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1 holangiocyte proliferation, and intrahepatic cholangiocarcinoma.
2 patients with previously treated IDH1-mutant cholangiocarcinoma.
3 nd plays a novel role in the pathogenesis of cholangiocarcinoma.
4 itaxel in blocking metastatic progression of cholangiocarcinoma.
5 t proteins on the cell surface of a model of cholangiocarcinoma.
6 ndergo a major liver resection for perihilar cholangiocarcinoma.
7 n patients with hepatocellular carcinoma and cholangiocarcinoma.
8 pressed in DRs of human cirrhotic livers and cholangiocarcinoma.
9 thologic examination, 10 patients (2.5%) had cholangiocarcinoma.
10 has potential as a therapeutic strategy for cholangiocarcinoma.
11 elp to identify novel therapeutic targets in cholangiocarcinoma.
12 oma with stem cell features and intrahepatic cholangiocarcinoma.
13 way is upregulated in patients with sporadic cholangiocarcinoma.
14 erations are involved in the pathogenesis of cholangiocarcinoma.
15 erihilar but not with intrahepatic or distal cholangiocarcinoma.
16 ting, and visualization for the treatment of cholangiocarcinoma.
17 mation and tumor burden in a murine model of cholangiocarcinoma.
18 tly decreased in malignancy, particularly in cholangiocarcinoma.
19 transformation and an origin of intrahepatic cholangiocarcinoma.
20 ting IDH1 mutations in advanced, IDH1-mutant cholangiocarcinoma.
21 Exclusion criteria were combined HCC and cholangiocarcinoma.
22 cular mechanisms of the miR-17-92 cluster in cholangiocarcinoma.
23 this model as well as in human intrahepatic cholangiocarcinoma.
24 erly assess liver masses in this setting for cholangiocarcinoma.
25 hepatic lithiasis, septic complications, and cholangiocarcinoma.
26 tic cholangiocarcinoma (ICC) or extrahepatic cholangiocarcinoma.
27 ocarcinoma and a combined hepatocellular and cholangiocarcinoma.
28 may be a potential therapeutic approach for cholangiocarcinoma.
29 hepatocellular carcinoma (HCC) and mixed HCC-cholangiocarcinoma.
30 gical characteristic similar to extrahepatic cholangiocarcinoma.
31 enhancement of cell migration in metastatic cholangiocarcinoma.
32 mixed hepatocellular carcinoma-mass-forming cholangiocarcinoma.
33 acute myeloid leukemia (AML), melanoma, and cholangiocarcinoma.
34 ell tolerated option for patients with mIDH1-cholangiocarcinoma.
35 ly treated nonresectable or metastatic mIDH1-cholangiocarcinoma.
36 cholangiocarcinomas, especially intrahepatic cholangiocarcinoma.
37 cellular carcinoma and 20% were intrahepatic cholangiocarcinoma.
38 zymes with clinico-radiological suspicion of cholangiocarcinoma.
39 2 occur in approximately 15% of intrahepatic cholangiocarcinomas.
40 (IDH) is recurrently mutated in intrahepatic cholangiocarcinomas.
41 utations may represent a distinct subtype of cholangiocarcinomas.
42 the genetic characterization of intrahepatic cholangiocarcinomas.
43 s encoding metabolic enzymes in intrahepatic cholangiocarcinomas.
44 stinction absent in ampullary carcinomas and cholangiocarcinomas.
45 he course of tissue injury, TAA also induced cholangiocarcinomas.
46 also reduce the number and size of attendant cholangiocarcinomas.
47 OR], 0.46 [95% CI, 0.35-0.61]; P < .001) and cholangiocarcinoma (2.6% vs 4.2% OR, 0.62 [95% CI, 0.35-
48 on-CRC = 37 (ocular/cutaneous melanoma = 32, cholangiocarcinoma = 3, appendiceal = 1, and breast = 1)
51 is a biomarker of increased invasiveness in cholangiocarcinoma, a primary liver cancer with scarce t
52 roximately 13% of patients with intrahepatic cholangiocarcinoma, a relatively uncommon cancer with a
53 curative in selected patients with perihilar cholangiocarcinoma after neoadjuvant chemoradiotherapy.
55 also evidence of mTOR pathway activation in cholangiocarcinoma, although its biological significance
56 implications of the finding in diagnosis of cholangiocarcinoma and 1.2 kb product in hepatobiliary d
57 Two false-positive cases of LR-5 included a cholangiocarcinoma and a combined hepatocellular and cho
58 S100A4 as a candidate therapeutic target in cholangiocarcinoma and establish a mechanistic rationale
59 inoma (HCC) and biliary tract cancers (i.e., cholangiocarcinoma and gallbladder carcinoma) are associ
60 Asia, there is an unprecedented link between cholangiocarcinoma and infection with the liver fluke Op
61 a novel tumor-suppressor role of miR-101 in cholangiocarcinoma and it suggests the possibility of ta
62 apoptosis through a Fas-related mechanism in cholangiocarcinoma and other cancer cell lines possibly
63 of human individuals with pancreatic cancer, cholangiocarcinoma and other malignant diseases of the b
65 and RUFY2-RET in lung cancer, FGFR2-CREB5 in cholangiocarcinoma and PPL-NTRK1 in thyroid carcinoma.
67 ned that macrophages generate WNT ligands in cholangiocarcinomas and depletion or inhibition of this
68 number of intrahepatic, perihilar and distal cholangiocarcinomas and gallbladder cancers in Japanese
69 increased risk of malignancy (in particular, cholangiocarcinoma) and biliary tract stone formation.
70 hepatocellular carcinoma, 1 had mass-forming cholangiocarcinoma, and 1 had mixed hepatocellular carci
71 liary obstruction is obligatory in perihilar cholangiocarcinoma, and advanced cytological tests such
72 astoma, acute myeloid leukemia, intrahepatic cholangiocarcinoma, and chondrosarcomas, led to intense
73 iple cancers, including lung adenocarcinoma, cholangiocarcinoma, and glioblastoma, is driving efforts
76 or exclusively on hepatolithiasis-associated cholangiocarcinoma, and those published in a language ot
77 only modest sensitivity for the diagnosis of cholangiocarcinoma, and treatment of biliary strictures
79 ng hepatocellular carcinoma and intrahepatic cholangiocarcinoma, are leading causes of cancer-related
80 Clinicians need to be aware of intrahepatic cholangiocarcinomas arising in cirrhosis and properly as
83 progresses slowly compared with intrahepatic cholangiocarcinoma because of surgical complexity and lo
84 , we found that primary cilia are reduced in cholangiocarcinoma by a mechanism involving histone deac
86 LC subtypes: hepatocellular carcinoma (HCC), cholangiocarcinoma (CC) and combined HCC/CC (CHC) tumors
88 ival were male sex, donor and recipient age, cholangiocarcinoma (CC) at LT, non-DBD donor and reduced
89 ith mixed hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC) characteristics that have a more
93 ding both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC), suggestive of progenitor cell o
96 ver tumors (angiosarcoma of the liver (ASL), cholangiocarcinoma (CCA) and hepatocellular carcinoma (H
97 rted that cilia are significantly reduced in cholangiocarcinoma (CCA) and that the experimental decil
98 Pancreatic ductal adenocarcinoma (PDAC) and cholangiocarcinoma (CCA) are both deadly cancers and the
101 the following intrahepatic and extrahepatic cholangiocarcinoma (CCA) cell lines, Mz-ChA-1, TFK-1, SG
102 ever, whether EF24 has anticancer effects on cholangiocarcinoma (CCA) cells and the mechanisms remain
106 s such as hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) has significantly changed in th
107 n of Carcinogenic Risks to Humans, 2012) for cholangiocarcinoma (CCA) in the Lower Mekong River Basin
119 limitation for the treatment of unresectable cholangiocarcinoma (CCA) is its poor response to chemoth
120 useful in the treatment of several cancers, cholangiocarcinoma (CCA) is refractory to this drug.
122 cancer liver metastases (CRCLM) and primary cholangiocarcinoma (CCA) models in BALB/c nude mice usin
126 etection of the highly aggressive malignancy cholangiocarcinoma (CCA) remains a challenge but has the
129 n of cancer-associated myofibroblasts within cholangiocarcinoma (CCA) stroma as well as their therape
130 h ErbB receptors have been widely studied in cholangiocarcinoma (CCA), a malignancy of the biliary tr
131 Notch and Wnt signaling are known drivers of cholangiocarcinoma (CCA), but the underlying factors tha
151 liary disease is linked to malignant cancer (cholangiocarcinoma, CCA) and affects millions of people
154 e-scale analysis, we implanted 93 HCCs and 8 cholangiocarcinomas (CCAs) to systematically analyze hos
157 ate into hepatocellular carcinomas (HCCs) or cholangiocarcinomas (CCs) in response to lineage-specifi
158 recently that, in a patient with metastatic cholangiocarcinoma, CD4 T cells specific for a peptide f
159 determined to be a key factor for promoting cholangiocarcinoma cell anaplasia, hyperproliferation, a
162 hance the chemotherapeutic effect on a human cholangiocarcinoma cell line and local drug deposition i
163 or cell surface proteins of the intrahepatic cholangiocarcinoma cell line CC-SW-1 was developed by mo
164 restored the expression of primary cilia in cholangiocarcinoma cell lines and decreased cell prolife
165 icotine also stimulated the proliferation of cholangiocarcinoma cell lines and promoted alpha7-nAChR-
166 7-nAChR), was more highly expressed in human cholangiocarcinoma cell lines compared with normal human
167 to established (EGI-1) and primary (CCA-TV3) cholangiocarcinoma cell lines expressing nuclear S100A4
168 c acid miRNA inhibitors was performed in six cholangiocarcinoma cell lines treated with cisplatin and
170 asts (TDFSM) was co-cultured with a pure rat cholangiocarcinoma cell strain (TDECC) derived from the
171 rative TDFSM myofibroblastic cells and TDECC cholangiocarcinoma cells accumulating within the gel mat
172 Green fluorescent protein-labeled human cholangiocarcinoma cells and cholangiocarcinomas in 24 m
173 ified as the bona fide targets of miR-101 in cholangiocarcinoma cells by both computational analysis
174 ns have been proven to be cytotoxic to human cholangiocarcinoma cells by inhibiting cell division and
175 R-17-92 cluster is highly expressed in human cholangiocarcinoma cells compared with the nonneoplastic
176 bers, miR-92a and miR-19a, in cultured human cholangiocarcinoma cells enhanced tumor cell proliferati
177 ied the effects of nicotine on the growth of cholangiocarcinoma cells in vitro and the progression of
178 a fide target of both miR-92a and miR-19a in cholangiocarcinoma cells via sequence prediction, 3' unt
179 the tumor mass, nuclear S100A4 expression by cholangiocarcinoma cells was significantly reduced, wher
180 al targets of the miR-17-92 cluster in human cholangiocarcinoma cells, including APAF-1 and PRDM2.
185 133 combined hepatocellular and intrahepatic cholangiocarcinoma (cHCC-ICC) cases, including separate,
186 and November 23, 2011 for bile duct injury, cholangiocarcinoma, choledochal cysts, or benign strictu
188 ssed at significantly higher levels in human cholangiocarcinoma compared with normal human control li
189 hocytes (TIL) from a patient with metastatic cholangiocarcinoma contained CD4+ T helper 1 (T(H)1) cel
195 t and survival in patients with extrahepatic cholangiocarcinoma (ECC), including perihilar cholangioc
196 ole of postoperative therapy in extrahepatic cholangiocarcinoma (EHCC) or gallbladder carcinoma (GBCA
198 rogenase-1 (IDH1) is mutated in up to 25% of cholangiocarcinomas, especially intrahepatic cholangioca
200 adult patients underwent LT for PSC without cholangiocarcinoma from 1984 to 2012, with follow-up thr
201 atients and in several other cancers such as cholangiocarcinoma, glioblastoma, or colorectal cancer.
202 e miR-17-92 cluster or miR-92a also enhanced cholangiocarcinoma growth in vivo in hairless outbred mi
204 ng hepatocellular carcinoma and intrahepatic cholangiocarcinoma, has become the second leading cause
206 ) assessment after liver resection for hilar cholangiocarcinoma (HC) is still controversial, and the
207 ch finally evolved to a giant hepatocellular-cholangiocarcinoma (HCC-CC) of the liver, successfully r
209 Development of PSC also increased risks of cholangiocarcinoma (HR, 28.46), hepatocellular carcinoma
210 ients had nodules demonstrating intrahepatic cholangiocarcinoma (I-CCA), nine had I-CCA nodules occur
215 hepatocellular liver cancer and intrahepatic cholangiocarcinoma (ICC) has increased and ranked 1st in
216 aimed to examine the burden of intrahepatic cholangiocarcinoma (ICC) in Thailand and identify the pr
221 resection (R0) for treatment of intrahepatic cholangiocarcinoma (ICC) is potentially curative, but th
223 er cancer, can be classified as intrahepatic cholangiocarcinoma (ICC) or extrahepatic cholangiocarcin
226 3, a frequent mutation found in intrahepatic cholangiocarcinoma (ICC), disables its role in enhancing
228 sive malignancy of mass-forming intrahepatic cholangiocarcinoma (ICC), we modeled ICC desmoplasia and
230 y and differential diagnosis of intrahepatic cholangiocarcinoma (iCCA) and hepatocellular carcinoma (
235 hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (iCCA), and other rare tumors, notabl
237 llular carcinomas (HCCs), three intrahepatic cholangiocarcinomas (ICCs), one neuroendocrine metastasi
243 n-labeled human cholangiocarcinoma cells and cholangiocarcinomas in 24 mice were treated with (a) com
245 as category LR-5, with the remainder of the cholangiocarcinomas in the sample appropriately characte
246 r developing an aggressive bile duct cancer, cholangiocarcinoma, in chronically infected patients.
247 l, a microtubule-stabilizing agent, inhibits cholangiocarcinoma invasiveness and metastatic spread.
253 rahepatic cholangiocarcinoma (ICC) and hilar cholangiocarcinoma (Klatskin tumors) is limited to surgi
256 diseased tissues (PDAC, ampullary carcinoma, cholangiocarcinoma, mucinous cystic neoplasm, chronic in
257 ed to hepatocellular carcinoma (n = 263) and cholangiocarcinoma (n = 36), the two most common liver c
259 diagnosis of malignant (pancreatic cancer or cholangiocarcinoma, n = 15) or nonmalignant (CP, n = 15)
260 s of malignant (pancreatic cancer, n = 20 or cholangiocarcinoma, n = 5) or nonmalignant (chronic panc
261 nd therapeutic approaches are undertaken for cholangiocarcinomas of different anatomical locations (i
264 rs or older and had histologically confirmed cholangiocarcinoma or muscle-invasive gallbladder cancer
265 ested a set of FISH probes on tumor tissues (cholangiocarcinoma or pancreatic carcinoma) and non-tumo
266 OR 0.319, 95% CI 0.107-0.949, p = 0.040) and cholangiocarcinomas (OR 0.185, 95% CI 0.049-0.696, p = 0
267 imaging abnormalities, biochemical changes, cholangiocarcinoma, or end-stage complications such as c
268 series, studies reporting on mixed types of cholangiocarcinoma, or exclusively on hepatolithiasis-as
269 the tumour group NPP7 activity was lowest in cholangiocarcinoma patients, being only 19% of that in g
270 holangiocarcinoma (ECC), including perihilar cholangiocarcinoma (pCCA) and distal cholangiocarcinoma
274 e helping to identify the genetic drivers of cholangiocarcinoma progression, which will unveil early
276 of this cell population in animal models of cholangiocarcinoma reduced tumor burden and proliferatio
277 permethylated in IDH(mut) AML, melanoma, and cholangiocarcinoma, relative to each of their IDH(wt) co
280 th hepatocellular carcinoma and intrahepatic cholangiocarcinoma revealed that combined and mixed type
281 anthoastrocytoma, anaplastic thyroid cancer, cholangiocarcinoma, salivary-duct cancer, ovarian cancer
282 on of miR-101 is decreased in 43.5% of human cholangiocarcinoma specimens and in all three cholangioc
283 genomic alterations typical of extrahepatic cholangiocarcinoma, such as TP53 (35.5%), KRAS (28.0%),
284 anscription factor is an oncogenic driver in cholangiocarcinoma that confers sensitivity to CDK4/6 in
287 broad spectrum of liver tumors, ranging from cholangiocarcinoma to hepatocellular carcinoma, which re
288 nAChR agonist) accelerated the growth of the cholangiocarcinoma tumors in our xenograft mouse model a
291 014 and May 12, 2017, 73 patients with mIDH1-cholangiocarcinoma were enrolled and received ivosidenib
292 At the end of study, the number and area of cholangiocarcinomas were significantly diminished in rat
293 ies (n = 12 pancreatic adenocarcinoma, n = 1 cholangiocarcinoma) were fluorescent (mean TBR 4.42 +/-
294 ty, sinonasal undifferentiated carcinoma and cholangiocarcinoma, which clustered by their embryonal o
295 tologically confirmed, advanced, IDH1-mutant cholangiocarcinoma who had progressed on previous therap
296 igatinib in previously treated patients with cholangiocarcinoma who have FGFR2 fusions or rearrangeme
297 es were reported for all patients with mIDH1-cholangiocarcinoma who were enrolled and received at lea
298 usly treated, locally advanced or metastatic cholangiocarcinoma with and without FGFR2 fusions or rea
300 carcinoma (PHCCA) is the most common type of cholangiocarcinoma with low resection rate and high morb