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The Scientific Basis of Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Chris O'Callaghan, Rachel Allen
Tumour suppressor genes restrict cell proliferation and induce repair or apoptosis in response to DNA damage. p53 is the classic example of a tumour suppressor gene, and is the most commonly mutated gene in tumours (Figure 2.11). DNA repair genes remove the damage induced by mutagenesis. Point mutations, translocations and gene amplification can all play a part in tumorigenesis. Chromosomal translocations can generate hybrid oncogenes, as seen with the Philadelphia chromosome in chronic myeloid leukaemia (see Chapter 15, Haematological disease).
Introduction to Cancer, Conventional Therapies, and Bionano-Based Advanced Anticancer Strategies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
The epigenetic theory of carcinogenesis refers to mechanisms that modify the expression of genes leading to carcinogenesis without modifying the primary DNA sequence. Normally, epigenetic processes are inherited and can be reversed, and they include alterations in DNA methylation and histone modifications. Disruption of epigenetic mechanisms can result in modified gene function and malignant transformation of cells [25]. Deregulated epigenetic processes can initiate genetic instability that results in the acquisition of mutations in tumor suppressor genes and in oncogenes. Furthermore, the studies have shown that epigenetic modifications in tumors are mainly of a clonal nature, which indicates the occurrence of these epigenetic disruptions in early cell generations [26].
Cancer and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Tormod S. Nilsen, Pernille Hojman, Henning Wackerhage
Cancer genes typically encode proteins that regulate the cell division, survival, growth or metabolism, termed the hallmarks of cancer, which we describe below. There are two main types of cancer genes: Oncogenes are genes whose gain-of-function by mutation promotes cancer.Tumour suppressor genes are genes whose loss of function by mutation or other factors promotes cancer.
The current status of gene therapy in bladder cancer
Published in Expert Review of Anticancer Therapy, 2023
Côme Tholomier, Alberto Martini, Sharada Mokkapati, Colin P. Dinney
Over the last several decades, multiple genetic alterations have been implicated in bladder carcinogenesis. Specific genes include oncogenes, growth factors, antiapoptotic genes, cell proliferation factors, tumor suppressor genes, cell cycle inhibitors, apoptotic genes, cell adhesion molecules, and drug resistance genes [35]. They can be classified into three distinct groups based on their function in tumor development (Table 2). Knowledge around these genetic alterations allowed for development of gene therapy strategies for bladder cancer, which are summarized in Table 3. For example, oncogenes can be inactivated using antisense oligonucleotides (ASOs) or ribozymes (RZs). Both can be designed to target only the gene of interest [36]. Specific to bladder cancer, multiple groups developed specific ASOs and RZs targeting c-Fos, ERBB2, and MYC oncogenes, to inhibit cancer cell growth, or sensitize the tumors to platinum-based chemotherapy [37–39]. Inversely, restoration or even overexpression of tumor suppressor genes was found to be of benefit and lead to cancer cell death. Multiple studies have focused on induction of wild-type p53 through adenoviral vectors, including a study in bladder cancer [40–42]. Similar results of enhanced tumor suppressor gene therapy were shown with adenoviral vector delivering the wild-type retinoblastoma (Rb) gene in an in-vivo bladder cancer murine model [43].
Orally delivered targeted nanotherapeutics for the treatment of colorectal cancer
Published in Expert Opinion on Drug Delivery, 2020
Xueqing Zhang, Heliang Song, Brandon S.B. Canup, Bo Xiao
Cancer is often related to the mutations in both oncogenes and tumor suppressor genes [59]. Therefore, the precise gene editing, including deleting, adding, and epigenetic modifications, might be an efficient approach for cancer treatments. Clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR associated protein 9 (Cas9) system has already shown its great potential in gene editing, and this gene-editing machinery can be delivered into cells by viral or non-viral vectors [60]. The high immunogenicity of viral vectors has a negative impact on their application in gene editing. On the contrary, non-viral vectors such as lipid-based NPs, MSNs, and polymeric NPs, are much less immunogenic, and these NPs can be easily optimized according to the conformation of CRISPR/Cas9 complex [61].
Remodeling the cancer epigenome: mutations in the SWI/SNF complex offer new therapeutic opportunities
Published in Expert Review of Anticancer Therapy, 2019
Krystal A Orlando, Vinh Nguyen, Jesse R Raab, Tara Walhart, Bernard E Weissman
The finding of frequent mutations of subunits of the SWI/SNF chromatin remodeling complex by the TCGA and other tumor sequencing projects across a broad range of cancers has sparked renewed interest in targeting the epigenome with new treatment options. Because many of these mutations result in loss of function, efforts at identifying therapeutic vulnerabilities have suffered the same hurdles encountered for tumor suppressor genes such as BRCA1, RB1 or TP53. While recent studies have implicated the underlying mechanisms by which mutant SWI/SNF subunits can drive tumorigenesis, this knowledge has translated into limited novel treatment options. The only options that have led to drugs in clinical trials for these cancers have come from characterizing downstream signaling pathways altered by these mutations or through synthetic lethality screens of tumor cell lines. Therefore, accelerating the pace of research for understanding how mutations in SWI/SNF subunits drive the development of nearly 25% of human cancers should become a high priority.