China
Africa
Explore chapters and articles related to this topic
Pharmacokinetics, Biodistribution, and Therapeutic Applications of Recently Developed siRNA and DNA Repair Genes Recurrence
Published in Loutfy H. Madkour, Nanoparticle-Based Drug Delivery in Cancer Treatment, 2022
A plausible explanation is that pathways involving retinoic acid receptors and/or retinoid X receptors are also downregulated in these neoplasms. In these analyses, low expression of retinoic acid receptor beta (RARB) was associated with a significantly lesser RFS (log-rank P = 0.03). Consistent with this observation, recent studies demonstrated that RARB expression was downregulated in papillary thyroid cancer and RARB silencing increased cell viability, decreased expression of NIS, and suppressed iodine uptake in thyroid cancer cells [182,183]. A more promising strategy may be targeting the MAPK signaling pathway. Accumulating evidence suggests that MAPK inhibition may provide better results in terms of iodine uptake and tumor response [184–186]. Further research is necessary to provide a more personalized approach, tailored to specific molecular alterations in individual patient tumors.
Treatment Options for Chemical Sensitivity
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
An intriguing question remains the extent to which NHRs modulate circadian systems according to changing environmental conditions, such as humoral or nutritional factors. For example, variation in the concentration of glucocorticoid hormone, retinoic acid, heme, and fatty acids affect GRs, retinoic acid receptor (RAR), REV-ERBα, neuronal Per-Arnt-Sim (PAS) doman protein 2 (NPAS2), and PPARs. Therefore, variation in cellular concentrations of any one of these ligands may influence Bmal1 transcription, and thereby modulate local cellular circadian rhythms. Within the brain, heme and carbon monoxide may modulate NPAS2 activity,86 whereas within the vascular cells, retinoic acid influences circadian oscillations through activation of RARα and RXRα.87 Similarly, rhythmic variation in NHR ligands may exert distinct effects on local tissue clock function at different times in the day–night cycle.
Pulmonary reactions to chemotherapeutic agents: the ‘chemotherapy lung’
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Fabien Maldonado, Andrew H Limper
ATRA has been used with excellent results for the treatment of promyelocytic leukaemia, or acute myeloblastic leukaemia M3 according to the French/American/British classification. The basis for this treatment is the presence of a mutation in the retinoic acid receptor-alpha gene in patients with these disorders, which to a certain extent can be corrected by high doses of ATRA. ATRA thus allows for the maturation of leukaemic cells and can therefore induce disease remission. It is usually used in association with other agents, namely daunorubicin and cytosine arabinoside. ATRA may also prevent the onset of disseminated intravascular coagulation which frequently complicates this type of leukaemia.
Overview of biological mechanisms of human carcinogens
Published in Journal of Toxicology and Environmental Health, Part B, 2019
Nicholas Birkett, Mustafa Al-Zoughool, Michael Bird, Robert A. Baan, Jan Zielinski, Daniel Krewski
Areca quid chewing and arecoline elevate the expression of calcium-binding proteins, which might be involved in oral submucous fibrosis, a pre-cancerous lesion (Yu et al. 2013). Areca-nut extract up-regulate cyclooxygenase inflammatory signaling in the oral cavity (Chiang et al. 2008). and induce the TGF-β pathway during the progression of oral submucous fibrosis (Khan et al. 2012). Extracts of lime-based betel quid were shown to induce cell transformation (Lin et al. 2003). Arecoline produced alterations in expression of several genes catalyzing histone methylation, acetylation, and demethylation in human K-562 myelogenous leukemia cells (Lin et al. 2011). Silencing of the Rarb (retinoic acid receptor β) gene, by hyper-methylation, was reported in areca nut-induced oral squamous cell carcinoma in mice (Lai et al. 2014).
Progresses and emerging trends of arsenic research in the past 120 years
Published in Critical Reviews in Environmental Science and Technology, 2021
Chengjun Li, Jiahui Wang, Bing Yan, Ai-Jun Miao, Huan Zhong, Wei Zhang, Lena Qiying Ma
Since being suggested as an effective drug for APL (Sun et al., 1992) with proven efficacy (Chen et al., 1997; Chen, et al., 1996), ATO has attracted worldwide interest throughout the 2000s. In recent years, there have been numerous clinical trials exploring this promising drug. For example, Zhang et al. (2010b) further proved that ATO controlled the fate of the PML-RARα (a fusion protein containing sequences from the PML zinc finger protein and retinoic acid receptor alpha) oncoprotein by directly binding PML, providing new insights into the drug’s mechanism of action and its specificity for APL. In the early 2010s, the possibility of the combined use of ATO and ATRA, which was firstly mentioned in Sanz et al. (2005) but without a reported experiment, had been explored with a promising complete remission rate (Iland et al., 2012; Lo-Coco et al., 2013). More recent clinical trials have demonstrated that the immense majority of APL patients can be cured by the combination of two targeted therapies (Abaza et al., 2017) with the mouse model explaining its mechanisms (Ablain et al., 2014; Vitaliano-Prunier et al., 2014), suggesting that APL is now curable (de Thé et al., 2017). However, despite the ATRA/ATO combination being able to cure the vast majority of APL patients, including both high-risk and low-risk patients with APL (Abaza et al., 2017; de Thé et al., 2017; Platzbecker, et al., 2017), there is still a significant fraction of APL patients (high-risk subgroups, elderly and frail patients) failing to achieve disease eradication (Pallavi et al., 2019). Therefore, exploration of the underlying mechanisms and additional recommended treatments for these patient groups are needed, which could be the research trends in the next few years.
Effects of tobacco compound 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) on the expression of epigenetically regulated genes in lung carcinogenesis
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Sun Woo Jin, Jong Seung Im, Jae Hyeon Park, Hyung Gyun Kim, Gi Ho Lee, Se Jong Kim, Seung Jun Kwack, Kyu-Bong Kim, Kyu Hyuck Chung, Byung Mu Lee, Sam Kacew, Hye Gwang Jeong, Hyung Sik Kim
The establishments of epigenetic alterations induced by NNK exposure may help elucidate possible molecular mechanisms underlying tobacco smoking-induced lung tumorigenesis. Previous investigators demonstrated that methylation of the retinoic acid receptor (RAR)-β and death-associated protein kinase gene might be detected in adenocarcinomas induced following NNK exposure (Breitling 2013; McCartney et al. 2018; Vuillemenot et al. 2004). Although epigenetic alterations play an important role in development of smoking-related diseases, the molecular mechanism through which substances present in tobacco smoke initiate lung tumorigenesis remains unclear.