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Nano-biosensors: A Custom-built Diagnosis
Published in Paula V. Messina, Luciano A. Benedini, Damián Placente, Tomorrow’s Healthcare by Nano-sized Approaches, 2020
Paula V. Messina, Luciano A. Benedini, Damián Placente
Cancer is an epigenetic disease. In fact, epigenetic changes, particularly DNA methylation, are predisposed to change and are suitable candidates to elucidate how specific environmental aspects may raise the risk of cancer. The delicate organization of methylation and chromatin states that regulates the normal cellular homeostasis of gene expression patterns becomes unrecognizable in the cancer cell. The genome of the transformed cell undergoes, simultaneously, a global genomic hypomethylation and a dense hypermethylation of the CpG islands (high frequency of CpG sites in genome, regions of DNA where a cytosine nucleotide is followed by a guanine nucleotide in the linear sequence of bases along its 5’ → 3’ direction) associated with gene regulatory regions. These dramatic changes may lead to chromosomal instability, activation of endogenous parasitic sequences, loss of imprinting, illegitimate expression, aneuploidy, and mutations, and may contribute to the transcriptional silencing of tumour suppressor genes. The aberrant CpG island methylation can also be used as a biomarker of malignant cells and as a predictor of their behaviour (Esteller and Herman 2002). Thus, the attainment of abnormalities’ estimation in the living cells gene expression of identifying cancer at the cellular level in an early stage before metastasis holds a great promise for increasing the survival of cancer patients (Laird 2003).
Chronic Arsenic Exposure to Drinking Water
Published in M. Manzurul Hassan, Arsenic in Groundwater, 2018
Cancer cells are characterized by an unstable genome, and genomes of certain cells are susceptible in accumulating DNA damage at an accelerated rate, developing a wide range of genetic abnormalities, and ultimately becoming cancerous. Genomic instability can be CIN (chromosome instability) and MIN (microsatellite instability) (Bhattacharjee et al., 2013c; Hudler, 2012). CIN is associated with mitotic errors such as chromosomal rearrangements or segregational anomalies and is most commonly observed in human cancer, while MIN is associated with DNA level instability seen in tumors (Bhattacharjee et al., 2013c) (Figure 4.5). As a nonmutagenic human carcinogen, arsenic has very strong clastogenic properties that can lead to its carcinogenic potential (Bustaffa et al., 2014; Collotta et al., 2013; Engström et al., 2011). The most prominent example of genetic variation influencing arsenic metabolism capacity is the 10q24.32 locus, which harbors the As3MT (arsenite methyltransferase enzyme) gene. Genetic variants have shown consistent association with arsenic metabolism capacity. Studies have reported associations between 10q24.32 metabolism-related SNP and skin lesion risk (Agusa et al., 2011).
Theranostic: Cancer Diagnosis and Therapy
Published in Mohammad E. Khosroshahi, Applications of Biophotonics and Nanobiomaterials in Biomedical Engineering, 2017
Cancer is a complicated disease caused by genetic instability and accumulation of multiple molecular alterations causing the cells to introduce uncontrolled proliferation, genomic, and chromosomal instability, and is the leading cause of death worldwide. In 2007, it was estimated that about 10 million cases of cancer occurred globally, with nearly 1.43 million new cases and 560,000 deaths projected to occur in the US in the year 2008 (American Cancer Society 2008). According to Cancer Research Society of Canada, about 196,900 new cases of cancer were expected in 2015 in Canada, i.e., 1 person every 3 minutes, every day. Similarly, Cancer Statistics Center of American Cancer Society predicted that in 2016, there will be an estimated 1,685,210 new cancer cases diagnosed, and 595,690 cancer deaths in the US. The projected numbers of new cancer cases and deaths in 2016 should not be compared with previous years to track cancer trends because they are model-based and vary from year to year for reasons other than changes in cancer occurrence. Age-standardized incidence and death rates should be used to measure cancer trends. Metastasis of cancerous cells from the primary site (i.e., tumor) to other organs in the body is governed by their ability to leave the tumor and invade through membranes and tissues, survive in circulation by avoiding immune attack and residing in surrounding tissues. To maintain growth, cancer cells need to initiate the formation of new blood vessels, hence providing a constant supply of nutrients. After a cancer is metastasized in the body, it becomes almost impossible to treat and often leads to patient mortality.
Genotoxicity biomarkers in car repair workers from Barranquilla, a Colombian Caribbean City
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Jaime Luna-Carrascal, Milton Quintana-Sosa, Jesus Olivero-Verbel
Biomarkers of genotoxicity of a group of auto repair workers were compared with those of an unexposed group. The exposed group showed a significantly higher degree of DNA damage (tail intensity), as well as increased number of MN in peripheral blood lymphocytes and oral cavity epithelial cells. Similarly other investigators noted that for oral mucosal epithelial cells (Pedro et al. 2019; Siebel and Basso Da Silva 2010), and peripheral blood lymphocytes with DNA damage occurred after diesel fuel emissions exposure (Duan et al. 2016; Londoño-Velasco et al. 2019; Zhang et al. 2015). Components such as MN in the oral mucosa and lymphocytes constitute genotoxic responses due to prolonged exposure to various air pollutants (Espitia-Pérez et al. 2016), as observed in this study. Further, the frequency of these MN might be associated with primary oxidative damage to DNA (Espitia-Pérez et al. 2018a), and activation of cellular systems in response to this insult (Vilas Boas et al. 2018; Wang et al. 2019). Indeed, the presence of MN and other nuclear abnormalities are manifestations of chromosomal instability that are frequently detected in cancer (Bonassi et al. 2007). Therefore, the elevated frequency of MN formation in epithelial and blood matrices may represent early carcinogenesis events (Bonassi et al. 2007; Pardini et al. 2017). Considering the adverse effects at the cellular level, cumulative exposures and risks from co-exposures should not be underestimated (Batterman et al. 2014).