期刊
PHYSIOLOGY
卷 23, 期 6, 页码 350-359出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physiol.00031.2008
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资金
- National Cancer Institute [1U54 CA-126513, RO1 CA-093405, R01 CA-120979]
- Mildred-Scheel-Stiftung, Deutsche Krebshilfe, Germany
Chronic inflammation-induced carcinogenesis is a commonly accepted entity and is frequently seen within the gastrointestinal tract, although the underlying mechanisms remain unclear. Alterations in specific oncogenes and tumor suppressor genes are known to be responsible for malignant transformation. Nevertheless, the inflammatory microenvironment classically affects tumor promotion in its role as an altered stem cell niche and can also affect tumor initiation and tumor progression. The origin of the tumor cells is often attributed to stem cells, a unique subpopulation within tumors that possess the ability to initiate tumor growth and sustain self-renewal, as well as is largely responsible for their metastatic potential. Here, we review the link between inflammation and gastrointestinal carcinogenesis and the relationship between stem cells and cancer stem cells.
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