China
Africa
Explore chapters and articles related to this topic
Antiviral Drugs as Tools for Nanomedicine
Published in Devarajan Thangadurai, Saher Islam, Charles Oluwaseun Adetunji, Viral and Antiviral Nanomaterials, 2022
Genetic changes are the cause of cancer especially DNA damage and genomic instability (Ferguson et al. 2015; Basu 2018). A few are due to genetic inheritance However, mostly the environment, i.e. anything outside the human body that interacts with it, lifestyle, or behavioural exposures lead to cancer. In general, cancer is not contagious in humans, though it can be caused by viruses and cancer bacteria. Avoiding exposure to such factors can contribute to a 75–80% reduction in cancer deaths. Environmental factors include exposure to different chemical and physical agents; for example, tobacco (accounts ~30% of cancer deaths), pollutants, diet and obesity (accounts ~35% of cancer deaths), infections (accounts ~20% of cancer deaths) and radiation (accounts ~10% of cancer deaths) (Merlo et al. 2012; Parsa 2012).
Avoiding Risk
Published in Kenneth L. Mossman, Radiation Risks in Perspective, 2006
Genomic instability refers to the acquisition of genetic damage in cells derived from cells damaged directly by exposure to carcinogens, such as ionizing radiation. Instability manifests itself in many ways, including changes in chromosome numbers, changes in chromosome structure, and gene mutations and amplification. Bystander effects are the most likely drivers of genomic instability. Effects can be observed at delayed times after irradiation and manifests in the progeny of exposed cells multiple generations after the initial insult. Genomic instability is important in the cancer initia tion process and appears to be a critical element in cancer progression and metastasis.
Nonviral Therapeutic Approaches for Modulation of Gene Expression: Nanotechnological Strategies to Overcome Biological Challenges
Published in Ana Rute Neves, Salette Reis, Nanoparticles in Life Sciences and Biomedicine, 2018
Ana M. Cardoso, Ana L. Cardoso, Maria C. Pedroso de Lima, Amalia S. Jurado
Following the discovery of antibiotics, which allowed the eradication of most kinds of infections, gene-related diseases gained a high relevance in the context of medical research—the neurodegenerative disorders sporadic Alzheimer’s disease (AD) and Parkinson’s disease (PD) being the most prevalent, whose etiology remains elusive. Both of these disorders are characterized by increased expression of proteins (amyloid-p peptide [Ap] and a-synuclein [a-syn], respectively), whose cytoplasmic and extracellular aggregates have been assigned as responsible for the disease progression [1–3]. Therefore, strategies that modulate dysregulated expression of genes, such as those coding for proteins involved in Ap and a-syn production and degradation or coding for regulatory elements of these pathways, are expected to efficiently counteract the development of these diseases. Although cancer has been described to have occurred in the primordial days of humanity [4], in recent years it has become one of the leading health concerns, the annual cancer cases being predicted to afflict 22 million people in 2032 [5]. Genomic instability, which characterizes cancer cells, facilitates gene mutation and, thus, aberrant gene expression [6]. Despite the differences in the genetic profiles displayed by various cancer types, some pathways are transversally affected, sharing a set of characteristics designated as “cancer hallmarks.” These include sustained proliferation ability, resistance to cell death, increased angiogenesis, invasion ability, and metastasis formation [7], which have been reported to be facilitated by a pro-inflammatory status [7] and energy metabolism dysregulation, the latter being regarded as a stemness promoter [8].
Effect of Gene 33/Mig6/ERRFI1 on hexavalent chromium-induced transformation of human bronchial epithelial cells depends on the length of exposure
Published in Journal of Environmental Science and Health, Part C, 2022
Cen Li, Dina Edeni, Sarah Platkin, Raymond Liu, Jiangwei Li, Maheen Hossain, Mozibur Rahman, Humayun Islam, John L. Phillips, Dazhong Xu
Progressive accumulation of genetic and/or epigenetic changes as a result of genomic instability is a hallmark of the carcinogenesis and cancer progression.18 This notion was classically depicted by the two-hit carcinogenesis theory, which applies to both genetic and epigenetic alterations and to both individuals with or without genetic predispositions.43 Recent evidence from genomic analyses of human cancer specimens further substantiates the concept of tumor evolution by revealing gradual genomic changes that accompany tumor progression.44,45 Cr(VI) carcinogenesis should inevitably follow this route. The ability of Cr(VI) to promote genomic instability facilitates the genomic changes in lung epithelial cells throughout the course of Cr(VI) exposure, which eventually lead to phenotypic alterations and neoplastic transformation. Results from the present study confirm the progressive nature of the neoplastic transformation of lung bronchial epithelial cells in response to chronic Cr(VI) exposure and reveal the adaptation of these cells to the deletion of Gene 33, a known tumor suppressor in the lung, during the course of chronic Cr(VI) exposure that lead to neoplastic transformation of these cells. The adaptation eliminated many of the early biological effects of the Gene 33 deletion.
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
Arsenicals do not react directly with DNA. The major underlying carcinogenic mechanisms observed at low concentrations are rapid induction of oxidative DNA damage and inhibition of DNA repair. Some forms of arsenic induce chromosomal aberrations in vitro, but this is significant only at toxic doses. Chronic low-dose exposure in animal models produces genomic instability and leads to chromosomal aberrations and micronucleus formation. AsIII interferes with spindle function during mitosis. Increased mutagenesis is observed as a consequence of enhanced genomic instability.
Absolute telomere length in peripheral blood lymphocytes of workers exposed to construction environment
Published in International Journal of Environmental Health Research, 2023
Paula Rohr, Isabela Campanelli dos Santos, André van Helvoort Lengert, Marcos Alves de Lima, Rui Manuel Reis, Fernando Barbosa, Henrique Cesar Santejo Silveira
Genomic instability is defined as an increased tendency of the genome to acquire mutations or other genetic changes to occur during the cell division (Langie et al. 2015). Thus, the genomic instability is an important hallmark of cancer that has a potential to orchestrate the others hallmarks capabilities to enable cancer driving (Hanahan and Weinberg 2011). Many biomarkers could be used to measure genomic instability, such as DNA strand breaks, chromosome aberrations, micronucleus frequencies, and telomere length (TL) (Laffon et al. 2021).