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1  is related to histopathological features of preneoplastic aberrant crypt foci (ACF), gene expression
2 ce of mPGES-1 reduced the size and number of preneoplastic aberrant crypt foci (ACF).
3 al hepatectomy but no signs of neoplastic or preneoplastic abnormalities for up to 18 months.
4                                          The preneoplastic "acidic" MUC2 mucin was detected only in t
5 ic analysis of cuSCC development through the preneoplastic AK stage using matched human samples and a
6 sion increased the rate of apoptosis of both preneoplastic and carcinomatous mammary epithelial cells
7 crease in the proliferation rate and size of preneoplastic and early neoplastic lesions, although hav
8 n and progesterone receptors was observed in preneoplastic and early neoplastic lesions, suggesting a
9 ent of the adult pancreas as well as in both preneoplastic and malignant lesions.
10 d mice to permit the growth of primary human preneoplastic and malignant plasma cells together with n
11 solated from a tumor stimulate the growth of preneoplastic and neoplastic cells in xenograft models.
12  consistently elevated in myc-overexpressing preneoplastic and neoplastic cells, most involved in pro
13 h for preferential induction of apoptosis in preneoplastic and neoplastic cells.
14 emble human ESCC, we visualized the probe in preneoplastic and neoplastic esophageal lesions using ne
15 alization of IGFBP-3 in the preponderance of preneoplastic and neoplastic esophageal lesions.
16 t was modified and improved to yield ovarian preneoplastic and neoplastic lesions that pathogenetical
17  CCSA-4 in the detection of individuals with preneoplastic and neoplastic lesions using ELISAs.
18 spring were examined at four time points for preneoplastic and neoplastic lesions.
19 ty acid oxidation and gluconeogenesis in rat preneoplastic and neoplastic liver lesions, when compare
20 hepatectomy and is strongly overexpressed in preneoplastic and neoplastic mouse liver.
21                                      We used preneoplastic and neoplastic mouse models of prostate ca
22 reduced the production of NO in NMBA-induced preneoplastic and papillomatous esophageal lesions when
23 ures associated with the early inflammatory, preneoplastic and tumour stages.
24 clinical trials for a variety of neoplastic, preneoplastic, and inflammatory conditions.
25 cumulation of MKlp2 in normal proliferating, preneoplastic, and transformed hepatocytes suggests that
26 of Akt activity is necessary for survival of preneoplastic as well as transformed lung epithelial cel
27                                        These preneoplastic B lymphocytes did not progress to detectab
28 o implicated acidic pH in the development of preneoplastic Barrett's esophagus in human.
29  Akt and Mcl-1 are strongly expressed in the preneoplastic bile duct inflammatory disease primary scl
30 ated in luminal progenitor cells resident in preneoplastic BRCA1(mut/+) breast tissue.
31 ate whole-body quantitative SPECT imaging of preneoplastic breast cancer tissue using (111)In-labeled
32 3 region had the highest frequency of LOH in preneoplastic breast epithelium (36%), followed by 3p21.
33  HER2/neu, which has also been identified in preneoplastic breast lesions, has been shown to regulate
34 elta3 are overexpressed in breast cancer and preneoplastic breast tissue.
35 cular alterations that have been examined in preneoplastic bronchial epithelium.
36 their presence is hypothesized to facilitate preneoplastic cell growth and tumor formation in older i
37     Similarly, senescent fibroblasts promote preneoplastic cell growth in vitro and in vivo.
38 factors directly responsible for stimulating preneoplastic cell growth, we carried out whole-genome t
39 PN is necessary for paracrine stimulation of preneoplastic cell growth.
40  recombinant OPN was sufficient to stimulate preneoplastic cell growth.
41              These results indicate that the preneoplastic cell populations found in this genetically
42                       DB[a,l]P-induced early preneoplastic cell proliferation correlated with H-ras a
43                                              Preneoplastic cells (PNCs) are found in most ptc mutants
44                                        Early preneoplastic cells (sup+) exhibit increased susceptibil
45 ty to apoptosis, which is lost in late stage preneoplastic cells (sup-).
46 ory phenotype, prevents the proliferation of preneoplastic cells and has beneficial roles in tissue r
47 n but facilitating progression and growth of preneoplastic cells and subclinical cancers, which are c
48         Alterations in cyclin D1 activity in preneoplastic cells could represent an early biomarker o
49 ivo models to study the interaction of human preneoplastic cells in the bone marrow microenvironment
50  characteristic structural reorganization of preneoplastic cells may involve changes in the microtubu
51           Most ptc1+/- mice form clusters of preneoplastic cells on the surface of the mature cerebel
52 d by proliferation so that the population of preneoplastic cells remains constant.
53 stitutive expression of Dss1 in JB6 Cl 41-5a preneoplastic cells strongly increased focus formation a
54 h prevents paraspeckle formation, sensitized preneoplastic cells to DNA-damage-induced cell death and
55          In approximately 15% of mice, these preneoplastic cells will become fast-growing, lethal tum
56 s in mtDNA among normal stem cells, immortal/preneoplastic cells, and tumorigenic cells.
57  that blocks Akt signaling in neoplastic and preneoplastic cells.
58 ell proliferation and result in promotion of preneoplastic cells.
59 , and drive the expansion of intraurothelial preneoplastic cells.
60  in both apoptosis and cell proliferation in preneoplastic cells.
61 ests that the methylation was occurring as a preneoplastic change.
62 TVrtTA-TetOPELP1 Tg mice had hyperplasia and preneoplastic changes as early as 12 weeks, and ER-posit
63                      Although the sequential preneoplastic changes have been defined for centrally ar
64                                              Preneoplastic changes in gene expression result from alt
65                                    Prominent preneoplastic changes in glandular tissue adjacent to th
66                            Identification of preneoplastic changes in histologically normal epitheliu
67 ted whether 4D-ELF would be able to identify preneoplastic changes in the colonocytes of the azoxymet
68 he bone marrow to peripheral organs predicts preneoplastic changes in the gastric microenvironment.
69 incomplete understanding of how CS initiates preneoplastic changes in the normal airway hinders early
70 Silencing TRIM29 in MCF10A cells resulted in preneoplastic changes that included loss of polarity in
71  follow a stepwise progression through early preneoplastic changes that ultimately culminated in fran
72  Bacterial colonization, gastric atrophy and preneoplastic changes were assessed histologically and c
73 rding the molecular characterization of lung preneoplastic changes, especially for squamous cell carc
74 postinoculation (p.i.) time on inflammation, preneoplastic changes, invasive lesions, and helicobacte
75 branching, hyperplasia, dysplasia, and other preneoplastic changes, which are indicative of increased
76                             We conclude that preneoplastic clones do not derive from long-lived, self
77 alcoholic steatohepatitis (NASH) is a common preneoplastic condition of hepatocellular carcinoma (HCC
78 model of human chronic atrophic gastritis, a preneoplastic condition.
79 se findings are relevant to human tumors and preneoplastic conditions accompanied by altered IGF2 exp
80 age-PCGT methylation signature is present in preneoplastic conditions and may drive gene expression c
81 nt and progression of neoplasia from in situ preneoplastic conditions to invasive disease was analyse
82                                         Even preneoplastic cystic structures may harbor entire loss o
83 educing prevalence of noninvasive cancer and preneoplastic disease.
84 ion of exocrine acinar cells into pancreatic preneoplastic ductal lesions by oncogenic Kras and/or pa
85 nhibited the formation of estrogen-dependent preneoplastic ductal lesions induced by 7,12-dimethylben
86                                              Preneoplastic ductal metaplasia developed in mice lackin
87 s of bone marrow and lymph nodes from young (preneoplastic) E micro -c-myc transgenic mice revealed i
88 er) was determined by a factorial design and preneoplastic endpoints in chemically induced rats and v
89 es were used to analyze the clonal growth of preneoplastic, enzyme-altered foci during liver carcinog
90  JB6 Cl 41-5a and TPA-resistant JB6 Cl 30-7b preneoplastic epidermal cell lines showed a remarkable g
91                    Although EBV infection of preneoplastic epithelial cells is not immortalizing, EBV
92 s from 45 primary breast cancers, 47 mammary preneoplastic epithelial foci, and 18 breast cancer cell
93 y significant reductions in the formation of preneoplastic esophageal lesions, decreased tumor incide
94 L at the earliest stage of development, or a preneoplastic event, requiring a second hit for neoplast
95 clonality in these populations, suggesting a preneoplastic expansion of CD5(+) B cell clones, with th
96 e results suggest that dysplasia arises in a preneoplastic field of chronic inflammation, which leads
97                       We hypothesized that a preneoplastic field of inflammation, telomere shortening
98 mocysteine concentrations and development of preneoplastic foci in the liver (increased placental glu
99 high likelihood of clonal relatedness of the preneoplastic foci to the tumors.
100 imulation platform to describe the growth of preneoplastic foci under experimental manipulations of i
101  F2rl2 and is associated with development of preneoplastic foci.
102 ant, protective effect on the development of preneoplastic fundic lesions and invasive carcinoma attr
103  of Th17-1 cells compared with the marrow in preneoplastic gammopathy (monoclonal gammopathy of undet
104              Here we show that patients with preneoplastic gammopathy mount a vigorous T cell respons
105      Moreover, xenografts from patients with preneoplastic gammopathy showed progressive growth, sugg
106 or decreasing pattern of expression from the preneoplastic ganglia to end stage tumors.
107 t mouse model to detect molecular changes in preneoplastic gastric dysplasia.
108  and the development of hypergastrinemia and preneoplastic gastric lesions.
109 in 17 (G17) offers the possibility to detect preneoplastic gastric mucosal conditions.
110 omas and hyperplastic EGL lesions, formed by preneoplastic GCPs.
111 ather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off
112 ns that originally drove the plasticity of a preneoplastic genome.
113 sine kinase inhibitors inhibit the growth of preneoplastic HBEC cells, suggesting their potential for
114    At regions of endothelial-enriched spots, preneoplastic HBECs undergo branching ductal-alveolar mo
115 creases size and number of aflatoxin-induced preneoplastic hepatic lesions in rats by >90%.
116 ese factors may enhance the survival of both preneoplastic hepatocytes and activated hepatic stellate
117 likely essential for the clonal expansion of preneoplastic hepatocytes to HCC, while Ctnnb1 mutations
118 3 impaired Akt and p44/42 phosphorylation in preneoplastic HER2-overexpressing mammary glands and in
119  we found reduced BCMO1 expression in normal preneoplastic intestine of folate-deficient tumor-prone
120 s effective in preventing the progression of preneoplastic intraepithelial lesions to invasive pancre
121 43%, respectively), proliferation rates, and preneoplastic lesion development.
122 s cell metaplasia is considered the critical preneoplastic lesion for gastric cancer.
123  and multiplicity, proliferation indices and preneoplastic lesion formation.
124 biquitous isoform, p110beta, did not prevent preneoplastic lesion initiation.
125 creatic ductal adenocarcinoma (PDAC) and its preneoplastic lesion intraductal papillary mucinous neop
126 liferative state is thought to represent the preneoplastic lesion of small-cell lung carcinoma.
127                                           No preneoplastic lesion or LOH was found in normal gallblad
128 id in the diagnosis and surveillance of this preneoplastic lesion.
129  in those with dysplasia compared with other preneoplastic lesions (0.31 vs 0.22; P = 0.042).
130 ase in PKC betaII expression was observed in preneoplastic lesions (aberrant crypt foci, 3.7-fold) co
131 nting the stepwise carcinogenic process from preneoplastic lesions (cirrhosis and dysplasia) to HCC,
132 D1(-/-) females developed significantly more preneoplastic lesions (eg, epithelial hyperplasias and m
133 easuring inhibition of formation of putative preneoplastic lesions (glutathione S-transferase P posit
134 e, the effect of resveratrol on formation of preneoplastic lesions (induced by 7,12-dimethylbenz(a)an
135 ents with gallstones had a high frequency of preneoplastic lesions and accumulation of LOH at various
136 , and senescence are frequently activated in preneoplastic lesions and are barriers to progression to
137 llomaviruses (HPVs) are linked to anogenital preneoplastic lesions and cancer.
138 1 occurred at a much lower frequency in both preneoplastic lesions and HCCs and were mutually exclusi
139 rinsulinism that leads to the development of preneoplastic lesions and hepatocellular carcinoma (HCC)
140 and TRalpha1 and their target genes in early preneoplastic lesions and hepatocellular carcinoma (HCCs
141 a pivotal role for RelA in regulating OIS in preneoplastic lesions and implicate the RelA/CXCL1/CXCR2
142 Keap1 mutations were present in 71% of early preneoplastic lesions and in 78.6% and 59.3% of early an
143 tors Ena/VASP, is overexpressed in high-risk preneoplastic lesions and in primary breast tumors and h
144 e incidence and reduced the latency of other preneoplastic lesions and increased cellular turnover in
145  that cured meat promotes carcinogen-induced preneoplastic lesions and increases specific biomarkers
146 s strongly ectopically expressed in advanced preneoplastic lesions and invasive human PDAC.
147         In rodent models, carcinogen-induced preneoplastic lesions and mammary tumors are inhibited.
148 ressor PTEN by accelerating the formation of preneoplastic lesions and mammary tumors.
149 he development of pancreatic intraepithelial preneoplastic lesions and progression to adenocarcinoma
150 wever, DDR signaling was strongly induced in preneoplastic lesions arising from individual mammary ce
151 s required to drive the development of human preneoplastic lesions as well as invasive adenocarcinoma
152 85% reduction in the hepatic focal burden of preneoplastic lesions at 1 micromol/kg body weight and a
153 t and amino acid defined (CDAA) diet develop preneoplastic lesions at 65 weeks and hepatocellular car
154  LOH was present in 2.1% to 47.8% of all the preneoplastic lesions at different loci.
155       We found that igf2 is not expressed in preneoplastic lesions but is induced as these lesions pr
156        Igf2 is not required for formation of preneoplastic lesions but is necessary for progression t
157 ic ductal cancers to arise from Kras-induced preneoplastic lesions by increasing epithelial cell prol
158  is highly up-regulated in the epithelium of preneoplastic lesions compared with benign epithelium, b
159                       Twenty-one of 47 (45%) preneoplastic lesions demonstrated 3p LOH, including 12
160                                              Preneoplastic lesions developed in BPA-exposed female of
161 s the progression of KRAS-induced pancreatic preneoplastic lesions in mice with pancreas-specific Cre
162 c epithelia, we evaluated the development of preneoplastic lesions in ovariectomized wild-type (WT) a
163 cific agents can suppress cured meat-induced preneoplastic lesions in rats and associated biomarkers
164 EITC had a protective effect on NMBA-induced preneoplastic lesions in the rat esophagus.
165 ms underlying the fate of the enzyme-altered preneoplastic lesions in the resistant hepatocyte (RH) m
166       CXCR2 upregulation is also observed in preneoplastic lesions in vivo.
167             Liver biopsy also helps identify preneoplastic lesions including large cell and small cel
168 umor initiation promoting the progression of preneoplastic lesions into tumors is well established.
169 ts also suggest that a hypothyroid status of preneoplastic lesions may contribute to their progressio
170 ed to development of multiple neoplastic and preneoplastic lesions of different organs.
171 hic gastritis (NAG), and is ineffective once preneoplastic lesions of multifocal atrophic gastritis (
172 ify EZH2 as a potential marker for detecting preneoplastic lesions of the breast in vivo and as a pos
173 s well as the level of prostaglandin E(2) in preneoplastic lesions of the esophagus at week 25.
174                                   Studies of preneoplastic lesions or early-stage cancer showed absen
175 Ralpha1 down-regulation was observed only in preneoplastic lesions positive for the progenitor cell m
176 genes in HCC were similarly altered in early preneoplastic lesions positive for the stem/progenitor c
177    There are three main morphologic forms of preneoplastic lesions recognized in the lung: squamous d
178 static epithelial cells and the formation of preneoplastic lesions resembling prostatic intraepitheli
179  OPN is expressed in senescent stroma within preneoplastic lesions that arise following 7,12-dimethyl
180 n of PKCepsilon in the mouse prostate causes preneoplastic lesions that display significant NF-kappaB
181 f murine prostate cancer, beginning from the preneoplastic lesions to distant metastases that suggest
182 d status favors the onset and progression of preneoplastic lesions to HCC.
183  contributes to the onset and progression of preneoplastic lesions towards malignancy.
184 quent stages of tumor development when early preneoplastic lesions transition into adenomas.
185 ated with GBC was tested from microdissected preneoplastic lesions using microsatellite markers.
186 tion between inflammation and hyperplasia or preneoplastic lesions was not identified.
187  was accompanied by increased apoptosis, and preneoplastic lesions were cleared by focal degenerative
188                                 Furthermore, preneoplastic lesions with eosinophilic phenotype freque
189 sible benefit of improved early detection of preneoplastic lesions with methylene blue chromoendoscop
190 ghly resistant to azoxymethane (AOM)-induced preneoplastic lesions, aberrant crypt foci.
191 morphologic features, increased incidence of preneoplastic lesions, and accelerated mammary tumor dev
192            Heme iron increased the number of preneoplastic lesions, but dietary heterocyclic amines a
193                In the initial development of preneoplastic lesions, cellular proliferation is control
194  been useful for the detection of cancer and preneoplastic lesions, for staging of inflammatory and a
195 d alveoli are polyclonal, and putative early preneoplastic lesions, hyperplastic alveolar nodules (HA
196     Tetraploid cells are frequently found in preneoplastic lesions, including intestinal cancers aris
197  genetic lesions with the formation of these preneoplastic lesions, recent data suggest that the tumo
198 ion, as well as TP33 copy number, in gastric preneoplastic lesions.
199 noncancerous colonocytes, resulting in fewer preneoplastic lesions.
200 umor subtypes, and its occurrence in "early" preneoplastic lesions.
201  diseases, such as prostatic hyperplasia and preneoplastic lesions.
202 tatic epithelium leads to the development of preneoplastic lesions.
203 terations were also present in head and neck preneoplastic lesions.
204 inst established tumor as well as developing preneoplastic lesions.
205 A insertions, and it can be found mutated in preneoplastic lesions.
206 on of the gallbladder specimens was done for preneoplastic lesions.
207  microenvironment that can be used to detect preneoplastic lesions.
208 ase in the activation of STAT3 in pancreatic preneoplastic lesions; STAT3 is a transcription factor r
209 lin D1, the incidence and overall volume of ;preneoplastic' lesions were significantly decreased.
210  associated with the malignant conversion of preneoplastic liver lesions.
211 nisms that generate metastatic stem cells in preneoplastic liver tissue are not well understood.
212                   CD133(+) LSCs derived from preneoplastic livers of beta2SP(+/-) mice treated with i
213 formation and the likely clonal outgrowth of preneoplastic lung epithelial cells that occurs in the c
214  association with IGF-1R activation in human preneoplastic lung lesions in smokers.
215  of these genes (82) was also changed in the preneoplastic mammary glands compared to wild-type contr
216 llular signal-regulated kinase activation in preneoplastic mammary glands from compound mutant mice.
217 sion of the luminal progenitor population in preneoplastic mammary glands of Her2/neu transgenic mice
218                                  Analyses of preneoplastic mammary tissue collected 1 month after DFM
219 ed expression profiles of mammary tumors and preneoplastic mammary tissue from MMTV-Neu transgenic mi
220 ne that spans the progression from normal to preneoplastic mammary tissue.
221 gamma target genes Adfp, Fabp4, and Pdhk4 in preneoplastic mammary tissue.
222                                          The preneoplastic mammary tissues of the PyMT/Fet-/- mice sh
223         Hence, these antibodies may serve as preneoplastic markers for HCC in HBV carriers with chron
224 of specific genes and their potential use as preneoplastic markers was further validated using an ind
225 ia, and increased staining for stem cell and preneoplastic markers.
226 orphogenesis and growth of normal MCF10A and preneoplastic MCF10AT1-EIII8 (referred as EIII8) human b
227                   Interestingly, although in preneoplastic Mdr2(-/-) livers RAGE ablation did not aff
228 of neutrophils that trigger proliferation of preneoplastic melanocytes.
229 signaling by inhibition of MEK might reverse preneoplastic metaplasia in the stomach.
230 sought to uncover new biomarkers for stomach preneoplastic metaplasias and neoplastic lesions by gene
231 mplex regulation of tumor development by the preneoplastic microenvironment, but also that this regul
232 duced neoplastic transformation in JB6-Cl.41 preneoplastic model.
233 mice develop uterine hyperplasia and ovarian preneoplastic morphological changes at a high frequency.
234 d cyclooxygenase activity contributes to the preneoplastic morphological changes of the ovarian surfa
235 gical and genetic properties of the p53 null preneoplastic mouse mammary epithelium in a p53 wild-typ
236 ction among many preexisting, low-penetrance preneoplastic mutations or stable epigenetic variants, f
237                                  We isolated preneoplastic neuroendocrine cells from a mouse model of
238 ons include differential susceptibilities of preneoplastic neuroglial cell types in different brain r
239 is as an endogenous anti-tumor signal in the preneoplastic niche.
240 t, FMD diet) fed to rats is known to produce preneoplastic nodules (PNNs) after 36 weeks and hepatoce
241                For many years the finding of preneoplastic nodules in the liver during experimental i
242 developed HCC whereas WT mice developed only preneoplastic nodules suggesting that loss of MT acceler
243 evelops nonalcoholic steatohepatitis (NASH), preneoplastic nodules, and hepatocellular carcinoma (HCC
244 ung cancer, either through direct actions on preneoplastic or neoplastic cells or through indirect ac
245 may provide a selective clonal advantage for preneoplastic or neoplastic hepatocytes and contribute t
246  is sufficient to lead to the development of preneoplastic or neoplastic lesions.
247 on of transforming growth factor beta, and a preneoplastic or tumor state of the hepatocytes influenc
248                                          The preneoplastic outgrowth lines were immortal and exhibite
249 the ovarian surface epithelium gives rise to preneoplastic ovarian lesions with an endometrioid gland
250 quently detected in the superficial cells of preneoplastic over non-neoplastic epithelia (P<0.0001),
251 th downstream MAPK/ERK pathway activation in preneoplastic pancreatic epithelium, whereas nontumorige
252                   Only a small percentage of preneoplastic pancreatic intraductal neoplasia lesions l
253 ithelium led to the development of increased preneoplastic pathology, however the role of specific NF
254 rming oncogenic H-ras mutations in the early preneoplastic period.
255 ssue architecture, which plays a role in the preneoplastic phenotype and contributes to epithelial tu
256 clusion, increased mTOR activity conferred a preneoplastic phenotype to the HepaRG cells by altering
257 are an essential hematopoietic component for preneoplastic polyp development and are a novel target f
258  ability of Kras to reprogram acini into PDA preneoplastic precursors.
259 ith increasing severity of histopathological preneoplastic/preinvasive changes.
260 e specific parental allele lost comparing 42 preneoplastic/preinvasive foci with those lost in the lu
261 in 77% of the lung cancers, 70% of normal or preneoplastic/preinvasive lesions associated with lung c
262 r, and 49% of 47 normal, mildly abnormal, or preneoplastic/preinvasive lesions found in smokers witho
263 ne the transcriptome of very early stages of preneoplastic progression in an in vivo model that mimic
264                  The function of EZH2 during preneoplastic progression in the mammary gland is unknow
265 Using an inducible transgenic mouse model of preneoplastic progression in the mammary gland, we disco
266 ts in an inducible transgenic mouse model of preneoplastic progression.
267                                Evaluation of preneoplastic proliferative lesions in the pancreata fro
268                     Neither pancreatitis nor preneoplastic proliferative lesions was found in monkeys
269 classical in vitro assays yet several unique preneoplastic properties were frequently observed, inclu
270 TRbeta1 and of its target genes in Krt-19(+) preneoplastic rat lesions and was associated with nodule
271 aR, VDR, CYP27B1, and CYP24A1 as modifiable, preneoplastic risk biomarkers for colorectal neoplasms.
272                         In addition, when 21 preneoplastic samples showing LOH were compared to their
273 ce uniformly contain intraganglionic, likely preneoplastic, Schwann cell proliferations.
274 fic CTLs capable of eliminating Mut H-ras(+) preneoplastic skin cells, demonstrating that immunosurve
275 genically mutated cells proliferate in early preneoplastic skin.
276                              We identified a preneoplastic stage in the patched (ptc) mutant mouse, a
277                              During the long preneoplastic stage, in which the liver is often the sit
278  mice as early as 32 weeks that persisted at preneoplastic stage.
279 ession was elevated at the proliferative and preneoplastic stages in X/c-myc bitransgenic livers, whe
280 or types, the influence of the stroma during preneoplastic stages is unknown.
281 hough folate supplementation administered in preneoplastic stages may lower the risk of colorectal ca
282 ver, whether the immune system can recognize preneoplastic stages of human cancer is not known.
283 permissive microenvironment at the earliest, preneoplastic stages of MB.
284  catalytic activity is critical in the early preneoplastic stages of the liver because DeltaEGFR mice
285 d in the p53 null mammary outgrowth lines at preneoplastic stages, and in all its derived tumors.
286 taining heterozygosity; and is seen in early preneoplastic stages, which demonstrate clonal relatedne
287 expression of Runx2 in the thymus leads to a preneoplastic state defined by an accumulation of cells
288  used the human P493-6 B cells, which have a preneoplastic state dependent on the Epstein-Barr viral
289 with adjacent VLS lesions, in 5 of which VIN preneoplastic tissue was also present (patient age, 64.3
290 ets claudin-4 expression in frank tumors and preneoplastic tissue, and cCPE imaging may be used as an
291 ction by conferring TNFalpha resistance to a preneoplastic TNFalpha sensitive cell, while simultaneou
292  these results show that RhoA can induce the preneoplastic transformation of hMECs by altering multip
293 o overcome senescence checkpoints and induce preneoplastic transformation of human mammary epithelial
294 MEC strains led to their immortalization and preneoplastic transformation.
295 y epithelium using a unique in vivo model of preneoplastic transformation.
296 = 0.003) with a 40% reduction in a marker of preneoplastic transformation.
297 ly bursal development and progresses through preneoplastic transformed follicles to metastatic lympho
298 with myc, may be important for generation of preneoplastic transformed follicles.
299 es multi-staged tumorigenesis beginning with preneoplastic-transformed follicles (TF) and progressing
300 creatic acinar-to-ductal metaplasia (ADM), a preneoplastic transition in oncogenic Kras-driven pancre

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