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IARC Monographs on the Evaluation of... 1999
Review
Topics: Animals; Carcinogenicity Tests; Carcinogens; Disease Models, Animal; Epidemiologic Studies; Global Health; Humans; Maximum Allowable Concentration; Methylene Chloride; Mice; Neoplasms; Neoplasms, Experimental; Rats
PubMed: 10476448
DOI: No ID Found -
IARC Monographs on the Evaluation of... 1999
Review
Topics: Acrylonitrile; Animals; Carcinogenicity Tests; Carcinogens; Cohort Studies; Disease Models, Animal; Environmental Exposure; Global Health; Humans; Maximum Allowable Concentration; Mice; Neoplasms; Neoplasms, Experimental; Rats; Risk Factors
PubMed: 10476445
DOI: No ID Found -
IARC Monographs on the Evaluation of... 1999
Review
Topics: Animals; Carcinogenicity Tests; Carcinogens; Humans; Hydrocarbons, Brominated; Mutagenicity Tests; Mutagens; Neoplasms, Experimental; Salmonella typhimurium; Trihalomethanes
PubMed: 10476403
DOI: No ID Found -
IARC Monographs on the Evaluation of... 1993
Review
Topics: Animals; Antineoplastic Agents; Carcinogens; Cyclohexenes; Food Analysis; Humans; Kidney Neoplasms; Limonene; Plants; Terpenes
PubMed: 8411619
DOI: No ID Found -
IARC Monographs on the Evaluation of... 2000
Review
Topics: Animals; Carcinogenicity Tests; Carcinogens; Cricetinae; Disease Models, Animal; Environmental Exposure; Epoxy Compounds; Female; Humans; Male; Maximum Allowable Concentration; Mice; Neoplasms, Experimental; Propanols; Rats
PubMed: 11100412
DOI: No ID Found -
IARC Monographs on the Evaluation of... 1999
Review
Topics: Animals; Carcinogenicity Tests; Carcinogens; Chromosome Aberrations; Dioxanes; Humans; Mutagenicity Tests; Mutagens; Neoplasms; Neoplasms, Experimental; Salmonella typhimurium
PubMed: 10476463
DOI: No ID Found -
Anais Da Academia Brasileira de Ciencias Dec 2007The use of chemical compounds benefits society in a number of ways. Pesticides, for instance, enable foodstuffs to be produced in sufficient quantities to satisfy the... (Review)
Review
The use of chemical compounds benefits society in a number of ways. Pesticides, for instance, enable foodstuffs to be produced in sufficient quantities to satisfy the needs of millions of people, a condition that has led to an increase in levels of life expectancy. Yet, at times, these benefits are offset by certain disadvantages, notably the toxic side effects of the chemical compounds used. Exposure to these compounds can have varying effects, ranging from instant death to a gradual process of chemical carcinogenesis. There are three stages involved in chemical carcinogenesis. These are defined as initiation, promotion and progression. Each of these stages is characterised by morphological and biochemical modifications and result from genetic and/or epigenetic alterations. These genetic modifications include: mutations in genes that control cell proliferation, cell death and DNA repair--i.e. mutations in proto-oncogenes and tumour suppressing genes. The epigenetic factors, also considered as being non-genetic in character, can also contribute to carcinogenesis via epigenetic mechanisms which silence gene expression. The control of responses to carcinogenesis through the application of several chemical, biochemical and biological techniques facilitates the identification of those basic mechanisms involved in neoplasic development. Experimental assays with laboratory animals, epidemiological studies and quick tests enable the identification of carcinogenic compounds, the dissection of many aspects of carcinogenesis, and the establishment of effective strategies to prevent the cancer which results from exposure to chemicals.
Topics: Animals; Carcinogens; Cell Transformation, Neoplastic; Humans; Neoplasms; Risk Factors
PubMed: 18066431
DOI: 10.1590/s0001-37652007000400004 -
EMBO Reports Mar 2015A key goal of cancer therapeutics is to selectively target the genetic lesions that initiate and maintain cancer cell proliferation and survival. While most cancers... (Review)
Review
A key goal of cancer therapeutics is to selectively target the genetic lesions that initiate and maintain cancer cell proliferation and survival. While most cancers harbor multiple oncogenic mutations, a wealth of preclinical and clinical data supports that many cancers are sensitive to inhibition of single oncogenes, a concept referred to as 'oncogene addiction'. Herein, we describe the clinical evidence supporting oncogene addiction and discuss common mechanistic themes emerging from the response and acquired resistance to oncogene-targeted therapies. Finally, we suggest several opportunities toward exploiting oncogene addiction to achieve curative cancer therapies.
Topics: Antineoplastic Agents; Cell Proliferation; Cell Survival; Drug Delivery Systems; Drug Resistance, Neoplasm; Genes, Essential; Humans; Models, Biological; Neoplasms; Oncogenes
PubMed: 25680965
DOI: 10.15252/embr.201439949 -
Environmental Science and Pollution... Sep 2022The etiology of the majority of human cancers is associated with a myriad of environmental causes, including physical, chemical, and biological factors. DNA damage... (Review)
Review
The etiology of the majority of human cancers is associated with a myriad of environmental causes, including physical, chemical, and biological factors. DNA damage induced by such mutagens is the initial step in the process of carcinogenesis resulting in the accumulation of mutations. Mutational events are considered the major triggers for introducing genetic and epigenetic insults such as DNA crosslinks, single- and double-strand DNA breaks, formation of DNA adducts, mismatched bases, modification in histones, DNA methylation, and microRNA alterations. However, DNA repair mechanisms are devoted to protect the DNA to ensure genetic stability, any aberrations in these calibrated mechanisms provoke cancer occurrence. Comprehensive knowledge of the type of mutagens and carcinogens and the influence of these agents in DNA damage and cancer induction is crucial to develop rational anticancer strategies. This review delineated the molecular mechanism of DNA damage and the repair pathways to provide a deep understanding of the molecular basis of mutagenicity and carcinogenicity. A relationship between DNA adduct formation and cancer incidence has also been summarized. The mechanistic basis of inflammatory response and oxidative damage triggered by mutagens in tumorigenesis has also been highlighted. We elucidated the interesting interplay between DNA damage response and immune system mechanisms. We addressed the current understanding of DNA repair targeted therapies and DNA damaging chemotherapeutic agents for cancer treatment and discussed how antiviral agents, anti-inflammatory drugs, and immunotherapeutic agents combined with traditional approaches lay the foundations for future cancer therapies.
Topics: Carcinogens; DNA; DNA Damage; DNA Repair; Humans; Mutagens; Neoplasms
PubMed: 34611806
DOI: 10.1007/s11356-021-16726-w -
Report on Carcinogens : Carcinogen... 2011
Topics: Animals; Asbestos; Carcinogens; Humans; Neoplasms
PubMed: 21836646
DOI: No ID Found