期刊
CURRENT OPINION IN GENETICS & DEVELOPMENT
卷 18, 期 1, 页码 11-18出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.gde.2007.12.007
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资金
- NCI NIH HHS [R01 CA115880-01A1, R01CA84232, R01 CA115880-02, R01 CA084232, R01 CA115880-03, R01 CA115880, R01CA118550] Funding Source: Medline
Precancerous and malignant cells can induce an immune response which results in the destruction of transformed and/or malignant cells, a process known as immune surveillance. However, immune surveillance is not always successful, resulting in 'edited' tumors that have escaped immune surveillance. Immunoediting is not simply because of the absence of antitumor immunity, but is because of protumor immunity that blocks antitumor adaptive and innate responses, and promotes conditions that favor tumor progression. Several immune protumor effector mechanisms are upregulated by chronic inflammation, leading to the hypothesis that inflammation promotes carcinogenesis and tumor growth by altering the balance between protumor and antitumor immunity, thereby preventing the immune system from rejecting malignant cells, and providing a tumor-friendly environment for progressive disease.
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