Interplay between inflammation and cancer

被引:0
|
作者
Khandia, Rekha [1 ]
Munjal, Ashok [1 ]
机构
[1] Barkatullah Univ, Dept Genet, Bhopal, Madhya Pradesh, India
来源
关键词
TRAIL-INDUCED APOPTOSIS; INFILTRATING DENDRITIC CELLS; MEDIATED UP-REGULATION; NF-KAPPA-B; BREAST-CANCER; COLORECTAL-CANCER; DEATH RECEPTORS; T-CELLS; MACROPHAGE POLARIZATION; TRICHOMONAS-VAGINALIS;
D O I
10.1016/bs.apcsb.2019.09.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
During the 19th century, for the first time, the linkage between inflammation and cancer was established. Inflammatory microenvironment is an essential component of the tumor microenvironment. Chronic inflammation due to persistent infection due to the microbes, viruses, helminths or constant exposure to non-infectious factors like smoke, silica or asbestos eventually might result in carcinogenesis. In tumor microenvironment, various inflammatory cells such as T lymphocytes (occasionally B cells), dendritic cells, macrophages, monocytes, neutrophils and natural killer (NK) cells are present. As a mediator of immune surveillance and host defense TRAIL cytokines are produced which upon binding with death receptors (DRs) initiate a cascade of apoptotic pathways. Anti-inflammatory drugs such as aspirin, celecoxib, diclofenac, diflunisal and ibuprofen etc. are being used against cancer, indicating the interplay between both the mechanisms. A deeper understanding of common pathways implicated between both the inflammation and cancer may pave the way to fight against both of these deleterious ailments.
引用
收藏
页码:199 / 245
页数:47
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