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1 he operative treatment of pancreatic cancer (pancreatic ductal adenocarcinoma).
2 -492, which is recognised as a biomarker for pancreatic ductal adenocarcinoma.
3 o be used for the detection and prognosis of pancreatic ductal adenocarcinoma.
4 s) and cell-free DNA (cfDNA), with regard to pancreatic ductal adenocarcinoma.
5 ment of treatment response, and follow-up of pancreatic ductal adenocarcinoma.
6 mples obtained from patients with metastatic pancreatic ductal adenocarcinoma.
7 mportant prognostic factor for patients with pancreatic ductal adenocarcinoma.
8 and increased survival compared with typical pancreatic ductal adenocarcinoma.
9 preoperative therapy and pancreatectomy for pancreatic ductal adenocarcinoma.
10 rapy in 730 evaluable patients with resected pancreatic ductal adenocarcinoma.
11 new standard of care following resection for pancreatic ductal adenocarcinoma.
12 tility and is believed to be dysregulated in pancreatic ductal adenocarcinomas.
13 tor 1 (NTSR1) is overexpressed in most human pancreatic ductal adenocarcinomas.
15 by CXCR4 causes immune suppression in human pancreatic ductal adenocarcinoma and colorectal cancer b
16 he mechanisms of immunotherapy resistance in pancreatic ductal adenocarcinoma and discuss strategies
17 pancreatic neoplasms are resectable stage I pancreatic ductal adenocarcinoma and high-risk precursor
18 analysis in a family with multiple cases of pancreatic ductal adenocarcinoma and identify a germline
19 of comprehensive genomic characterization of pancreatic ductal adenocarcinoma and its precursor lesio
21 of chronic pancreatitis and occurs in 25% of pancreatic ductal adenocarcinomas and 40% of acinar cell
22 s and murine models of renal cell carcinoma, pancreatic ductal adenocarcinoma, and melanoma triggered
25 OCR were DUOX 1 and 2, which are silenced in pancreatic ductal adenocarcinoma, but upregulated with P
27 those for managing recalcitrant tumors like pancreatic ductal adenocarcinoma, cause off-target toxic
31 advances show the accelerated pace at which pancreatic ductal adenocarcinoma drugs are achieving suc
32 ectors, as attractive therapeutic targets in pancreatic ductal adenocarcinoma, especially in BAP1-def
35 adenocarcinoma incidence is rising and that pancreatic ductal adenocarcinoma has the highest case-fa
36 Whole-exome and whole-genome sequencing of pancreatic ductal adenocarcinomas have confirmed the cri
37 es that are effective for most patients with pancreatic ductal adenocarcinoma, important incremental
38 s the regression, and delays the regrowth of pancreatic ductal adenocarcinoma in a patient-derived xe
39 l be major breakthroughs in the treatment of pancreatic ductal adenocarcinoma in the next 5-10 years.
40 imate, in conjunction with the findings that pancreatic ductal adenocarcinoma incidence is rising and
41 intraductal papillary mucosal neoplasms and pancreatic ductal adenocarcinoma including the character
45 stration, olaparib for germline BRCA-mutated pancreatic ductal adenocarcinoma is expected to be appro
53 requently following preoperative therapy for pancreatic ductal adenocarcinoma, it is associated with
54 the factors that lead to the development of pancreatic ductal adenocarcinoma, its progression, and t
56 d that B7-H3.CAR-Ts controlled the growth of pancreatic ductal adenocarcinoma, ovarian cancer and neu
59 e optimal neoadjuvant therapy for resectable pancreatic ductal adenocarcinoma (PDA) and the impact on
60 ent on the uptake of extracellular proteins, pancreatic ductal adenocarcinoma (PDA) cells were select
61 Lineage plasticity is a prominent feature of pancreatic ductal adenocarcinoma (PDA) cells, which can
62 AIMS: Approximately 50% of all patients with pancreatic ductal adenocarcinoma (PDA) develop diabetes
72 though the estimated time for development of pancreatic ductal adenocarcinoma (PDA) is more than 20 y
74 cribe lipid accumulation in the TME areas of pancreatic ductal adenocarcinoma (PDA) populated by CD8+
83 sion of exosomes at the distal tumor site of pancreatic ductal adenocarcinoma (PDAC) ablated the deve
85 ne resectable (BR) and locally advanced (LA) pancreatic ductal adenocarcinoma (PDAC) after neoadjuvan
86 emcitabine alone in patients with metastatic pancreatic ductal adenocarcinoma (PDAC) and a Karnofsky
88 ge mitochondria and are cystic precursors to pancreatic ductal adenocarcinoma (PDAC) and cholangiocar
89 and induced cell death in KRAS-mutated human pancreatic ductal adenocarcinoma (PDAC) and colon cancer
90 nsmembrane mucin, is aberrantly expressed in pancreatic ductal adenocarcinoma (PDAC) and generally co
92 g that cAMP pathway is commonly activated in pancreatic ductal adenocarcinoma (PDAC) and its premalig
93 pithelial-to-mesenchymal transition (EMT) in Pancreatic Ductal Adenocarcinoma (PDAC) and of mesenchym
94 s and have emerged as therapeutic targets in pancreatic ductal adenocarcinoma (PDAC) and other cancer
95 reduced metastasis and prolonged survival in pancreatic ductal adenocarcinoma (PDAC) and our genomic
96 l variation in use of surgery for stage I-II pancreatic ductal adenocarcinoma (PDAC) and the associat
97 ance of the SIII in patients with resectable pancreatic ductal adenocarcinoma (PDAC) and the effects
98 KRAS are the hallmark genetic alterations in pancreatic ductal adenocarcinoma (PDAC) and the key driv
101 ch chronic stress promote the development of pancreatic ductal adenocarcinoma (PDAC) are poorly defin
102 ying adaptive targeted therapy resistance in pancreatic ductal adenocarcinoma (PDAC) are poorly under
103 tudies have reported a role for HNF1alpha in pancreatic ductal adenocarcinoma (PDAC) but it is contro
104 Here, we present non-invasive detection of pancreatic ductal adenocarcinoma (PDAC) by 5-hydroxymeth
107 perates to prevent cellular proliferation in pancreatic ductal adenocarcinoma (PDAC) cells, patient-d
113 ng metabolic abnormalities that occur before pancreatic ductal adenocarcinoma (PDAC) diagnosis could
114 and to liver metastasis, which in turn makes pancreatic ductal adenocarcinoma (PDAC) difficult to tre
115 unotherapy has only limited efficacy against pancreatic ductal adenocarcinoma (PDAC) due to the prese
128 mprovements in the outcomes of patients with pancreatic ductal adenocarcinoma (PDAC) have lagged behi
159 overall five-year survival of patients with pancreatic ductal adenocarcinoma (PDAC) is dismal, there
170 to its late diagnosis and dismal prognosis, pancreatic ductal adenocarcinoma (PDAC) is one of the mo
174 efficacy of systemic cancer therapeutics in pancreatic ductal adenocarcinoma (PDAC) is partly attrib
185 ly invasive distal pancreatectomy (MIDP) for pancreatic ductal adenocarcinoma (PDAC) on outcome by a
186 r-associated macrophages in a mouse model of pancreatic ductal adenocarcinoma (PDAC) originate from b
187 , we found that in cancer cells derived from pancreatic ductal adenocarcinoma (PDAC) PAR2 protein is
188 rapies have demonstrated limited efficacy in pancreatic ductal adenocarcinoma (PDAC) patients despite
193 multiple factors are known to contribute to pancreatic ductal adenocarcinoma (PDAC) progression, the
194 preoperative therapy and pancreatectomy for pancreatic ductal adenocarcinoma (PDAC) prolongs surviva
207 n multi-spectral images of multiplex-labeled pancreatic ductal adenocarcinoma (PDAC) tissue samples.
208 ls of KDM3A and DCLK1 messenger RNA in human pancreatic ductal adenocarcinoma (PDAC) tissues and asso
209 patients with locally advanced or metastatic pancreatic ductal adenocarcinoma (PDAC) treated with FOL
210 metabolic tracing to demonstrate that mouse pancreatic ductal adenocarcinoma (PDAC) tumors and human
211 Here, we provide evidence that a subset of pancreatic ductal adenocarcinoma (PDAC) tumors are wired
214 ine resectable (BR) or locally advanced (LA) pancreatic ductal adenocarcinoma (PDAC) undergoing total
215 s associated with humoral immune response in pancreatic ductal adenocarcinoma (PDAC) using in-depth p
216 hereas a dilated pancreatic duct (>3 mm) and pancreatic ductal adenocarcinoma (PDAC) were associated
217 n the management of patients with resectable pancreatic ductal adenocarcinoma (PDAC) when risks of po
219 modestly improved the survival prospects of pancreatic ductal adenocarcinoma (PDAC), additional enga
221 in the proto-oncogene KRAS are a hallmark of pancreatic ductal adenocarcinoma (PDAC), an aggressive m
222 is deemed instrumental to the progression of pancreatic ductal adenocarcinoma (PDAC), as exemplified
224 djuvant radiotherapy (RT) after resection of pancreatic ductal adenocarcinoma (PDAC), especially for
225 ains a primary challenge in the treatment of pancreatic ductal adenocarcinoma (PDAC), exploiting oxid
227 o a dearth of precision-medicine research in pancreatic ductal adenocarcinoma (PDAC), the main type o
229 h 1 (PD-1) inhibitors have limited effect in pancreatic ductal adenocarcinoma (PDAC), underscoring th
232 system x(C) (-) is a critical dependency of pancreatic ductal adenocarcinoma (PDAC), which is a lead
234 or HNF1A harbors susceptibility variants for pancreatic ductal adenocarcinoma (PDAC), while KDM6A, en
235 besity is a major modifiable risk factor for pancreatic ductal adenocarcinoma (PDAC), yet how and whe
266 a samples obtained from patients affected by pancreatic ductal adenocarcinoma (PDAC, n = 58), pancrea
268 KRAS mutations are present in over 90% of pancreatic ductal adenocarcinomas (PDAC), and drive thei
269 ID1A mutations occur in approximately 10% of pancreatic ductal adenocarcinomas (PDAC), but whether th
271 dulating heterogeneity in pancreatic cancer (pancreatic ductal adenocarcinoma [PDAC]) model systems,
277 llenge to select treatment for patients with pancreatic ductal adenocarcinomas (PDACs) based on genom
287 analyze somatic noncoding alterations in 308 pancreatic ductal adenocarcinomas (PDAs) and identify co
288 rent understanding of the pathophysiology of pancreatic ductal adenocarcinoma, recent advances in the
289 (AAV)-driven somatic genome-editing model of pancreatic ductal adenocarcinoma reported by Ideno et al
290 clear definition of "early recurrence" after pancreatic ductal adenocarcinoma resection is currently
291 abilized by CDK5-mediated phosphorylation in pancreatic ductal adenocarcinoma, resulting in the dereg
292 nalyzed ductal and neuroendocrine markers in pancreatic ductal adenocarcinoma, revealing heterogeneou
295 lucose uptake, and glycolysis in three human pancreatic ductal adenocarcinoma tumor xenografts with d
296 Here we demonstrate that, within colon and pancreatic ductal adenocarcinoma tumors, efficient strom
298 ike cells isolated from patients affected by pancreatic ductal adenocarcinoma, was observed, pointing
300 patients with histopathologically confirmed pancreatic ductal adenocarcinoma who received preoperati