PMID- 23293472
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130108
LR  - 20211021
IS  - 0971-6580 (Print)
IS  - 0976-5131 (Electronic)
IS  - 0971-6580 (Linking)
VI  - 19
IP  - 3
DP  - 2012 Sep
TI  - Tobacco exposure may enhance inflammation in prostate carcinoma patients: an 
      explorative study in north Indian population.
PG  - 310-8
LID - 10.4103/0971-6580.103681 [doi]
AB  - Prostate cancer is responsible for major deaths globally after lung cancer. 
      However, etiology of prostate cancer is still unknown. Individual risk and 
      incidence of prostate cancer may result from the interaction of genetic 
      susceptibility with exposure to environmental factors such as infectious agents, 
      tobacco, occupational exposure, dietary carcinogens, and/or hormonal imbalances 
      leading to injury of the prostate and to the development of chronic inflammation. 
      About 30% of all human cancers are caused by tobacco smoking and inhaled 
      pollutants. Inflammation is now regarded as an important hallmark of cancer. The 
      present study has been aimed to explore the pro-inflammatory levels in prostate 
      carcinoma patients by examining the serum levels of novel cytokine interleukin-18 
      (IL-18) expression in tobacco exposed population. A total of 578 (n = 284 biopsy 
      proven prostate cancer patients, n = 294 controls with and without tobacco 
      exposed population) were recruited. Serum IL-18 (Interleukin-18) level was done 
      by ELISA. The IL-18 levels between cancer patients and controls within same mode 
      tobacco exposure as tobacco smoking (overall) showed significant difference (P < 
      0.0001) and further we compared within stratified group, it significantly differ 
      (P < 0.0001) in bidi and cigarette smoking than control non users. Furthermore, 
      IL-18 levels in tobacco chewers (overall) with gutkha and khaini chewers showed 
      significant difference (P < 0.01) than controls non users. Moreover, the IL-18 
      levels between cancer patients and controls with in of combined mode chewers 
      smokers and alcohol (CSA), smokers with alcohol showed significant difference (P 
      < 0.01) than controls. The IL-18 levels also differed significantly (P < 0.05) 
      with smokers and chewers in higher stages of III and IV, and showed non 
      significant with in lower stages. Tobacco exposure enhance the inflammation in 
      prostate carcinoma patients in stratified group as it have been represented as a 
      risk factors in various cancers, but this study provide further its role that 
      seems to influence inflammation especially in prostate carcinoma.
FAU - Dwivedi, Shailendra
AU  - Dwivedi S
AD  - Department of Pharmacology and Therapeutics, Chhatrapati Sahuji Maharaj Medical 
      University (Erstwhile KGMU), Lucknow, India.
FAU - Goel, Apul
AU  - Goel A
FAU - Mandhani, Anil
AU  - Mandhani A
FAU - Khattri, Sanjay
AU  - Khattri S
FAU - Pant, Kamlesh Kumar
AU  - Pant KK
LA  - eng
PT  - Journal Article
PL  - India
TA  - Toxicol Int
JT  - Toxicology international
JID - 101191279
PMC - PMC3532779
OTO - NOTNLM
OT  - Interleukin-18
OT  - NF-KB
OT  - prostate cancer
OT  - tobacco chewers
OT  - tobacco smokers
COIS- Conflict of Interest: None declared.
EDAT- 2013/01/08 06:00
MHDA- 2013/01/08 06:01
PMCR- 2012/09/01
CRDT- 2013/01/08 06:00
PHST- 2013/01/08 06:00 [entrez]
PHST- 2013/01/08 06:00 [pubmed]
PHST- 2013/01/08 06:01 [medline]
PHST- 2012/09/01 00:00 [pmc-release]
AID - TI-19-310 [pii]
AID - 10.4103/0971-6580.103681 [doi]
PST - ppublish
SO  - Toxicol Int. 2012 Sep;19(3):310-8. doi: 10.4103/0971-6580.103681.