ライフサイエンスコーパス: pancreatic cancer

1 ce and functionality in a xenograft model of pancreatic cancer.

2 up to three years before the development of pancreatic cancer.

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

4 atitis (CP) and a markedly increased risk of pancreatic cancer.

5 ly reducing invasive capacity of KRAS-mutant pancreatic cancer.

6 in 4 (BRD4) to drug the 'undruggable' MYC in pancreatic cancer.

7 er and a potential target for the therapy in pancreatic cancer.

8 sed in patients with (borderline-)resectable pancreatic cancer.

9 traepithelial neoplasia stage I (PanIN-I) of pancreatic cancer.

10 enopausal breast cancer, and isoleucine with pancreatic cancer.

11 g to overcome resistance to immunotherapy in pancreatic cancer.

12 iated with a poor prognosis in patients with pancreatic cancer.

13 and anticancer responses in murine and human pancreatic cancer.

14 nd 3D multicellular tumor spheroid models of pancreatic cancer.

15 radiation and platinum-based chemotherapy in pancreatic cancer.

16 both IPMNs and MCNs are direct precursors to pancreatic cancer.

17 tions for second-line therapy for metastatic pancreatic cancer.

18 more effective therapy for the treatment of pancreatic cancer.

19 mising candidate agents for the treatment of pancreatic cancer.

20 to aid in the early detection and staging of pancreatic cancer.

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

22 ght be developed as a therapeutic target for pancreatic cancer.

23 the treatment of gemcitabine-resistant human pancreatic cancer.

24 l inhibitors for more effective treatment of pancreatic cancer.

25 R172H/+ Pdx1-Cre-driven (KPC) mouse model of pancreatic cancer.

26 egimens that should be effective in treating pancreatic cancer.

27 on and pharmacological denervation to target pancreatic cancer.

28 dy to demonstrate usefulness of the HDRA for pancreatic cancer.

29 ic MYC expression for effective treatment of pancreatic cancer.

30 ltidrug treatment for patients with advanced pancreatic cancer.

31 resents a risk factor for the development of pancreatic cancer.

32 benefit in a widely accepted mouse model of pancreatic cancer.

33 ion in patients with (borderline-)resectable pancreatic cancer.

34 and sonodynamic therapy for the treatment of pancreatic cancer.

35 ts with microsatellite stable colorectal and pancreatic cancer.

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

37 ing further development for the treatment of pancreatic cancer.

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

39 2014, a total of 8,354 participants died of pancreatic cancer.

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

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

42 fy mechanisms of MEK inhibitor resistance in pancreatic cancer.

43 ies for targeting this aggressive subtype of pancreatic cancer.

44 g survival of patients with locally advanced pancreatic cancer.

45 developed to slow or inhibit progression of pancreatic cancer.

46 mic disorders, including Crohn's disease and pancreatic cancer.

47 the phenotype and clinical features of human pancreatic cancers.

48 cluding esophageal, gastric, colorectal, and pancreatic cancers.

49 reatment of BRCA-mutated breast, ovarian and pancreatic cancers.

50 This curbed chemoresistance in KRAS-mutant pancreatic cancers.

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

52 Only high-dose opium use was associated with pancreatic cancer (2.66, 1.23-5.74).

53 17 months from diagnosis of locally advanced pancreatic cancer (95% confidence interval [CI]: 15 mont

54 Pancreatic Cancer Action Network and Perthera.

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

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

57 mors in mice, as well as in a mouse model of pancreatic cancer and a subset of primary human tumors.

58 ificant clinical challenge for patients with pancreatic cancer and contributes to a high rate of recu

59 mitations, and pitfalls in the management of pancreatic cancer and discusses current research in nove

60 or (KYT) programme includes US patients with pancreatic cancer and enables patients to undergo commer

61 from a genetically engineered mouse model of pancreatic cancer and found soluble vascular cell adhesi

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

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

64 acy of percutaneous IRE for locally advanced pancreatic cancer and locally recurring pancreatic cance

65 RNA contributes to therapeutic resistance in pancreatic cancer and that targeting this pathway could

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

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

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

69 inone oxidoreductase 1 (NQO1) is frequent in pancreatic cancer, and it offers promising tumor-selecti

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

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

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

73 evelopment, but its expression and impact in pancreatic cancer are unknown.

74 ngs for other cancers such as colorectal and pancreatic cancers are either too cytotoxic or insuffici

75 While most pancreatic cancers arise sporadically, a small subset of

76 ectrochemical biosensor for the detection of pancreatic cancer-associated microRNA, miR-196b.

77 roid cancer, was hypersecreted in metastatic pancreatic cancer at least 16.5 months pre-diagnosis.

78 ueried from the nationwide prospective Dutch Pancreatic Cancer Audit.

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

80 KRAS is the most commonly mutated gene in pancreatic cancer, but clinical agents that directly tar

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

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

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

84 Ps have the potential to improve outcomes of pancreatic cancer by overcoming transporter-mediated che

85 in (BAP1) functions as a tumor suppressor in pancreatic cancer by promoting the activity of the Hippo

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

87 y diagnosed with metastatic breast, lung, or pancreatic cancer, CEACAM5 was a persistent longitudinal

88 biomimetic models and 98% for aptamer-based pancreatic cancer cell detection.

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

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

91 Pancreatic cancer cell lines (PD2560) were orthotopicall

92 release and remarkable cytotoxicity in human pancreatic cancer cell lines and Kras(G12D); Trp52(R172H

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

94 methylation of 11 KRAS-mutant and dependent pancreatic cancer cell lines and observed strikingly sim

95 trate that UBAP2 is highly expressed in both pancreatic cancer cell lines and tumor tissues of PDAC p

96 was knocked down in primary cancer cells and pancreatic cancer cell lines by using small hairpin RNAs

97 Metastatic human pancreatic cancer cell lines had increased levels of PPP

98 We performed studies with the human pancreatic cancer cell lines PATU-8988T, BxPC-3, PANC-1,

99 Pancreatic cancer cell lines were analyzed by gene-expre

100 Three different human pancreatic cancer cell lines were compared to normal pan

101 s in reduced phosphorylation of cortactin in pancreatic cancer cell lines, resulting in increased in

102 Taking advantage of prostate and pancreatic cancer cell models known to have high basal R

103 CSCs were isolated from pancreatic cancer cell populations using flow cytometry

104 HSP70-BCL2 signaling axis that is crucial to pancreatic cancer cell survival and therapeutic resistan

105 Pancreatic cancer cells (mT3) from KPC mice (C57BL/6), w

106 The spheroids were generated by co-culturing pancreatic cancer cells and pancreatic stellate cells in

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

108 yl CPs also reduce the metabolic activity of pancreatic cancer cells and the growth of a Panc-1 xenog

109 d whether it regulates production of sEVs in pancreatic cancer cells and their ability to form premet

110 correlated with MUC1 and MUC4 expression in pancreatic cancer cells and tumor tissue.

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

112 t small extracellular vesicles secreted from pancreatic cancer cells could initiate malignant transfo

113 Pancreatic cancer cells depleted of PAF1 formed smaller

114 Loss of Rab27a in pancreatic cancer cells did not decrease tumor growth in

115 MUC1 knockdown in pancreatic cancer cells enhanced unfolded protein respon

116 Pancreatic cancer cells exhibited increased pyruvate car

117 Pancreatic cancer cells from these tumors had higher inv

118 HIF1A-knockout pancreatic cancer cells had increased expression of prot

119 reduces metastases derived from prostate and pancreatic cancer cells in a FBXL7-dependent manner.

120 eir ability to form premetastatic niches for pancreatic cancer cells in mice.

121 Loss of HIF1A from pancreatic cancer cells increases their invasive and met

122 rates that the actin architecture of TMTs in pancreatic cancer cells is fundamentally different from

123 urthermore, the silencing of MUC5AC in human pancreatic cancer cells reduced their tumorigenic propen

124 ned media experiments revealed that squamous pancreatic cancer cells secrete factors that recruit neu

125 le for exploiting metabolic reprogramming in pancreatic cancer cells to confer therapeutic opportunit

126 PPP1R1B significantly reduced the ability of pancreatic cancer cells to form lung metastases in mice.

127 aminase inhibitors sensitized chemoresistant pancreatic cancer cells to gemcitabine, thereby improvin

128 such as penfluridol, block PRL signaling in pancreatic cancer cells to reduce their proliferation, i

129 CXCL10 as proteins that promote migration of pancreatic cancer cells toward sensory neurons.

130 AXL from the plasma membrane to endosomes in pancreatic cancer cells treated with the AXL ligand grow

131 Glutamine-deficient pancreatic cancer cells up-regulate classic EMT regulato

132 The increased sortilin level in pancreatic cancer cells was confirmed by immunohistochem

133 Combined treatment of pancreatic cancer cells with EGFR and STAT3 inhibitors p

134 Pancreatic cancer cells with ITGA3 or ITGB1 knockdown ha

135 Pancreatic cancer cells with loss or inhibition of PRKD1

136 Pancreatic cancer cells with PRLR knockdown formed signi

137 ed PRL-induced JAK2 signaling; incubation of pancreatic cancer cells with these compounds reduced the

138 trongly reduced the adhesion and invasion of pancreatic cancer cells without affecting cell survival

139 ns of intracellular zinc and is increased in pancreatic cancer cells, in cell lines and mice.

140 antly reduced accumulation of gemcitabine in pancreatic cancer cells, increased growth of xenograft t

141 cause for resistance to STAT3 inhibitors in pancreatic cancer cells, regardless of KRAS mutation sta

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

143 atment increases the release of sVCAM-1 from pancreatic cancer cells, which attracts macrophages into

144 cer, QD394, with significant cytotoxicity in pancreatic cancer cells.

145 inhibition creates enhanced cytotoxicity in pancreatic cancer cells.

146 invasive and colony forming capabilities of pancreatic cancer cells.

147 a-lapachone, another NQO1 substrate, against pancreatic cancer cells.

148 s antitumor activities, particularly against pancreatic cancer cells.

149 in combination with gemcitabine for killing pancreatic cancer cells.

150 s expressed and secreted by murine and human pancreatic cancer cells.

151 PRL increases proliferation and migration of pancreatic cancer cells.

152 n orthotopic implantation of MUC5AC-depleted pancreatic cancer cells.

153 significant change in the aggressiveness of pancreatic cancer cells.

154 molecular mechanism leading to resistance in pancreatic cancer cells.

155 er ENT1, which reduced gemcitabine uptake by pancreatic cancer cells.

156 ment of two novel mAbs against CFPAC-1 human pancreatic cancer cells.

157 subsequent degradation of the p53 protein in pancreatic cancer cells.

158 s in regulating pro-metastatic propensity of pancreatic cancer cells: by generating pro-metastatic en

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

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

161 is hypermethylated in advanced prostate and pancreatic cancers, correlating with decreased FBXL7 mRN

162 at age 45 years, we estimated that 28% of US pancreatic cancer deaths among persons born in 1970-1974

163 6 positive, cell culture-derived, breast and pancreatic cancer-derived exosomes, respectively, when t

164 1cre, KC), which mirrors the early stages of pancreatic cancer development.

165 ther, our study supports a biphasic model of pancreatic cancer development: an AGO2-independent early

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

167 rapy for resectable or borderline resectable pancreatic cancer did not show a significant overall sur

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

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

170 ancreatic cancer; however, its relevance for pancreatic cancer early detection or for monitoring subj

171 reatic innervation is an important factor in pancreatic cancer etiology and progression.

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

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

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

175 ishing newly diagnosed cases with resectable pancreatic cancer from healthy controls (64% sensitivity

176 fibrosis and to differentiate patients with pancreatic cancer from those with pancreatitis.

177 In the locally advanced pancreatic cancer group, 18 participants received no the

178 pression of HNF1alpha leads to inhibition of pancreatic cancer growth and progression, which indicate

179 n D1 expression, and inhibited mutp53-driven pancreatic cancer growth both in vitro and in vivo.

180 About 25% of pancreatic cancers harbour actionable molecular alterati

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

182 Background Patients with locally advanced pancreatic cancer have a dismal prognosis, with a median

183 is an established circulating biomarker for pancreatic cancer; however, its relevance for pancreatic

184 8.46), hepatocellular carcinoma (HR, 21.00), pancreatic cancer (HR, 5.26), and gallbladder cancer (HR

185 vasive IPMNs and MCNs as origins of invasive pancreatic cancer, identifying potential drivers of inva

186 an attractive target for the development of pancreatic cancer imaging agents.

187 nced pancreatic cancer and locally recurring pancreatic cancer in a prospective phase II trial.

188 t (m)2) is associated with increased risk of pancreatic cancer in epidemiologic studies.

189 d slight increases in incidence of liver and pancreatic cancer in some high-income regions.

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

191 n with a review of the clinical landscape of pancreatic cancer, including genetic and environmental r

192 The incidence of pancreatic cancer increases with age, suggesting that ch

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

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

195 ht into the divergent roles of MAGEA6 during pancreatic cancer initiation and progression.

196 these data show that sortilin contributes to pancreatic cancer invasion and could eventually be targe

197 alternative strategy for early detection of pancreatic cancer involves visualization of high-grade p

198 Pancreatic cancer is a disease with limited therapeutic

199 Pancreatic cancer is a lethal disease owing to its intri

200 Pancreatic cancer is an aggressive malignancy, often dia

201 tratification after primary chemotherapy for pancreatic cancer is challenging and prediction models,

202 Pancreatic cancer is characterized by an extensive and c

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

204 A screening program to find early-stage pancreatic cancer is needed but has been challenging to

205 ab27a itself in the metastatic propensity of pancreatic cancer is not well understood.

206 Pancreatic cancer is one of the most complex types of ca

207 Pancreatic cancer is one of the world's leading causes o

208 Pancreatic cancer is the fourth leading cause of cancer-

209 Pancreatic cancer is the fourth leading cause of death w

210 Because pancreatic cancer is typically advanced at the time of d

211 Pancreatic cancer is usually advanced and drug resistant

212 Here, in a mouse model of mutant KRAS-driven pancreatic cancer, loss of AGO2 allows precursor lesion

213 to inhibit cell growth and proliferation in pancreatic cancer, lymphocytic leukemia, and multiple my

214 of sensory and sympathetic neurons supports pancreatic cancer metabolism during nutrient-deprived co

215 ple negative breast cancer MDA-MB-231, human pancreatic cancer MIAPaCa-2, and human colorectal cancer

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

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

218 In a pancreatic cancer model, a DNA hypomethylating drug incr

219 ntly improved survival in the aggressive KPC pancreatic cancer model.

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

221 deed found to activate apoptosis in multiple pancreatic cancer models, whereas the free antibody did

222 We examined the association between BMI and pancreatic cancer mortality among 963,317 adults who wer

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

224 etically engineered mouse models of lung and pancreatic cancer, oncogenic KRAS is insufficient to dri

225 Pancreatic cancer, one of the deadliest human malignanci

226 We exploited this paradigm to target pancreatic cancer, one of the major unmet needs in oncol

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

228 cer cell and fibroblast metabolism in murine pancreatic cancer organoid-fibroblast co-cultures and tu

229 al importance for the operative treatment of pancreatic cancer (pancreatic ductal adenocarcinoma).

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

231 me-wide association studies comprising 2,039 pancreatic cancer patients and 32,592 controls in the Ja

232 In breast and pancreatic cancer patients we find that low FAK expressi

233 The National Cancer Database was queried for pancreatic cancer patients who underwent pancreaticoduod

234 However, treatment of advanced pancreatic cancer patients with STAT3 inhibitors often m

235 keletal muscle fiber cross-sectional area in pancreatic cancer patients.

236 ssociated with longer survival in metastatic pancreatic cancer patients.

237 reatment with STAT3 and EGFR inhibitors, for pancreatic cancer patients.

238 ion and muscle fiber cross-sectional area in pancreatic cancer patients.

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

240 mutant alleles (~1 copy) in blood samples of pancreatic cancer patients.

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

242 Continuing recalcitrance to therapy cements pancreatic cancer (PC) as the most lethal malignancy, wh

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

244 icated metabolic rewiring as a necessity for pancreatic cancer (PC) growth, invasion, and chemotherap

245 Pancreatic cancer (PC) is difficult to defeat due to mec

246 Today, pancreatic cancer (PC) remains a major health problem in

247 Pancreatic cancer (PC) remains a therapeutic challenge b

248 uppressor gene linked to breast cancer (BC), pancreatic cancer (PC), and ovarian cancer (OC) suscepti

249 -9) is a prognostic marker for patients with pancreatic cancer (PC), but its value as a treatment bio

250 Phase I studies in pancreatic cancer (PDAC) utilizing P-AscH(-) have demons

251 ced metabolic reprogramming is a hallmark of pancreatic cancer (PDAC), yet the metabolic drivers of m

252 tment of palbociclib with a MEK inhibitor in pancreatic cancer PDX models upregulated p27 and further

253 n update to the ASCO guideline on metastatic pancreatic cancer pertaining to recommendations for ther

254 itumor activity of HDACi in glioblastoma and pancreatic cancer preclinical models.

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

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

257 Successful treatment of pancreatic cancer remains a challenge due to desmoplasia

258 Surgery for metastatic pancreatic cancer remains controversial as the survival

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

260 tion was done on 2 patients with ovarian and pancreatic cancer, respectively.

261 treatment in the spontaneous mouse model of pancreatic cancer, revealed that sVCAM-1 promotes tumor

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

263 91; 95% CI, 1.40 to 6.04; P = 4.1 x 10(-3)), pancreatic cancer (RR, 2.37; 95% CI, 1.24 to 4.50; P = 8

264 ity in a small but heterogenous set of human pancreatic cancer samples.

265 the evolution of the metastatic capacity of pancreatic cancer.See related article by Rozeveld et al.

266 In pancreatic cancer, selective autophagy instead reroutes

267 oO-Tn was further applied to the analysis of pancreatic cancer sera, where Tn-glycoproteins were iden

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

269 ion, DUOX was significantly downregulated in pancreatic cancer specimens compared with normal pancrea

270 In pancreatic cancer specimens from patients, increased lev

271 g the lysine methyltransferase SMYD2 and the pancreatic cancer stem cell regulator RORC in all three

272 presence of a subset of PDAC cells known as pancreatic cancer stem cells (CSCs), which are more resi

273 cal and clinical significance of eradicating pancreatic cancer stem cells (PCSC) and its components u

274 Heterozygous mice also develop pancreatic cancer suggesting a haploinsufficient tumor s

275 2 gene variants are probably associated with pancreatic cancer susceptibility in populations of East

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

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

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

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

280 reatic and other cancer cell lines and human pancreatic cancer tissue microarrays.

281 DH11 messenger RNA in human pancreatitis and pancreatic cancer tissues and cells with normal pancreas

282 report that PRMT1 expression is increased in pancreatic cancer tissues and is associated with higher

283 ved extracellular vesicles play in spreading pancreatic cancer to other organs, due to the highly met

284 that PGD-driven suppression of TXNIP allows pancreatic cancers to avidly consume glucose.

285 in first-line therapy is an urgent issue in pancreatic cancer treatment.

286 pplications for IL-17RB-targeting therapy in pancreatic cancer treatment.

287 n2) is known to increase the invasiveness of pancreatic cancer tumor cells, but the mechanisms by whi

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

289 The association between T2DM and pancreatic cancer was also observed in a meta-analysis o

290 AM-1 in the plasma of patients with advanced pancreatic cancer was an independent prognostic factor f

291 ineered mouse models of Kras-driven lung and pancreatic cancer was deleterious to tumor initiation an

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

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

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

295 nts with resectable or borderline resectable pancreatic cancer were randomly assigned to receive preo

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

297 a, and increased the number of patients with pancreatic cancer who can undergo surgery.Many research

298 Of 1856 patients with pancreatic cancer who were referred to the KYT programme

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

300 xpression analysis showed that patients with pancreatic cancer with high stromal expression of Prrx1