2021
DOI: 10.1038/d41586-021-00211-y
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Mutation alters chromatin changes during injury response to drive cancer

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Cited by 2 publications
(1 citation statement)
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“…Cancer cells diverged from inflamed epithelium by cell-autonomous transcriptional switches (e.g., NR1H4 − MYC + ) and by chromosomal instability (e.g., chr19 segmental aberrations), whereas retaining the memory of epithelial plasticity, suggestive of sustaining co-option of ‘wound healing’ programs akin to generalized CIACs 61 . The metaplastic subgroup (subtype I) peculiarly showed KRAS-related pathway activation, together with KRAS G12D -induced tumorigenesis in our metaplastic gallbladder organoid, implying the necessity of genomic aberrations for metaplasia-induced carcinogenesis, presumably via abnormal chromatin remodeling 62 . In comparison to the ordinarily slowly self-renewal gallbladder stem cells (once every ~625 days) 63 , inflammation spawns gallbladder transit-amplifying stem cells 64 , possibly further reprogrammed into tumor-initiating stem cells by persistent inflammatory signals (e.g., NF-κB as a master) 65 , which have been pervasively identified in subtype II mEPCs.…”
Section: Discussionmentioning
confidence: 80%
“…Cancer cells diverged from inflamed epithelium by cell-autonomous transcriptional switches (e.g., NR1H4 − MYC + ) and by chromosomal instability (e.g., chr19 segmental aberrations), whereas retaining the memory of epithelial plasticity, suggestive of sustaining co-option of ‘wound healing’ programs akin to generalized CIACs 61 . The metaplastic subgroup (subtype I) peculiarly showed KRAS-related pathway activation, together with KRAS G12D -induced tumorigenesis in our metaplastic gallbladder organoid, implying the necessity of genomic aberrations for metaplasia-induced carcinogenesis, presumably via abnormal chromatin remodeling 62 . In comparison to the ordinarily slowly self-renewal gallbladder stem cells (once every ~625 days) 63 , inflammation spawns gallbladder transit-amplifying stem cells 64 , possibly further reprogrammed into tumor-initiating stem cells by persistent inflammatory signals (e.g., NF-κB as a master) 65 , which have been pervasively identified in subtype II mEPCs.…”
Section: Discussionmentioning
confidence: 80%