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IARC Monographs on the Evaluation of... 2000
Review
Topics: Animals; Carcinogens; Disease Models, Animal; Environmental Exposure; Ethanolamines; Female; Humans; Industrial Oils; Male; Maximum Allowable Concentration; Mice; Neoplasms; Rats; Reproduction
PubMed: 11100407
DOI: No ID Found -
IARC Monographs on the Evaluation of... 1999
Review
Topics: Animals; Carcinogenicity Tests; Carcinogens; Humans; Insecticides; Mutagenicity Tests; Mutagens; Neoplasms; Neoplasms, Experimental; Propane
PubMed: 10476458
DOI: No ID Found -
IARC Monographs on the Evaluation of... 1999
Review
Topics: Acetaldehyde; Animals; Carcinogenicity Tests; Carcinogens; Humans; Mutagenicity Tests; Mutagens; Neoplasms; Neoplasms, Experimental; Occupational Exposure
PubMed: 10476449
DOI: No ID Found -
IARC Monographs on the Evaluation of... 1999
Review
Topics: 2-Propanol; Animals; Carcinogenicity Tests; Carcinogens; Humans; Neoplasms; Neoplasms, Experimental; Occupational Exposure
PubMed: 10476373
DOI: No ID Found -
International Journal of Molecular... May 2022The tobacco-specific -nitrosamines 4-(-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) and '-nitrosonornicotine (NNN) always occur together and exclusively in tobacco... (Review)
Review
The tobacco-specific -nitrosamines 4-(-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) and '-nitrosonornicotine (NNN) always occur together and exclusively in tobacco products or in environments contaminated by tobacco smoke. They have been classified as "carcinogenic to humans" by the International Agency for Research on Cancer. In 1998, we published a review of the biochemistry, biology and carcinogenicity of tobacco-specific nitrosamines. Over the past 20 years, considerable progress has been made in our understanding of the mechanisms of metabolism and DNA adduct formation by these two important carcinogens, along with progress on their carcinogenicity and mutagenicity. In this review, we aim to provide an update on the carcinogenicity and mechanisms of the metabolism and DNA interactions of NNK and NNN.
Topics: Carcinogens; DNA Adducts; Humans; Nitrosamines; Nicotiana; Tobacco Products
PubMed: 35563500
DOI: 10.3390/ijms23095109 -
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 -
Oncogene Mar 2020Insulin-like growth factor (IGF) binding protein 2 (IGFBP2) was discovered and identified as an IGF system regulator, controlling the distribution, function, and... (Review)
Review
Insulin-like growth factor (IGF) binding protein 2 (IGFBP2) was discovered and identified as an IGF system regulator, controlling the distribution, function, and activity of IGFs in the pericellular space. IGFBP2 is a developmentally regulated gene that is highly expressed in embryonic and fetal tissues and markedly decreases after birth. Studies over the last decades have shown that in solid tumors, IGFBP2 is upregulated and promotes several key oncogenic processes, such as epithelial-to-mesenchymal transition, cellular migration, invasion, angiogenesis, stemness, transcriptional activation, and epigenetic programming via signaling that is often independent of IGFs. Growing evidence indicates that aberrant expression of IGFBP2 in cancer acts as a hub of an oncogenic network, integrating multiple cancer signaling pathways and serving as a potential therapeutic target for cancer treatment.
Topics: Gene Expression Regulation, Neoplastic; Humans; Insulin-Like Growth Factor Binding Protein 2; Oncogenes; Signal Transduction
PubMed: 31925333
DOI: 10.1038/s41388-020-1154-2 -
Comptes Rendus Biologies Sep 2023Replication stress is an alteration in the progression of replication forks caused by a variety of events of endogenous or exogenous origin. In precancerous lesions,... (Review)
Review
Replication stress is an alteration in the progression of replication forks caused by a variety of events of endogenous or exogenous origin. In precancerous lesions, this stress is exacerbated by the deregulation of oncogenic pathways, which notably disrupts the coordination between replication and transcription, and leads to genetic instability and cancer development. It is now well established that transcription can interfere with genome replication in different ways, such as head-on collisions between polymerases, accumulation of positive DNA supercoils or formation of R-loops. These structures form during transcription when nascent RNA reanneals with DNA behind the RNA polymerase, forming a stable DNA:RNA hybrid. In this review, we discuss how these different cotranscriptional processes disrupt the progression of replication forks and how they contribute to genetic instability in cancer cells.
Topics: Transcription, Genetic; R-Loop Structures; DNA Replication; DNA; Oncogenes; RNA; Neoplasms
PubMed: 37779381
DOI: 10.5802/crbiol.123 -
Report on Carcinogens : Carcinogen... 2011
Topics: Animals; Carcinogens; Humans; Neoplasms; Phenylenediamines
PubMed: 21850141
DOI: No ID Found -
Report on Carcinogens : Carcinogen... 2011
Topics: Animals; Carcinogens; Chloroform; Humans; Neoplasms; Solvents
PubMed: 21850127
DOI: No ID Found