ライフサイエンスコーパス: pancreatic

1 ary sclerosing cholangitis) (5.5% vs. 0.1%), pancreatic (1.7% vs. 0%) and rheumatic diseases (7.2% vs

2 In summary, CTSD is expressed in pancreatic acinar and inflammatory cells, undergoes subc

3 Pancreatic acinar cell carcinoma (ACC) is an aggressive

4 In conclusion, human cadaveric pancreatic acini maintain physiological functions and ha

5 for the treatment of advanced or metastatic pancreatic adenocarcinoma and advanced epithelial ovaria

6 18)F-FTT uptake was seen in one subject with pancreatic adenocarcinoma and another with liver cancer.

7 d the anti-cancer effect of PSM and PSB over pancreatic adenocarcinoma cells and glioblastoma cells.

8 st demonstrated that breast cancer cells and pancreatic adenocarcinoma cells generated micromolar lev

9 2 and May 2014, 137 patients with metastatic pancreatic adenocarcinoma for whom gemcitabine-based che

10 Pancreatic adenocarcinoma is moderately responsive to ge

11 ve cohort study, 1122 participants developed pancreatic adenocarcinoma over 4.2 million person-years.

12 Cancer Data Base was queried for T1-3N0-1M0 pancreatic adenocarcinoma patients who underwent PD.

13 the pathogenesis of cancers such as lung and pancreatic adenocarcinomas.

14 Pancreatic allograft thrombosis (PAT) remains the leadin

15 QA) on digestion of potato starch by porcine pancreatic alpha amylase (PPAA) was investigated using i

16 However, Kv11.1 is also present in pancreatic alpha and beta cells and intestinal L and K c

17 s critical to mammalian survival, is that of pancreatic alpha and beta cells producing glucagon and i

18 ucagon hypersecretion involving expansion of pancreatic alpha-cell mass.

19 5'-flanking conserved sequences that control pancreatic and beta-cell type-specific transcription, wh

20 ly in dogs, produced significantly increased pancreatic and biliary fluid rich in bicarbonate.

21 /TAZ in pancreatic cancer tissues as well as pancreatic and breast cancer cell lines.

22 was accompanied by a marked augmentation of pancreatic and intestinal BF responses.

23 Using pancreatic and ovarian cancer cells with ST6Gal-I knockd

24 otherapies in preclinical models of advanced pancreatic and ovarian cancer.

25 nular pancreas is a rare and often neglected pancreatic anomaly due to a lack of awareness of this en

26 nking perturbations of the gut microbiome to pancreatic autoimmunity.

27 Inadequate pancreatic beta cell function underlies type 1 and type

28 ABSTRACT: Development of pancreatic beta cell mass before birth is essential for

29 Finally, db/db-PI3Kgamma(-/-) mice have more pancreatic beta cells and larger islets than db/db mice,

30 s (T1D) manifests when the insulin-producing pancreatic beta cells are destroyed as a consequence of

31 Pancreatic beta cells are functionally programmed to rel

32 ke cells.Our incomplete understanding of how pancreatic beta cells form limits the generation of beta

33 atopoietic stem cells, and insulin-releasing pancreatic beta cells through a signaling pathway involv

34 is secreted in conjunction with insulin from pancreatic beta cells to regulate glucose metabolism.

35 aracterized by the autoimmune destruction of pancreatic beta cells.

36 tory subunit is expressed in human and mouse pancreatic beta cells.

37 Pancreatic beta-cell apoptosis and proliferation were al

38 /-) mice exhibit glycemic dysregulations and pancreatic beta-cell dysfunctions, we evaluated islet fu

39 While mitophagy is critical to pancreatic beta-cell function, the posttranslational sig

40 Pancreatic beta-cell insulin production is orchestrated

41 Insulin production by the pancreatic beta-cell is required for normal glucose home

42 Although treatment with the pancreatic beta-cell toxin streptozotocin induced hyperg

43 The pancreatic beta-cell transcriptome is highly sensitive t

44 rst-in-class surrogate imaging biomarker for pancreatic beta-cells by targeting the protein GPR44.

45 Elevated cholesterol content within pancreatic beta-cells has been shown to reduce beta-cell

46 nsulin-resistant conditions such as obesity, pancreatic beta-cells proliferate to prevent blood gluco

47 R fetus produce developmental adaptations in pancreatic beta-cells that impair fetal insulin secretio

48 elivery of insulin mimicking the function of pancreatic beta-cells to achieve meticulous control of b

49 atty acid-induced apoptosis in human and rat pancreatic beta-cells, as well as in human and murine pa

50 NAs and proapoptotic Bcl-2 proteins in human pancreatic beta-cells, broadening our understanding of c

51 The expression and function of NMDARs in pancreatic beta-cells, by contrast, are poorly understoo

52 In pancreatic beta-cells, mitochondrial bioenergetics contr

53 endotoxemia upregulates miR-155-5p in murine pancreatic beta-cells, which improved glucose metabolism

54 ate progression to autoimmune destruction of pancreatic beta-cells.

55 ce glucose-stimulated insulin secretion from pancreatic beta-cells.

56 leading to deleterious downstream effects in pancreatic beta-cells.

57 developing novel approaches to regenerating pancreatic beta-cells.

58 e of genomic analysis, with prostate, renal, pancreatic, breast, and colon cancer as the most common

59 ted in a mouse model of KRAS/mut p53-induced pancreatic cancer (KPC mice).

60 invasive IPMNs showed that family history of pancreatic cancer (P = 0.027) and high-grade dysplasia (

61 with histologically proved locally advanced pancreatic cancer 5 cm or smaller (13 women, 12 men; med

62 In a pancreatic cancer allograft model, co-injection of PDAC

63 e electroporation (IRE) for locally advanced pancreatic cancer and (b) evaluate the quality of life (

64 " with an enhanced capacity to both suppress pancreatic cancer and transactivate select p53 target ge

65 ay to Carbohydrate Antigen 19-9 (CA 19-9), a pancreatic cancer biomarker, produce optically tunable s

66 help overcome the gemcitabine resistance in pancreatic cancer by regulating ER stress and stemness.

67 ion network derived by integrating 560 human pancreatic cancer cases across seven studies.

68 over 50% when tested against a panel of four pancreatic cancer cell lines in vitro.

69 ility, we analyzed the proteomes of 10 human pancreatic cancer cell lines to a depth of >8,700 quanti

70 metry assays in BXPC-3 and PANC-1 cells, two pancreatic cancer cell lines with high and low TF expres

71 eal was conducted in a cohort of low-passage pancreatic cancer cell lines, primary patient-derived xe

72 in phosphorylation and signaling pathways in pancreatic cancer cells after gemcitabine treatment usin

73 l pancreas cells, as well as in KRAS mutated pancreatic cancer cells and was essential for ER homoeos

74 a strategy to suppress the KRAS oncogene in pancreatic cancer cells by means of small molecules bind

75 riptolide, HIF-1alpha protein accumulated in pancreatic cancer cells even though hypoxic response was

76 Pancreatic cancer cells have extensively reprogrammed me

77 acropinocytosis can be a nutrient source for pancreatic cancer cells, but it is not fully understood

78 Using pancreatic cancer cells, we demonstrate that inhibition

79 antimetastatic and cytotoxic to human L3.6pl pancreatic cancer cells.

80 roidal tissue growths of connexin43-positive pancreatic cancer Colo357 cells during light-controlled

81 reased the levels of proliferation more than pancreatic cancer derived MDSC.

82 on, which have remained elusive, we analyzed pancreatic cancer development in mice expressing p53 tra

83 guishing patients with early- and late-stage pancreatic cancer from healthy donors and patients with

84 ; 95% CI, 3.0% to 5.8%) of 854 patients with pancreatic cancer had a deleterious germline mutation, 3

85 ts delineating rewired metabolic networks in pancreatic cancer have revealed new in-roads to develop

86 We assessed associations between diet and pancreatic cancer incidence in the National Institutes o

87 e et al. show that metastatic progression of pancreatic cancer involves large-scale enhancer reprogra

88 significantly reduced, but also the onset of pancreatic cancer is delayed.

89 lusion Percutaneous IRE for locally advanced pancreatic cancer is generally well tolerated, although

90 Pancreatic cancer is molecularly diverse, with few effec

91 Differentiating it from pancreatic cancer is of paramount importance.

92 -initiated GEMM tumors from one lung and two pancreatic cancer models, we discover that significant i

93 nthesis, correlates with better prognosis in pancreatic cancer patients on fluoropyrimidine analogs.

94 correlated with poor gemcitabine response in pancreatic cancer patients.

95 genetically engineered mouse model and human pancreatic cancer patients.

96 cation, and treatment response assessment in pancreatic cancer patients.

97 ded to overcome the genetic heterogeneity of pancreatic cancer predisposition.

98 ranscription factor is a critical barrier to pancreatic cancer progression.

99 he next 2 years, and three challenges to the pancreatic cancer research community as it moves toward

100 However, the role of HOTAIR in pancreatic cancer resistance to anticancer agents is unk

101 r non-aspirin NSAIDs was not associated with pancreatic cancer risk, even after considering several l

102 ith the FOLFIRINOX protocol in patients with pancreatic cancer should not be withhold from patients s

103 Pancreatic cancer statistics are dismal, with a 5-year s

104 e performed routinely in patients undergoing pancreatic cancer surgery with the aim to achieve a R0 r

105 Deleterious germline mutations contribute to pancreatic cancer susceptibility and are well documented

106 , 31 (3.5%) of which affected known familial pancreatic cancer susceptibility genes: BRCA2 (12 patien

107 21-activated kinase 4 (PAK4) is amplified in pancreatic cancer tissue.

108 ely with LATS but negatively with YAP/TAZ in pancreatic cancer tissues as well as pancreatic and brea

109 esent study determined the role of HOTAIR in pancreatic cancer TRAIL resistance and investigated the

110 livery vehicle for the targeted treatment of pancreatic cancer using combined antimetabolite and sono

111 Recommendations All patients with resected pancreatic cancer who did not receive preoperative thera

112 KRAS mutations are common in pancreatic cancer, but directly targeting the KRAS prote

113 In orthotopic xenograft models of pancreatic cancer, combining PDP with nanoliposomal irin

114 Given the long latency period of pancreatic cancer, exploring the influence of early and

115 me, and the incidence of acute pancreatitis, pancreatic cancer, medullary thyroid carcinoma, and seri

116 seen in severe hypoglycaemia, pancreatitis, pancreatic cancer, or medullary thyroid cancer reported

117 nt mechanism of resistance to gemcitabine in pancreatic cancer, whereby increased glycolytic flux lea

118 ations that coincide with the development of pancreatic cancer.

119 he most widely used single-agent therapy for pancreatic cancer.

120 ome after resection and adjuvant therapy for pancreatic cancer.

121 maging, but up to half may be forerunners of pancreatic cancer.

122 ing of 26 metastases from four patients with pancreatic cancer.

123 immunosuppressive tumor microenvironment in pancreatic cancer.

124 ted in both primary and metastatic models of pancreatic cancer.

125 ic modification that has not been studied in pancreatic cancer.

126 reast cancer, lung cancer, glioblastoma, and pancreatic cancer.

127 ified FOLFIRINOX in patients with metastatic pancreatic cancer.

128 TF(+) MVs and VTE has been observed only in pancreatic cancer.

129 m clinical trial design for immunotherapy in pancreatic cancer.

130 families in which multiple members have had pancreatic cancer.

131 ers is a novel regulatory mechanism in human pancreatic cancer.

132 rly defined strategy to target mutant p53 in pancreatic cancer.

133 a therapeutic window for obesity-associated pancreatic cancer.Obesity is an established risk factor

134 ng and in the development and progression of pancreatic cancer; however, the details of such function

135 Defining mutation load in individual pancreatic cancers and the optimal assay for patient sel

136 nology has been studied for the treatment of pancreatic carcinoma and has shown a significant surviva

137 Hierarchical clustering using pancreatic cell lineage genes was used to assign cells i

138 tipotent and contribute progeny to all major pancreatic cell lineages, we also identify numerous unip

139 tress and pro-inflammation between different pancreatic cell types.

140 pancreas, potentially explaining the loss of pancreatic cells and decreased pancreatic weight.

141 e findings suggest that insulin secretion in pancreatic cells is regulated by Ca(2+) and ROS signalin

142 liferative in benign and well-differentiated pancreatic cells, TGFbeta appears to promote the progres

143 es, and senescent cells, as well as a 2-step pancreatic clamping with a [U-(13)C]palmitate infusion t

144 nes, primary patient-derived xenografts, and pancreatic controls and revealed strikingly altered patt

145 The cellular content of pancreatic cyst fluid aspirate is often suboptimal for a

146 Purpose Pancreatic cystic lesions are common incidental findings

147 robustly identify premalignant and malignant pancreatic cystic lesions.

148 uencing and targeted sequencing of the major pancreatic cysts has identified unique mutational profil

149 l is effective for the treatment of mucinous pancreatic cysts.

150 beta cells, resembling that observed during pancreatic development.

151 bound in both peptide complexes after peptic-pancreatic digestion.

152 from healthy donors and patients with benign pancreatic disease.

153 in the ducts, which could otherwise lead to pancreatic disease.

154 e pancreas will shed light in the origins of pancreatic diseases and may suggest novel therapeutic ap

155 ng, MCF-7 breast, HL-60 leukemia, MIA PaCa-2 pancreatic, DU145 prostate, HeLa cervical and CaCo-2 col

156 ed IPMNs) of the pancreatic system is a main pancreatic duct (MPD) diameter of 5.0 mm or greater on c

157 BSTRACT: A computational model of guinea-pig pancreatic duct epithelium was developed to determine th

158 Here we used long-term partial pancreatic duct ligation (PDL) as a model to study CPRD.

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

160 Pancreatic ductal adenocarcinoma (PDA) is a deadly cance

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

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

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

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

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

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

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

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

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

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

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

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

173 Pancreatic ductal adenocarcinoma (PDAC) has generally a

174 Pancreatic ductal adenocarcinoma (PDAC) has single-digit

175 Pancreatic ductal adenocarcinoma (PDAC) is a highly leth

176 Pancreatic ductal adenocarcinoma (PDAC) is an aggressive

177 Pancreatic ductal adenocarcinoma (PDAC) is characterized

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

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

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

181 Pancreatic ductal adenocarcinoma (PDAC) remains a highly

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

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

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

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

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

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

188 Purpose Metastatic pancreatic ductal adenocarcinoma is characterized by exc

189 Pancreatic ductal adenocarcinoma, even when diagnosed ea

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

191 mportant prognostic factor for patients with pancreatic ductal adenocarcinoma.

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

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

194 ancreatic ductal progenitor cells (HPNE) and pancreatic ductal cells (HPDE).

195 l as phosphorylated SOX9 expression in human pancreatic ductal progenitor cells (HPNE) and pancreatic

196 ogether, our data showed that A2AARs control pancreatic dysfunction in HFD-induced obesity.

197 ri-miR-9-BMSCs) can significantly reduce the pancreatic edema, infiltration, hemorrhage, necrosis, th

198 Finally, in vitro differentiation of pancreatic endocrine cells derived from human pluripoten

199 Pancreatic endothelial cells from NOD-Idd22 animals expr

200 es developed in 10.6%; 50.4% reported taking pancreatic enzymes; 54.6% reported needing antacids.

201 es colonic tumorigenesis, through activating pancreatic ER kinase/eukaryotic translation initiation f

202 sue and extracellular matrix, inducing local pancreatic fibrosis and an inflammatory response.

203 ministration of pasireotide for reduction of pancreatic fistula (PF).

204 er drainage as first intervention for severe pancreatic fistula after pancreatoduodenectomy was assoc

205 s that RPD is noninferior to OPD in terms of pancreatic fistula development and other major postopera

206 significant PF (International Study Group on Pancreatic Fistula Grade B or C) and hospital-related in

207 ver, its impact on major outcomes, including pancreatic fistula, has yet to be adequately compared wi

208 reases the occurrence of clinically relevant pancreatic fistula.

209 First intervention for pancreatic fistula: catheter drainage or relaparotomy.

210 Organ/space SSIs appear to be related to pancreatic fistulae, which are not modifiable.

211 elp to clarify the mechanism responsible for pancreatic HCO3(-) secretion, a vital process that preve

212 found to be better after duodenum-preserving pancreatic head resection (DPPHR) than after partial pan

213 argin status for survival after resection of pancreatic-head ductal adenocarcinoma.

214 flammatory cytokine GM-CSF, concomitant with pancreatic infiltration of inflammatory monocytes that t

215 d that a low dose Cae (5 ug/kg) could induce pancreatic injury in HTG mice while there was no obvious

216 y disease leading to pain, maldigestion, and pancreatic insufficiency.

217 Patients with pancreatic-insufficient cystic fibrosis (PI-CF) are at i

218 ticosterone had a significant enhancement in pancreatic insulin-positive area, but a marked decrease

219 t of the autophagy pathway, in beta cells by pancreatic intra-ductal AAV8-shAtg7 infusion in C57BL/6

220 of mice is sufficient to induce formation of pancreatic intraepithelial neoplasia (PanINs)-a precurso

221 n exhibited diminished SC chemoattraction to pancreatic intraepithelial neoplasia and increased abdom

222 TIMP1 was upregulated in patients with pancreatic intraepithelial neoplasias grade 3 and PDAC l

223 of precancerous pancreatic lesions, known as pancreatic intraepithelial neoplasms (PanIN), and descri

224 However, our comprehensive analysis of pancreatic islet bioenergetics reveals that Drp1 does no

225 ular regulatory program to correctly specify pancreatic islet cell fates.

226 Organ growth and pancreatic islet cell proliferation and mass were examin

227 To validate the approach, single rat pancreatic islet cells were rapidly analyzed with optica

228 development with expected stratification of pancreatic islet mass were examined in relation to indiv

229 shown to be a surrogate imaging biomarker of pancreatic islet mass.

230 ecretion, steatosis, metabolic inflammation, pancreatic islet morphometry, islet cellular composition

231 Pancreatic islet transplantation is a promising clinical

232 hormone, is released from alpha-cells of the pancreatic islet.

233 nduce free cholesterol accumulation in human pancreatic islets and the INS-1 insulinoma cell line.

234 AD, and islet amyloid polypeptide (IAPP) in pancreatic islets in T2D.

235 The liver as transplantation site for human pancreatic islets is a harsh microenvironment for islets

236 n vitro, we tested whether EVs isolated from pancreatic islets of healthy patients and patients with

237 in depletion of the resident macrophages of pancreatic islets of Langerhans that lasted for several

238 PP) is responsible for cell depletion in the pancreatic islets of Langherans, and for multiple pathol

239 Pancreatic islets produce and secrete cytokines and chem

240 We found that rat and human pancreatic islets release the intracellular beta-cell au

241 most highly expressed SOX family protein in pancreatic islets, and mutations in Sox4 are associated

242 In human type 1 diabetes pancreatic islets, fasting conditions reduce PKA and mTO

243 The transplantation of pancreatic islets, following the Edmonton Protocol, is a

244 delta-1, the dominant alpha2delta subunit in pancreatic islets, results in glucose intolerance and di

245 small fraction of genomic CpG sites in human pancreatic islets, the tissue of primary pathogenic impo

246 le-genome DNA methylation landscape in human pancreatic islets, to identify differentially methylated

247 c beta-cells, as well as in human and murine pancreatic islets, via AKT/BCL2 signaling.

248 iRNAs that are modulated by glucose in mouse pancreatic islets.

249 TRMs formed a protective barrier surrounding pancreatic islets.

250 8067 overlaps a predicted enhancer region in pancreatic islets.

251 Animals were followed for >80 weeks and pancreatic lesions were evaluated histologically and imm

252 tion in the microenvironment of precancerous pancreatic lesions, known as pancreatic intraepithelial

253 in the adult pancreas that can commit to the pancreatic lineage following proliferation and mesenchym

254 Pancreatic lipase (PL) plays a central role in fat metab

255 nt capacity, stronger inhibitory activity on pancreatic lipase and comparable and lower activity on a

256 00CW near-infrared fluorescence to delineate pancreatic, liver, or intestinal inflammation in living

257 The immunomodulatory character of pancreatic lysates of patients with cancer differs from

258 adenocarcinomas, 1 low-grade intraepithelial pancreatic neoplasia, and 1 case of polycystic kidney di

259 detection research in high-germline risk for pancreatic neoplasia, elucidating early ontogeny in BRCA

260 prescribed by her oncologist for metastatic pancreatic neuroendocrine and kidney tumors.

261 Prognostic biomarkers for the pancreatic neuroendocrine tumors are needed.

262 linger et al reported 2 female patients with pancreatic neuroendocrine tumors, WDS, and achlorhydria.

263 Pancreatic Ngf overexpression accelerated tumor developm

264 ress induced a pro-inflammatory phenotype in pancreatic normal, cancer and stellate cells.

265 in a large number of tumor entities such as pancreatic or colon carcinoma.

266 e morbidity among patients undergoing hepato-pancreatic or colorectal procedures.

267 s for NETs of ileal or jejunal origin and of pancreatic origin are presented.

268 es to overactive Wnt signaling in subsets of pancreatic, ovarian, gastric, and colorectal tumors.

269 e introduced conditional, Pdx1-Cre-mediated, pancreatic PAK4 gene depletion in the mouse, verified by

270 Tcf7l2 was selectively inactivated in their pancreatic pericytes exhibited impaired glucose toleranc

271 the proportion of chromosomal alterations in pancreatic primary tumors and liver metastases.

272 hat Nkx2.2 is not only required in the early pancreatic progenitors, but has additional essential act

273 s of Kras mutant neoplastic ductal cells and pancreatic regeneration after acute pancreatitis.

274 Readmission after pancreatic resection is common and can largely be attrib

275 For pancreatic resections, costs were 5.5% higher (95% CI, 0

276 ession of pancreatic tumors in mice carrying pancreatic-specific KRAS activation.

277 Recent findings implicate pancreatic stellate cells (PSC) as prominent mediators o

278 Pancreatic stellate cells (PSCs) are key mediators in th

279 itions, the activation of myofibroblast-like pancreatic stellate cells (PSCs) plays a predominant rol

280 ve analysis included 201 patients undergoing pancreatic surgery at a university-based tertiary referr

281 s were conducted at a high-volume, academic, pancreatic surgery specialty center-in a standardized fa

282 e main and branch ducts (mixed IPMNs) of the pancreatic system is a main pancreatic duct (MPD) diamet

283 ncreatitis developed a pseudoaneurysm of the pancreatic tail, diagnosed as a splenic artery pseudoane

284 xpression profiles of patient-derived normal pancreatic tissue (n = 77) and PDA samples (n = 103).

285 As a result, Atf3(-/-) pancreatic tissue displayed increased tissue damage and

286 tress, and lipid metabolism were measured in pancreatic tissue, acinar cells, and isolated mitochondr

287 and PDAC lesions relative to matched normal pancreatic tissue.

288 Pancreatic tissues were collected and analyzed by histol

289 We illustrate them using bovine pancreatic trypsin inhibitor and present a new, detailed

290 s directed at aberrant signaling pathways in pancreatic tumor cells may improve the poor outcome of p

291 We also describe relationships between the pancreatic tumor extracellular matrix, the vasculature,

292 trix metalloproteinases 1 (TIMP1) in primary pancreatic tumors and metastases using both in vitro tec

293 Pancreatic tumors are renowned for their extremely hypox

294 E inhibits the initiation and progression of pancreatic tumors in mice carrying pancreatic-specific K

295 s without conferring a specific phenotype to pancreatic tumors or changing the status of the tumor su

296 c driving force for Brca2-deficiency-induced pancreatic tumors.

297 the maintenance of amino acid levels within pancreatic tumors.

298 maging with DPA-713-IRDye800CW showed strong pancreatic uptake, focal liver uptake, and gastrointesti

299 Pancreatic VDCC uptake of (52)Mn(2+) was successfully ma

300 g the loss of pancreatic cells and decreased pancreatic weight.