China
Africa
Explore chapters and articles related to this topic
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].
Radiation Carcinogenesis: Animal Model
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
The frequency of radiation-induced cancer has been extensively studied in animals. However, the dose–response curves markedly vary from one tumor type to another.1 This suggests that other environmental factors, such as cocarcinogens, tumor promoters, and antitumor promoters, may influence the processes of radiation-induced carcinogenesis, thereby shaping the dose–response curve. The factors that influence carcinogenesis include (1) age, (2) sex, (3) genetic constitution, (4) capacity to repair DNA damage, (5) carcinogen metabolism, (6) immunological status, and (7) dietary factors.
Chemical Carcinogenesis as a Consequence of Alterations in the Structure and Function of DNA
Published in Philip L. Grover, Chemical Carcinogens and DNA, 2019
In addition, we do not believe, on the basis of the theory to be presented, that all carcinogenic events need both the initiation and promotion phases. There might be some which require only initiation; some which require both initiation and promotion; while others would require only promotion.** A summary of the two-stage concept of carcinogenesis is presented with the following definitions. Carcinogenesis = initiation and/or promotion.Initiation = DNA damage + “mutation fixation”.Anti-initiation = prevention of DNA damage and its repair by “error-prone” mechanisms.Promotion = gene modulation (gene repression or derepression).Antipromotion = negation of tumor promoter functions.
Mechanistic analysis of endothelial lipase G promotion of the occurrence and development of cervical carcinoma by activating the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B/mechanistic target of rapamycin kinase signalling pathway
Published in Journal of Obstetrics and Gynaecology, 2023
Jing Huang, Renci Liu, Yiwen Zhang, Xiujie Sheng
The International Agency for Research on Carcinoma (IARC) of the World Health Organisation released the latest data in 2020. The total number of new carcinomas in the world was about 19.29 million, and the number of cervical carcinomas was 600,000 cases, which accounted for 3.1% (2021). Cervical carcinoma has its unique biological characteristics, such as invasiveness and metastasis, abnormal cell differentiation, proliferation, and loss of growth control. It can be divided into three processes: Carcinogenesis, carcinoma promotion, and evolution. Cervical carcinoma might occur through a long multi-factor and multi-step process; therefore, earlier diagnosis and effective treatment strategies have become an urgent need to prolong the survival period of patients with cervical carcinoma and to improve their quality of life.
Integrated analysis of mRNA–m6A–protein profiles reveals novel insights into the mechanisms for cadmium-induced urothelial transformation
Published in Biomarkers, 2021
Bin Wu, Xu Jiang, Yapeng Huang, Xiaoling Ying, Haiqing Zhang, Bixia Liu, Zhuo Li, Dengfeng Qi, Weidong Ji, Xingming Cai
Chemical carcinogenesis is the process by which chemical substances induce normal cells to undergo malignant transformation and develop into tumours. Chemical carcinogens can bind to DNA and induce mutations in cancer susceptibility genes, leading to the development of carcinogenesis (Luch 2005). Advancements in systems biology help identify and predict interactions within cells, which can be partly represented as gene networks. Analysis of these complex networks offers useful insights into biological signalling pathways. Chemical carcinogenesis causes changes in gene expression, and transcriptome analysis provides information on tissues or cells at a particular period or time point (Kim et al. 2012). In addition to changes at the DNA and transcriptional levels, chemical carcinogens can also cause epigenetic changes, such as in 5-methylcytosine (5mC) and N6-methyladenosine (m6A) (Yang et al. 2019), microRNAs (Li et al. 2019b) and long-noncoding RNAs (Li et al. 2019a). These changes contribute to carcinogenesis by regulating gene expression. Protein expression is the last step for genes to function in biological processes. It is controlled by complex regulatory systems, thus making the proteome highly dynamic (Aslam et al. 2017) and accounting for the inconsistency in gene expression at the transcription level and at the protein level.
Relationship between the Monocyte Chemo-attractant Protein-1 gene rs1024611 A>G Polymorphism and Cancer Susceptibility: A Meta-analysis Involving 14,617 Subjects
Published in Immunological Investigations, 2021
Zhan Chen, Shiping Yin, Liang Zheng, Weifeng Tang, Mingqiang Kang, Wei Wei, Kang Sui
Malignancies are the major global health concern. Recent years have witnessed a steep rise in incidences and mortality rates of malignancies (Torre et al. 2016). In 2018, around 18.1 million cases of cancer were diagnosed, and 9.6 million cancer-related deaths were reported (Bray et al. 2018). Despite this, the etiology of cancer remains underexplored. Numerous studies have demonstrated that genetic and environmental risk factors play a crucial role in the onset of carcinogenesis. Recent epidemiological studies demonstrated that chronic inflammation and infections are associated with various malignancies (Bilen et al. 2019; Jones and Jenkins 2018; Tomic et al. 2019). According to a report, the infection and chronic inflammatory condition might lead to the onset of 25% of total malignancies (Hussain and Harris 2007).