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Introduction to Cancer, Conventional Therapies, and Bionano-Based Advanced Anticancer Strategies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Carcinogenesis is the process by which the transformation of normal cells into cancer/tumor takes place. Tumor is an abnormal mass of tissue due to the uncontrolled growth of cells. Tumor can be benign (not cancer) or malignant (cancer). The roles of genes involved include the inhibition of cellular proliferation, which encompasses the function of tumor suppressor genes, and positive signaling of migration and proliferation, which contains oncogenes’ function. In addition, other genes concerned involve these with roles in apoptosis control and DNA repair [4]. One of the most known models involved in carcinogenesis is the RAS gene activation. The activation mechanism of the RAS protooncogenes is normally via point mutations at either one or many activating positions within the sequence. The elevated expression of the RAS gene may lead to the transformation of normal cells, which induces the formation of tumors [5].
Chemical Orthogonal Space
Published in Mihai V. Putz, New Frontiers in Nanochemistry, 2020
There are three operational stages associated with the carcinogenesis process: initiation, promotion and progression, each stage having a distinct mechanism and QSAR characteristics. In this context, the selection of appropriate molecular descriptors has an important role in a meaningful QSAR formulation (Putz et al., 2011a, Benigni et al., 2007). From their study, Putz et al., (2011a) determined that mutagenicity can be considered an interaction mechanism of the electrophilic ligand-receptor type which implies a covalent binding between the ligand molecule SA and receptor. They also determined that the residual QSAR analysis can be improved by the structural alert or molecular fragment analysis (Putz et al., 2011a).
Quick Methods: Structure-Activity Relationships and Short-Term Bioassay
Published in Samuel C. Morris, Cancer Risk Assessment, 2020
While the predominant notion of carcinogenesis involves damage to DNA as an initiating factor, some chemicals appear to induce cancer without involving DNA, perhaps through interruption of cell-to-cell communication or simply by increasing cell proliferation. Short-term tests such as the cell transformation assay (Heidelberger et al., 1983) have been developed to detect such chemicals. There is still a need for further improvement in detecting promoting activity in short-term tests (NAS, 1986).
The anticancer activity of metal oxides and phytochemical-enriched medicinal nano-spheres (MNS); a comparative evaluation
Published in Inorganic and Nano-Metal Chemistry, 2022
Masoud Homayouni Tabrizi, Seyed Mohammad Reza Seyedi, Zeynab Mokhtareeizadeh
Pro-oxidants and antioxidants are the two main effectors, which significantly influence the cell’s growth, proliferation, and death. The imbalance in pro-oxidant/antioxidant levels has been well known as one of the main causes of carcinogenesis. Therefore, the necessity of an antioxidant defense system (ADS) is obviously comprehensible for cells. There is a complex network of ADS effectors consisting of antioxidant enzymes and molecules. (Gpx), (SOD), and (CAT) are the axial known antioxidant enzymes that significantly regulate the pro-oxidant antioxidant balance (PAB) in cells. In a cancer cell, the ADS network has been improved to decrease the PAB index and prevent the cell cycle stop in response to its high metabolism rate.[6,31] However, there is a maximum threshold for buffering the metabolic-mediated imbalance of reactive oxygen specious (ROS) in cancer cells. The ROS levels higher than cancer antioxidant buffering system (CABS) capacity conducts the cells to a programmed cell death pathway or apoptosis. This can be considered as the first point of the cancer cell’s strategy for surviving under such stressful conditions. This is while the normal cells are far susceptible than cancer types in oxidative tensions due to their weaker ADS. Therefore, as the second key requirement for a suitable anticancer compound, the antioxidant activity is an obligatory condition to protect the normal cells.[5]
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
The primary mechanism of carcinogenesis is through genotoxicity. Busulfan binds covalently to cellular macromolecules including DNA, RNA, and proteins. Consequently, this drug is capable of producing mono-adducts, intrastrand DNA–DNA cross-links, and DNA–protein cross-links. In vitro studies with human and rodent cells treated with busulfan showed formation of chromosomal aberrations, sister chromatid exchange, and mutations. In vivo treatment of rodents with busulfan induced dominant lethal mutations, and increased the frequency of chromosomal aberrations or micronuclei in bone marrow, intestine, embryonic liver, and germ cells. Patients treated with busulfan for chronic myeloid leukemia were found to exhibit elevated frequencies of sister chromatid exchange and chromosomal aberrations in their peripheral blood lymphocytes. Evidence suggests that busulfan directly induces losses or deletions affecting chromosomes 5 or 7 (e.g. loss of heterozygosity for TP53). Chromosomal alterations and deletions were reported in a variety of experimental models and in lymphocytes of exposed humans.
Toxicity in vitro reveals potential impacts of microplastics and nanoplastics on human health: A review
Published in Critical Reviews in Environmental Science and Technology, 2022
Qingying Shi, Jingchun Tang, Rutao Liu, Lan Wang
Noteworthy, the unrepaired or misrepaired DNA lesions lead to mutagenic processes. If these mutations modulate key genes involved in genomic integrity maintenance, or cell cycle control, then carcinogenesis might be initiated. Therefore, it should be considered that if MPs and NPs are able to induce genotoxicity, then these plastics might also have the capacity to initiate carcinogenesis due to alterations imposed on the genetic material (Fadeel et al., 2017).