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Radionuclides and heavy metals
Published in Rym Salah-Tazdaït, Djaber Tazdaït, Phyto and Microbial Remediation of Heavy Metals and Radionuclides in the Environment, 2022
Rym Salah-Tazdaït, Djaber Tazdaït
There are three groups of genes whose mutation usually leads to cancer formation. (1) The oncogenes (LMP-1, URG4/URGCP, etc.) are the mutated versions of the proto-oncogenes, which normally positively regulate cell division. In contrary to the proto-oncogenes, the oncogenes are active in a way that is excessive or inappropriate (Dodurga, Seçme, and Şatıroğlu-Tufan 2018, 12). In the case of oncogenes, a single mutant allele may be sufficient to modify the phenotype of the cell. (2) The mutator genes such as BRCA1 or BRCA2 constitute a class of genes that play a fundamental role in DNA repair and replication; they are thus responsible for maintaining the integrity of the genome. The mutated versions of these genes lead to several cellular disorders, including malignant transformations (Clark and Pazdernik 2016, 611). (3) Tumor-suppressor genes or anti-oncogenes (RB1, NF2, APC, DPC4, etc.) are, as the name suggests, a group of genes that act by inhibiting tumour development. The two mutant alleles of a mutator gene or an anti-oncogene can lead to uncontrolled cell proliferation (Caldas and Venkitaraman 2001, 232–4).
Experimental Results on Cellular and Subcellular Systems Exposed to Low-Frequency and Static Magnetic Fields
Published in Ben Greenebaum, Frank Barnes, Biological and Medical Aspects of Electromagnetic Fields, 2018
Myrtill Simkó, Mats-Olof Mattsson
Environmental conditions have recently been strongly associated with epigenetic regulation of gene expression. This includes ionizing radiation where it has been suggested that genomic instability caused by radiation is due to changes in methylation patterns of the DNA (Aypar et al. 2011). Also other environmental toxicants have been shown to influence DNA methylation (Kim et al. 2012). These authors showed that several toxicants caused both global hypomethylation and specific hypermethylation of various tumor suppressor genes. The latter phenomenon, in turn, leads to the tumor suppressor genes being more difficult to transcribe and therefore tumor development including cancer is facilitated. Interestingly, the normal cellular metabolism, when producing redox intermediates, can have a direct effect on epigenetic signaling (Cyr & Domann 2011). These authors have pointed to a strong link between metabolism and epigenetics in the pathogenesis of cardiovascular disease, Alzheimer’s disease, certain types of cancer, and environmental toxicology.
Artificial Neural Networks and Prognosis in Prostate Cancer
Published in Raouf N.G. Naguib, Gajanan V. Sherbet, Artificial Neural Networks in Cancer Diagnosis, Prognosis, and Patient Management, 2001
In addition to established clinical prognostic markers, several new factors are emerging which may have a varying degree of significance in predicting outcome. Amongst these novel experimental markers are the genes regulating programmed cell death, otherwise known as apoptosis. These include the tumour suppressor gene p53 and the proto-oncogene bcl-2. It is now evident that the effects of androgen suppression in prostate cancer are mediated via apoptosis. Deregulation of the genetic pathway leading to programmed cell death may confer hormone-resistant prostate cancer which is incurable. Our group has demonstrated previously that the combination of bcl-2 overexpression and p53 nuclear accumulation by immunohistochemistry correlates strongly with hormone refractory prostate cancer [1,2]. In the study described herein, we incorporated experimental with conventional markers to assess the sensitivity of neural networks in predicting outcome following appropriate training. The results were compared with those obtained from conventional statistical methods.
Green fabrication of silver nanoparticles mediated by Bistorta officinalis aqueous extract: putative mechanism for apoptosis-inducing properties
Published in Inorganic and Nano-Metal Chemistry, 2022
Reyhaneh Shali, Ali Neamati, Masoud Homayouni Tabrizi, Ayda Etminan, Sara Ghandehari, Maryam Karimi Noghondar
Cancer is a multifactorial disease and many factors, including genetic and environmental factors, play a role in its occurrence. Inactivation of tumor suppressor genes and activation of oncogenes due to genetic and epigenetic changes is one of the most important known factors for cancer.[1,2] One of the most important limitations in the treatment of cancer with conventional methods[3] is the acquired resistance of the tumor to drugs, which has made cancer treatment a serious challenge. Due to the increase in mutations and genetic instability in cancer cells and their rapid genetic changes, these cells quickly become resistant to drugs. Therefore, further research on the discovery of new treatment strategies to overcome the drug resistance of cancers seems necessary.[4] Nanotechnology, by covering the fields of chemistry, medicine, engineering and biology, seeks to identify solutions for the management of cancer.[5] Recently, the use of nanoparticles has received a lot of attention due to its high reactivity, increase in surface to volume ratio and some unique properties.[6] Despite the many benefits to nanotechnology, a limited number of nanoproducts are currently used, and the most important limitation of nanoparticle use is its toxicity and their unknown immunological reactions in the body.[7]
MicroRNA-122 overexpression promotes apoptosis and tumor suppressor gene expression induced by microcystin-leucine arginine in mouse liver
Published in International Journal of Environmental Health Research, 2022
Rui Wang, Haohao Liu, Xingde Du, Ya Ma, Zhihui Tian, Shiyu Zhang, Linjia Shi, Hongxiang Guo, Huizhen Zhang
The tumor suppressor genes, Rb, PTEN, P21 and P53, play a very important negative regulatory role in controlling cell growth, proliferation and differentiation Macleod (2000). In this study, tumor suppressor genes Rb, PTEN, P21 and P53 were increased after MC-LR exposure. This may be related to the self-repair of mice, which resists the cancer-promoting effects of MC-LR. However, after transfection of miR-122 agomir, the expressions of tumor suppressor genes were further increased. Based on these, it can be concluded that the reduction of miR-122 can promote the risk of hepatocarcinogenesis induced by MC-LR through inhibiting the increase of tumor suppressor genes.