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Radiobiological Evaluation and Optimisation of Treatment Plans
Published in W. P. M. Mayles, A. E. Nahum, J.-C. Rosenwald, Handbook of Radiotherapy Physics, 2021
Tucker et al. (2013) demonstrated that single nucleotide polymorphisms (SNPs) can significantly improve the prediction of radiation pneumonitis by the LKB model. In a study on clinical risk factors, Tucker at al. (2008) showed that the generalised Lyman model including patient smoking history yielded NTCPs differing by up to 27% from those solely based on dose-volume data. Valdagni et al. (2009) tried to understand why, despite rectal DVHs predictive of a low risk of late rectal bleeding (LRB), certain prostate cancer patients nevertheless suffered from LRB whereas others with DVHs predictive of a high risk did not bleed. They identified two genes that were especially predictive of enhanced radiosensitivity and one that was predictive of enhanced radioresistance. Studies such as these may result in NTCP models that yield different predictions for ‘biologically different' patients with very similar DVHs (see Section 44.3.6). Ultimately, such improved models ought to be employed in the various levels of radiobiological optimisation discussed here (Rancati et al. 2011; Tommasino et al. 2017; West et al. 2007; Burnet et al. 2019).
Radiation Hormesis in Immunity
Published in T. D. Luckey, Radiation Hormesis, 2020
Radioresistance is a little understood and somewhat controversial phenomena. When exposed to lethal doses of radiation, animals previously exposed to ionizing radiation show less mortality within the next 30 d than control animals (Table 5.1). Within an undetermined time frame, different types of radiation, different rates of exposure, or different total dose appears to invoke subsequent radioresistance. Several reports indicated that either acute or chronic whole-body exposure to ionizing radiation provided considerable protection to subsequent lethal doses, 4 to 7 Gy, of acute irradiation. Resistance was associated with the induction of repair enzymes and geater immune competence.407,895 The mechanisms involve both intracellular and intercellular reactions.93,274,411,822,1004 Numerous reports of increased radioresistance in mammals and a variety of other organisms give validity to the concept.527,895 Results observed include decreased chromosomal damage.492,821,1004
Cellular Radiation Damage
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
In comparing the radiosensitivity of different types of cells, tissues, or organs, one must define the criterion of radiation damage. A statement about the radiosensitivity of cells without reference to the criterion of radiation damage is meaningless. Some cells may be radioresistant as judged by one criterion of damage, but highly radiosensitive by another. A few principles that allow one to predict the radiosensitivity of cells are described in this chapter. Some major references are listed at the end of the chapter.3,10
Effects of prolonged treatment of TGF-βR inhibitor SB431542 on radiation-induced signaling in breast cancer cells
Published in International Journal of Radiation Biology, 2022
Poonam Yadav, Priya Kundu, Vipul K. Pandey, Prayag J. Amin, Jisha Nair, Bhavani S. Shankar
Radioresistance of tumors and normal tissue toxicity remains the foremost problems of radiation oncology despite several improvements in localized delivery systems. Radioresistance of tumors in turn leads to remission and disease progression and normal tissue toxicity results in several side-effects (Atun et al. 2015; Baumann et al. 2016; Domina et al. 2018). Understanding the cellular and molecular changes during this process is crucial to devise strategies to overcome radioresistance. Several investigators have reported changes that vary from DNA damage and its consequent repair (Schiavoni et al. 2013) to activate various signal transduction pathways (Zhong et al. 2000; Noordhuis et al. 2009; Kim HS et al. 2012; Theys et al. 2013). Additionally, several pro-survival proteins/enzymes have also been implicated in conferring radioresistance (Ozeki et al. 2004; Grdina et al. 2015; Wang SS et al. 2015).
Activation of COL11A1 by PRRX1 promotes tumor progression and radioresistance in ovarian cancer
Published in International Journal of Radiation Biology, 2021
Miaomiao Zhu, Chenxia Ye, Jing Wang, Guangxia Yang, Xiaoyan Ying
Ovarian cancer is the leading deadly gynecologic cancer, with 5-year survival ranging from 30 to 92% (Greenlee et al. 2001; Jemal et al. 2008). Ovarian cancer is hard to be diagnosed in the early stage (the International Federation of Gynecology and Obstetrics stages: Stage 1 and II) due to the lack of specific symptoms. Most patients are diagnosed with advanced-stage disease (Stage III and IV), in which malignancy has already disseminated throughout the peritoneal cavity (Dinh et al. 2008). With the combination of surgery and chemotherapy at diagnosis, the majority of patients will have a complete response to the first-line treatment. However, most patients eventually develop recurrent within 5 years, with the progressive development of chemoresistance, which may be caused by accumulated mutations or altered tumor microenvironment (Yang et al. 2018). The evolution of radiation techniques with lower toxicity plays an emerging role in ovarian cancer treatment, such as stereotactic body radiotherapy (SBRT), intensity-modulated radiotherapy (IMRT) and low-dose fractionated radiotherapy with the combination of chemotherapy and targeted therapy (Fields et al. 2017; DeSelm et al. 2018). Unfortunately, similar to chemotherapy, responses to subsequent radiotherapy may decline due to the inevitable development of resistance to radiotherapy. The mechanisms underlying radioresistance remain largely elusive.
Role of miRNAs in regulating responses to radiotherapy in human breast cancer
Published in International Journal of Radiation Biology, 2021
Zhi Xiong Chong, Swee Keong Yeap, Wan Yong Ho
Radioresistance arises when the irradiated cancer cells turn on alternative mechanisms that promote them to survive, proliferate, invade, and escape from cellular death (Tang et al. 2018). Radioresistant tumor cells had been shown to induce cell cycle (G2/M) arrest both in vivo and in vitro (Gogineni et al. 2011; Anastasov et al. 2012). This might contribute to radioresistance as the arrest in the cell cycle provides time for the damaged DNA to be repaired, allowing cancer cells to continue proliferating (Gogineni et al. 2011; Tang et al. 2018). Therefore, radioresistant cancer cells can also exhibit enhanced DNA damage repair capacity, as evidenced by the upregulation of key genes involved in DNA repair pathways such as Chk1 (Jiang et al. 2019), ATM (Bian et al. 2020), RAD1, BRCA1, and BRCA2 (Balbous et al. 2016).