TY - JOUR
T1 - Tobacco Smoking and Liver Cancer Risk
T2 - Potential Avenues for Carcinogenesis
AU - Jain, Divya
AU - Chaudhary, Priya
AU - Varshney, Nidhi
AU - Bin Razzak, Khandaker Sabit
AU - Verma, Devret
AU - Khan Zahra, Tasnim Reza
AU - Janmeda, Pracheta
AU - Sharifi-Rad, Javad
AU - Daştan, Sevgi Durna
AU - Mahmud, Shafi
AU - Docea, Anca Oana
AU - Calina, Daniela
N1 - Publisher Copyright:
© 2021 Divya Jain et al.
PY - 2021
Y1 - 2021
N2 - Smoking a cigarette generates over 4000 chemicals that have a deleterious impact on each part of the human body. It produces three main severe effects on the liver organ: oncogenic, immunological, and indirect or direct toxic effects. It results in the production of cytotoxic substances, which raises fibrosis and necro-inflammation. Additionally, it also directs the production of pro-inflammatory cytokines tumour necrosis factor alfa (TNF-α) and interleukins (IL-1β, IL-6) that will be responsible for the chronic liver injury. Furthermore, it gives rise to secondary polycythemia and successively raises the turnover and mass of red cells, which might be a common factor responsible for the development of oxidative stress in the liver due to iron overload. It also produces chemicals that are having oncogenic properties and raises the risk of liver cancer especially in sufferers of chronic hepatitis C. Smoking modulates both humoral and cell-mediated responses by restricting the proliferation of lymphocytes and inducing their apoptosis and ultimately decreasing the surveillance of cancer cells. Moreover, it has been determined that heavy smoking impacts the response of hepatitis C patients to interferon (IFN) therapy through different mechanisms, which can be improved by phlebotomy. Efforts are being made in different nations in decreasing the prevalence of smoking to improve premature death and ill effects of their nation's individuals.
AB - Smoking a cigarette generates over 4000 chemicals that have a deleterious impact on each part of the human body. It produces three main severe effects on the liver organ: oncogenic, immunological, and indirect or direct toxic effects. It results in the production of cytotoxic substances, which raises fibrosis and necro-inflammation. Additionally, it also directs the production of pro-inflammatory cytokines tumour necrosis factor alfa (TNF-α) and interleukins (IL-1β, IL-6) that will be responsible for the chronic liver injury. Furthermore, it gives rise to secondary polycythemia and successively raises the turnover and mass of red cells, which might be a common factor responsible for the development of oxidative stress in the liver due to iron overload. It also produces chemicals that are having oncogenic properties and raises the risk of liver cancer especially in sufferers of chronic hepatitis C. Smoking modulates both humoral and cell-mediated responses by restricting the proliferation of lymphocytes and inducing their apoptosis and ultimately decreasing the surveillance of cancer cells. Moreover, it has been determined that heavy smoking impacts the response of hepatitis C patients to interferon (IFN) therapy through different mechanisms, which can be improved by phlebotomy. Efforts are being made in different nations in decreasing the prevalence of smoking to improve premature death and ill effects of their nation's individuals.
UR - https://www.scopus.com/pages/publications/85122256870
U2 - 10.1155/2021/5905357
DO - 10.1155/2021/5905357
M3 - Artículo de revisión
AN - SCOPUS:85122256870
SN - 1687-8450
VL - 2021
JO - Journal of Oncology
JF - Journal of Oncology
M1 - 5905357
ER -