期刊
MOLECULAR ONCOLOGY
卷 11, 期 1, 页码 79-96出版社
WILEY
DOI: 10.1016/j.molonc.2016.09.008
关键词
cancer; epigenetic; metastasis
类别
资金
- Medical Research Council
- Medical Research Council [MC_UP_1101/4, MC_UU_12022/7] Funding Source: researchfish
- MRC [MC_UU_12022/7] Funding Source: UKRI
Genetic analyses of cancer progression in patient samples and model systems have thus far failed to identify specific mutational drivers of metastasis. Yet, at least in experimental systems, metastatic cancer clones display stable traits that can facilitate progression through the many steps of metastasis. How cancer cells establish and maintain the transcriptional programmes required for metastasis remains mostly unknown. Emerging evidence suggests that metastatic traits may arise from epigenetically altered transcriptional output of the oncogenic signals that drive tumour initiation and early progression. Molecular dissection of such mechanisms remains a central challenge for a comprehensive understanding of the origins of metastasis.
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