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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)
49 n/endometrial/vulvar cancers, 3; and de novo cholangiocarcinoma, 4).
50 ctal liver metastases (7%), and intrahepatic cholangiocarcinoma (6%).
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.
54       Effective treatments for patients with cholangiocarcinoma after progression on gemcitabine-base
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
64  be translated to distinguish between distal cholangiocarcinoma and pancreatic cancers.
65 and RUFY2-RET in lung cancer, FGFR2-CREB5 in cholangiocarcinoma and PPL-NTRK1 in thyroid carcinoma.
66              Because of the bad prognosis of cholangiocarcinoma and the sizeable morbidity-mortality
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
74                     Patient 2 had metastatic cholangiocarcinoma, and his findings resolved after 2 we
75 2) was found in sarcoma, esophageal, breast, cholangiocarcinoma, and lung cancer.
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
78                       The factors that drive cholangiocarcinoma are poorly understood, though chronic
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
81                                        Using cholangiocarcinoma as a desmoplastic tumor model, we inv
82                                        Using cholangiocarcinoma as a model, we found that primary cil
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
85 e myeloid leukaemia (AML), low-grade glioma, cholangiocarcinoma (CC) and chondrosarcoma (CS).
86 LC subtypes: hepatocellular carcinoma (HCC), cholangiocarcinoma (CC) and combined HCC/CC (CHC) tumors
87           Hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC) are the most common liver cancer
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
90                             The prognosis of cholangiocarcinoma (CC) is dismal.
91                         However, its role in cholangiocarcinoma (CC) is not established.
92                                              Cholangiocarcinoma (CC) is typically diagnosed at an adv
93 ding both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC), suggestive of progenitor cell o
94 ced EMT also increases local invasiveness of cholangiocarcinomas (CC), but prevents metastases.
95 mation of both hepatocellular carcinomas and cholangiocarcinomas (CC).
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
99            Desmoplastic malignancies such as cholangiocarcinoma (CCA) are characterized by a dense st
100                Subjects with advanced PSC or cholangiocarcinoma (CCA) at baseline were excluded.
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
103                                              Cholangiocarcinoma (CCA) cells paradoxically express the
104 eIF2alpha in non-malignant cholangiocyte and cholangiocarcinoma (CCA) cells.
105                                              Cholangiocarcinoma (CCA) encompasses a heterogeneous col
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
108                                              Cholangiocarcinoma (CCA) includes a heterogeneous group
109                                              Cholangiocarcinoma (CCA) is a bile duct cancer that orig
110                                              Cholangiocarcinoma (CCA) is a devastating disease due to
111                                              Cholangiocarcinoma (CCA) is a devastating liver tumour a
112                                              Cholangiocarcinoma (CCA) is a highly invasive cancer, di
113                                              Cholangiocarcinoma (CCA) is a highly malignant epithelia
114                                              Cholangiocarcinoma (CCA) is a lethal hepatobiliary neopl
115                                              Cholangiocarcinoma (CCA) is an aggressive and heterogene
116                                 Intrahepatic cholangiocarcinoma (CCA) is characterized by an abundant
117                                              Cholangiocarcinoma (CCA) is characterized by an abundant
118                The tumor microenvironment of cholangiocarcinoma (CCA) is composed of numerous cells,
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.
121                                              Cholangiocarcinoma (CCA) is the second most common malig
122  cancer liver metastases (CRCLM) and primary cholangiocarcinoma (CCA) models in BALB/c nude mice usin
123                                              Cholangiocarcinoma (CCA) mortality rates are increasing
124                                              Cholangiocarcinoma (CCA) presents significant diagnostic
125 with other liver cancers, mortality rates of cholangiocarcinoma (CCA) remain unknown.
126 etection of the highly aggressive malignancy cholangiocarcinoma (CCA) remains a challenge but has the
127           Whether NAFLD is a risk factor for cholangiocarcinoma (CCA) remains inconclusive.
128    Whether aspirin use is protective against cholangiocarcinoma (CCA) remains unclear.
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
132           Desmoplastic malignancies, such as cholangiocarcinoma (CCA), have an abundant tumor immune
133                                              Cholangiocarcinoma (CCA), in contrast, is characterized
134                                              Cholangiocarcinoma (CCA), or tumor of the biliary tree,
135  pancreatic ductal adenocarcinoma (PDAC) and cholangiocarcinoma (CCA), respectively.
136  million people in Southeast Asia and causes cholangiocarcinoma (CCA).
137 n pathogenesis of opisthorchiasis-associated cholangiocarcinoma (CCA).
138 nd epigenetic regulation of miR-34a in human cholangiocarcinoma (CCA).
139 sociated with poor survival of patients with cholangiocarcinoma (CCA).
140 eptor (FGFR) oncogenic signaling pathways in cholangiocarcinoma (CCA).
141 sses both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA).
142 olangitis (PSC) are at an increased risk for cholangiocarcinoma (CCA).
143  where chronic infection frequently leads to cholangiocarcinoma (CCA).
144 gical resection or liver transplantation for cholangiocarcinoma (CCA).
145 cinoma with liver metastases (CRLM), but not cholangiocarcinoma (CCA).
146 ory cholangiopathy frequently complicated by cholangiocarcinoma (CCA).
147 tant role in the pathogenesis and biology of cholangiocarcinoma (CCA).
148  the development of non-Hodgkin lymphoma and cholangiocarcinoma (CCA).
149 logic resection or liver transplantation for cholangiocarcinoma (CCA).
150                           BACKGROUND & AIMS: Cholangiocarcinomas (CCA) are resistant to chemotherapy,
151 liary disease is linked to malignant cancer (cholangiocarcinoma, CCA) and affects millions of people
152                                              Cholangiocarcinomas (CCAs) are hepatobiliary cancers wit
153                                              Cholangiocarcinomas (CCAs) comprise a mucin-secreting fo
154 e-scale analysis, we implanted 93 HCCs and 8 cholangiocarcinomas (CCAs) to systematically analyze hos
155           Hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCC) are the most common liver tumor
156 lecular mechanisms underlying the genesis of cholangiocarcinomas (CCs) are poorly understood.
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
160 se of the in situ tumor, as well as promoted cholangiocarcinoma cell growth and progression.
161 egion) prevented miR-92a- or miR-19a-induced cholangiocarcinoma cell growth.
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
169 holangiocarcinoma specimens and in all three cholangiocarcinoma cell lines used in this study.
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.
181                                       Unlike cholangiocarcinoma cells, neither CAF nor quiescent fibr
182  similar effects in quiescent fibroblasts or cholangiocarcinoma cells.
183 lation and transcription activation in human cholangiocarcinoma cells.
184                                          For cholangiocarcinoma, centers that performed a low volume
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
187            Here we report data for the mIDH1-cholangiocarcinoma cohort.
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
190 rihilar cholangiocarcinoma (pCCA) and distal cholangiocarcinoma (dCCA).
191                                              Cholangiocarcinoma developed in 2 of the 29 PSC patients
192 th hepatocellular carcinoma and intrahepatic cholangiocarcinoma development.
193 ignaling, two important pathways involved in cholangiocarcinoma development.
194  and periampullary tumors (ampulloma, distal cholangiocarcinoma, duodenal adenocarcinoma).
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
197                            For patients with cholangiocarcinoma, endoscopic drainage is superior in c
198 rogenase-1 (IDH1) is mutated in up to 25% of cholangiocarcinomas, especially intrahepatic cholangioca
199  can arise in the liver as hepatocellular or cholangiocarcinoma forms.
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
203                                              Cholangiocarcinoma has a high mortality and morbidity.
204 ng hepatocellular carcinoma and intrahepatic cholangiocarcinoma, has become the second leading cause
205                         Mixed hepatocellular cholangiocarcinomas have emerged as a distinct subtype o
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
208 as a promising option for unresectable hilar cholangiocarcinoma (hCCA).
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
211                                 Intrahepatic cholangiocarcinoma (ICC) accounts for 12% of cases and h
212                                 Intrahepatic cholangiocarcinoma (ICC) and hepatocellular carcinoma (H
213           Curative treatment of intrahepatic cholangiocarcinoma (ICC) and hilar cholangiocarcinoma (K
214 ollowing surgical management of intrahepatic cholangiocarcinoma (ICC) are limited.
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
217                                 Intrahepatic cholangiocarcinoma (ICC) is a highly malignant, heteroge
218                                 Intrahepatic cholangiocarcinoma (ICC) is a primary cancer of the live
219                                 Intrahepatic cholangiocarcinoma (ICC) is a severe malignant tumor in
220                                 Intrahepatic cholangiocarcinoma (ICC) is asevere malignant tumor in w
221 resection (R0) for treatment of intrahepatic cholangiocarcinoma (ICC) is potentially curative, but th
222                                 Intrahepatic cholangiocarcinoma (ICC) likely originates from the bili
223 er cancer, can be classified as intrahepatic cholangiocarcinoma (ICC) or extrahepatic cholangiocarcin
224 .0% and 70.0% for patients with intrahepatic cholangiocarcinoma (ICC) respectively.
225 diabetes, smoking, obesity, and intrahepatic cholangiocarcinoma (ICC) risk remain inconclusive.
226 3, a frequent mutation found in intrahepatic cholangiocarcinoma (ICC), disables its role in enhancing
227                In patients with intrahepatic cholangiocarcinoma (ICC), the oncologic benefit of surge
228 sive malignancy of mass-forming intrahepatic cholangiocarcinoma (ICC), we modeled ICC desmoplasia and
229 atocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC).
230 y and differential diagnosis of intrahepatic cholangiocarcinoma (iCCA) and hepatocellular carcinoma (
231                                 Intrahepatic cholangiocarcinoma (iCCA) has over the last 10-20 years
232                                 Intrahepatic cholangiocarcinoma (iCCA) is a contraindication to liver
233                                 Intrahepatic cholangiocarcinoma (iCCA) is a fatal bile duct cancer wi
234                                 Intrahepatic cholangiocarcinoma (iCCA) is the second most common prim
235 hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (iCCA), and other rare tumors, notabl
236                    About 15% of intrahepatic cholangiocarcinomas (ICCs) express constitutively active
237 llular carcinomas (HCCs), three intrahepatic cholangiocarcinomas (ICCs), one neuroendocrine metastasi
238 rapies for localized inoperable intrahepatic cholangiocarcinoma (IHCC) are ineffective.
239 t common genetic alterations in intrahepatic cholangiocarcinoma (IHCC), a deadly liver cancer.
240 cinoma (HCC) in 128 (4-year cumI: 10.5%) and cholangiocarcinoma in 3.
241 cinoma cells in vitro and the progression of cholangiocarcinoma in a mouse xenograft model.
242 uced, which were similar to that observed in cholangiocarcinoma in TCGA and Oncomine databases.
243 n-labeled human cholangiocarcinoma cells and cholangiocarcinomas in 24 mice were treated with (a) com
244                         The remainder of the cholangiocarcinomas in the sample (n = 8) were appropria
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.
248                                              Cholangiocarcinoma is a relatively rare cancer of the bi
249                                 Intrahepatic cholangiocarcinoma is a treatment refractory malignancy
250 icotine's involvement in the pathogenesis of cholangiocarcinoma is controversial.
251                               Because distal cholangiocarcinoma is difficult to distinguish from panc
252                                              Cholangiocarcinoma is the second most common primary liv
253 rahepatic cholangiocarcinoma (ICC) and hilar cholangiocarcinoma (Klatskin tumors) is limited to surgi
254                Two patients (one PSC and one cholangiocarcinoma) lacking NPP7 activity had only the 1
255                           Here, we show that cholangiocarcinoma metastasis is characterized by down-r
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
258               The most common malignancy was cholangiocarcinoma (n = 594); patients of advanced age a
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
262                   Patients with extrahepatic cholangiocarcinoma or gallbladder cancer and a microscop
263 ation therapy for patients with extrahepatic cholangiocarcinoma or gallbladder cancer.
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
271                   Liver surgery in perihilar cholangiocarcinoma (PHC) is associated with high postope
272           Importance: Resection of perihilar cholangiocarcinoma (PHC) is high-risk surgery, with repo
273                                    Perihilar cholangiocarcinoma (PHCCA) is the most common type of ch
274 e helping to identify the genetic drivers of cholangiocarcinoma progression, which will unveil early
275 ed the novel hypothesis that menin regulates cholangiocarcinoma proliferation.
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
278 eases, although the implication of miRNAs in cholangiocarcinoma remains to be defined further.
279                                              Cholangiocarcinoma represents a diverse group of epithel
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
285                                              Cholangiocarcinoma, the second most common liver cancer,
286 determine the expression of miR-101 in human cholangiocarcinoma tissues and cell lines.
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
289                                Only a single cholangiocarcinoma was misdiagnosed as category LR-5, wi
290        Response rates for CRC, melanoma, and cholangiocarcinoma were 68.2%, 57.1%, and 100% respectiv
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
299 ivation of AKT and YAP in bile ducts induced cholangiocarcinoma with liver metastases.
300 carcinoma (PHCCA) is the most common type of cholangiocarcinoma with low resection rate and high morb

 
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