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Scaling Insulin-Producing Cells by Multiple Strategies
Eiji Yoshihara,Jinhyuk Choi,Fritz Cayabyab,Harvey Perez 대한내분비학회 2024 Endocrinology and metabolism Vol.39 No.2
In the quest to combat insulin-dependent diabetes mellitus (IDDM), allogenic pancreatic islet cell therapy sourced from deceased donors represents a significant therapeutic advance. However, the applicability of this approach is hampered by donor scarcity and the demand for sustained immunosuppression. Human induced pluripotent stem cells are a game-changing resource for generating synthetic functional insulin-producing β cells. In addition, novel methodologies allow the direct expansion of pancreatic progenitors and mature β cells, thereby circumventing prolonged differentiation. Nevertheless, achieving practical reproducibility and scalability presents a substantial challenge for this technology. As these innovative approaches become more prominent, it is crucial to thoroughly evaluate existing expansion techniques with an emphasis on their optimization and scalability. This manuscript delineates these cutting-edge advancements, offers a critical analysis of the prevailing strategies, and underscores pivotal challenges, including cost-efficiency and logistical issues. Our insights provide a roadmap, elucidating both the promises and the imperatives in harnessing the potential of these cellular therapies for IDDM.
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FXR Regulates Intestinal Cancer Stem Cell Proliferation
Fu, Ting,Coulter, Sally,Yoshihara, Eiji,Oh, Tae Gyu,Fang, Sungsoon,Cayabyab, Fritz,Zhu, Qiyun,Zhang, Tong,Leblanc, Mathias,Liu, Sihao,He, Mingxiao,Waizenegger, Wanda,Gasser, Emanuel,Schnabl, Bernd,Atk Elsevier 2019 Cell Vol.176 No.5
<P><B>Summary</B></P> <P>Increased levels of intestinal bile acids (BAs) are a risk factor for colorectal cancer (CRC). Here, we show that the convergence of dietary factors (high-fat diet) and dysregulated WNT signaling (APC mutation) alters BA profiles to drive malignant transformations in Lgr5-expressing (Lgr5<SUP>+</SUP>) cancer stem cells and promote an adenoma-to-adenocarcinoma progression. Mechanistically, we show that BAs that antagonize intestinal farnesoid X receptor (FXR) function, including tauro-β-muricholic acid (T-βMCA) and deoxycholic acid (DCA), induce proliferation and DNA damage in Lgr5<SUP>+</SUP> cells. Conversely, selective activation of intestinal FXR can restrict abnormal Lgr5<SUP>+</SUP> cell growth and curtail CRC progression. This unexpected role for FXR in coordinating intestinal self-renewal with BA levels implicates FXR as a potential therapeutic target for CRC.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Genetic and dietary risk factors for colorectal cancer converge on the BA-FXR axis </LI> <LI> FXR controls proliferating Lgr5<SUP>+</SUP> intestinal stem cells </LI> <LI> FXR agonists curtail colorectal cancer progression </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>
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