ライフサイエンスコーパス: pancreatic cancer

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

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

3 e between endothelium and pericytes in human pancreatic cancer.

4 stroma might be used to treat patients with pancreatic cancer.

5 osolic calcium, and eventually cell death in pancreatic cancer.

6 families in which multiple members have had pancreatic cancer.

7 (23%) in colorectal cancer, and six (6%) in pancreatic cancer.

8 testing efficacy of IVC in treating advanced pancreatic cancer.

9 n with gemcitabine in patients with advanced pancreatic cancer.

10 for the treatment of chemotherapy-refractory pancreatic cancer.

11 ypes, such as melanoma, lung, colorectal and pancreatic cancer.

12 neoplasms, have the potential to progress to pancreatic cancer.

13 n the treatment of various cancers including pancreatic cancer.

14 ed with gemcitabine monotherapy for resected pancreatic cancer.

15 ermline mutation of BRCA2 induces hereditary pancreatic cancer.

16 itoring was developed to treat mouse ectopic pancreatic cancer.

17 t antisense RNA (HOTAIR) is overexpressed in pancreatic cancer.

18 ic potential in many malignancies, including pancreatic cancer.

19 mbined sonodynamic/antimetabolite therapy in pancreatic cancer.

20 d oncogenic signaling as well as stemness in pancreatic cancer.

21 se of these drugs is associated with risk of pancreatic cancer.

22 a reduction in survival among patients with pancreatic cancer.

23 fy T-cell antigens in long-term survivors of pancreatic cancer.

24 did not improve overall survival in advanced pancreatic cancer.

25 nd fluorouracil) in patients with metastatic pancreatic cancer.

26 ipants died, with cause of death as terminal pancreatic cancer.

27 tients with invasive malignancies, including pancreatic cancer.

28 igation as a potential therapeutic target in pancreatic cancer.

29 racil/folinic acid in patients with resected pancreatic cancer.

30 ositron emission tomography (PET) imaging of pancreatic cancer.

31 a critical, actionable therapeutic target in pancreatic cancer.

32 t a strategy to overcome TRAIL resistance in pancreatic cancer.

33 dolescence and midlife to be associated with pancreatic cancer.

34 huge potential as drug delivery vehicles for pancreatic cancer.

35 biomarker candidates for early detection of pancreatic cancer.

36 longs survival in orthotopic models of human pancreatic cancer.

37 gemcitabine alone in advanced or metastatic pancreatic cancer.

38 s been the first line systemic treatment for pancreatic cancer.

39 making a larger contribution than lactate in pancreatic cancer.

40 he FDA for gemcitabine-refractory metastatic pancreatic cancer.

41 ations that coincide with the development of pancreatic cancer.

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

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

44 ome after resection and adjuvant therapy for pancreatic cancer.

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

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

47 immunosuppressive tumor microenvironment in pancreatic cancer.

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

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

50 ified FOLFIRINOX in patients with metastatic pancreatic cancer.

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

52 rcinoma, gallstones, acute pancreatitis, and pancreatic cancer.

53 which are in involved in the pathogenesis of pancreatic cancer.

54 m clinical trial design for immunotherapy in pancreatic cancer.

55 role in tumorigenesis and chemo-response in pancreatic cancer.

56 ng is associated with increased incidence of pancreatic cancer.

57 atients with locally advanced and metastatic pancreatic cancer.

58 with Kras(G12D) to promote highly metastatic pancreatic cancer.

59 o oncogenic Kras(G12D), a common mutation in pancreatic cancer.

60 d risk of colorectal, endometrial, lung, and pancreatic cancers.

61 77030 due to prostate cancer; 1157878 due to pancreatic cancer; 209314 due to uterine cancer; 421628

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

63 ranscription factor that is overexpressed in pancreatic cancer, activates UPR and results in chronic

64 er excluding 13 genes known to predispose to pancreatic cancer (adjusted odds ratio, 1.35; P = .045).

65 gnificance: In an established mouse model of pancreatic cancer, administration of the promising exper

66 "Pancreatic Cancer: Advances in Science and Clinical Care

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

68 the two major oncogenic signaling pathway in pancreatic cancer along with a decreased tumor initiatin

69 Purpose To update the Potentially Curable Pancreatic Cancer: American Society of Clinical Oncology

70 A possible reduction in risk for pancreatic cancer among people with diabetes who regular

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

72 on, and inhibition of glycolysis in MiaPaCa2 pancreatic cancer and A673 sarcoma cells.

73 y ATAC-seq and gene expression by RNA-seq in pancreatic cancer and control samples.

74 t debilitating and fatal diseases, including pancreatic cancer and diabetes.

75 s study, we evaluated the cross-talk between pancreatic cancer and its TAS in primary human cell cult

76 sis for colorectal, lung, female breast, and pancreatic cancer and melanoma in patients who resided i

77 These findings, and those in pancreatic cancer and melanoma models, indicate that dis

78 TAT1-Tyr701 occurs in PBMC derived from both pancreatic cancer and melanoma patients.

79 n immunocompetent orthotopic mouse models of pancreatic cancer and melanoma, we found that CAR T cell

80 uppressed cancer in multiple mouse models of pancreatic cancer and significantly increased overall su

81 However, the functionality of PAK4 in pancreatic cancer and the contribution made by HGF signa

82 ranscriptional response of oncogenic KRAS in pancreatic cancer and to understand their clinical relev

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

84 igh-penetrant genetic factor associated with pancreatic cancer and we also identified candidate pancr

85 alpha 1 (ITGA1) is frequently upregulated in pancreatic cancers and associated precursor lesions.

86 n independent cohorts of breast, ovarian and pancreatic cancers and demonstrated its efficacy in alte

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

88 s between diabetes, diabetes management, and pancreatic cancer, and identifies areas where additional

89 33 patients had reported a family history of pancreatic cancer, and most did not have a cancer family

90 R0 and R1 margin status after resection for pancreatic cancer are controversial.

91 sults call into question the degree to which pancreatic cancers are addicted to KRAS by illustrating

92 osis have shown promising efficacy, but many pancreatic cancers are resistant to TRAIL therapy.

93 In this study, we use pancreatic cancer as a case study to examine the practic

94 at is as accurate a serological biomarker of pancreatic cancer as the cancer antigen CA19-9.

95 ed the first 10 patients with a diagnosis of pancreatic cancer, based on tissue analysis, and 10 cons

96 ation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge.

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

98 An analysis of human pancreatic cancer biopsies was concordant with these fin

99 1alpha was upregulated in human melanoma and pancreatic cancer biopsy specimens in correlation with m

100 ght still have potential in the treatment of pancreatic cancer but further development requires the i

101 t form of the GTPase KRAS is a key driver of pancreatic cancer but remains a challenging therapeutic

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

103 type 2 diabetes (T2DM) is a risk factor for pancreatic cancer, but increasing epidemiological data p

104 important modality for the local control of pancreatic cancer, but pancreatic cancer cell radioresis

105 Here we investigated how Atm contributes to pancreatic cancer by deleting this gene in a murine mode

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

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

108 urate, a major metabolite of aspirin, in 396 pancreatic cancer cases and 784 matched individuals with

109 Through the end of 2006, a total of 1,322 pancreatic cancer cases occurred (average follow up time

110 enome sequencing data from 437 patients with pancreatic cancer (cases) and 1922 individuals not known

111 E-selectin-mediated rolling facilitates pancreatic cancer cell adhesion to hyaluronic acid.

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

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

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

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

116 In Ras mutant pancreatic cancer cell lines, the phosphorylation and di

117 l cycle progression and apoptosis in several pancreatic cancer cell lines.

118 T5C) as favoring the mesenchymal identity in pancreatic cancer cell lines.

119 knockdown of Cad-11 in cancer cells reduced pancreatic cancer cell migration.

120 Using ovarian and pancreatic cancer cell models with ST6Gal-I overexpressi

121 d the contribution made by HGF signalling to pancreatic cancer cell motility remain to be elucidated.

122 osphorylate AKT Furthermore, USP49 inhibited pancreatic cancer cell proliferation and enhanced cellul

123 ied from Spirulina, effectively inhibits the pancreatic cancer cell proliferation in vitro and xenogr

124 the local control of pancreatic cancer, but pancreatic cancer cell radioresistance remains a serious

125 Upon exposure of TAS to pancreatic cancer cell-conditioned media, we documented

126 The in vitro therapeutic studies in pancreatic cancer cells (PANC-1 and CAPAN-1) demonstrate

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

128 We demonstrated that pancreatic cancer cells and glioblastoma cells were spec

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

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

131 Taken together, these data suggest that pancreatic cancer cells consume extracellular protein, i

132 Moreover, this association in pancreatic cancer cells correlated with functional cross

133 UN-KC-6141 cells (pancreatic cancer cells derived from Pdx1-Cre;LSL-Kras(G

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

135 We observed that TRAIL-resistant pancreatic cancer cells had higher levels of HOTAIR expr

136 f HOTAIR expression, whereas TRAIL-sensitive pancreatic cancer cells had lower HOTAIR levels.

137 Furthermore, we demonstrate that pancreatic cancer cells have a specific motility respons

138 itro proliferation caused by GLS inhibition, pancreatic cancer cells have adaptive metabolic networks

139 Pancreatic cancer cells have extensively reprogrammed me

140 ffect of FASN inhibitors with gemcitabine in pancreatic cancer cells in culture and orthotopic implan

141 55A/T159A/S280A) suppressed tumorigenesis in pancreatic cancer cells in vitro and in vivo to a greate

142 es as an important source of amino acids for pancreatic cancer cells in vivo.

143 ted from chronic pancreatitis tissues and in pancreatic cancer cells metastasized to the liver.

144 We then used microraft arrays to select pancreatic cancer cells that proliferate in spite of cyt

145 assess agonist properties, and in AR42J rat pancreatic cancer cells to determine receptor binding ch

146 ntial targets and strategies for sensitizing pancreatic cancer cells to gemcitabine.

147 ivation by its agonist clofibrate sensitizes pancreatic cancer cells to radiation by modulating cell

148 ate-mediated PPARalpha activation sensitizes pancreatic cancer cells to radiation through the Wnt/bet

149 igh HOTAIR levels increase the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via e

150 rmacological ascorbate induced cell death in pancreatic cancer cells with diverse mutational backgrou

151 therapeutic target, clearly interfering with pancreatic cancer cells' aggressiveness.

152 lencing of YAP in Sk-Hep1, SNU182, HepG2, or pancreatic cancer cells, as well as incubation with thio

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

154 n catabolism and macropinocytosis in situ by pancreatic cancer cells, but not by adjacent, non-cancer

155 Using pancreatic cancer cells, we demonstrate that inhibition

156 Pancreatic cancer cells, which use macropinocytosed prot

157 ver, gemcitabine can promote the stemness of pancreatic cancer cells.

158 fter beta-lapachone treatment of NQO1+ human pancreatic cancer cells.

159 sion was significantly increased in PSCs and pancreatic cancer cells.

160 tein synthesis, and cell size in ovarian and pancreatic cancer cells.

161 ants in human and genetically defined murine pancreatic cancer cells.

162 NFkappaB and apoptotic signaling pathways in pancreatic cancer cells.

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

164 juvant treatment to sensitize chemoresistant pancreatic cancer cells.

165 systematically evaluated and then applied to pancreatic cancer cells.

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

167 iants in coding regions that affect risk for pancreatic cancer, combining data from 5 studies.

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

169 er cases and 784 matched individuals without pancreatic cancer (controls).

170 or death for patients without development of pancreatic cancer, date of surgery for patients with his

171 mor xenografts and in an orthotopic model of pancreatic cancer delayed tumor development.

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

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

174 ere, the authors interrogate the proteome of pancreatic cancer endothelium via phage display and iden

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

176 FOLFOX (mFOLFOX) in patients with metastatic pancreatic cancer for whom gemcitabine-based therapy had

177 odels such as for pancreatitis and different pancreatic cancer forms.

178 ia-telangiectasia-mutated) increase Familial Pancreatic Cancer (FPC) susceptibility, and ATM somatic

179 ospective US cohorts who were diagnosed with pancreatic cancer from 1984 to 2008.

180 breast, colorectal, non-small-cell lung, or pancreatic cancer from 2009 to 2012 (N = 25,032) were id

181 ould best discriminate between patients with pancreatic cancer from controls.

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

183 atic cancer and we also identified candidate pancreatic cancer genes.

184 We interrogated 385 pancreatic cancer genomes to define hypermutation and it

185 tudy was conducted in 9 centers of the Dutch Pancreatic Cancer Group from January 1, 2005, to Septemb

186 Furthermore, blockade of BRD4 inhibited pancreatic cancer growth in vivo.

187 ; 95% CI, 3.0% to 5.8%) of 854 patients with pancreatic cancer had a deleterious germline mutation, 3

188 Pancreatic cancer has a devastating prognosis, with an o

189 umors and metastases within individuals with pancreatic cancer have exposed the complex clonal dynami

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

191 35% of patients with pancreatic cancer have unresectable locally advanced dis

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

193 fit of additional resection in patients with pancreatic cancer in case of positive FS to achieve clea

194 rs (prostate cancers in TRAMP and PTEN mice, pancreatic cancer in KPC mice), we identified two subpop

195 D use was not associated with future risk of pancreatic cancer in participants from several large pro

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

197 MUC16 neoantigens in long-term survivors of pancreatic cancer, including clones with specificity to

198 ate CTCs from blood samples of patients with pancreatic cancer, including immunoaffinity and label-fr

199 As the incidence of pancreatic cancer increases, there is an urgent need to

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

201 Pancreatic cancer is a lethal disease with poor prognosi

202 Pancreatic cancer is a malignant neoplasm with a high mo

203 Pancreatic cancer is accompanied by a fibrotic reaction

204 Pancreatic cancer is among the most lethal cancers with

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

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

207 Pancreatic cancer is molecularly diverse, with few effec

208 Differentiating it from pancreatic cancer is of paramount importance.

209 the main causations of the poor prognosis of pancreatic cancer is the lack of effective chemotherapie

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

211 In pancreatic cancer, macropinocytosis is driven by oncogen

212 Here, we further revealed its anti-pancreatic cancer mechanisms and conducted a phase I/IIa

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

214 We demonstrate that pancreatic cancer metabolism is adaptive and that target

215 xenograft model, IL-35 promotes spontaneous pancreatic cancer metastasis in an ICAM1-dependent manne

216 CP cargo, alpha5 integrin, does not suppress pancreatic cancer metastasis-indicating a role for RCP-d

217 tential role of Cad-11 in PSC activation and pancreatic cancer metastasis.

218 ssion of ITGA1-specific collagens within the pancreatic cancer microenvironment significantly correla

219 ras(G12D) and Pdx-1CreLSL-Kras(G12D)p53(L/L) pancreatic cancer models to ablate KLF10 expression and

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

221 ncreasing disease progression in spontaneous pancreatic cancer mouse model, and a correlation of high

222 als in Europe for CBD stenosis of malignant (pancreatic cancer, n = 20 or cholangiocarcinoma, n = 5)

223 ment and secretion of GDNF are essential for pancreatic cancer neural spread.

224 taxel to human albumin, exhibits efficacy in pancreatic cancer, non-small cell lung cancer and breast

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

226 amino acid and nucleotide synthesis, whereas pancreatic cancer obtains amino acids from catabolism of

227 Pancreatic cancer occurs more frequently in older patien

228 tive patients with a diagnosis of malignant (pancreatic cancer or cholangiocarcinoma, n = 15) or nonm

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

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

231 nd toxic effects in Syrian hamster models of pancreatic cancer (PaCa).

232 A is significantly associated with decreased pancreatic cancer patient survival rate.

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

234 1 expression identifies mutant KRAS lung and pancreatic cancer patients with the worst survival outco

235 gic pancreatic cancer researchers as well as pancreatic cancer patients, survivors, and advocates.

236 ith poor prognoses and decreased survival in pancreatic cancer patients.

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

238 correlated with poor gemcitabine response in pancreatic cancer patients.

239 genetically engineered mouse model and human pancreatic cancer patients.

240 ociated with different long-term outcomes in pancreatic cancer patients.

241 ed PPARalpha expression in tissue samples of pancreatic cancer patients.

242 ronic inflammation (CI) is a risk factor for pancreatic cancer (PC) including the most common type, d

243 nase Axl is associated with poor outcomes in pancreatic cancer (PDAC), where it coordinately mediates

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

245 on of RNS could be an important strategy for pancreatic cancer prevention.

246 events involved in chronic pancreatitis and pancreatic cancer progression and metastasis remain poor

247 hat beta-adrenergic signaling is involved in pancreatic cancer progression.

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

249 ancer, breast cancer, colorectal cancer, and pancreatic cancer published between Jan 1, 2011, and Dec

250 of PPARalpha and its biological function in pancreatic cancer radiosensitivity have not been previou

251 went surgical resection for locally advanced pancreatic cancer ranged from 0% to 43%.

252 A total of 2,054 (86%) died, with pancreatic cancer recorded as the underlying cause of de

253 Although the prognosis in pancreatic cancer remains grim in part due to poor respo

254 Pancreatic cancer remains one of the great challenges in

255 nt atmosphere of the meeting, a coalition of pancreatic cancer research and support foundations parti

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

257 , translational, clinical, and epidemiologic pancreatic cancer researchers as well as pancreatic canc

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

259 els of salicylurate were not associated with pancreatic cancer risk (odds ratio, 1.08; 95% CI, 0.72-1

260 ular aspirin use was associated with reduced pancreatic cancer risk among participants with diabetes

261 and EPHA1) and 7 genes had associations with pancreatic cancer risk, based on the sequence-kernel ass

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

263 fore baseline, was inversely associated with pancreatic cancer risk.

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

265 ss-talk may offer a viable strategy to treat pancreatic cancer.Significance: In an established mouse

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

267 rier family 22 member 17 (SLC22A17) in human pancreatic cancer stellate cells (PSC), key mediators of

268 etry revealed that AGR2 was overexpressed in pancreatic cancer stem cells (CSC) compared with non-ste

269 the difference in treating pancreatitis and pancreatic cancer successfully.

270 hlight the functional importance of IKBKE in pancreatic cancer, support the evaluation of IKBKE as a

271 c KRAS mutations and poor prognosis in human pancreatic cancer, supporting a potential tumour-suppres

272 oprotein and is necessary and sufficient for pancreatic cancer suppression, like p53.

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

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

275 These deleterious pancreatic cancer susceptibility gene mutations, some of

276 Conclusion Germline mutations in pancreatic cancer susceptibility genes are commonly iden

277 ncer, we sequenced 32 genes, including known pancreatic cancer susceptibility genes, in DNA prepared

278 , 31 (3.5%) of which affected known familial pancreatic cancer susceptibility genes: BRCA2 (12 patien

279 Considering the poor prognosis of pancreatic cancer, the detection of a pancreatic cyst ca

280 21-activated kinase 4 (PAK4) is amplified in pancreatic cancer tissue.

281 monstrate that PPARalpha is overexpressed in pancreatic cancer tissues and clofibrate-mediated PPARal

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

283 nificantly higher expression of PPARalpha in pancreatic cancer tissues than in tumor-adjacent tissues

284 show that, in human chronic pancreatitis and pancreatic cancer tissues, Cad-11 expression was signifi

285 C obtained from mice and patients with CP or pancreatic cancer to examine the effect of Jak/STAT and

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

287 In genetically engineered lung and pancreatic cancer tumours in fasted mice, the contributi

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

289 hose expression is essential to maintain the pancreatic cancer vasculature through a VEGF-independent

290 The Vandetanib in Pancreatic Cancer (ViP) trial was a phase 2 double-blind

291 creased expression of USP49 in patients with pancreatic cancer was associated with decreased FKBP51 e

292 itled Diabetes, Pancreatogenic Diabetes, and Pancreatic Cancer was held at the American Diabetes Asso

293 tations in patients with apparently sporadic pancreatic cancer, we sequenced 32 genes, including know

294 ptor (TFRC) and beta-Glucuronidase (GUSB) in pancreatic cancer were identified to be stable as well.

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

296 gests a target to limit neural remodeling in pancreatic cancer, which contributes to poorer quality o

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

298 propriate adjuvant regimen for patients with pancreatic cancer who have undergone an R0 or R1 resecti

299 invasion using a premalignant mouse model of pancreatic cancer with conditional knockout of p120 cate

300 nes are commonly identified in patients with pancreatic cancer without a significant family history o