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1 apancreatic trypsinogen activation and cause hereditary pancreatitis.
2 trypsinogen (PRSS1) cause autosomal dominant hereditary pancreatitis.
3 e cationic trypsinogen gene in patients with hereditary pancreatitis.
4 trypsinogen activation are not the cause of hereditary pancreatitis.
5 ce of patients with sporadic pancreatitis or hereditary pancreatitis.
6 e cationic trypsinogen (Tg) of patients with hereditary pancreatitis.
7 s and one was proven by DNA analysis to have hereditary pancreatitis.
8 trypsinogen (Tg-1) has been associated with hereditary pancreatitis.
9 omechanism of the Asn-21 --> Ile mutation in hereditary pancreatitis.
10 lack of association of PRSS2 mutations with hereditary pancreatitis.
11 might be of pathophysiological relevance in hereditary pancreatitis, a human inborn disorder associa
12 SS1 are frequently detected in patients with hereditary pancreatitis, a rare genetic disease of the p
14 s in CKDN2A and PRSS1 mutation carriers with hereditary pancreatitis and at age 35 years in the setti
15 f PRSS1 mutations as pathogenic mediators of hereditary pancreatitis and indicate that persistent pan
17 ibition can contribute to the development of hereditary pancreatitis associated with the Arg(117) -->
18 tely 1% of people diagnosed with CP may have hereditary pancreatitis, associated with cationic trypsi
19 r hand, the results clearly demonstrate that hereditary pancreatitis-associated mutations do not lead
20 recombinant human cationic trypsinogen with hereditary pancreatitis-associated mutations N29I, N29T,
21 ine cationic trypsinogen or PRSS1 mutations (hereditary pancreatitis), BRCA2 mutations (usually in as
26 alization of the gene for autosomal dominant hereditary pancreatitis (HP) to a small region of the lo
29 trypsinogen mutants associated with classic hereditary pancreatitis (N29I, N29T, V39A, R122C, and R1
30 first trypsinogen mutation in families with hereditary pancreatitis, pancreatic genetics has made ra
31 ng all patients with Peutz-Jeghers syndrome, hereditary pancreatitis, patients with CDKN2A gene mutat
32 s hereditary breast ovarian cancer syndrome, hereditary pancreatitis, Peutz-Jeghers syndrome, familia
34 ivation, mutations in PRSS2 are not found in hereditary pancreatitis suggesting that activation of th
35 he disease-causing mutation in kindreds with hereditary pancreatitis that lack the previously identif
36 tic proteases have been previously linked to hereditary pancreatitis, this is the first known instanc
37 ations and the initiation and progression of hereditary pancreatitis, we have sought to generate a tr