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1 n, ductal hyperplasia, or dysplastic lesions/pancreatic intraepithelial neoplasia.
2 ular complexes (TC), mucinous metaplasia, or pancreatic intraepithelial neoplasia.
3 within the pancreatic ducts, referred to as pancreatic intraepithelial neoplasias.
4 );Pdx1-Cre mice, but did not alter growth of pancreatic intraepithelial neoplasias.
5 e expression of oncogenic KRAS, premalignant pancreatic intraepithelial neoplasia 1 (PanIN1) lesions
6 owed substantial reduction of ADM as well as pancreatic intraepithelial neoplasia-1 (PanIN-1), PanIN-
8 n exhibited diminished SC chemoattraction to pancreatic intraepithelial neoplasia and increased abdom
9 adenocarcinoma specimens, but also in human pancreatic intraepithelial neoplasia and metaplastic duc
10 thelial cells in culture and for Kras-driven pancreatic intraepithelial neoplasia and PDAC formation
11 lasia lesions, but progression to high-grade pancreatic intraepithelial neoplasias and PDAC is blocke
12 f p110alpha and RAC1 were increased in human pancreatic intraepithelial neoplasias and PDAs compared
13 eased ADM, decreased formation of high-grade pancreatic intraepithelial neoplasias, and accelerated d
14 stologically analyzed for formation of IPMN, pancreatic intraepithelial neoplasias, and PDAC, in addi
16 tion drastically attenuates the formation of pancreatic intraepithelial neoplasia induced by mutant K
17 creatic carcinomas (93%), 3 of 18 high-grade pancreatic intraepithelial neoplasia lesions (17%), and
18 sia lesions (17%), and 0 of the 69 low-grade pancreatic intraepithelial neoplasia lesions expressed S
19 ar-to-ductal metaplasia (ADM)-a precursor of pancreatic intraepithelial neoplasia lesions that can pr
20 uncovered induction of NFATc2 in late-stage pancreatic intraepithelial neoplasia lesions with increa
21 or Atg7 accumulate low-grade, pre-malignant pancreatic intraepithelial neoplasia lesions, but progre
24 er, rather than reduced, number of low-grade pancreatic intraepithelial neoplasia (mPanIN) lesions.
25 acinar-to-ductal metaplasia (ADM), malignant pancreatic intraepithelial neoplasia (mPanIN), and PDAC
26 more, AGR2 is coexpressed with MUC1 in mouse pancreatic intraepithelial neoplasia (mPanIN)-like lesio
27 significantly accelerated the progression of pancreatic intraepithelial neoplasias (mPanIN) and promo
28 y elevated Ras activity and in sparse murine pancreatic intraepithelial neoplasias (mPanINs) that did
32 on starting at either noninvasive precursor (pancreatic intraepithelial neoplasia) or the PDAC stage
33 elated significantly with the progression of pancreatic intraepithelial neoplasias (P = 0.001) and de
35 nervous system (CNS) occurs as early as the pancreatic intraepithelial neoplasia (PanIN) 2 stage.
36 ), KPC(Pdx1), and KC(iMist1) mouse models of pancreatic intraepithelial neoplasia (PanIN) and analyze
37 ng, cells that underwent ADM can progress to pancreatic intraepithelial neoplasia (PanIN) and eventua
38 sine kinase is overexpressed in premalignant pancreatic intraepithelial neoplasia (PanIN) and in the
39 rcinoma (PDA) develops predominantly through pancreatic intraepithelial neoplasia (PanIN) and intradu
40 ncreatic development and is induced in mouse pancreatic intraepithelial neoplasia (PanIN) and pancrea
41 reatitis and might be viewed as a prelude to pancreatic intraepithelial neoplasia (PanIN) and pancrea
42 ative real-time polymerase chain reaction in pancreatic intraepithelial neoplasia (PanIN) and PDAC sa
44 the presence of oncogenic KRAS, accelerates pancreatic intraepithelial neoplasia (PanIN) formation a
45 that attenuates acinar-to-ductal metaplasia, pancreatic intraepithelial neoplasia (PanIN) formation,
48 tion of beta-catenin blocks the formation of pancreatic intraepithelial neoplasia (PanIN) in the pres
49 120 catenin progressively develop high-grade pancreatic intraepithelial neoplasia (PanIN) lesions and
50 ppressed in both pancreatic cancer cells and pancreatic intraepithelial neoplasia (PanIN) lesions in
52 ry for the transition from early to advanced pancreatic intraepithelial neoplasia (PanIN) lesions, we
53 ing acinar-to-ductal metaplasia and in early pancreatic intraepithelial neoplasia (PanIN) lesions.
54 ADM lesions then convert to precancerous pancreatic intraepithelial neoplasia (PanIN) that progre
55 While KRAS(G12D) alone elicited premalignant pancreatic intraepithelial neoplasia (PanIN) that progre
56 ons in the pancreas, with characteristics of pancreatic intraepithelial neoplasia (PanIN), a precurso
57 potential OIS biomarkers in human and murine pancreatic intraepithelial neoplasia (PanIN), and found
58 ere collected and analyzed for inflammation, pancreatic intraepithelial neoplasia (PanIN), and PDAC.
59 ar-regulated kinase, inflammation, fibrosis, pancreatic intraepithelial neoplasia (PanIN), and PDACs.
60 ng that PDAC and its preinvasive precursors, pancreatic intraepithelial neoplasia (PanIN), arise via
61 ncreatic epithelium accelerated formation of pancreatic intraepithelial neoplasia (PanIN), increased
62 e microarrays, methylation analysis of early pancreatic intraepithelial neoplasia (PanIN), mouse mode
63 fects of fascin deficiency on development of pancreatic intraepithelial neoplasia (PanIn), PDAC, and
64 oblotting indicates that RON is expressed in pancreatic intraepithelial neoplasia (PanIN), primary, a
65 t N-cadherin is expressed in human and mouse pancreatic intraepithelial neoplasia (PanIN), suggesting
66 (ADM), pancreatic acinar cells give rise to pancreatic intraepithelial neoplasia (PanIN), the most c
67 e formation of PDA and its precursor lesion, pancreatic intraepithelial neoplasia (PanIN), we examine
69 ll identity, thus resisting the formation of pancreatic intraepithelial neoplasia (PanIN)-derived PDA
82 well-defined precursor ductal lesions called pancreatic intraepithelial neoplasia (PanIN-1A, -1B, -2,
84 and premalignant pancreatic ductal cells [96 pancreatic intraepithelial neoplasias (PanIN) from 46 pa
86 We studied the formation and maintenance of pancreatic intraepithelial neoplasia (PanINs) in p48Cre;
87 th the initiation and expansion of low-grade pancreatic intraepithelial neoplasia (PanINs), likely th
88 that reconstitute hallmark features of human pancreatic intraepithelial neoplasia (PanINs), the precu
89 of mice is sufficient to induce formation of pancreatic intraepithelial neoplasia (PanINs)-a precurso
91 and promotes the development of premalignant pancreatic intraepithelial neoplasias (PanINs) and cysti
92 ary human pancreatic ductal adenocarcinomas, pancreatic intraepithelial neoplasias (PanINs) and norma
93 -mediated acinar-to-ductal metaplasia (ADM), pancreatic intraepithelial neoplasias (PanINs) and ultim
94 status, while analysis of precursor lesions, pancreatic intraepithelial neoplasias (PanINs), demonstr
95 partment was sufficient for the formation of pancreatic intraepithelial neoplasias (PanINs), putative
96 of focal premalignant ductal lesions, termed pancreatic intraepithelial neoplasias (PanINs), whereas
98 gically identifiable intraductal precursors [pancreatic intraepithelial neoplasias (PanINs)] that und
99 Pdx1-Cre;LSL-KrasG12D model by exacerbating pancreatic intraepithelial neoplasias, promoting facial
100 ates that inactivation of this GTPase at the pancreatic intraepithelial neoplasia stage promotes panc
101 of MUC4 expression has also been observed in pancreatic intraepithelial neoplasia, suggesting its ass
102 veloped a greater number and higher grade of pancreatic intraepithelial neoplasias than KC mice, and
103 pressed in human pancreatic cancer cells and pancreatic intraepithelial neoplasia, the early lesion o
104 ehog signaling caused extensive formation of pancreatic intraepithelial neoplasias, the earliest stag
105 for oncogenic KRAS in both the formation of pancreatic intraepithelial neoplasias, the most common p
106 ed in human PDAC tissues and in premalignant pancreatic intraepithelial neoplasia tissues isolated fr
108 rmore, Hes1 is an essential component of the pancreatic intraepithelial neoplasias-to-PDAC route in K
110 innervation increased dramatically when only pancreatic intraepithelial neoplasia were apparent.
111 12D)-induced acinar-to-ductal metaplasia and pancreatic intraepithelial neoplasias, which rapidly pro
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