期刊
NATURE GENETICS
卷 47, 期 9, 页码 1038-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.3357
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资金
- National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre
- Cancer Research UK
- Medical Research Council
- Cancer Research UK [15874] Funding Source: researchfish
- Medical Research Council [G1002565] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0611-10065, 05/12/01] Funding Source: researchfish
- Versus Arthritis
- Cancer Research UK [20406] Funding Source: researchfish
- MRC [G1002565] Funding Source: UKRI
The molecular genetic relationship between esophageal adenocarcinoma (EAC) and its precursor lesion, Barrett's esophagus, is poorly understood. Using whole-genome sequencing on 23 paired Barrett's esophagus and EAC samples, together with one in-depth Barrett's esophagus case study sampled over time and space, we have provided the following new insights: (i) Barrett's esophagus is polyclonal and highly mutated even in the absence of dysplasia; (ii) when cancer develops, copy number increases and heterogeneity persists such that the spectrum of mutations often shows surprisingly little overlap between EAC and adjacent Barrett's esophagus; and (iii) despite differences in specific coding mutations, the mutational context suggests a common causative insult underlying these two conditions. From a clinical perspective, the histopathological assessment of dysplasia appears to be a poor reflection of the molecular disarray within the Barrett's epithelium, and a molecular Cytosponge technique overcomes sampling bias and has the capacity to reflect the entire clonal architecture.
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