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1  have increased levels of Cdc25A and develop hepatic cysts).
2 at somatic loss of Pkd1 results in renal and hepatic cysts.
3  intragenic, somatic mutations are common in hepatic cysts.
4 te cilia that regulate progressive growth of hepatic cysts.
5 ominant polycystic kidney disease, developed hepatic cysts.
6 95%, with internal septations present in the hepatic cysts.
7 recognized and treated differently than most hepatic cysts.
8                                              Hepatic cysts and bile duct proliferation, characteristi
9  Additionally, DEN(N2ICD) mice develop large hepatic cysts, dysplasia of the biliary epithelium, and
10                     More prominent in women, hepatic cysts emerge after the onset of puberty and dram
11 garding mechanism, the epithelium that lines hepatic cysts exhibited markedly higher levels of phosph
12 d by the gradual development of fluid-filled hepatic cysts formed from cholangiocytes and commonly re
13 ue of somatostatin known to inhibit cAMP) in hepatic cyst growth using an in vitro model of cystogene
14  would be positioned to modulate the rate of hepatic cyst growth.
15                      Volumes of total liver, hepatic cysts, hepatic parenchyma, and total kidney were
16  patients with polycystic liver disease with hepatic cysts identified by magnetic resonance imaging a
17 stic kidney disease (ADPKD) increases liver, hepatic cyst, or kidney volume.
18 by overlapping phenotypes, such as renal and hepatic cysts, skeletal defects, retinal degeneration an
19 arcinomas, metastases tumours, haemangiomas, hepatic cysts were chosen and evaluated.
20                                              Hepatic cysts were lined by single or multiple layers of
21 han 90% of patients older than 35 years have hepatic cysts, which may cause abdominal discomfort and
22 otopic liver transplantation for symptomatic hepatic cysts with excellent long-term results and minim