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Recent publication of Hegyi and Sahin-Tóth reported that CPA1 p.n256K mutant mice developed chronic pancreatitis (CP) through endoplasmic reticulum stress.1 This, along with other animal models based on CP genetic variants, revealed that the clinical course and mechanism of CP are better recapitulated with in vivo methods.2
Previously, we found that SPINK1 c.194+2T>C mutation is the most frequently observed variant in Chinese patients with idiopathic CP. Function of c.194+2T>C variant has been characterised through in vitro studies as resulting in the absence of serine protease inhibitor secretion.3 4 However, the unavailability of SPINK1 c.194+2T>C animal model hindered the study into its role in CP development. To date, the only in vivo study focused on phenotype of homozygous Spink1 (also known as Spink3) deleted mice and found that they died of autophagic acinar cell death within 15 days after birth.5 Considering over 80% of Chinese CP patients with SPINK1 c.194+2T>C variant carry heterozygous mutation,6 we hypothesise that a heterozygous c.194+2T>C variant animal model may practically sketch the clinical pattern of …
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