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2 eoadjuvant therapy for resectable pancreatic ductal adenocarcinoma (PDA) and the impact on surgical o
3 uptake of extracellular proteins, pancreatic ductal adenocarcinoma (PDA) cells were selected for grow
4 sticity is a prominent feature of pancreatic ductal adenocarcinoma (PDA) cells, which can occur via d
9 The immune microenvironment of pancreatic ductal adenocarcinoma (PDA) is comprised of a heterogene
10 estimated time for development of pancreatic ductal adenocarcinoma (PDA) is more than 20 years, PDAs
11 accumulation in the TME areas of pancreatic ductal adenocarcinoma (PDA) populated by CD8+ T cells in
17 le (BR) and locally advanced (LA) pancreatic ductal adenocarcinoma (PDAC) after neoadjuvant FOLFIRINO
18 alone in patients with metastatic pancreatic ductal adenocarcinoma (PDAC) and a Karnofsky performance
20 dria and are cystic precursors to pancreatic ductal adenocarcinoma (PDAC) and cholangiocarcinoma (CCA
21 cell death in KRAS-mutated human pancreatic ductal adenocarcinoma (PDAC) and colon cancer lines, whi
22 pathway is commonly activated in pancreatic ductal adenocarcinoma (PDAC) and its premalignant lesion
23 o-mesenchymal transition (EMT) in Pancreatic Ductal Adenocarcinoma (PDAC) and of mesenchymal-to-epith
24 in use of surgery for stage I-II pancreatic ductal adenocarcinoma (PDAC) and the association between
26 reported a role for HNF1alpha in pancreatic ductal adenocarcinoma (PDAC) but it is controversial.
27 present non-invasive detection of pancreatic ductal adenocarcinoma (PDAC) by 5-hydroxymethylcytosine
29 prevent cellular proliferation in pancreatic ductal adenocarcinoma (PDAC) cells, patient-derived xeno
41 in the outcomes of patients with pancreatic ductal adenocarcinoma (PDAC) have lagged behind advances
64 e diagnosis and dismal prognosis, pancreatic ductal adenocarcinoma (PDAC) is one of the most devastat
75 distal pancreatectomy (MIDP) for pancreatic ductal adenocarcinoma (PDAC) on outcome by a propensity-
76 demonstrated limited efficacy in pancreatic ductal adenocarcinoma (PDAC) patients despite their succ
79 actors are known to contribute to pancreatic ductal adenocarcinoma (PDAC) progression, the role of lo
88 ontrast, neoantigen expression in pancreatic ductal adenocarcinoma (PDAC) results in exacerbation of
90 th locally advanced or metastatic pancreatic ductal adenocarcinoma (PDAC) treated with FOLFIRINOX, an
91 tracing to demonstrate that mouse pancreatic ductal adenocarcinoma (PDAC) tumors and human PDAC cell
92 provide evidence that a subset of pancreatic ductal adenocarcinoma (PDAC) tumors are wired to integra
94 lated pancreatic duct (>3 mm) and pancreatic ductal adenocarcinoma (PDAC) were associated with a bett
95 nstrumental to the progression of pancreatic ductal adenocarcinoma (PDAC), as exemplified by the freq
97 ary challenge in the treatment of pancreatic ductal adenocarcinoma (PDAC), exploiting oxidative stres
98 inhibitors have limited effect in pancreatic ductal adenocarcinoma (PDAC), underscoring the need to c
100 To expand the TAA landscape of pancreatic ductal adenocarcinoma (PDAC), we performed tandem mass s
101 ) (-) is a critical dependency of pancreatic ductal adenocarcinoma (PDAC), which is a leading cause o
103 rbors susceptibility variants for pancreatic ductal adenocarcinoma (PDAC), while KDM6A, encoding Lysi
104 major modifiable risk factor for pancreatic ductal adenocarcinoma (PDAC), yet how and when obesity c
120 btained from patients affected by pancreatic ductal adenocarcinoma (PDAC, n = 58), pancreatic neuroen
122 auses immune suppression in human pancreatic ductal adenocarcinoma and colorectal cancer by impairing
123 ms of immunotherapy resistance in pancreatic ductal adenocarcinoma and discuss strategies to directly
124 neoplasms are resectable stage I pancreatic ductal adenocarcinoma and high-risk precursor neoplasms,
125 n a family with multiple cases of pancreatic ductal adenocarcinoma and identify a germline truncating
126 nsive genomic characterization of pancreatic ductal adenocarcinoma and its precursor lesions, and we
128 nts undergoing pancreatectomy for pancreatic ductal adenocarcinoma between 2000 and 2013 were include
133 how the accelerated pace at which pancreatic ductal adenocarcinoma drugs are achieving successful cli
135 noma incidence is rising and that pancreatic ductal adenocarcinoma has the highest case-fatality rate
137 onjunction with the findings that pancreatic ductal adenocarcinoma incidence is rising and that pancr
138 l papillary mucosal neoplasms and pancreatic ductal adenocarcinoma including the characterization of
140 laparib for germline BRCA-mutated pancreatic ductal adenocarcinoma is expected to be approved soon in
149 ition of "early recurrence" after pancreatic ductal adenocarcinoma resection is currently lacking.
150 ls of PRKD1 were reduced in human pancreatic ductal adenocarcinoma tissues compared with nontumor tis
151 ke, and glycolysis in three human pancreatic ductal adenocarcinoma tumor xenografts with differing ph
152 emonstrate that, within colon and pancreatic ductal adenocarcinoma tumors, efficient stromagenesis re
155 OX 1 and 2, which are silenced in pancreatic ductal adenocarcinoma, but upregulated with P-AscH(-) tr
156 attractive therapeutic targets in pancreatic ductal adenocarcinoma, especially in BAP1-deficient or l
157 effective for most patients with pancreatic ductal adenocarcinoma, important incremental progress ha
158 s that lead to the development of pancreatic ductal adenocarcinoma, its progression, and the interpla
159 3.CAR-Ts controlled the growth of pancreatic ductal adenocarcinoma, ovarian cancer and neuroblastoma
161 tanding of the pathophysiology of pancreatic ductal adenocarcinoma, recent advances in the understand
162 ven the likely systemic nature of pancreatic ductal adenocarcinoma, the oncologic benefit of achievin
163 solated from patients affected by pancreatic ductal adenocarcinoma, was observed, pointing to this cl
168 ons occur in approximately 10% of pancreatic ductal adenocarcinomas (PDAC), but whether these mutatio
176 ere we show that ILC2s infiltrate pancreatic ductal adenocarcinomas (PDACs) to activate tissue-specif
178 pancreatitis and occurs in 25% of pancreatic ductal adenocarcinomas and 40% of acinar cell carcinomas
179 me and whole-genome sequencing of pancreatic ductal adenocarcinomas have confirmed the critical drive
180 A highly aggressive subset of pancreatic ductal adenocarcinomas undergo trans-differentiation int
183 tion of grade 1 and 2 invasive cancers (both ductal and lobular), but no change in the detection of g
184 differentiated cell types, including acinar, ductal and myoepithelial cells, that are maintained in a
188 r E-cadherin promotes metastasis of invasive ductal breast carcinoma by enhancing the survival of tum
190 dian age was 62 y (range, 31-90 y), most had ductal carcinoma (95%), and most were estrogen receptor-
193 common histologic subtypes were infiltrating ductal carcinoma (IDC, 84.9%) and luminal A (LA, 49.1%);
194 the lesions to be benign (n = 55), invasive ductal carcinoma (n = 51), invasive lobular carcinoma (n
197 new mechanistic insight into progression of ductal carcinoma and support clinical application of MNK
199 sversion present in human genomic DNA from a ductal carcinoma cell line, a mutation commonly found in
200 et their differentiation and perturbation in ductal carcinoma in situ (DCIS) are poorly understood.
202 ow-up (mean = 8.4 y), 2,225 invasive and 623 ductal carcinoma in situ (DCIS) cases were identified.
204 iR-223 expression was lost in microdissected ductal carcinoma in situ (DCIS) from patients with lumin
209 e (PPV) of biopsy, using invasive cancer and ductal carcinoma in situ (DCIS) to define a positive ref
210 st cancers progress from relatively indolent ductal carcinoma in situ (DCIS) to invasive ductal carci
211 on on the re-intervention rate in women with ductal carcinoma in situ (DCIS) undergoing breast-conser
212 g surgery for node-negative breast cancer or ductal carcinoma in situ (DCIS) were randomly assigned t
213 ied, including invasive breast cancer (IBC), ductal carcinoma in situ (DCIS), and adjacent benign tis
216 ws intended to highlight the relationship of ductal carcinoma in situ as a precursor to breast cancer
218 eased during the past 2 decades, whereas the ductal carcinoma in situ detection rate increased less r
219 ofractionation in patients with non-low-risk ductal carcinoma in situ following breast-conserving sur
220 reast epithelial tissue and hormone-negative ductal carcinoma in situ lesions but were uncoupled in t
221 early breast cancer or extensive/high-grade ductal carcinoma in situ planned for standard radioactiv
222 damage repair pathway and provides a link in ductal carcinoma in situ progression to invasive ductal
223 orial introduces this month's special Breast Ductal Carcinoma in Situ Theme Issue, a series of review
224 inhibitors to delay progression of indolent ductal carcinoma in situ to invasive ductal carcinoma.
226 r older with completely excised non-low-risk ductal carcinoma in situ were randomly assigned, by use
227 preventing breast cancer (both invasive and ductal carcinoma in situ) in the post-treatment period.
228 developed breast cancer (invasive, n = 129; ductal carcinoma in situ,n = 47) over a median follow-up
232 nsmembrane protease, serine 13), in invasive ductal carcinoma patient tissue samples compared to norm
233 lecular level, the proliferation of invasive ductal carcinoma through breast tissue is beyond the ran
234 al carcinoma in situ progression to invasive ductal carcinoma through loss of SIM2s, increased genomi
239 vation that most breast cancers are invasive ductal carcinomas and express E-cadherin in primary tumo
242 riple-negative grade 3 cancers; two invasive ductal carcinomas that were estrogen and progesterone re
245 jor axes, one that encompasses a gradient of ductal cell differentiation stages, and another featurin
246 in HPNE cells (human noncancerous pancreatic ductal cell line); we evaluated cell migration, invasion
247 lowing severe or chronic liver injury, adult ductal cells (cholangiocytes) contribute to regeneration
248 6A9 is predominantly expressed in pancreatic ductal cells and frequently coexpressed with CF transmem
249 te that an increase in SLC26A9 expression in ductal cells of the pancreas delays the age at onset of
250 quencing (scRNA-seq) of ALK3(bright+)-sorted ductal cells, a fraction that harbors BMP-responsive pro
251 eatic tumors, we find that subpopulations of ductal cells, macrophages, dendritic cells and cancer ce
252 rentiated cells, including myoepithelial and ductal cells, that appear to dedifferentiate to a progen
253 olic homeostasis in Yap-deficient neoplastic ductal cells, which gradually re-differentiate into acin
254 vating PIK3CA(H1047R) mutation each produces ductal changes observed in invasive progression, yet wit
255 traductal administration overcomes the rapid ductal clearance of CPX, prolongs mammary tissue persist
256 ver, the molecular mechanisms by which adult ductal-committed cells acquire cellular plasticity, init
257 Infants with single ventricle anatomy and ductal-dependent pulmonary blood flow palliated with eit
258 t or BT shunt as palliation for infants with ductal-dependent pulmonary blood flow, adjusted for base
261 nosis is based on pancreatic calcifications, ductal dilatation, and atrophy visualized by imaging wit
263 addition, oestrogen, which is essential for ductal elongation during puberty, upregulates CCR1 expre
265 receptor ACKR2 contributes to the control of ductal epithelial branching in the developing mammary gl
266 ncreatic cell lines versus normal pancreatic ductal epithelial cells, as shown by Western blot analys
267 es were observed in the bile duct, including ductal epithelial proliferation, micropapillary growth o
270 in chronic pancreatitis, other than by using ductal features alone as described in the Cambridge clas
272 nt of percutaneously diagnosed pure atypical ductal hyperplasia (ADH) is an unresolved clinical issue
273 landscape of normal breast tissue, atypical ductal hyperplasia (ADH), DCIS and invasive breast cance
274 apparent complete lesion removal), atypical ductal hyperplasia diagnosed with percutaneous needle bi
277 ATDC is required for KRAS-driven acinar-ductal metaplasia (ADM) and its progression to pancreati
278 kappaB-Ras deficiency promotes acinar-to-ductal metaplasia (ADM) during tumour initiation as well
279 tructures, the ductal phenotype of acinar-to-ductal metaplasia (ADM), and dysplasia with Dice coeffic
282 lls increased their expression of markers of ductal metaplasia; these effects of IL22 were prevented
284 lacement pumps, each linked to a contractile ductal network, milk begins its passage toward the depen
286 70% water formulations moderately increased ductal penetration, but minimally altered stratum corneu
287 tool segments normal acinar structures, the ductal phenotype of acinar-to-ductal metaplasia (ADM), a
289 loss of Anks6 causes ciliary abnormalities, ductal plate remodeling defects and periportal fibrosis
290 l cells are most similar to human acinar and ductal populations, that a PrU-like population is conser
291 ication, characterisation, and monitoring of ductal progenitor cells during development and progressi
292 omplex, is co-expressed with SOX9 by foregut ductal progenitors in the developing human liver and pan
294 bed in Jag1 mutants until later stages, when ductal remodeling fails, and signs of acinar-to-ductal m
295 ate-mapping analysis revealed that, although ductal stem cells marked by cytokeratin K14 and Axin2 un
296 xploration (LCBDE) deals with gallstones and ductal stones in one session, the limited availability o
300 scopy (SOPCP) enables direct biliopancreatic ductal visualization, targeted tissue sampling, and ther