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Application of Carbon Nanotubes in Cancer Vaccines as Drug Delivery Tools
Published in Loutfy H. Madkour, Nanoparticle-Based Drug Delivery in Cancer Treatment, 2022
The way the CNTs interact with nucleic acids has been extensively studied for their potential applications. Both antisense oligonucleotides and small interfering RNA (siRNA) are very promising fragments for gene silencing, applicable for the treatment of many diseases. They can in fact inhibit protein expression, potentially blocking many cellular pathways. Cancer therapy is one of the possible applications, when the targets are oncogenes or genes involved, for instance, in angiogenesis or chemotherapy resistance. One of the first studies in this field was performed a few years ago [181]. Cationic SWCNTs were used to complex siRNA, able to silence the expression of telomerase reverse transcriptase and thus inhibit cell growth. This activity was proved in vitro, on different cell lines, both murine and human, and in vivo, after intra-tumor injection in xenografted mice.
Basic Chemical Hazards to Human Health and Safety — II
Published in Jack Daugherty, Assessment of Chemical Exposures, 2020
Oncogenes. Cellular genes that bring about cancer during the normal growth and development are protooncogenes. Transduced oncogenes of acute transforming retroviruses were protooncogenes. Oncogenes can also be formed from protooncogenes by mechanisms other than retroviral involvement, however. Point mutations or DNA rearrangements, such as translocations or gene amplifications, also lead to oncogenes. Certain types of oncogenes are activated by specific chemical dosages. Others are activated during neoplastic progression. The loss of specific regulatory functions, such as tumor suppressor genes, is believed to be a step in neoplastic transformations. The activation of ras protooncogenes by point mutation in a tumor induced by a specific chemical may occur early in the tumorigenesis and may even be the initiation step. DNA damaging potential of chemicals to the H-ras and K-ras genes has been implicated in carcinogenesis, both in the induction of tumors and the progression from benign to malignant tumors.
Environmental Disease
Published in Gary S. Moore, Kathleen A. Bell, Living with the Earth, 2018
Gary S. Moore, Kathleen A. Bell
Cancer develops from multiple mutations in the DNA, often in the genes producing proteins that control cell division. Some of these genes are tumor suppressor genes, which produce proteins that can repair defective cells or help destroy damaged cells. When these genes undergo mutation, the DNA repair system breaks down. In a typical pathway leading to cancer, a chemical agent such as benzo(a)pyrene (BP), associated with smoking cigarettes, combines with human DNA to form an adduct (carcinogenic residues bound to DNA) that leads to increased mutations that eventually accumulate and lead to cancer. The smoke from cigarettes contains as many as 4,000 compounds with more than 40 of these known to be carcinogenic. Included among these are BP, benzene, and arsenic. The act of smoking (or being exposed to passive smoke) brings these substances into intimate contact with the delicate tissue of the respiratory tract. Other defective genes (such as ras) produce proteins that inappropriately stimulate cell division. Collectively, these cancer-causing genes are called oncogenes.
Identification of cancer types from gene expressions using learning techniques
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Swati B. Bhonde, Sharmila K. Wagh, Jayashree R. Prasad
Cancer is caused by variations or changes in gene regulators that regulate cell division and development, resulting in highly expressed genes (Daniel and Shumer 2017). In such cases, a group of genes known as oncogenes plays an important role in the transformation of normal cells into cancerous cells (Basavegowda and Dagnew 2020). Somatic mutations, Copy Numbers (CNs), profiles, and various epigenetic changes are distinct in each kind of tumor (Greene and Costello 2020). As a consequence, cell differentiation, environmental factors, and genetic inheritance by parents may interrupt Gene Expression (GE). Changes in GE can affect the development of proteins, which can affect normal cell behavior (Hajieskandar and Mohammadzadeh 2020). The damaged cells begin to reproduce at a faster rate than normal, eventually forming a tumor in the affected region. Such tumors may sometimes develop into cancer (Jang et al. 2020). This is one of the reasons why cancer cases are steadily growing year after year, eventually becoming the world’s second leading cause of death (Echle et al. 2021). Despite its importance in directing patient care, histologic-based cancer diagnosis remains difficult in many patients, especially in those who first present with metastatic, poorly differentiated neoplasms, where unclear or inaccurate classification may harm treatment options and outcomes (Carrasco Pro et al. 2020).