anjana Pandey, Saumya Srivastava, Recent Advances in Cancer Diagnostics and Therapy, 2022
Anjana Pandey, Saumya Srivastava
Another drug targeting the mammalian rapamycin (mTOR) pathway is rapamycin (Rapamune, Wyeth Ayerst). Rapamycin specifically inhibits the mTOR and works downstream of AKT (Hay and Sonenberg, 2004). Clinical trials of mTOR inhibitors were carried out in breast cancer patients and other solid tumors (Hidalgo and Rowinsky, 2000; Chan et al., 2005; Nagata et al., 2004).
Nanotechnology-Mediated Radiation Therapy
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Autophagy has been observed as a regulatory cellular homeostatic process that protects genome integrity, and prevents the accumulation of misfolded proteins and action of damaged organelles through a lysosomal pathway [62, 63]. Autophagic cell death takes place upon induction of autophagy in cells treated with radiation. Literary evidences have shown that, in cancer cells, those receiving chemotherapy and radiotherapy, treatment response often results in tumor inhibition via the involvement of autophagy-related proteins (ATG) depending on factors like time and type of treatment by inhibiting autophagy [64, 65]. To reverse the pro-cell survival mechanisms exerted by autophagy, in certain cancer cells treatment with autophagy inhibitors combined with chemotherapy and radiotherapy will succumb the cancer cells toward cell death [66]. Cancer cells receiving ionizing radiation sometimes do not die via the usual programmed cell death apoptotic pathway, which could be due to the intrinsic resistance toward apoptosis on account of mutations in p53 and bax [67]. In this scenario, autophagy is activated as the type II programmed cell death pathway making it a pro-cell death mechanism. Administration of mammalian target of rapamycin (mTOR) inhibitors such as Everolimus induces autophagy and sensitizes cancer cells to ionizing radiation [68]. Consistent reports supporting the role of autophagic cell death in radiation-induced cancer cells, where it functions as pro-cell death phenomenon suggests that a blockade in the autophagy process might lead to a decrease in the cell death of the irradiated cells [69]. Autophagy is characterized by the formation of autophagosomes, a double membrane-bound vesicular structure that assists in the sequestration of old and damaged organelles by lysosomal degradation [53]. Though numerous signaling finds association in the initiation of the autophagy process, the PI3K-Akt-mTOR pathway is the crucial one, which is also studied to be connected with the induction of autophagy in radiation-induced cells [70]. It has become imperative to develop future cancer treatments in a way to modulate autophagic signaling pathways for improving radiotherapeutic outcomes in cancer patients to reap the maximum benefits of the treatment process.
6-(2-Morpholinoethyl)-thiazolo[3,2-a]pyrimidin-5-one: A novel scaffold for the synthesis of potential PI3kα inhibitors
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Ahmed R. Ali, Eman R. El-Bendary, Mariam A. Ghaly, Ihsan A. Shehata
It was established that compounds 4a and 4b demonstrated high correlation levels with rapamycin (NSC S226080) with PCC values of 0.607 and 0.629, respectively. Considerable correlations between compounds 4c, 5a, 5b, 5c, 6a, 6b, and 6c, and rapamycin were noted with PCC values of 0.523, 0.507, 0.496, 0.53, 0.448, 0.453, and 0.538, respectively. Such similarity in COMPARE results could indicate the resemblance in mechanisms of action with rapamycin. Rapamycin is reported to be mTOR inhibitor which is considered to be a key enzyme in regulation of cellular metabolism, growth, and proliferation [29,30] .
Surface modification of ureteral stents: development history, classification, function, and future developments
Published in Expert Review of Medical Devices, 2023
Kaiguo Xia, Xudong Shen, Xiaojie Ang, Bingbing Hou, Yang Chen, Kaiping Zhang, Zongyao Hao
Rapamycin is a macrolide antibiotic with immunosuppressive properties and an mTOR inhibitor that inhibits epithelial cell proliferation. Ho D [80] et al. dissolved rapamycin in polylactic acid and immersed it on the surface of a degradable stent to manufacture a rapamycin drug-eluting stent, then a ureteral thermal injury model was constructed in rabbits, and rapamycin drug-eluting stents and ordinary stents were placed respectively, and the results showed that rapamycin drug-eluting biodegradable stent can effectively improve collagen deposition after ureteral thermal injury, which is an important way to reduce ureteral stricture.