ライフサイエンスコーパス: pancreatic

1 few LDs were found in normal human juvenile pancreatic acinar and islet cells, with numbers subseque

2 Alterations in calcium signaling in pancreatic acinar cells can result in pancreatitis.

3 mice given cerulein injections had increased pancreatic activation of trypsinogen and more edema, inf

4 Higher pancreatic activity of trypsin increases the severity of

5 currence after curative-intent resection for pancreatic adenocarcinoma (PDAC).

6 This study assesses how the volume of pancreatic-adjacent operations (PAO) impacts the outcome

7 a possible genetic modifier contributing to pancreatic agenesis and demonstrates the usefulness of u

8 in human serum is a key indicator of various pancreatic ailments and an affordable point-of-care dete

9 on the generation of stem cell-derived human pancreatic alpha (SC-alpha) cells from pluripotent stem

10 ization of Pg in relation to mouse and human pancreatic alpha- and beta-cells using 3-D confocal and

11 man Salivary alpha-amylase (HSA) and Porcine Pancreatic alpha-amylase (PPA).

12 inhibition of Wnt signaling in Wnt-addicted pancreatic and colorectal cancer models.

13 ardiac outflow tract defects, sometimes with pancreatic and diaphragmic malformations.

14 To compare pancreatic and hepatic steatosis quantified by proton de

15 hanged, autocrine SHH interference in colon, pancreatic, and lung cell lines triggered cell death thr

16 eas, widely prescribed for diabetes, inhibit pancreatic ATP-sensitive K(+) (K(ATP) ) channels to incr

17 Strikingly, severe pancreatic atrophy accompanied tumor progression in Ddr1

18 Pancreatic Bap1 deficiency causes acinar atrophy but com

19 is caused by single gene mutations reducing pancreatic beta cell number or impairing beta cell funct

20 onal potential of the GLP-1/GLP-1R system in pancreatic beta cells has led to the development of esta

21 though most effort has focused on generating pancreatic beta cells, considerable evidence indicates t

22 at SPARC promoted GSIS by inhibiting RGS4 in pancreatic beta cells.

23 coupled to the prostaglandin EP3 receptor in pancreatic beta cells.

24 ulation in the insulin secretory granules of pancreatic beta cells.

25 ding to the destruction of insulin producing pancreatic beta cells.

26 tor that may contribute to the initiation of pancreatic beta-cell destruction during the development

27 e 2 diabetes, a process which contributes to pancreatic beta-cell dysfunction and death.

28 chronic metabolic stress, may contribute to pancreatic beta-cell failure.

29 the insulin receptor; however, its impact on pancreatic beta-cell function is unknown.

30 of glucose uptake by skeletal muscle, and of pancreatic beta-cell phenotype in mice.

31 Insulin-secreting pancreatic beta-cells express the machinery for DA synth

32 Fine-tuning of insulin release from pancreatic beta-cells is essential to maintain blood glu

33 sceptibility locus, but its specific role in pancreatic beta-cells is largely unknown.

34 ibe the impact of induced Sbp2 deficiency in pancreatic beta-cells on selenoprotein transcript profil

35 is regulated by calcium (Ca(2+) ) entry into pancreatic beta-cells through voltage-dependent Ca(2+) (

36 a global disease caused by the inability of pancreatic beta-cells to secrete adequate insulin.

37 ge (e.g., the liver, vasculature, heart, and pancreatic beta-cells).

38 Within the pancreatic beta-cells, insulin secretory granules (SGs)

39 P2Y14 was expressed in both human and rodent pancreatic beta-cells.

40 al and pathological conditions, including in pancreatic beta-cells.

41 in situ hybridisation for RFX6 in the dorsal pancreatic bud of a Carnegie stage 14 human embryo.

42 ceeded in participants with locally advanced pancreatic cancer (17 months) and those with local recur

43 d followed by in vivo treatment of xenograft pancreatic cancer (BxPC-3) tumours in a murine model.

44 reatic cancer cell line, Dartmouth-Hitchcock Pancreatic Cancer (DHPC)-018.

45 o high levels of target miR-1291-5p in human pancreatic cancer (PC) cells.

46 Pancreatic cancer (PC) remains a therapeutic challenge b

47 ange, 56-69 years]; 40 with locally advanced pancreatic cancer and 10 with local recurrence) were inc

48 diagnosis from 129 subjects with resectable pancreatic cancer and 275 controls (100 healthy subjects

49 collected up to 5 years before diagnosis of pancreatic cancer and from 875 matched controls from the

50 Family history of pancreatic cancer and high-grade IPMN was identified as

51 next discuss current treatment paradigms for pancreatic cancer and the shortcomings of targeted thera

52 Patients with pancreatic cancer are often divided into one of four cat

53 tions between selected GP2 gene variants and pancreatic cancer are replicated in 10,822 additional ca

54 my (2014-2017) were extracted from the Dutch Pancreatic Cancer Audit.

55 Comparison of resectable pancreatic cancer cases to subjects with chronic pancrea

56 ave equivalent potency to gemcitabine in the pancreatic cancer cell line MIA PaCa-2.

57 protrusions, which we classify as TMTs, in a pancreatic cancer cell line, Dartmouth-Hitchcock Pancrea

58 In studies of pancreatic cancer cell lines and mice, we found that ZIP

59 Pancreatic cancer cell lines were analyzed by gene-expre

60 show that KP372-1 sensitizes NQO1-expressing pancreatic cancer cells and spares immortalized normal p

61 ous trans-differentiation of human and mouse pancreatic cancer cells can influence the phenotype of n

62 MUC1 knockdown in pancreatic cancer cells enhanced unfolded protein respon

63 or subsequent utilization during invasion of pancreatic cancer cells, representing a potential target

64 molecular mechanism leading to resistance in pancreatic cancer cells.

65 inhibition creates enhanced cytotoxicity in pancreatic cancer cells.

66 As the incidence of pancreatic cancer continues to increase, new treatment s

67 1cre, KC), which mirrors the early stages of pancreatic cancer development.

68 The alkylating warhead of the pancreatic cancer drug streptozotocin (SZN) contains an

69 CA19-9 can serve as an anchor marker for pancreatic cancer early detection applications.

70 AC and may provide insights to understanding pancreatic cancer etiology.

71 CT of patients with metastasized ovarian and pancreatic cancer for follow-up to therapy with (90)Y-FA

72 Pancreatic cancer has a dismal prognosis, and there is n

73 Risk factors for developing pancreatic cancer include family history, obesity, type

74 anding molecular pathways that contribute to pancreatic cancer initiation and progression provides th

75 Pancreatic cancer is characterized by an extensive and c

76 The prognosis for patients with pancreatic cancer is extremely poor, as they are resista

77 ine treatment causes profound changes in the pancreatic cancer microenvironment, including elevated T

78 ylating agent causes profound changes in the pancreatic cancer microenvironment, including increased

79 or camptothecin (CPT) down-regulated FLIP in pancreatic cancer models and enhanced apoptosis induced

80 aged 18 years or older with biopsy-confirmed pancreatic cancer of any stage, enrolled in the KYT prog

81 as-induced metaplastic cells, which leads to pancreatic cancer onset and progression.

82 To comprehend the contribution of Muc5ac in pancreatic cancer pathology, we genetically ablated it i

83 vely correlated with the overall survival of pancreatic cancer patients.

84 l to be an effective neoadjuvant therapy for pancreatic cancer patients.

85 nerves by cancer cells has a driving role in pancreatic cancer progression.

86 The overall prognosis for pancreatic cancer remains dismal and potent chemotherape

87 ge 50 years is more strongly associated with pancreatic cancer risk than BMI at older ages, and they

88 We obtained 93 pancreatic cancer specimens (tumor and adjacent nontumor

89 ancer of the pancreas (ASCP) is a subtype of pancreatic cancer that has a worse prognosis and greater

90 uggest IL-17RB can be a potential target for pancreatic cancer therapy.

91 has been reported as a major contributor in pancreatic cancer tumorigenesis and chemoresistance.

92 In addition, pancreatic cancer was found to be higher under the press

93 cancer, liver cancer, colorectal cancer, and pancreatic cancer were 5% (95% CI: 3-8%), 12% (95% CI: 8

94 lorectal cancer, KRAS in gastric cancer, and pancreatic cancer were mostly associated gene alteration

95 These lesions progress to metastatic pancreatic cancer with high frequency.

96 males, 1% to 4%; 95% CI males, 2% to 5%) for pancreatic cancer, and 1% (95% CI, 0.2% to 5%) for male

97 rectal cancer, liver cancer, stomach cancer, pancreatic cancer, and esophageal cancer are leading cau

98 stantial effect on survival in patients with pancreatic cancer, and that molecularly guided treatment

99 rate for resectable or borderline resectable pancreatic cancer, but the overall benefit is unproven.

100 agents that are used to treat breast cancer, pancreatic cancer, colorectal cancer, or non-small cell

101 Oncogenic KRAS, a critical driver of pancreatic cancer, promotes metabolic reprogramming and

102 In pancreatic cancer, selective autophagy instead reroutes

103 equence of squamous trans-differentiation in pancreatic cancer, thus highlighting an instructive role

104 6 positive, cell culture-derived, breast and pancreatic cancer-derived exosomes, respectively, when t

105 tive therapeutic intervention for mitigating pancreatic cancer-induced cachexia.

106 geal cancer, colon cancer, rectal cancer and pancreatic cancer.

107 ing further development for the treatment of pancreatic cancer.

108 the development of high-grade dysplasia and pancreatic cancer.

109 s a drug of choice in the treatment of human pancreatic cancer.

110 (HSL) in regulating the aggressive nature of pancreatic cancer.

111 ancer, but its benefits have not extended to pancreatic cancer.

112 fy mechanisms of MEK inhibitor resistance in pancreatic cancer.

113 2014, a total of 8,354 participants died of pancreatic cancer.

114 ily history of breast, ovarian, prostate, or pancreatic cancer.

115 Here we report that patients whose pancreatic cancers express elevated levels of Death Rece

116 About 25% of pancreatic cancers harbour actionable molecular alterati

117 igrations of several solid cancers including pancreatic cancers that require high DPAGT1 expression i

118 We previously reported that metastatic pancreatic cancers were dependent on the glucose-metabol

119 often observed in association with invasive pancreatic cancers, but their origins and evolutionary r

120 This curbed chemoresistance in KRAS-mutant pancreatic cancers.

121 cell atlas can be interrogated to understand pancreatic cell biology and provides a crucial reference

122 l cells underpin the generation of different pancreatic cell types.

123 In lung and pancreatic cells, gene ontology analyses of DM promoters

124 ive cargo in beta-cells as compared to other pancreatic cells; importantly, Zn(II)-mediated hydrolysi

125 TO varies considerably between pancreatic centers, demonstrating the potential benefit

126 In pancreatic CSCs, PAF1 interacts with DDX3 and PHF5A to r

127 zed trial of patients undergoing EUS-FNA for pancreatic cyst evaluation, we found the risk of infecti

128 ciprofloxacin vs placebo in patients with a pancreatic cyst requiring EUS-FNA at multiple centers in

129 Clinical, EUS and pancreatic cystic fluid (PCF) data were prospectively re

130 eedle aspiration (EUS-FNA) is recommended in pancreatic cystic lesions (PCLs) with worrisome features

131 Our primary outcome was the presence of pancreatic cysts on initial surveillance in patients wit

132 onic pancreatitis; and 125 with noncancerous pancreatic cysts).

133 BEST PRACTICE ADVICE 6: Pancreatic debridement should be avoided in the early, a

134 ibe a requirement for MAFB late in the human pancreatic developmental program and identify it as a di

135 extensive translation of lncRNAs during hESC pancreatic differentiation and provides a blueprint for

136 report that MAFB knockout hPSCs have normal pancreatic differentiation capacity up to the progenitor

137 etermined using an in vitro simulated peptic-pancreatic digestion, followed by measurement of ferriti

138 generalizability across murine cohorts with pancreatic disease.

139 e samples to map the cellular foundations of pancreatic diseases.

140 on was defined as a new IPMN, increased main pancreatic duct (MPD) size, and increased size of an exi

141 cancer cells and spares immortalized normal pancreatic duct cells, hTERT-HPNE.

142 From approx. 130 weeks post pancreatic duct ligation, all animals were supplemented

143 12-week-old female diabetic Balb/c mice via pancreatic duct.

144 e optimal neoadjuvant therapy for resectable pancreatic ductal adenocarcinoma (PDA) and the impact on

145 Pancreatic ductal adenocarcinoma (PDA) is among the most

146 Pancreatic ductal adenocarcinoma (PDA) is an aggressive

147 Pancreatic ductal adenocarcinoma (PDAC) and cholangiocar

148 ying adaptive targeted therapy resistance in pancreatic ductal adenocarcinoma (PDAC) are poorly under

149 Here, we present non-invasive detection of pancreatic ductal adenocarcinoma (PDAC) by 5-hydroxymeth

150 Patients with pancreatic ductal adenocarcinoma (PDAC) have high plasma

151 mprovements in the outcomes of patients with pancreatic ductal adenocarcinoma (PDAC) have lagged behi

152 Pancreatic ductal adenocarcinoma (PDAC) is a genetically

153 Pancreatic ductal adenocarcinoma (PDAC) is a leading cau

154 Pancreatic ductal adenocarcinoma (PDAC) is an aggressive

155 KRAS mutant pancreatic ductal adenocarcinoma (PDAC) is characterized

156 Pancreatic ductal adenocarcinoma (PDAC) is characterized

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

158 to its late diagnosis and dismal prognosis, pancreatic ductal adenocarcinoma (PDAC) is one of the mo

159 Pancreatic ductal adenocarcinoma (PDAC) is typically dia

160 Pancreatic ductal adenocarcinoma (PDAC) remains one of t

161 Pancreatic ductal adenocarcinoma (PDAC) remains one of t

162 The prognosis for pancreatic ductal adenocarcinoma (PDAC) remains poor des

163 er metastatic potential than the more common pancreatic ductal adenocarcinoma (PDAC) subtype.

164 patients with locally advanced or metastatic pancreatic ductal adenocarcinoma (PDAC) treated with FOL

165 To expand the TAA landscape of pancreatic ductal adenocarcinoma (PDAC), we performed ta

166 besity is a major modifiable risk factor for pancreatic ductal adenocarcinoma (PDAC), yet how and whe

167 hanisms that regulate AXL over-expression in pancreatic ductal adenocarcinoma (PDAC).

168 colytic viruses are promising agents against pancreatic ductal adenocarcinoma (PDAC).

169 may contribute to stagnant survival rates in pancreatic ductal adenocarcinoma (PDAC).

170 ineffective for improving early detection of pancreatic ductal adenocarcinoma (PDAC).

171 n oncogenic Kras murine model of spontaneous pancreatic ductal adenocarcinoma (PDAC).

172 Pancreatic ductal adenocarcinoma carries a dismal progno

173 intraductal papillary mucosal neoplasms and pancreatic ductal adenocarcinoma including the character

174 ike cells isolated from patients affected by pancreatic ductal adenocarcinoma, was observed, pointing

175 of chronic pancreatitis and occurs in 25% of pancreatic ductal adenocarcinomas and 40% of acinar cell

176 tility and is believed to be dysregulated in pancreatic ductal adenocarcinomas.

177 Pancreatic ductal carcinoma (PDAC) is a highly lethal ca

178 d that SLC26A9 is predominantly expressed in pancreatic ductal cells and frequently coexpressed with

179 s important to identify and ligate accessory pancreatic ducts since persistence of accessory ducts wi

180 ted, and found that nine are dispensable for pancreatic endocrine cell development.

181 e why individuals with MRS specifically lack pancreatic endocrine cells, we micro-CT imaged a 12-week

182 sponsive insulin delivery systems that mimic pancreatic endocrine function could enhance health and i

183 ive for the long-term, longitudinal study of pancreatic endocrine regeneration.

184 cifically labels a subset of PDX1-expressing pancreatic endoderm.

185 e 2 diabetes overlap with putative endocrine pancreatic enhancers, suggesting that these SNPs modulat

186 Stricture of pancreatic-enteric anastomoses is a major late complicat

187 in nutrient malabsorption and requires oral pancreatic enzyme replacement.

188 ligation, all animals were supplemented with pancreatic enzymes and vitamins resulting in blood conce

189 The physiological activity of pancreatic enzymes in the ileum has been studied in heal

190 The interplay between pancreatic epithelium and the surrounding microenvironme

191 vious studies demonstrate that activation of pancreatic ER kinase (PERK) protects oligodendrocytes ag

192 Most infants with cystic fibrosis (CF) have pancreatic exocrine insufficiency that results in nutrie

193 d subcutaneous adipose tissue, and liver and pancreatic fat at MRI.

194 The hepatic fat fraction was 4.9% and the pancreatic fat fraction was 7.9%.

195 unction enzymes, fetuin-A, body composition, pancreatic fat, intramyocellular lipids, fecal SCFAs, bl

196 lation must address the challenges of severe pancreatic fibrosis and young donor age.

197 Older age (OR-1.07), grade B/C pancreatic fistula (OR-3.84), and epidural use (OR-3.12)

198 Secondary outcomes were postoperative pancreatic fistula (POPF), delayed gastric emptying (DGE

199 ctrum of individual patient presentations of pancreatic fistula risk, and to define the utility of mi

200 The presence of postoperative pancreatic fistula was a significant risk factor for bot

201 Any efforts to reduce postoperative pancreatic fistula would decrease the incidence of incis

202 y ducts will lead to maintenance of exocrine pancreatic function.

203 ts that cholinergic stimulation of islets by pancreatic ganglia resets these endocrine units, produci

204 lamic stem/progenitor cells produce multiple pancreatic, gastrointestinal and hypothalamic peptides i

205 Reliance on rodents for understanding pancreatic genetics, development and islet function coul

206 elopment were splanchnic vein thrombosis and pancreatic head parenchymal necrosis.

207 Amylin, a pancreatic hormone and neuropeptide, acts principally in

208 elevated blood glucose is not due to altered pancreatic hormone release.

209 stigated the respective roles of glucose and pancreatic hormones on AMPK activation in mouse primary

210 slet amyloid polypeptide (IAPP) is linked to pancreatic inflammation, beta-cell degeneration, and the

211 injury and improved survival independent of pancreatic injury.

212 ence of epilepsy and the absence of exocrine pancreatic insufficiency and hypoplasia of nasal alae.

213 Exocrine pancreatic insufficiency was successfully induced in 12

214 nc-1, and Panc-28 cells and samples of human pancreatic intraepithelial neoplasia (PanIN), along with

215 PRKD1(KO)-KC mice developed more pancreatic intraepithelial neoplasia, at a faster rate,

216 rs of stromal activation entirely surrounded pancreatic intraepithelial neoplasias in KPC/Cdh11(+/+)

217 of statins in the reduction of systemic and pancreatic intraluminal inflammation, we hypothesized th

218 entified novel putative biomarkers for early pancreatic islet aberrations preceding T2D.

219 The case here is the pancreatic islet beta-cell presented with excessive leve

220 driver gene mutations, including significant pancreatic islet cell adaptation in obesity-associated t

221 ose levels, insulin sensitivity and restored pancreatic islet cell mass, neuronal innervation and mic

222 electrical activity of beta-cells within the pancreatic islet drives oscillatory insulin secretion.

223 on potential amplitude as a key regulator of pancreatic islet hormone secretion.

224 -quantitative confocal analysis of non-fixed pancreatic islet microscopy we demonstrated that ODND pr

225 ogeneous cell populations that display mixed pancreatic islet phenotypes and immaturity.

226 owledge on the creation of three-dimensional pancreatic islet structures in both microscale and micro

227 The pancreatic islet, consisting of 1-2% mass of the whole p

228 Pancreatic islet-like distributions of islet hormones we

229 We found that pancreatic islets are innervated by vagal sensory axons

230 inflammatory processes are also activated in pancreatic islets from obese animals and humans with obe

231 Pancreatic islets from rats encapsulated in the device a

232 Pulsatile insulin from pancreatic islets is crucial for glucose homeostasis, bu

233 Silencing of this intronic circular RNA in pancreatic islets leads to a decrease in the expression

234 on selenoprotein transcript profiles in the pancreatic islets of C57BL/6J mice.

235 hate transporter present in MIN6m9 cells and pancreatic islets, prevented this flush.

236 sing the mouse insulinoma MIN6 cell line and pancreatic islets, we investigated the effects of G prot

237 l outer plexiform layer, Purkinje cells, and pancreatic islets.

238 This study shows that pancreatic lesions are characterized by specific exosoma

239 diagnostic modality for characterisation of pancreatic lesions.

240 pancreatic transcription factors that drive pancreatic lineage specification.

241 All extracts inhibited pancreatic lipase (IC(50) between 1.15 and 0.59 mg/mL),

242 tandards, were assessed on the inhibition of pancreatic lipase and interference on the bioaccessibili

243 Outcome measures included pancreatic lipase levels, the systemic inflammatory resp

244 ic (anti-alpha-amylase, -alpha-glucosidase, -pancreatic lipase) and antioxidant potential (FRAP, ORAC

245 individual live T cells from thymus, spleen, pancreatic lymph nodes, and islets before and after diab

246 ctional conservation between mouse and human pancreatic mesenchyme by testing identified mesenchymal

247 Pancreatic MRI protocols are mostly qualitative due to t

248 ICE ADVICE 5: Drainage and/or debridement of pancreatic necrosis is indicated in patients with infect

249 venous antibiotics with ability to penetrate pancreatic necrosis should be favored (eg, carbapenems,

250 The pancreatic neoadjuvant Massachusetts-score (PANAMA-score

251 erstand the relevance of these signatures in pancreatic neoplasms.

252 evaluated (eg, ATM and DAXX) are limited to pancreatic NETs and are most likely not informative.

253 ing the hypothesis of a calcitriol producing pancreatic neuroendocrine tumor.

254 ing the hypothesis of a calcitriol-producing pancreatic neuroendocrine tumor.

255 tumoral pancreas, and aorta were recorded on pancreatic parenchymal phase (PPP) dual-energy CT 70-keV

256 he correlations remained significant between pancreatic PDFF and hepatic PDFF (R(S)=0.632, p<0.001) a

257 patic PDFF (R(S)=0.632, p<0.001) and between pancreatic PDFF and liver steatosis (R(S)=0.608, p<0.001

258 (4) receptor (Y(4)R) is unique as it prefers pancreatic polypeptide over NPY and peptide YY.

259 rogenitor stage, but favor somatostatin- and pancreatic polypeptide-positive cells at the expense of

260 naling controls proliferation of multipotent pancreatic progenitor cells (MPCs) and their segregation

261 ervation, we show that ZBED2 can repress the pancreatic progenitor transcriptional program, enhance m

262 with intravenous contrast using a dual phase pancreatic protocol is typically the best method to dete

263 rapy on the surgical complication rate after pancreatic resection.

264 Genes involved in the "pancreatic secretion" pathway are the most strongly diff

265 We characterized the anatomical pattern of pancreatic sensory innervation by combining viral tracin

266 owever, current culture conditions for human pancreatic slices (HPSs) have only been tested for short

267 y and immunohistochemistry were performed in pancreatic specimens after total pancreatectomy due to c

268 Gastric (stage II/III), pancreatic (stage I/II/III), and rectal cancers (stage I

269 Pancreatic steatosis can be considered a marker of metab

270 The learning curve of experienced pancreatic surgeons for PAR was 15 such procedures.

271 Of the 15,182 patients who completed a pancreatic surgery between 2016 and 2018, 6114 (40%) rec

272 s one of the most common complications after pancreatic surgery.

273 a retrospective study of HRIs who underwent pancreatic surveillance at a single institution between

274 complications and after placing experimental pancreatic sutures in the pancreatic tail of C57/Bl6 mic

275 For these organs, the mean pancreatic T(2) values were nearly 40% at 1.5 T and < 12

276 acing experimental pancreatic sutures in the pancreatic tail of C57/Bl6 mice.

277 tic lipid DB-position fragment ions in mouse pancreatic tissue with down to 10 mum pixel size allows

278 U) and increased number of leukocytes in the pancreatic tissue.

279 CGA database, paired PDA and adjacent normal pancreatic tissues, PDA tissue array and cell lines were

280 ere increased in PDAC compared with nontumor pancreatic tissues.

281 the actin cytoskeleton and the expression of pancreatic transcription factors that drive pancreatic l

282 ntensive efforts have focused on elucidating pancreatic transcriptional programs that can drive the d

283 his study was to quantify the risk of SCI in pancreatic transplantation.

284 ly confirmed cases relative to the number of pancreatic transplants from UK registry data during the

285 Pancreatic triglyceride lipase (PNLIP) increased in adip

286 Pancreatic tumor cells release small extracellular vesic

287 d infiltration of lymphocytes throughout the pancreatic tumor compared to untreated animals.

288 IL22 to be increased during pancreatitis and pancreatic tumor development and to be required for tumo

289 bine leads to extensive reprogramming of the pancreatic tumor microenvironment and that patients who

290 Human pancreatic tumor tissues were implanted into interscapul

291 In one pancreatic tumor, there were many more L1 insertions in

292 Treatment of orthotopic pancreatic tumor-bearing mice with gemcitabine alone or

293 IL17 is involved in pancreatic tumorigenesis, but its role in invasive PDAC

294 ion of T-regulatory and exhausted T cells in pancreatic tumors and increases numbers of memory CD4+ a

295 Compared with pancreatic tumors in KPC/Cdh11(+/+) mice, tumors of KPC/

296 ese sEVs promote metastasis of xenograft and pancreatic tumors to lung in mice.

297 mice did not develop precancerous lesions or pancreatic tumors.

298 y but combines with oncogenic Ras to produce pancreatic tumors.

299 col is typically the best method to detect a pancreatic tumour and to determine surgical resectabilit

300 earch efforts are focusing on modulating the pancreatic tumour microenvironment to enhance the effica