Degradation of SARS-CoV-2 Receptor ACE2 by Tobacco Carcinogens

2020 ◽  
Author(s):  
Gui-Zhen Wang ◽  
Qun Zhao ◽  
Fan Liang ◽  
Chen Zhang ◽  
Hui Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
2004 ◽  
Vol 43 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Claudia I Henschke ◽  
Olli S Miettinen
Keyword(s):  

ISRN Oncology ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Rajiv Lochan ◽  
Helen L. Reeves ◽  
Anne K. Daly ◽  
Richard M. Charnley

The extremely poor outcome from pancreas cancer is well known. However, its aetiology less well appreciated, and the molecular mechanisms underlying this are poorly understood. Tobacco usage is one of the strongest risk factors for this disease, and this is a completely avoidable hazard. In addition, there are well described hereditary diseases which predispose, and familial pancreas cancer. We have sought here to summarise the role of tobacco-derived carcinogens and the mode of their tumorigenic action on the pancreas. There is compelling evidence from animal and human studies (laboratory including cell line studies and epidemiologic) that tobacco derived carcinogens cause pancreas cancer. However, the manner in which they do so is not entirely apparent. There is also compelling evidence that synergism with genetic and other life-style factors—like diet obesity—results in a multifactorial causation of the disease. Ascertaining the role of tobacco carcinogens in the development of this cancer and their interaction with other risk factors will enable novel therapeutic and preventative strategies to improve outcome from this appalling malignancy.


2016 ◽  
Author(s):  
Ludmil B. Alexandrov ◽  
Young Seok Ju ◽  
Kerstin Haase ◽  
Peter Van Loo ◽  
Iñigo Martincorena ◽  
...  

ABSTRACTTobacco smoking increases the risk of at least 15 classes of cancer. We analyzed somatic mutations and DNA methylation in 5,243 cancers of types for which tobacco smoking confers an elevated risk. Smoking is associated with increased mutation burdens of multiple distinct mutational signatures, which contribute to different extents in different cancers. One of these signatures, mainly found in cancers derived from tissues directly exposed to tobacco smoke, is attributable to misreplication of DNA damage caused by tobacco carcinogens. Others likely reflect indirect activation of DNA editing by APOBEC cytidine deaminases and of an endogenous clock-like mutational process. The results are consistent with the proposition that smoking increases cancer risk by increasing the somatic mutation load, although direct evidence for this mechanism is lacking in some smoking-related cancer types.ONE SENTENCE SUMMARYMultiple distinct mutational processes associate with tobacco smoking in cancer reflecting direct and indirect effects of tobacco smoke.


2005 ◽  
Vol 65 (18) ◽  
pp. 8548-8557 ◽  
Author(s):  
C. Clifford Conaway ◽  
Chung-Xiou Wang ◽  
Brian Pittman ◽  
Yang-Ming Yang ◽  
Joel E. Schwartz ◽  
...  

Author(s):  
Mario Pepe ◽  
Francesco Pelizza ◽  
Anne-Sophie Lamort ◽  
Nikolaos I. Kanellakis ◽  
Georgios T. Stathopoulos

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