医学
信号转导
贾纳斯激酶
结直肠癌
自噬
癌症研究
PI3K/AKT/mTOR通路
炎症性肠病
结肠炎
疾病
免疫学
生物信息学
癌症
内科学
细胞因子
细胞生物学
细胞凋亡
生物
遗传学
标识
DOI:10.1016/j.dld.2022.08.012
摘要
Long-term colitis in people with inflammatory bowel disease (IBD) may lead to colon cancer called colitis-associated colorectal cancer (CAC). Since the advent of preclinical prototypes of CAC, various immunological messaging cascades have been identified as implicated in developing this disease. The toll-like receptor (TLR)s, Janus kinase (JAK)-signal transducer and activator of transcription (STAT), Nuclear factor-kappa B (NF-κB), mammalian target of rapamycin complex (mTOR), autophagy, and oxidative stress are only a few of the molecular mechanisms that have been recognized as major components to CAC progression. These pathways may also represent attractive medicinal candidates for the prevention and management of CAC. CAC signaling mechanisms at the molecular level and how their dysregulation may cause illness are summarized in this comprehensive overview.
科研通智能强力驱动
Strongly Powered by AbleSci AI