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1 d in livers of animal models and humans with polycystic liver disease.
2 Mutations in polycystins are a cause of polycystic liver disease.
3 tal diseases including Alagille Syndrome and polycystic liver disease.
4 gous gene models of human autosomal dominant polycystic liver disease.
5 ibitors might be used to treat patients with polycystic liver disease.
6 ese proteins might inhibit cyst expansion in polycystic liver disease.
7 regulator of cell proliferation may underlie polycystic liver disease.
8 mortalized B lymphoblasts from patients with polycystic liver disease.
9 mic reticulum (ER), cause autosomal dominant polycystic liver disease.
10 hen mutated, causes human autosomal dominant polycystic liver disease.
11 presents a potential therapeutic approach in polycystic liver disease.
12 ogenic variants sometimes resulted in severe polycystic liver disease.
13 cyst epithelium of a subset of patients with polycystic liver disease.
14 Mutations in PC2 are associated with polycystic liver diseases.
15 ts with breast abnormalities, 1 patient with polycystic liver disease, 1 patient with esophageal thic
17 nical profile of isolated autosomal dominant polycystic liver disease (ADPLD) using nonaffected famil
19 ficant cause of ESRD, and autosomal dominant polycystic liver diseases (ADPLD), which result in signi
22 in vitro key features of Alagille syndrome, polycystic liver disease and cystic fibrosis (CF)-associ
23 have been associated with autosomal dominant polycystic liver disease and implicated in ADPKD, while
24 e previously been described in patients with polycystic liver disease and in some cases cystic kidney
25 olycystic kidney disease, autosomal dominant polycystic liver disease, and the third form of ADPKD.
26 al history, manifestations, and treatment of polycystic liver disease are based on the disease as it
27 underdiagnosed and genetically distinct from polycystic liver disease associated with ADPKD but with
28 y-eight of the 49 individuals diagnosed with polycystic liver disease before participation in the stu
30 ith extensive hepatic involvement with adult polycystic liver disease can have an excellent outcome w
31 ylase 6 inhibitors in cholangiocarcinoma and polycystic liver disease cells demonstrated synergistic
34 whereas in isolated PCLD (autosomal dominant polycystic liver disease), disrupted cell adhesion may b
35 lysis of a randomized trial of patients with polycystic liver disease due to ADPKD, lanreotide for 12
36 osomal dominant polycystic kidney disease or polycystic liver disease; efficacy does not depend on si
38 ative or indeterminate diagnosis, those with polycystic liver disease had slightly higher levels of s
39 hort of 265 patients with autosomal dominant polycystic liver disease harboring pathogenic variants i
42 Mutations in the gene encoding SEC63 cause polycystic liver disease in humans; however, it is not c
43 al presentation and histological features of polycystic liver disease in the presence or absence of A
44 ycystic kidney disease or autosomal dominant polycystic liver disease, indicating that there are comm
45 pies to delay progression of kidney disease; polycystic liver disease; intracranial aneurysms and oth
56 resent a therapeutic route for patients with polycystic liver disease, most of whom would not be amen
57 ion and biochemical properties of normal and polycystic liver disease mutant forms of hepatocystin we
58 ns were solitary giant liver cysts (n = 16), polycystic liver disease (n = 9), hydatid cyst (n = 6),
59 al hepatic fibrosis (two), cystinosis (one), polycystic liver disease (one), A-1-A deficiency (one),
60 ng mutation in hepatocystin observed in some polycystic liver disease patients produces a protein tha
61 seen in the rare inherited disorder isolated polycystic liver disease (PCLD) and are recognized as th
65 mains the curative treatment for symptomatic Polycystic Liver Disease (PCLD) patients and is associat
67 of resective and fenestration procedures for polycystic liver disease (PCLD), we present the first se
70 resent review summarizes recent knowledge on polycystic liver diseases (PCLDs), mechanisms of hepatic
78 c tools or biomarkers are urgently needed in polycystic liver disease (PLD) to monitor disease progre
79 ical trials have shown that in patients with polycystic liver disease (PLD), short-term treatment wit
82 ncreased level of intracranial aneurysms and polycystic liver disease (PLD), which can be severe and
87 malized age-adjusted total liver volumes and polycystic liver disease-related hospitalization (liver
92 ly unresolved clinical diagnosis of ADPKD or polycystic liver disease to identify a candidate gene, A
93 d from healthy individuals and patients with polycystic liver disease to reproduce the effects of the
94 s analysis, we studied the 175 patients with polycystic liver disease with hepatic cysts identified b