ライフサイエンスコーパス: pancreatic ductal adenocarcinoma

1 (EP-3533) to image and quantify fibrosis in pancreatic ductal adenocarcinoma.

2 s with unique qualities as T-cell targets in pancreatic ductal adenocarcinoma.

3 d other adenocarcinomas like lung cancer and pancreatic ductal adenocarcinoma.

4 intraductal papillary mucinous neoplasia and pancreatic ductal adenocarcinoma.

5 ically engineered mouse model (KPC mouse) of pancreatic ductal adenocarcinoma.

6 mportant prognostic factor for patients with pancreatic ductal adenocarcinoma.

7 oader BRCA genetic testing for patients with pancreatic ductal adenocarcinoma.

8 are usually associated with pancreatitis and pancreatic ductal adenocarcinoma.

9 and increased survival compared with typical pancreatic ductal adenocarcinoma.

10 preoperative therapy and pancreatectomy for pancreatic ductal adenocarcinoma.

11 rapy in 730 evaluable patients with resected pancreatic ductal adenocarcinoma.

12 new standard of care following resection for pancreatic ductal adenocarcinoma.

13 prominent risk factor for the development of pancreatic ductal adenocarcinoma.

14 ry mucinous neoplasia (14 patients, 35%) and pancreatic ductal adenocarcinoma (2 patients, 5%).

15 ormal tissue obtained from 854 patients with pancreatic ductal adenocarcinoma, 288 patients with othe

16 therapy resistance are cardinal features of pancreatic ductal adenocarcinoma, a commonly lethal mali

17 This is particularly true of pancreatic ductal adenocarcinoma, a highly lethal diseas

18 ents who undergo pancreaticoduodenectomy for pancreatic ductal adenocarcinoma, additional resection t

19 resectable or locally advanced biopsy-proven pancreatic ductal adenocarcinoma, an Eastern Cooperative

20 ive patients (12.5%) required surgery (3 for pancreatic ductal adenocarcinoma and 2 for intraductal p

21 id pressures, however, are relatively low in pancreatic ductal adenocarcinoma and cannot account for

22 rtained clinic-based cohort of patients with pancreatic ductal adenocarcinoma and describe the clinic

23 progression of pancreatic intraneoplasia to pancreatic ductal adenocarcinoma and liver metastasis in

24 ring genes essential to tumorigenesis in the pancreatic ductal adenocarcinoma and lung adenocarcinoma

25 Using mouse models for pancreatic ductal adenocarcinoma and lung adenocarcinoma

26 8 years, with locally advanced or metastatic pancreatic ductal adenocarcinoma, and Eastern Cooperativ

27 abetes secondary to chronic pancreatitis and pancreatic ductal adenocarcinoma, and highlight several

28 endai criteria negative), 8 of 11 (73%) with pancreatic ductal adenocarcinoma, and in 0 of 19 patient

29 s and murine models of renal cell carcinoma, pancreatic ductal adenocarcinoma, and melanoma triggered

30 We use pancreatic ductal adenocarcinoma as an in vitro and an i

31 (PKD1) are linked to oncogenic signaling in pancreatic ductal adenocarcinoma, but a direct functiona

32 process for the management of patients with pancreatic ductal adenocarcinoma by providing a complete

33 reas OPD patients had a higher percentage of pancreatic ductal adenocarcinoma cases, and greater prop

34 those for managing recalcitrant tumors like pancreatic ductal adenocarcinoma, cause off-target toxic

35 ed in up to 30% of cancers, including 90% of pancreatic ductal adenocarcinomas, causing it to be cons

36 hough VSV is effective against a majority of pancreatic ductal adenocarcinoma cell (PDAC) cell lines,

37 ng the proliferation of KRas-dependent human pancreatic ductal adenocarcinoma cell lines.

38 pIC can also trigger apoptosis in pancreatic ductal adenocarcinoma cells (PDAC) but its me

39 ssed by pancreatic stellate cells (PSCs) and pancreatic ductal adenocarcinoma cells (PDACs), drives t

40 Furthermore, pancreatic ductal adenocarcinoma cells, whose growth dep

41 tibodies decreased the viability of cultured pancreatic ductal adenocarcinoma cells.

42 ic cancer cells and serum from patients with pancreatic ductal adenocarcinoma contain genomic DNA.

43 Human pancreatic ductal adenocarcinomas contain somatic mutati

44 ductal-neuroendocrine lineage plasticity in pancreatic ductal adenocarcinoma, contributing to poor s

45 thelial neoplasia (PanINs), the precursor to pancreatic ductal adenocarcinoma, could generate new str

46 Pancreatic ductal adenocarcinoma, even when diagnosed ea

47 NLS or shRNA knockdown of renalase inhibited pancreatic ductal adenocarcinoma growth.

48 f type 3c diabetes are chronic pancreatitis, pancreatic ductal adenocarcinoma, haemochromatosis, cyst

49 A genetic signature of pancreatic ductal adenocarcinoma has been identified.

50 he stromal response to cancers, particularly pancreatic ductal adenocarcinoma, has evolved from that

51 Integrated genomic analysis of 456 pancreatic ductal adenocarcinomas identified 32 recurren

52 romoted Myo10 expression in cancer cells and pancreatic ductal adenocarcinoma in mice, whereas suppre

53 can serve as an effective cell of origin for pancreatic ductal adenocarcinoma in the setting of gain-

54 2a) was required for progression of IPMNs to pancreatic ductal adenocarcinomas in Acvr1b(flox/flox);L

55 to Kras(G12D)-driven transformation and form pancreatic ductal adenocarcinomas in vivo after Cdkn2a i

56 ies incorporating resected tissue from human pancreatic ductal adenocarcinoma into a reporter-carryin

57 Pancreatic ductal adenocarcinoma is a lethal cancer with

58 Pancreatic ductal adenocarcinoma is a notoriously diffic

59 Pancreatic ductal adenocarcinoma is an aggressive malign

60 Purpose Metastatic pancreatic ductal adenocarcinoma is characterized by exc

61 Beset by poor prognosis, pancreatic ductal adenocarcinoma is classified as famili

62 Effective treatment of pancreatic ductal adenocarcinoma is hindered by lack of

63 Pancreatic ductal adenocarcinoma is on pace to become th

64 The frequency of familial pancreatic ductal adenocarcinoma is small, but its impor

65 One treatment strategy for pancreatic ductal adenocarcinoma is to modify, rather th

66 requently following preoperative therapy for pancreatic ductal adenocarcinoma, it is associated with

67 In contrast to pancreatic ductal adenocarcinoma, no recurrent point mut

68 In the subset of 522 (51%) pancreatic ductal adenocarcinomas, operative approach wa

69 iations of pancreatic neuroendocrine tumors, pancreatic ductal adenocarcinomas, or 1 of several types

70 In a cohort of patients with pancreatic ductal adenocarcinoma, overall survival was i

71 LTSs) (>/=10 years) following a diagnosis of pancreatic ductal adenocarcinoma (PADC) and identifies t

72 lyzed heterocellular KRAS(G12D) signaling in pancreatic ductal adenocarcinoma (PDA) cells.

73 Approximately 50% of all patients with pancreatic ductal adenocarcinoma (PDA) develop diabetes

74 AIMS: Approximately 50% of all patients with pancreatic ductal adenocarcinoma (PDA) develop diabetes

75 or (HGF)/Met signaling has critical roles in pancreatic ductal adenocarcinoma (PDA) development and p

76 Pancreatic ductal adenocarcinoma (PDA) develops predomin

77 Pancreatic ductal adenocarcinoma (PDA) has a dismal prog

78 Pancreatic ductal adenocarcinoma (PDA) has a dismal prog

79 Patients with pancreatic ductal adenocarcinoma (PDA) have a poor progn

80 protein EPAC1 promotes invasion/migration of pancreatic ductal adenocarcinoma (PDA) in vitro.

81 To define the role of KLF4 in pancreatic ductal adenocarcinoma (PDA) initiation, we us

82 Pancreatic ductal adenocarcinoma (PDA) is a deadly cance

83 Pancreatic ductal adenocarcinoma (PDA) is a highly letha

84 Pancreatic ductal adenocarcinoma (PDA) is a lethal disea

85 The poor clinical outcome in pancreatic ductal adenocarcinoma (PDA) is attributed to

86 The tumor microenvironment (TME) in pancreatic ductal adenocarcinoma (PDA) is characterized

87 Pancreatic ductal adenocarcinoma (PDA) is classically re

88 on therapy in the treatment of patients with pancreatic ductal adenocarcinoma (PDA) is controversial.

89 The initiation of pancreatic ductal adenocarcinoma (PDA) is linked to acti

90 Pancreatic ductal adenocarcinoma (PDA) is one of the mos

91 Pancreatic ductal adenocarcinoma (PDA) is the most letha

92 tosis (programmed necrosis), but its role in pancreatic ductal adenocarcinoma (PDA) is unclear.

93 The pathogenesis of pancreatic ductal adenocarcinoma (PDA) requires high lev

94 Previously, it has been shown that pancreatic ductal adenocarcinoma (PDA) tumors exhibit hi

95 s of major importance in the pathobiology of pancreatic ductal adenocarcinoma (PDA), and specific con

96 lycoprotein that is overexpressed in >80% of pancreatic ductal adenocarcinoma (PDA), induced a pro-an

97 embryonic signaling pathways is frequent in pancreatic ductal adenocarcinoma (PDA), making developme

98 llular matrix (ECM) is a defining feature of pancreatic ductal adenocarcinoma (PDA), where ECM signal

99 We investigated this duality in pancreatic ductal adenocarcinoma (PDA), which, with othe

100 reatment option for patients with stage I/II pancreatic ductal adenocarcinoma (PDA), yet many studies

101 ease progression and therapeutic response in pancreatic ductal adenocarcinoma (PDA).

102 ctin 1 is highly expressed on macrophages in pancreatic ductal adenocarcinoma (PDA).

103 y 40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA).

104 er.Obesity is an established risk factor for pancreatic ductal adenocarcinoma (PDA).

105 tumor cells may improve the poor outcome of pancreatic ductal adenocarcinoma (PDA).

106 Obesity is an established risk factor for pancreatic ductal adenocarcinoma (PDA).

107 sion of exosomes at the distal tumor site of pancreatic ductal adenocarcinoma (PDAC) ablated the deve

108 Pancreatic ductal adenocarcinoma (PDAC) after complete s

109 used genetically engineered mouse models of pancreatic ductal adenocarcinoma (PDAC) and found that m

110 nsmembrane mucin, is aberrantly expressed in pancreatic ductal adenocarcinoma (PDAC) and generally co

111 LCN2 is upregulated in patients with pancreatic ductal adenocarcinoma (PDAC) and in obese ind

112 m of our study was to analyze the miRNome of pancreatic ductal adenocarcinoma (PDAC) and its preneopl

113 Pancreatic ductal adenocarcinoma (PDAC) and other carcin

114 reduced metastasis and prolonged survival in pancreatic ductal adenocarcinoma (PDAC) and our genomic

115 Patients with pancreatic ductal adenocarcinoma (PDAC) and preoperative

116 EMMs) have greatly expanded our knowledge of pancreatic ductal adenocarcinoma (PDAC) and serve as a c

117 olin was overexpressed in human specimens of pancreatic ductal adenocarcinoma (PDAC) and that the ove

118 KRAS are the hallmark genetic alterations in pancreatic ductal adenocarcinoma (PDAC) and the key driv

119 Nineteen patients (5%) had distinct pancreatic ductal adenocarcinoma (PDAC) and were exclude

120 The relationships between diabetes and pancreatic ductal adenocarcinoma (PDAC) are complex.

121 Most patients with pancreatic ductal adenocarcinoma (PDAC) are diagnosed wi

122 Early-detection tests for pancreatic ductal adenocarcinoma (PDAC) are needed.

123 ch chronic stress promote the development of pancreatic ductal adenocarcinoma (PDAC) are poorly defin

124 The mechanisms of initiation of pancreatic ductal adenocarcinoma (PDAC) are still largel

125 Pancreatic ductal adenocarcinoma (PDAC) carries the most

126 Pancreatic ductal adenocarcinoma (PDAC) cells (PCC) have

127 RAIL-R2 overexpression or knockdown in human pancreatic ductal adenocarcinoma (PDAC) cells and their

128 In adaptation to oncogenic signals, pancreatic ductal adenocarcinoma (PDAC) cells undergo ep

129 Subpopulations of human pancreatic ductal adenocarcinoma (PDAC) cells were simil

130 tic vesicular stomatitis virus (VSV) against pancreatic ductal adenocarcinoma (PDAC) cells.

131 ternative route for discharging lactate from pancreatic ductal adenocarcinoma (PDAC) cells.

132 Increased PI 3-kinase (PI3K) signaling in pancreatic ductal adenocarcinoma (PDAC) correlates with

133 and to liver metastasis, which in turn makes pancreatic ductal adenocarcinoma (PDAC) difficult to tre

134 The genome of pancreatic ductal adenocarcinoma (PDAC) frequently conta

135 Pancreatic ductal adenocarcinoma (PDAC) has a grim progn

136 Pancreatic ductal adenocarcinoma (PDAC) has a poor progn

137 rrant expression of the kinase IKKepsilon in pancreatic ductal adenocarcinoma (PDAC) has been associa

138 Pancreatic ductal adenocarcinoma (PDAC) has generally a

139 d effects of altered activities of miRNAs in pancreatic ductal adenocarcinoma (PDAC) has not been don

140 forms serve in the systemic dissemination of pancreatic ductal adenocarcinoma (PDAC) has not been inv

141 ensive alternative splicing (AS) analysis of pancreatic ductal adenocarcinoma (PDAC) has not been per

142 Pancreatic ductal adenocarcinoma (PDAC) has single-digit

143 ntially curative R0 resection, patients with pancreatic ductal adenocarcinoma (PDAC) have a poor prog

144 The incidence and death rate of pancreatic ductal adenocarcinoma (PDAC) have increased i

145 Immunotherapy approaches for pancreatic ductal adenocarcinoma (PDAC) have met with li

146 The exact nature and dynamics of pancreatic ductal adenocarcinoma (PDAC) immune compositi

147 mmadelta T cells from healthy donors to kill pancreatic ductal adenocarcinoma (PDAC) in vitro and in

148 erates with oncogenic signaling to influence pancreatic ductal adenocarcinoma (PDAC) initiation, prog

149 o-ductal metaplasia (ADM) is a key event for pancreatic ductal adenocarcinoma (PDAC) initiation.

150 Patients with pancreatic ductal adenocarcinoma (PDAC) invariably succu

151 Pancreatic ductal adenocarcinoma (PDAC) is a deadly canc

152 Pancreatic ductal adenocarcinoma (PDAC) is a devastating

153 Pancreatic ductal adenocarcinoma (PDAC) is a genomically

154 Pancreatic ductal adenocarcinoma (PDAC) is a highly aggr

155 Pancreatic ductal adenocarcinoma (PDAC) is a highly aggr

156 Pancreatic ductal adenocarcinoma (PDAC) is a highly leth

157 Pancreatic ductal adenocarcinoma (PDAC) is a lethal form

158 Dense fibrotic stroma associated with pancreatic ductal adenocarcinoma (PDAC) is a major obsta

159 (miR-10b) expression in the cancer cells in pancreatic ductal adenocarcinoma (PDAC) is a marker of d

160 The hallmark of pancreatic ductal adenocarcinoma (PDAC) is abundant desm

161 The malignant progression of pancreatic ductal adenocarcinoma (PDAC) is accompanied b

162 Pancreatic ductal adenocarcinoma (PDAC) is almost unifor

163 Pancreatic ductal adenocarcinoma (PDAC) is an aggressive

164 Pancreatic ductal adenocarcinoma (PDAC) is an aggressive

165 Pancreatic Ductal Adenocarcinoma (PDAC) is an aggressive

166 Pancreatic ductal adenocarcinoma (PDAC) is an aggressive

167 Pancreatic ductal adenocarcinoma (PDAC) is characterized

168 Pancreatic ductal adenocarcinoma (PDAC) is characterized

169 Pancreatic ductal adenocarcinoma (PDAC) is characterized

170 Pancreatic ductal adenocarcinoma (PDAC) is characterized

171 Pancreatic ductal adenocarcinoma (PDAC) is characterized

172 Pancreatic ductal adenocarcinoma (PDAC) is characterized

173 The management of pancreatic ductal adenocarcinoma (PDAC) is extremely poo

174 cally advanced/borderline resectable (LA/BR) pancreatic ductal adenocarcinoma (PDAC) is not standardi

175 epidemic in obesity and metabolic syndrome, pancreatic ductal adenocarcinoma (PDAC) is on track to b

176 Pancreatic ductal adenocarcinoma (PDAC) is one of the de

177 Pancreatic ductal adenocarcinoma (PDAC) is one of the de

178 Pancreatic ductal adenocarcinoma (PDAC) is one of the de

179 Pancreatic ductal adenocarcinoma (PDAC) is one of the mo

180 The therapeutic resistance of pancreatic ductal adenocarcinoma (PDAC) is partly ascrib

181 efficacy of systemic cancer therapeutics in pancreatic ductal adenocarcinoma (PDAC) is partly attrib

182 t the role of sympathetic nerve signaling in pancreatic ductal adenocarcinoma (PDAC) is poorly unders

183 Pancreatic ductal adenocarcinoma (PDAC) is strikingly re

184 Pancreatic ductal adenocarcinoma (PDAC) is the fourth le

185 Pancreatic ductal adenocarcinoma (PDAC) is the fourth-le

186 to the effective treatment of patients with pancreatic ductal adenocarcinoma (PDAC) is the molecular

187 A hallmark of pancreatic ductal adenocarcinoma (PDAC) is the presence

188 Pancreatic ductal adenocarcinoma (PDAC) is typically dia

189 t their role in the malignant progression of pancreatic ductal adenocarcinoma (PDAC) is uncertain.

190 erstanding the initiation and progression of pancreatic ductal adenocarcinoma (PDAC) may provide ther

191 stromal signals regulate the development of pancreatic ductal adenocarcinoma (PDAC) may suggest nove

192 Pancreatic ductal adenocarcinoma (PDAC) metastasizes by

193 Pancreatic ductal adenocarcinoma (PDAC) metastasizes to

194 investigated the ontogeny of TAMs in murine pancreatic ductal adenocarcinoma (PDAC) models.

195 e effects of alcohol drinking and smoking on pancreatic ductal adenocarcinoma (PDAC) mortality are co

196 Pancreatic ductal adenocarcinoma (PDAC) offers an optima

197 r-associated macrophages in a mouse model of pancreatic ductal adenocarcinoma (PDAC) originate from b

198 , we found that in cancer cells derived from pancreatic ductal adenocarcinoma (PDAC) PAR2 protein is

199 we investigated how eIF5A proteins regulate pancreatic ductal adenocarcinoma (PDAC) pathogenesis.

200 efficacy of the bromodomain inhibitor JQ1 in pancreatic ductal adenocarcinoma (PDAC) patient-derived

201 and otastat potassium" in chemotherapy-naive pancreatic ductal adenocarcinoma (PDAC) patients with pe

202 Tissue architecture contributes to pancreatic ductal adenocarcinoma (PDAC) phenotypes.

203 ls of non-small-cell lung cancer (NSCLC) and pancreatic ductal adenocarcinoma (PDAC) reduces tumor gr

204 Outcomes for patients with pancreatic ductal adenocarcinoma (PDAC) remain poor.

205 Pancreatic ductal adenocarcinoma (PDAC) remains a highly

206 Pancreatic ductal adenocarcinoma (PDAC) remains a lethal

207 Despite some advances, pancreatic ductal adenocarcinoma (PDAC) remains generall

208 To explore the role of pancreatic ductal adenocarcinoma (PDAC) size on surgical

209 e, we found miR-206 to be abrogated in human pancreatic ductal adenocarcinoma (PDAC) specimens and ce

210 trated that pancreatic stellate cells within pancreatic ductal adenocarcinoma (PDAC) stroma secrete l

211 s report, we demonstrate in a mouse model of pancreatic ductal adenocarcinoma (PDAC) that inhibiting

212 n multi-spectral images of multiplex-labeled pancreatic ductal adenocarcinoma (PDAC) tissue samples.

213 nstrate that IL-35 is overexpressed in human pancreatic ductal adenocarcinoma (PDAC) tissues, and tha

214 ed in patients suspected of being at risk of pancreatic ductal adenocarcinoma (PDAC) to better define

215 nflammation that accompanies early phases of pancreatic ductal adenocarcinoma (PDAC) would produce pa

216 ocrine pancreas that promotes development of pancreatic ductal adenocarcinoma (PDAC), a deadly pancre

217 a conditional oncogenic Kras mouse model of pancreatic ductal adenocarcinoma (PDAC), a malignancy th

218 Pancreatic ductal adenocarcinoma (PDAC), a particularly

219 In this study, we examined the metabolism of pancreatic ductal adenocarcinoma (PDAC), a poorly vascul

220 modestly improved the survival prospects of pancreatic ductal adenocarcinoma (PDAC), additional enga

221 in the proto-oncogene KRAS are a hallmark of pancreatic ductal adenocarcinoma (PDAC), an aggressive m

222 Gemcitabine is commonly used to treat pancreatic ductal adenocarcinoma (PDAC), and we hypothes

223 the backbones for chemotherapy treatment in pancreatic ductal adenocarcinoma (PDAC), but patients of

224 KRAS is the most frequently mutated gene in pancreatic ductal adenocarcinoma (PDAC), but the mechani

225 KN2A) occur in approximately 80% of sporadic pancreatic ductal adenocarcinoma (PDAC), contributing to

226 long been the standard of care for treating pancreatic ductal adenocarcinoma (PDAC), despite its poo

227 ligand overexpressed by neoplastic cells in pancreatic ductal adenocarcinoma (PDAC), drives formatio

228 During the progression of pancreatic ductal adenocarcinoma (PDAC), heterogeneous s

229 Many somatic mutations have been detected in pancreatic ductal adenocarcinoma (PDAC), leading to the

230 lthough smoking is a leading risk factor for pancreatic ductal adenocarcinoma (PDAC), little is known

231 In pancreatic ductal adenocarcinoma (PDAC), mutant KRAS sti

232 he development and metastatic progression of pancreatic ductal adenocarcinoma (PDAC), one of the dead

233 (SIRT6) that is critical for suppression of pancreatic ductal adenocarcinoma (PDAC), one of the most

234 Incidence of and mortality from pancreatic ductal adenocarcinoma (PDAC), the most common

235 y of metastasis in an autochthonous model of pancreatic ductal adenocarcinoma (PDAC), using lineage t

236 MT2D are subject to deletion and mutation in pancreatic ductal adenocarcinoma (PDAC), where these les

237 invasive and widely metastatic phenotype of pancreatic ductal adenocarcinoma (PDAC).

238 ral population-based cohort of patients with pancreatic ductal adenocarcinoma (PDAC).

239 M), a precursor lesion to the development of pancreatic ductal adenocarcinoma (PDAC).

240 ed clinical benefit to date in patients with pancreatic ductal adenocarcinoma (PDAC).

241 echnologies to identify oncogenic drivers of pancreatic ductal adenocarcinoma (PDAC).

242 atitis is the most important risk factor for pancreatic ductal adenocarcinoma (PDAC).

243 ism pathways were shown to be deregulated in pancreatic ductal adenocarcinoma (PDAC).

244 survival in a large cohort of patients with pancreatic ductal adenocarcinoma (PDAC).

245 than Met at inhibiting cell proliferation in pancreatic ductal adenocarcinoma (PDAC).

246 approaches to attenuate CXCL4L1 in models of pancreatic ductal adenocarcinoma (PDAC).

247 and p16 inactivation are required to develop pancreatic ductal adenocarcinoma (PDAC).

248 reatic intraepithelial neoplasia (PanIN) and pancreatic ductal adenocarcinoma (PDAC).

249 domain, during pathogenesis of Kras-induced pancreatic ductal adenocarcinoma (PDAC).

250 h drug resistance in many cancers, including pancreatic ductal adenocarcinoma (PDAC).

251 e survival after pancreaticoduodenectomy for pancreatic ductal adenocarcinoma (PDAC).

252 unction as a safeguard during development of pancreatic ductal adenocarcinoma (PDAC).

253 care in the adjuvant treatment of resectable pancreatic ductal adenocarcinoma (PDAC).

254 three highly distinct metabolic subtypes in pancreatic ductal adenocarcinoma (PDAC).

255 ts and mice, but these have little effect on pancreatic ductal adenocarcinoma (PDAC).

256 The authors developed a Markov model of pancreatic ductal adenocarcinoma (PDAC).

257 roscopy (LapDP) or open surgery (OpenDP) for pancreatic ductal adenocarcinoma (PDAC).

258 ations in the KRAS oncogene are prevalent in pancreatic ductal adenocarcinoma (PDAC).

259 omas and are particularly prominent in human pancreatic ductal adenocarcinoma (PDAC).

260 umorigenicity in human colorectal cancer and pancreatic ductal adenocarcinoma (PDAC).

261 a signaling node frequently mutated in human pancreatic ductal adenocarcinoma (PDAC).

262 l roles in the initiation and progression of pancreatic ductal adenocarcinoma (PDAC).

263 Here we assessed the role of ESRP1 in pancreatic ductal adenocarcinoma (PDAC).

264 anIN1) lesions rarely become fully malignant pancreatic ductal adenocarcinoma (PDAC).

265 was also expressed in many tumors including pancreatic ductal adenocarcinoma (PDAC).

266 onditions promote chemotherapy resistance in pancreatic ductal adenocarcinoma (PDAC).

267 itions, is a major susceptibility factor for pancreatic ductal adenocarcinoma (PDAC).

268 pithelial neoplasias (PanINs) and ultimately pancreatic ductal adenocarcinoma (PDAC).

269 roscopic or robot-assisted approach, 24% for pancreatic ductal adenocarcinoma (PDAC).

270 ess is stimulated and leads to cell death in pancreatic ductal adenocarcinoma (PDAC).

271 um, ampulla, or distal CBD with those having pancreatic ductal adenocarcinoma (PDAC).

272 sion, is common in various cancers including pancreatic ductal adenocarcinoma (PDAC).

273 Pancreatic ductal adenocarcinomas (PDAC) harbor recurren

274 The majority of pancreatic ductal adenocarcinomas (PDAC) rely on the mRN

275 In pancreatic ductal adenocarcinomas (PDAC), lymphoid infil

276 ) is a fundamental driver in the majority of pancreatic ductal adenocarcinomas (PDAC).

277 lar matrix (D-ECM), is a puzzling feature of pancreatic ductal adenocarcinoma (PDACs).

278 or activated in most solid tumors, including pancreatic ductal adenocarcinomas (PDACs).

279 copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs).

280 (dMMR) is detected in a small proportion of pancreatic ductal adenocarcinomas (PDACs).

281 ating mutations in KRAS are detected in most pancreatic ductal adenocarcinomas (PDACs).

282 ncerous cystic lesions that can develop into pancreatic ductal adenocarcinomas (PDACs).

283 ) comprise the majority of the tumor bulk of pancreatic ductal adenocarcinomas (PDACs).

284 analyze somatic noncoding alterations in 308 pancreatic ductal adenocarcinomas (PDAs) and identify co

285 s by EXponential enrichment) targeting human pancreatic ductal adenocarcinoma (PL45).

286 a phase 2 study in patients with metastatic pancreatic ductal adenocarcinoma previously treated with

287 Eligible patients with metastatic pancreatic ductal adenocarcinoma previously treated with

288 nalyzed ductal and neuroendocrine markers in pancreatic ductal adenocarcinoma, revealing heterogeneou

289 by a multi-institutional group of experts in pancreatic ductal adenocarcinoma that included radiologi

290 In pancreatic ductal adenocarcinoma, the CCL2-CCR2 chemokin

291 In orthotopic mouse models of melanoma and pancreatic ductal adenocarcinoma, the compounds reduced

292 R55alpha expression was markedly elevated in pancreatic ductal adenocarcinoma tissues compared with a

293 Patients with pancreatic ductal adenocarcinoma treated within the inte

294 action between these two pathways in primary pancreatic ductal adenocarcinoma tumor cells and provide

295 atients with previously untreated metastatic pancreatic ductal adenocarcinoma were randomly assigned

296 elected, consecutive, incident patients with pancreatic ductal adenocarcinoma were recruited at a sin

297 eage marker heterogeneity in mouse models of pancreatic ductal adenocarcinoma, where lineage tracing

298 tic potential of Kras(G12D/+);Trp53(R172H/+) pancreatic ductal adenocarcinomas while increasing their

299 e safety profile in patients with metastatic pancreatic ductal adenocarcinoma who previously received

300 patients with histopathologically confirmed pancreatic ductal adenocarcinoma who received preoperati