期刊
CELL CYCLE
卷 8, 期 3, 页码 383-390出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.8.3.7542
关键词
epigenetics; epigenetic progenitor model; imprinting; colorectal cancer; signal transduction
类别
资金
- NIH [CA65145]
Our recent study of the mechanism by which an epigenetic alteration, loss of imprinting (LOI) of Igf2, increases tumor risk, revealed a strong relationship between IGF2 dosage, the dynamics of signaling along the IGF2 axis, cell proliferation and tumor risk. 1 Colon epithelia in a mouse model with LOI of Igf2 showed increased sensitivity to IGF1R blockade and abrogation of premalignant lesion development in LOI(+) mice. These results are consistent with the epigenetic progenitor model of cancer, 2 in which epigenetic changes precede and heighten risk of cancer in response to oncogenic mutations. Thus, one can envision a highly targeted and focused chemoprevention strategy targeted to signaling pathways in nonmalignant cells that have undergone an epigenetic lesion, rather than a broad approach toward reversing epigenetic lesions that may have unintended consequences affecting the whole epigenome.
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