Nr5a2 maintains acinar cell differentiation and constrains oncogenic Kras-mediated pancreatic neoplastic initiation (original) (raw)

“…The PdxCre late transgene is effective after the MPC stage, because β-galactosidase-labeled ductal cells have been rarely observed in PdxCre late ;R26R mice (Heiser et al, 2006). The effects of NR5A2-depletion at the post-MPC stage appear restricted to the completion of acinar differentiation and are consistent with the need for maintenance of acinar cell identity (Holmstrom et al, 2011;Flandez et al, 2014;von Figura et al, 2014).…”

Section: Discussionmentioning

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“…The PdxCre late transgene is effective after the MPC stage, because β-galactosidase-labeled ductal cells have been rarely observed in PdxCre late ;R26R mice (Heiser et al, 2006). The effects of NR5A2-depletion at the post-MPC stage appear restricted to the completion of acinar differentiation and are consistent with the need for maintenance of acinar cell identity (Holmstrom et al, 2011;Flandez et al, 2014;von Figura et al, 2014).…”

Section: Discussionmentioning

“…Cre , although some impairment of acinar terminal development was evident (von Figura et al, 2014). The PdxCre late transgene is effective after the MPC stage, because β-galactosidase-labeled ductal cells have been rarely observed in PdxCre late ;R26R mice (Heiser et al, 2006).…”

Section: Discussionmentioning

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“…Common variants of these genes have also been associated with risk of obesity (81) and type II diabetes (40,91) or fasting glucose level (60). On the other hand, emerging evidence suggest that these genes also act as an oncogene or tumor suppressor gene in pancreatic carcinogenesis (8,25,41,92). It is conceivable that genes involved in organ development and differentiation may contribute to the ability of tumor cells to proliferate and evade cell death as well as reprogram progenitor cells to a state that give rise to a tumor (64).…”

Section: Genetic Factorsmentioning