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1 ular complexes (TC), mucinous metaplasia, or pancreatic intraepithelial neoplasia.
2 velopment of acinar-to-ductal metaplasia and pancreatic intraepithelial neoplasia.
3 ion of acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia.
4 s, including acinar-to-ductal metaplasia and pancreatic intraepithelial neoplasia.
5 n, ductal hyperplasia, or dysplastic lesions/pancreatic intraepithelial neoplasia.
6  within the pancreatic ducts, referred to as pancreatic intraepithelial neoplasias.
7 );Pdx1-Cre mice, but did not alter growth of pancreatic intraepithelial neoplasias.
8  with high-grade dysplasia and some enlarged pancreatic intraepithelial neoplasias.
9 e expression of oncogenic KRAS, premalignant pancreatic intraepithelial neoplasia 1 (PanIN1) lesions
10 owed substantial reduction of ADM as well as pancreatic intraepithelial neoplasia-1 (PanIN-1), PanIN-
11                Its expression is lost at the pancreatic intraepithelial neoplasia 1b (PanIN1b)/PanIN2
12 both a reduction in the development of early pancreatic intraepithelial neoplasia and an increase in
13 n exhibited diminished SC chemoattraction to pancreatic intraepithelial neoplasia and increased abdom
14  adenocarcinoma specimens, but also in human pancreatic intraepithelial neoplasia and metaplastic duc
15 thelial cells in culture and for Kras-driven pancreatic intraepithelial neoplasia and PDAC formation
16 lasia lesions, but progression to high-grade pancreatic intraepithelial neoplasias and PDAC is blocke
17 f p110alpha and RAC1 were increased in human pancreatic intraepithelial neoplasias and PDAs compared
18 through expansion to dissemination from both pancreatic intraepithelial neoplasias and throughout PDA
19 ith RA96 distinguished chronic pancreatitis, pancreatic intraepithelial neoplasia, and varying grades
20 eased ADM, decreased formation of high-grade pancreatic intraepithelial neoplasias, and accelerated d
21 stologically analyzed for formation of IPMN, pancreatic intraepithelial neoplasias, and PDAC, in addi
22 oplasms and mucinous cystic neoplasms, while pancreatic intraepithelial neoplasias are rarely detecte
23             PRKD1(KO)-KC mice developed more pancreatic intraepithelial neoplasia, at a faster rate,
24                           Here, we show that pancreatic intraepithelial neoplasia driven by oncogenic
25       TIMP1 was upregulated in patients with pancreatic intraepithelial neoplasias grade 3 and PDAC l
26          In contrast, presence of high-grade pancreatic intraepithelial neoplasia (HG-PanIN) at the f
27 rs of stromal activation entirely surrounded pancreatic intraepithelial neoplasias in KPC/Cdh11(+/+)
28 tion drastically attenuates the formation of pancreatic intraepithelial neoplasia induced by mutant K
29 he downstream MAPK effector pathway, driving pancreatic intraepithelial neoplasia initiation.
30 creatic carcinomas (93%), 3 of 18 high-grade pancreatic intraepithelial neoplasia lesions (17%), and
31 sia lesions (17%), and 0 of the 69 low-grade pancreatic intraepithelial neoplasia lesions expressed S
32 ar-to-ductal metaplasia (ADM)-a precursor of pancreatic intraepithelial neoplasia lesions that can pr
33  uncovered induction of NFATc2 in late-stage pancreatic intraepithelial neoplasia lesions with increa
34  or Atg7 accumulate low-grade, pre-malignant pancreatic intraepithelial neoplasia lesions, but progre
35  associated with development of premalignant pancreatic intraepithelial neoplasia lesions.
36 l metaplasia and the subsequent formation of pancreatic intraepithelial neoplasia lesions.
37 er, rather than reduced, number of low-grade pancreatic intraepithelial neoplasia (mPanIN) lesions.
38 acinar-to-ductal metaplasia (ADM), malignant pancreatic intraepithelial neoplasia (mPanIN), and PDAC
39 more, AGR2 is coexpressed with MUC1 in mouse pancreatic intraepithelial neoplasia (mPanIN)-like lesio
40 significantly accelerated the progression of pancreatic intraepithelial neoplasias (mPanIN) and promo
41 y elevated Ras activity and in sparse murine pancreatic intraepithelial neoplasias (mPanINs) that did
42            Similarly, pancreatitis (n = 17), pancreatic intraepithelial neoplasia (n = 80), and pancr
43 e precursor lesions has been standardized as pancreatic intraepithelial neoplasia or PanIN.
44 -ductal metaplasia but did not develop mouse pancreatic intraepithelial neoplasia or tumors.
45 on starting at either noninvasive precursor (pancreatic intraepithelial neoplasia) or the PDAC stage
46 elated significantly with the progression of pancreatic intraepithelial neoplasias (P = 0.001) and de
47 ration (P < 0.0001) and dysplasia (increased pancreatic intraepithelial neoplasia, P < 0.01).
48  nervous system (CNS) occurs as early as the pancreatic intraepithelial neoplasia (PanIN) 2 stage.
49 ), KPC(Pdx1), and KC(iMist1) mouse models of pancreatic intraepithelial neoplasia (PanIN) and analyze
50 ng, cells that underwent ADM can progress to pancreatic intraepithelial neoplasia (PanIN) and eventua
51 sine kinase is overexpressed in premalignant pancreatic intraepithelial neoplasia (PanIN) and in the
52 rcinoma (PDA) develops predominantly through pancreatic intraepithelial neoplasia (PanIN) and intradu
53 ncreatic development and is induced in mouse pancreatic intraepithelial neoplasia (PanIN) and pancrea
54 reatitis and might be viewed as a prelude to pancreatic intraepithelial neoplasia (PanIN) and pancrea
55 ative real-time polymerase chain reaction in pancreatic intraepithelial neoplasia (PanIN) and PDAC sa
56                                              Pancreatic intraepithelial neoplasia (PanIN) are pancrea
57 t of Arid1a deficiency in the progression of pancreatic intraepithelial neoplasia (PanIN) by profilin
58 hesized a regulatory model of the acinar-ADM-pancreatic intraepithelial neoplasia (PanIN) continuum a
59 arly, an absence of ATF3 reduced spontaneous pancreatic intraepithelial neoplasia (PanIN) formation a
60  the presence of oncogenic KRAS, accelerates pancreatic intraepithelial neoplasia (PanIN) formation a
61 that attenuates acinar-to-ductal metaplasia, pancreatic intraepithelial neoplasia (PanIN) formation,
62              We previously demonstrated that pancreatic intraepithelial neoplasia (PanIN) formation,
63                          Increasing grade of pancreatic intraepithelial neoplasia (PanIN) has been as
64 velops in the earliest stages of preinvasive pancreatic intraepithelial neoplasia (PanIN) in the Kras
65 tion of beta-catenin blocks the formation of pancreatic intraepithelial neoplasia (PanIN) in the pres
66                                              Pancreatic intraepithelial neoplasia (PanIN) is a precur
67 ated macrophages contribute to fibrogenesis, pancreatic intraepithelial neoplasia (PanIN) lesion grow
68 120 catenin progressively develop high-grade pancreatic intraepithelial neoplasia (PanIN) lesions and
69 ppressed in both pancreatic cancer cells and pancreatic intraepithelial neoplasia (PanIN) lesions in
70            A second microarray containing 54 pancreatic intraepithelial neoplasia (PanIN) lesions was
71 ry for the transition from early to advanced pancreatic intraepithelial neoplasia (PanIN) lesions, we
72 tions and is also frequently associated with pancreatic intraepithelial neoplasia (PanIN) lesions.
73 ing acinar-to-ductal metaplasia and in early pancreatic intraepithelial neoplasia (PanIN) lesions.
74 ) and are considered the initiating event of pancreatic intraepithelial neoplasia (PanIN) precursor l
75 While KRAS(G12D) alone elicited premalignant pancreatic intraepithelial neoplasia (PanIN) that progre
76     ADM lesions then convert to precancerous pancreatic intraepithelial neoplasia (PanIN) that progre
77 etic axon sprouting has been observed around pancreatic intraepithelial neoplasia (PanIN), a common p
78                Recent evidence suggests that pancreatic intraepithelial neoplasia (PanIN), a microsco
79 ons in the pancreas, with characteristics of pancreatic intraepithelial neoplasia (PanIN), a precurso
80 nc-1, and Panc-28 cells and samples of human pancreatic intraepithelial neoplasia (PanIN), along with
81 potential OIS biomarkers in human and murine pancreatic intraepithelial neoplasia (PanIN), and found
82 ere collected and analyzed for inflammation, pancreatic intraepithelial neoplasia (PanIN), and PDAC.
83 ar-regulated kinase, inflammation, fibrosis, pancreatic intraepithelial neoplasia (PanIN), and PDACs.
84 plasia (ADM), accelerated the progression of pancreatic intraepithelial neoplasia (PanIN), and result
85 ng that PDAC and its preinvasive precursors, pancreatic intraepithelial neoplasia (PanIN), arise via
86 ncreatic epithelium accelerated formation of pancreatic intraepithelial neoplasia (PanIN), increased
87 e microarrays, methylation analysis of early pancreatic intraepithelial neoplasia (PanIN), mouse mode
88 fects of fascin deficiency on development of pancreatic intraepithelial neoplasia (PanIn), PDAC, and
89 oblotting indicates that RON is expressed in pancreatic intraepithelial neoplasia (PanIN), primary, a
90 t N-cadherin is expressed in human and mouse pancreatic intraepithelial neoplasia (PanIN), suggesting
91  (ADM), pancreatic acinar cells give rise to pancreatic intraepithelial neoplasia (PanIN), the most c
92       Kras mutation induces the formation of pancreatic intraepithelial neoplasia (PanIN), these lesi
93 e formation of PDA and its precursor lesion, pancreatic intraepithelial neoplasia (PanIN), we examine
94                      Using a murine model of pancreatic intraepithelial neoplasia (PanIN), we found t
95 acterize ECM proteins in normal pancreas and pancreatic intraepithelial neoplasia (PanIN)- and PDAC-b
96  pancreatic cancer is typically managed like pancreatic intraepithelial neoplasia (PanIN)-derived pan
97 ll identity, thus resisting the formation of pancreatic intraepithelial neoplasia (PanIN)-derived PDA
98 ma develops through precursor lesions termed pancreatic intraepithelial neoplasia (PanIN).
99  series of noninvasive duct lesions known as pancreatic intraepithelial neoplasia (PanIN).
100 ic adenocarcinoma and its precursor lesions: pancreatic intraepithelial neoplasia (PanIN).
101 rs to invasive pancreatic ductal carcinomas, pancreatic intraepithelial neoplasia (PanIN).
102 ctal metaplasia (ADM) and its progression to pancreatic intraepithelial neoplasia (PanIN).
103 smoking during initiation and development of pancreatic intraepithelial neoplasia (PanIN).
104 ieved to arise from precursor lesions termed pancreatic intraepithelial neoplasia (PanIN).
105 PDGs) have been hypothesized to give rise to pancreatic intraepithelial neoplasia (PanIN).
106 uman malignancies, including human PDACs and pancreatic intraepithelial neoplasia (PanIN).
107 sions, acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN).
108 t to originate from duct-like lesions called pancreatic intraepithelial neoplasia (PanIN).
109 rised of putative precursor lesions known as pancreatic intraepithelial neoplasia (PanIN).
110 reatic tumors and their putative precursors, pancreatic intraepithelial neoplasia (PanIN).
111 well-defined precursor ductal lesions called pancreatic intraepithelial neoplasia (PanIN-1A, -1B, -2,
112                                              Pancreatic intraepithelial neoplasias (PanIN) are the pr
113 and premalignant pancreatic ductal cells [96 pancreatic intraepithelial neoplasias (PanIN) from 46 pa
114 vasive, intraductal precursor lesions called pancreatic intraepithelial neoplasias (PanIN).
115  cancer involves visualisation of high-grade pancreatic intraepithelial neoplasias (PanIN-3), general
116  cancer involves visualization of high-grade pancreatic intraepithelial neoplasias (PanIN-3s), genera
117 elopment of advanced PDAC precursor lesions (pancreatic intraepithelial neoplasia [PanIN]-3) in male
118  We studied the formation and maintenance of pancreatic intraepithelial neoplasia (PanINs) in p48Cre;
119 eads to the early appearance of premalignant pancreatic intraepithelial neoplasia (PanINs) in tissues
120  pancreatic cancer and initiate precancerous pancreatic intraepithelial neoplasia (PanINs) when induc
121 th the initiation and expansion of low-grade pancreatic intraepithelial neoplasia (PanINs), likely th
122 that reconstitute hallmark features of human pancreatic intraepithelial neoplasia (PanINs), the precu
123 of mice is sufficient to induce formation of pancreatic intraepithelial neoplasia (PanINs)-a precurso
124  (ADM) and the development of pre-neoplastic pancreatic intraepithelial neoplasia (PanINs).
125  present in tubular complexes (TC) and early pancreatic intraepithelial neoplasia (PanINs).
126 and promotes the development of premalignant pancreatic intraepithelial neoplasias (PanINs) and cysti
127 ary human pancreatic ductal adenocarcinomas, pancreatic intraepithelial neoplasias (PanINs) and norma
128 -mediated acinar-to-ductal metaplasia (ADM), pancreatic intraepithelial neoplasias (PanINs) and ultim
129                                              Pancreatic intraepithelial neoplasias (PanINs) are the m
130  required for development and progression of pancreatic intraepithelial neoplasias (PanINs) are uncle
131 status, while analysis of precursor lesions, pancreatic intraepithelial neoplasias (PanINs), demonstr
132 partment was sufficient for the formation of pancreatic intraepithelial neoplasias (PanINs), putative
133 of focal premalignant ductal lesions, termed pancreatic intraepithelial neoplasias (PanINs), whereas
134 etaplasia (ADM), giving rise to premalignant pancreatic intraepithelial neoplasias (PanINs), which fi
135 s of Nupr1 protected from the development of pancreatic intraepithelial neoplasias (PanINs).
136 gically identifiable intraductal precursors [pancreatic intraepithelial neoplasias (PanINs)] that und
137 ze: 1.22 +/- 0.56 mm) alongside 54 low-grade pancreatic intraepithelial neoplasias (positive control
138  Pdx1-Cre;LSL-KrasG12D model by exacerbating pancreatic intraepithelial neoplasias, promoting facial
139 ssed member of the mucin family during early pancreatic intraepithelial neoplasia stage I (PanIN-I) o
140 ates that inactivation of this GTPase at the pancreatic intraepithelial neoplasia stage promotes panc
141 of MUC4 expression has also been observed in pancreatic intraepithelial neoplasia, suggesting its ass
142 veloped a greater number and higher grade of pancreatic intraepithelial neoplasias than KC mice, and
143 pressed in human pancreatic cancer cells and pancreatic intraepithelial neoplasia, the early lesion o
144 ehog signaling caused extensive formation of pancreatic intraepithelial neoplasias, the earliest stag
145  for oncogenic KRAS in both the formation of pancreatic intraepithelial neoplasias, the most common p
146 ed in human PDAC tissues and in premalignant pancreatic intraepithelial neoplasia tissues isolated fr
147 ytosine (5-HmC) in CAFs, in progression from pancreatic intraepithelial neoplasia to PDAC.
148 rmore, Hes1 is an essential component of the pancreatic intraepithelial neoplasias-to-PDAC route in K
149                          With recognition of pancreatic intraepithelial neoplasia, we see that chroni
150 innervation increased dramatically when only pancreatic intraepithelial neoplasia were apparent.
151 ors but also early pancreatic lesions called pancreatic intraepithelial neoplasias, which are challen
152 12D)-induced acinar-to-ductal metaplasia and pancreatic intraepithelial neoplasias, which rapidly pro

 
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