ライフサイエンスコーパス: cholangiocarcinoma

1 cellular carcinoma and 20% were intrahepatic cholangiocarcinoma.

2 way is upregulated in patients with sporadic cholangiocarcinoma.

3 erihilar but not with intrahepatic or distal cholangiocarcinoma.

4 ting, and visualization for the treatment of cholangiocarcinoma.

5 mation and tumor burden in a murine model of cholangiocarcinoma.

6 tly decreased in malignancy, particularly in cholangiocarcinoma.

7 transformation and an origin of intrahepatic cholangiocarcinoma.

8 Exclusion criteria were combined HCC and cholangiocarcinoma.

9 cular mechanisms of the miR-17-92 cluster in cholangiocarcinoma.

10 this model as well as in human intrahepatic cholangiocarcinoma.

11 erly assess liver masses in this setting for cholangiocarcinoma.

12 hepatic lithiasis, septic complications, and cholangiocarcinoma.

13 tic cholangiocarcinoma (ICC) or extrahepatic cholangiocarcinoma.

14 may be a potential therapeutic approach for cholangiocarcinoma.

15 hepatocellular carcinoma (HCC) and mixed HCC-cholangiocarcinoma.

16 Exclusion criteria were combined HCC and cholangiocarcinoma.

17 atients (5.2%) who presented with coexistent cholangiocarcinoma.

18 zebrafish ICC were similar to those of human cholangiocarcinoma.

19 gorithm for patients with suspected or known cholangiocarcinoma.

20 ls in the control of tumor cell apoptosis in cholangiocarcinoma.

21 ht be targets for prevention or treatment of cholangiocarcinoma.

22 tion for EUS is the diagnosis and staging of cholangiocarcinoma.

23 s in an orthotopic rat model of intrahepatic cholangiocarcinoma.

24 et is implicated in the progression of human cholangiocarcinoma.

25 the roles and mechanisms of miR-26a in human cholangiocarcinoma.

26 ts for the treatment of cholangiopathies and cholangiocarcinoma.

27 nd plays a novel role in the pathogenesis of cholangiocarcinoma.

28 zymes with clinico-radiological suspicion of cholangiocarcinoma.

29 itaxel in blocking metastatic progression of cholangiocarcinoma.

30 t proteins on the cell surface of a model of cholangiocarcinoma.

31 ndergo a major liver resection for perihilar cholangiocarcinoma.

32 n patients with hepatocellular carcinoma and cholangiocarcinoma.

33 pressed in DRs of human cirrhotic livers and cholangiocarcinoma.

34 thologic examination, 10 patients (2.5%) had cholangiocarcinoma.

35 has potential as a therapeutic strategy for cholangiocarcinoma.

36 elp to identify novel therapeutic targets in cholangiocarcinoma.

37 oma with stem cell features and intrahepatic cholangiocarcinoma.

38 2 occur in approximately 15% of intrahepatic cholangiocarcinomas.

39 (IDH) is recurrently mutated in intrahepatic cholangiocarcinomas.

40 utations may represent a distinct subtype of cholangiocarcinomas.

41 the genetic characterization of intrahepatic cholangiocarcinomas.

42 s encoding metabolic enzymes in intrahepatic cholangiocarcinomas.

43 stinction absent in ampullary carcinomas and cholangiocarcinomas.

44 he course of tissue injury, TAA also induced cholangiocarcinomas.

45 also reduce the number and size of attendant cholangiocarcinomas.

46 gulated chromatin remodeling in intrahepatic cholangiocarcinomas.

47 of the tumors that formed were intrahepatic cholangiocarcinomas.

48 marked reduction in concomitantly developed cholangiocarcinomas.

49 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-

50 on-CRC = 37 (ocular/cutaneous melanoma = 32, cholangiocarcinoma = 3, appendiceal = 1, and breast = 1)

51 n/endometrial/vulvar cancers, 3; and de novo cholangiocarcinoma, 4).

52 is a biomarker of increased invasiveness in cholangiocarcinoma, a primary liver cancer with scarce t

53 also evidence of mTOR pathway activation in cholangiocarcinoma, although its biological significance

54 implications of the finding in diagnosis of cholangiocarcinoma and 1.2 kb product in hepatobiliary d

55 e acute myeloid leukaemia, low-grade glioma, cholangiocarcinoma and CS methylation data identifies ca

56 S100A4 as a candidate therapeutic target in cholangiocarcinoma and establish a mechanistic rationale

57 We provide insight into the pathogenesis of cholangiocarcinoma and identify previously unrecognized

58 Asia, there is an unprecedented link between cholangiocarcinoma and infection with the liver fluke Op

59 a novel tumor-suppressor role of miR-101 in cholangiocarcinoma and it suggests the possibility of ta

60 apoptosis through a Fas-related mechanism in cholangiocarcinoma and other cancer cell lines possibly

61 of human individuals with pancreatic cancer, cholangiocarcinoma and other malignant diseases of the b

62 We found that HDAC6 is overexpressed in cholangiocarcinoma and overexpression of HDAC6 in normal

63 be translated to distinguish between distal cholangiocarcinoma and pancreatic cancers.

64 and RUFY2-RET in lung cancer, FGFR2-CREB5 in cholangiocarcinoma and PPL-NTRK1 in thyroid carcinoma.

65 btype 4 (IgG4)-associated cholangitis mimics cholangiocarcinoma and presence of more than 10 IgG4-pos

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 Biopsy revealed 47 HCCs, 6 HGDNs, 1 LGDNs, 1 cholangiocarcinoma, and 1 epithelioid hemangioendothelio

70 liary obstruction is obligatory in perihilar cholangiocarcinoma, and advanced cytological tests such

71 astoma, acute myeloid leukemia, intrahepatic cholangiocarcinoma, and chondrosarcomas, led to intense

72 iple cancers, including lung adenocarcinoma, cholangiocarcinoma, and glioblastoma, is driving efforts

73 Patient 2 had metastatic cholangiocarcinoma, and his findings resolved after 2 we

74 or exclusively on hepatolithiasis-associated cholangiocarcinoma, and those published in a language ot

75 miR-101 inhibits cholangiocarcinoma angiogenesis by direct targeting of V

76 a significant decrease in tumor growth in a cholangiocarcinoma animal model.

77 R-25 contributes to evasion of TRAIL-induced cholangiocarcinoma apoptosis.

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 Cs), which encompass intra- and extrahepatic cholangiocarcinomas as well as gallbladder carcinomas, a

84 novel therapeutic approach for intrahepatic cholangiocarcinoma, because this protein also appears to

85 eiving endoscopic biliary drainage for hilar cholangiocarcinoma between September 1995 and December 2

86 , we found that primary cilia are reduced in cholangiocarcinoma by a mechanism involving histone deac

87 r transplantation for unresectable perihilar cholangiocarcinoma caused the United Network of Organ Sh

88 e myeloid leukaemia (AML), low-grade glioma, cholangiocarcinoma (CC) and chondrosarcoma (CS).

89 LC subtypes: hepatocellular carcinoma (HCC), cholangiocarcinoma (CC) and combined HCC/CC (CHC) tumors

90 Hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC) are the most common liver cancer

91 ith mixed hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC) characteristics that have a more

92 The prognosis of cholangiocarcinoma (CC) is dismal.

93 However, its role in cholangiocarcinoma (CC) is not established.

94 Cholangiocarcinoma (CC) is the second most common primar

95 Cholangiocarcinoma (CC) is typically diagnosed at an adv

96 ding both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC), suggestive of progenitor cell o

97 ced EMT also increases local invasiveness of cholangiocarcinomas (CC), but prevents metastases.

98 mation of both hepatocellular carcinomas and cholangiocarcinomas (CC).

99 strictures and obstructive jaundice, making cholangiocarcinoma (CCA) an important differential diagn

100 Desmoplastic malignancies such as cholangiocarcinoma (CCA) are characterized by a dense st

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 selected patients with early-stage perihilar cholangiocarcinoma (CCA) following neoadjuvant chemoradi

106 Metastatic penile carcinoma derived from cholangiocarcinoma (CCA) has not been previously reporte

107 Cholangiocarcinoma (CCA) includes a heterogeneous group

108 Cholangiocarcinoma (CCA) is a biliary cancer arising fro

109 Cholangiocarcinoma (CCA) is a devastating disease due to

110 Cholangiocarcinoma (CCA) is a devastating liver tumour a

111 Cholangiocarcinoma (CCA) is a lethal hepatobiliary neopl

112 Intrahepatic cholangiocarcinoma (CCA) is characterized by an abundant

113 Cholangiocarcinoma (CCA) is characterized by an abundant

114 The tumor microenvironment of cholangiocarcinoma (CCA) is composed of numerous cells,

115 Cholangiocarcinoma (CCA) presents significant diagnostic

116 with other liver cancers, mortality rates of cholangiocarcinoma (CCA) remain unknown.

117 etection of the highly aggressive malignancy cholangiocarcinoma (CCA) remains a challenge but has the

118 Whether NAFLD is a risk factor for cholangiocarcinoma (CCA) remains inconclusive.

119 Whether aspirin use is protective against cholangiocarcinoma (CCA) remains unclear.

120 h ErbB receptors have been widely studied in cholangiocarcinoma (CCA), a malignancy of the biliary tr

121 PSC is associated with an increased risk of cholangiocarcinoma (CCA), gallbladder cancer, hepatocell

122 Cholangiocarcinoma (CCA), in contrast, is characterized

123 Cholangiocarcinoma (CCA), or tumor of the biliary tree,

124 he miR species found to be down-regulated in cholangiocarcinoma (CCA), participates in cancer homeost

125 olangitis (PSC) are at an increased risk for cholangiocarcinoma (CCA).

126 n pathogenesis of opisthorchiasis-associated cholangiocarcinoma (CCA).

127 nd epigenetic regulation of miR-34a in human cholangiocarcinoma (CCA).

128 where chronic infection frequently leads to cholangiocarcinoma (CCA).

129 sociated with poor survival of patients with cholangiocarcinoma (CCA).

130 eptor (FGFR) oncogenic signaling pathways in cholangiocarcinoma (CCA).

131 sses both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA).

132 million people in Southeast Asia and causes cholangiocarcinoma (CCA).

133 BACKGROUND & AIMS: Cholangiocarcinomas (CCA) are resistant to chemotherapy,

134 liary disease is linked to malignant cancer (cholangiocarcinoma, CCA) and affects millions of people

135 Cholangiocarcinomas (CCAs) are hepatobiliary cancers wit

136 Cholangiocarcinomas (CCAs) comprise a mucin-secreting fo

137 ssue microarray of liver fluke-induced human cholangiocarcinomas (CCAs).

138 Hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCC) are the most common liver tumor

139 s signaling pathway in the carcinogenesis of cholangiocarcinoma (CCC) is still unknown.

140 lecular mechanisms underlying the genesis of cholangiocarcinomas (CCs) are poorly understood.

141 ate into hepatocellular carcinomas (HCCs) or cholangiocarcinomas (CCs) in response to lineage-specifi

142 recently that, in a patient with metastatic cholangiocarcinoma, CD4 T cells specific for a peptide f

143 determined to be a key factor for promoting cholangiocarcinoma cell anaplasia, hyperproliferation, a

144 se of the in situ tumor, as well as promoted cholangiocarcinoma cell growth and progression.

145 egion) prevented miR-92a- or miR-19a-induced cholangiocarcinoma cell growth.

146 udies of cancer-associated fibroblastic cell/cholangiocarcinoma cell interactions that may more accur

147 nd matricellular protein-protein and protein-cholangiocarcinoma cell interactions, as well as hypoxia

148 hance the chemotherapeutic effect on a human cholangiocarcinoma cell line and local drug deposition i

149 or cell surface proteins of the intrahepatic cholangiocarcinoma cell line CC-SW-1 was developed by mo

150 restored the expression of primary cilia in cholangiocarcinoma cell lines and decreased cell prolife

151 icotine also stimulated the proliferation of cholangiocarcinoma cell lines and promoted alpha7-nAChR-

152 tify elevated miR-25 expression in malignant cholangiocarcinoma cell lines as well as patient samples

153 7-nAChR), was more highly expressed in human cholangiocarcinoma cell lines compared with normal human

154 to established (EGI-1) and primary (CCA-TV3) cholangiocarcinoma cell lines expressing nuclear S100A4

155 ity in human immortalized cholangiocytes and cholangiocarcinoma cell lines in vitro were pH and AE2 d

156 , was more effective in inhibiting growth of cholangiocarcinoma cell lines than trastuzumab.

157 holangiocarcinoma specimens and in all three cholangiocarcinoma cell lines used in this study.

158 Human cholangiocarcinoma cell lines were transduced with lenti

159 ata from the patients with data from 7 human cholangiocarcinoma cell lines, which were then exposed t

160 mechanism to explain how p38 promotes human cholangiocarcinoma cell proliferation and invasion.

161 asts (TDFSM) was co-cultured with a pure rat cholangiocarcinoma cell strain (TDECC) derived from the

162 rative TDFSM myofibroblastic cells and TDECC cholangiocarcinoma cells accumulating within the gel mat

163 Green fluorescent protein-labeled human cholangiocarcinoma cells and cholangiocarcinomas in 24 m

164 ession of miR-26a increased proliferation of cholangiocarcinoma cells and colony formation in vitro,

165 ified as the bona fide targets of miR-101 in cholangiocarcinoma cells by both computational analysis

166 R-17-92 cluster is highly expressed in human cholangiocarcinoma cells compared with the nonneoplastic

167 bers, miR-92a and miR-19a, in cultured human cholangiocarcinoma cells enhanced tumor cell proliferati

168 interactions between these stromal cells and cholangiocarcinoma cells in relation to promoting intrah

169 PH-loaded DCs generated cytotoxicity against cholangiocarcinoma cells in vitro and significantly supp

170 ied the effects of nicotine on the growth of cholangiocarcinoma cells in vitro and the progression of

171 deficient mice, overexpression of miR-26a by cholangiocarcinoma cells increased tumor growth and over

172 We analyzed growth of human cholangiocarcinoma cells that overexpress miR-26a or its

173 associated fibroblastic cells crosstalk with cholangiocarcinoma cells to promote intrahepatic cholang

174 a fide target of both miR-92a and miR-19a in cholangiocarcinoma cells via sequence prediction, 3' unt

175 the tumor mass, nuclear S100A4 expression by cholangiocarcinoma cells was significantly reduced, wher

176 tions, human immortalized cholangiocytes and cholangiocarcinoma cells were exposed to chenodeoxychola

177 effects of tubastatin-A were abolished when cholangiocarcinoma cells were rendered unable to regener

178 Initially, human cholangiocarcinoma cells were treated with various conce

179 al targets of the miR-17-92 cluster in human cholangiocarcinoma cells, including APAF-1 and PRDM2.

180 Unlike cholangiocarcinoma cells, neither CAF nor quiescent fibr

181 lmodulin (CaM) is recruited into the DISC in cholangiocarcinoma cells, suggesting a novel role of CaM

182 similar effects in quiescent fibroblasts or cholangiocarcinoma cells.

183 lation and transcription activation in human cholangiocarcinoma cells.

184 experiments confirmed uptake of MGd by human cholangiocarcinoma cells.

185 the pro-tumorigenic ability of p38 in human cholangiocarcinoma cells.

186 mote the proliferation and invasion of human cholangiocarcinoma cells.

187 an target of rapamycin signaling pathways in cholangiocarcinoma cells.

188 For cholangiocarcinoma, centers that performed a low volume

189 sponse of hepatocellular carcinoma (HCC) and cholangiocarcinoma (CGC) to sorafenib, a cationic drug.

190 and November 23, 2011 for bile duct injury, cholangiocarcinoma, choledochal cysts, or benign strictu

191 ssed at significantly higher levels in human cholangiocarcinoma compared with normal human control li

192 hocytes (TIL) from a patient with metastatic cholangiocarcinoma contained CD4+ T helper 1 (T(H)1) cel

193 Cholangiocarcinoma developed in 2 of the 29 PSC patients

194 th hepatocellular carcinoma and intrahepatic cholangiocarcinoma development.

195 ignaling, two important pathways involved in cholangiocarcinoma development.

196 s high throughout the course of intrahepatic cholangiocarcinomas development and low during hepatocel

197 nherent limitations of current approaches to cholangiocarcinoma diagnosis and staging have driven the

198 ole of postoperative therapy in extrahepatic cholangiocarcinoma (EHCC) or gallbladder carcinoma (GBCA

199 For patients with cholangiocarcinoma, endoscopic drainage is superior in c

200 can arise in the liver as hepatocellular or cholangiocarcinoma forms.

201 adult patients underwent LT for PSC without cholangiocarcinoma from 1984 to 2012, with follow-up thr

202 miR-26a promotes cholangiocarcinoma growth by inhibition of GSK-3beta and

203 xpression of miR-101 significantly inhibited cholangiocarcinoma growth in severe combined immunodefic

204 e miR-17-92 cluster or miR-92a also enhanced cholangiocarcinoma growth in vivo in hairless outbred mi

205 Cholangiocarcinoma has a high mortality and morbidity.

206 oblastic cells in the stroma of intrahepatic cholangiocarcinoma has recently been demonstrated to acc

207 ng hepatocellular carcinoma and intrahepatic cholangiocarcinoma, has become the second leading cause

208 Mixed hepatocellular cholangiocarcinomas have emerged as a distinct subtype o

209 ) assessment after liver resection for hilar cholangiocarcinoma (HC) is still controversial, and the

210 ch finally evolved to a giant hepatocellular-cholangiocarcinoma (HCC-CC) of the liver, successfully r

211 lity of treatment for hilar and intrahepatic cholangiocarcinoma (HCCA-ICCA).

212 ients had nodules demonstrating intrahepatic cholangiocarcinoma (I-CCA), nine had I-CCA nodules occur

213 Intrahepatic cholangiocarcinoma (ICC) and hepatocellular carcinoma (H

214 Curative treatment of intrahepatic cholangiocarcinoma (ICC) and hilar cholangiocarcinoma (K

215 ollowing surgical management of intrahepatic cholangiocarcinoma (ICC) are limited.

216 e initiation and development of intrahepatic cholangiocarcinoma (ICC) associated with hepatitis B and

217 hepatocellular liver cancer and intrahepatic cholangiocarcinoma (ICC) has increased and ranked 1st in

218 atocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) have increased in the United St

219 aimed to examine the burden of intrahepatic cholangiocarcinoma (ICC) in Thailand and identify the pr

220 Intrahepatic cholangiocarcinoma (ICC) is a highly malignant, heteroge

221 Intrahepatic cholangiocarcinoma (ICC) is a primary cancer of the live

222 PURPOSE OF REVIEW: Intrahepatic cholangiocarcinoma (ICC) is a treatment-refractory disea

223 resection (R0) for treatment of intrahepatic cholangiocarcinoma (ICC) is potentially curative, but th

224 Intrahepatic cholangiocarcinoma (ICC) is the second most common type

225 Intrahepatic cholangiocarcinoma (ICC) likely originates from the bili

226 er cancer, can be classified as intrahepatic cholangiocarcinoma (ICC) or extrahepatic cholangiocarcin

227 diabetes, smoking, obesity, and intrahepatic cholangiocarcinoma (ICC) risk remain inconclusive.

228 In patients with intrahepatic cholangiocarcinoma (ICC), the oncologic benefit of surge

229 sive malignancy of mass-forming intrahepatic cholangiocarcinoma (ICC), we modeled ICC desmoplasia and

230 atocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC).

231 Intrahepatic cholangiocarcinoma (iCCA) is a fatal bile duct cancer wi

232 hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (iCCA), and other rare tumors, notabl

233 Intrahepatic cholangiocarcinomas (ICCs) are primary liver tumors with

234 llular carcinomas (HCCs), three intrahepatic cholangiocarcinomas (ICCs), one neuroendocrine metastasi

235 rapies for localized inoperable intrahepatic cholangiocarcinoma (IHCC) are ineffective.

236 Intrahepatic cholangiocarcinoma (IHCC) is a primary cancer of the liv

237 t common genetic alterations in intrahepatic cholangiocarcinoma (IHCC), a deadly liver cancer.

238 ection in hepatocellular carcinoma and hilar cholangiocarcinoma improves survival.

239 cinoma (HCC) in 128 (4-year cumI: 10.5%) and cholangiocarcinoma in 3.

240 cinoma cells in vitro and the progression of cholangiocarcinoma in a mouse xenograft model.

241 n-labeled human cholangiocarcinoma cells and cholangiocarcinomas in 24 mice were treated with (a) com

242 r developing an aggressive bile duct cancer, cholangiocarcinoma, in chronically infected patients.

243 To establish a mouse model of resectable cholangiocarcinoma including the most frequent genetic a

244 Twenty-nine patients with unresectable cholangiocarcinoma, including 11 men (mean age, 60 years

245 l, a microtubule-stabilizing agent, inhibits cholangiocarcinoma invasiveness and metastatic spread.

246 Cholangiocarcinoma is a heterogeneous disease with a poo

247 PURPOSE OF REVIEW: Cholangiocarcinoma is a malignancy arising from biliary

248 Cholangiocarcinoma is a relatively rare cancer of the bi

249 Intrahepatic cholangiocarcinoma is a treatment refractory malignancy

250 Endoscopic biliary drainage of hilar cholangiocarcinoma is controversial with respect to the

251 icotine's involvement in the pathogenesis of cholangiocarcinoma is controversial.

252 Because distal cholangiocarcinoma is difficult to distinguish from panc

253 Cholangiocarcinoma is the second most common primary liv

254 rahepatic cholangiocarcinoma (ICC) and hilar cholangiocarcinoma (Klatskin tumors) is limited to surgi

255 Two patients (one PSC and one cholangiocarcinoma) lacking NPP7 activity had only the 1

256 a number of microRNAs have been described in cholangiocarcinoma, many additional microRNAs dysregulat

257 diseased tissues (PDAC, ampullary carcinoma, cholangiocarcinoma, mucinous cystic neoplasm, chronic in

258 ed to hepatocellular carcinoma (n = 263) and cholangiocarcinoma (n = 36), the two most common liver c

259 The most common malignancy was cholangiocarcinoma (n = 594); patients of advanced age a

260 diagnosis of malignant (pancreatic cancer or cholangiocarcinoma, n = 15) or nonmalignant (CP, n = 15)

261 s of malignant (pancreatic cancer, n = 20 or cholangiocarcinoma, n = 5) or nonmalignant (chronic panc

262 epatocellular carcinoma: n = 3, intrahepatic cholangiocarcinoma: n = 2, extrahepatic cholangiocarcino

263 atic cholangiocarcinoma: n = 2, extrahepatic cholangiocarcinoma: n = 2, malignant epithelioid hemangi

264 In a syngeneic rat model of cholangiocarcinoma, navitoclax treatment triggered CAF a

265 nd therapeutic approaches are undertaken for cholangiocarcinomas of different anatomical locations (i

266 SEMS insertion for the palliation of hilar cholangiocarcinoma offers higher technical and clinical

267 ested a set of FISH probes on tumor tissues (cholangiocarcinoma or pancreatic carcinoma) and non-tumo

268 imaging abnormalities, biochemical changes, cholangiocarcinoma, or end-stage complications such as c

269 series, studies reporting on mixed types of cholangiocarcinoma, or exclusively on hepatolithiasis-as

270 the tumour group NPP7 activity was lowest in cholangiocarcinoma patients, being only 19% of that in g

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 cells in relation to promoting intrahepatic cholangiocarcinoma progression is only just beginning to

274 e helping to identify the genetic drivers of cholangiocarcinoma progression, which will unveil early

275 angiocarcinoma cells to promote intrahepatic cholangiocarcinoma progression.

276 has recently been demonstrated to accelerate cholangiocarcinoma progression.

277 fibroblastic cells in promoting intrahepatic cholangiocarcinoma progression.

278 ed the novel hypothesis that menin regulates cholangiocarcinoma proliferation.

279 of this cell population in animal models of cholangiocarcinoma reduced tumor burden and proliferatio

280 eases, although the implication of miRNAs in cholangiocarcinoma remains to be defined further.

281 Cholangiocarcinoma represents a diverse group of epithel

282 anthoastrocytoma, anaplastic thyroid cancer, cholangiocarcinoma, salivary-duct cancer, ovarian cancer

283 transcriptomes from 104 surgically resected cholangiocarcinoma samples collected from patients in Au

284 on of miR-101 is decreased in 43.5% of human cholangiocarcinoma specimens and in all three cholangioc

285 53(KO) ;Tgfbr2(KO) mice develop both HCC and cholangiocarcinomas, suggesting that loss of p53, indepe

286 Cholangiocarcinoma, the second most common liver cancer,

287 on to measure expression of miR-26a in human cholangiocarcinoma tissues and cell lines (eg, CCLP1, SG

288 Human cholangiocarcinoma tissues and cell lines had increased

289 determine the expression of miR-101 in human cholangiocarcinoma tissues and cell lines.

290 mPGES-1 is overexpressed in human cholangiocarcinoma tissues.

291 broad spectrum of liver tumors, ranging from cholangiocarcinoma to hepatocellular carcinoma, which re

292 filing of 23 ICC and combined hepatocellular cholangiocarcinoma tumor specimens from Asian patients u

293 nAChR agonist) accelerated the growth of the cholangiocarcinoma tumors in our xenograft mouse model a

294 f treating 3 or more patients with perihilar cholangiocarcinoma using neoadjuvant therapy, followed b

295 endoscopic palliation in patients with hilar cholangiocarcinoma using self-expandable metallic stents

296 Through exomic sequencing of 32 intrahepatic cholangiocarcinomas, we discovered frequent inactivating

297 Response rates for CRC, melanoma, and cholangiocarcinoma were 68.2%, 57.1%, and 100% respectiv

298 At the end of study, the number and area of cholangiocarcinomas were significantly diminished in rat

299 Patients with perihilar cholangiocarcinoma who were treated with neoadjuvant the

300 ivation of AKT and YAP in bile ducts induced cholangiocarcinoma with liver metastases.