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1 e (ERK) 1/2 pathway stimulates the growth of liver cysts.
2 cystic area and a nonsignificant decrease in liver cysts.
3 form cyst formation and presence of adjacent liver cysts.
4 onophosphate (cAMP) in cholangiocytes lining liver cysts.
5 y disease that exhibit cholangiocyte-derived liver cysts.
6 ence, mutant hepatocystin is undetectable in liver cysts.
7 cm for solid nodules and 14 cm for solitary liver cysts.
8 brosis and portal hypertension as well as of liver cysts.
9 ant, resulting in a significant reduction in liver cysts.
10 cysts, limited kidney insufficiency, and few liver cysts.
11 1 %) patients underwent only fenestration of liver cysts.
13 th non-enlarged cystic kidneys and few or no liver cysts; 8 subjects reached end-stage kidney disease
15 predisposing to the combination of renal and liver cysts (AD-PKD1 and AD-PKD2) and mutations in a thi
16 Patients typically have hypertension and liver cysts, and 9% to 14% develop intracranial aneurysm
17 This disease is characterized by renal and liver cysts, and cardiovascular extrarenal manifestation
18 imary biliary cirrhosis, cholangiocarcinoma, liver cysts, and in the progression of biliary fibrosis
20 Sorafenib caused an unexpected increase in liver cyst area, cell proliferation (Ki67), and expressi
21 nhibitor rapamycin significantly reduced the liver cyst area, liver/body weight ratio, pericystic mic
22 sease (ARPKD), develop cholangiocyte-derived liver cysts associated with increased intracellular aden
26 GFR-2 inhibitor SU5416 significantly reduced liver cyst development, liver/body weight ratio, and exp
27 antly at increased risk of having any kidney/liver cyst diagnosis (Odds Ratio 2.42, 95% confidence in
30 conditions, electron microscopy of the ADPKD liver cyst epithelium revealed morphological features si
33 immunosorbent assay analysis of human ADPKD liver cyst fluid detected epithelial neutrophil attracta
35 he changes in signaling pathways involved in liver cyst formation and progression, and their impact o
36 kd2, and to provide evidence that kidney and liver cyst formation associated with Pkd2 deficiency occ
39 atment of liver and kidney cancers, inhibits liver cyst growth in PC2-defective mice, we treated PC2
40 hat there are common cellular mechanisms for liver cyst growth regardless of the underlying genetic c
41 thelial growth factor (VEGF), which promotes liver cyst growth via autocrine and paracrine mechanisms
42 Although the minimally invasive treatment of liver cysts has been reported, the laparoscopic approach
43 gle patient suffering from multiple infected liver cysts has provided the opportunity to observe and
45 ro and in vivo, as shown by the reduction of liver cysts in mice treated with combined octreotide and
48 multiple extrarenal complications, including liver cysts, intracranial aneurysms, and cardiac valvula
51 When given to epithelial cells isolated from liver cysts of Pkd2cKO mice (Pkd2cKO-cells), sorafenib p
52 polycystic liver disease (PCLD) consists of liver cysts that are radiologically and pathologically i
54 lesions were renal cysts, liver hemangiomas, liver cysts, thyroid nodules, and uterine leiomyomas.
59 isolated intrahepatic bile ducts (IBDUs) and liver cysts was analyzed by confocal and immunoelectron