ライフサイエンスコーパス: dysplastic

1 dition, 10 nevi developed of which nine were dysplastic.

2 entially all of the Apc-deficient cells were dysplastic.

3 esophageal epithelium (22 of 22) but not all dysplastic [6 of 43 (14%), P = 0.0001] and SCC [50 of 12

4 Dysplastic ACF, once postulated as the ACF destined for

5 Conversely, dysplastic adenomas (16%) stained intensely for GFP, and

6 Dysplastic adenomas accumulate beta-catenin and lose het

7 aberrant crypt foci and low- and high-grade dysplastic adenomas in the large intestine, similar to t

8 m patients with Lynch syndrome--78 low-grade dysplastic adenomas, 57 high-grade dysplastic adenomas,

9 ated adenomas/polyps, 70 sporadic high-grade dysplastic adenomas, and 19 hyperplastic polyps--and tis

10 low-grade dysplastic adenomas, 57 high-grade dysplastic adenomas, and 31 colon cancer samples.

11 et, larger, more numerous, and more severely dysplastic adenomas.

12 validation cohort (65 patients), 51 were non-dysplastic and 14 had high-grade dysplasia.

13 %, and 96.3%, respectively, for detection of dysplastic and cancerous esophageal lesions).

14 (DKO) kidneys were severely hypoplastic and dysplastic and demonstrated rapid, premature depletion o

15 ells were used to determine RA levels in non-dysplastic and dysplastic Barrett's cell lines and endos

16 The moderate-risk group comprised 27 non-dysplastic and eight high-grade dysplasia cases, whereas

17 t included colobomatous microphthalmos and a dysplastic and elevated disc without central cupping.

18 eloid cells, and residual myeloid cells were dysplastic and immunophenotypically abnormal.

19 de a clinically relevant model for detecting dysplastic and malignant clones within the crypt-structu

20 t deregulation of polarity pathways promotes dysplastic and neoplastic growth in mammals by disruptin

21 serine-arginine protein kinase 1 (SRPK1), in dysplastic and neoplastic pancreatic ductular cells.

22 rsed this inflammatory signature at both the dysplastic and neoplastic stages of ESCC development, an

23 assess odds of progression for patients with dysplastic and nondysplastic BE, based on biomarker stat

24 ge-related methylation was found in both the dysplastic and nondysplastic mucosa of patients with ulc

25 progenitor cells within the myriad types of dysplastic and normal cells in the bone marrow and perip

26 The dual dysplastic and proliferative features in these stem cell

27 hese rare "overlap" syndromes that have both dysplastic and proliferative pathological features, and

28 Lesions comprised rare foci of dysplastic and sloughed cells in respiratory bronchioles

29 His thymus was dysplastic and, although not depleted of T cells, showed

30 Granulocytes were consistently increased, dysplastic, and hypofunctional.

31 ina bifida is a NTD where the spinal cord is dysplastic, and the overlying spinal column is absent.

32 ntly labeled peptides or lectins to identify dysplastic areas of Barrett's epithelium.

33 s important to carefully map the size of the dysplastic areas, (3) patients that receive ablative or

34 as increased beta-catenin activation in non-dysplastic areas.

35 mutation for synchronous tumors and multiple dysplastic areas.

36 Dysplastic neurons, giant cells, and dysplastic astroglia express high levels of pS6 and demo

37 dysplastic neurons, giant neuroglial cells, dysplastic astroglia, and reactive astrocytes.

38 icantly higher in Barrett's metaplasia (BE), dysplastic Barrett's (D) and EAC than in NE (P<0.0000001

39 to determine RA levels in non-dysplastic and dysplastic Barrett's cell lines and endoscopic biopsies.

40 a and intestinal metaplasia in patients with dysplastic Barrett's esophagus (BE), and reduce rates of

41 lation (RFA) is an established treatment for dysplastic Barrett's esophagus (BE).

42 ternative to esophagectomy for patients with dysplastic Barrett's esophagus (BE).

43 ment of malignancy: benign metaplastic never-dysplastic Barrett's esophagus (NDBE; n=66) and high-gra

44 opic radiofrequency ablation could eradicate dysplastic Barrett's esophagus and decrease the rate of

45 Endoscopic eradication therapy for dysplastic Barrett's esophagus has become an encouraging

46 rial, we randomly assigned 127 patients with dysplastic Barrett's esophagus in a 2:1 ratio to receive

47 In patients with dysplastic Barrett's esophagus, radiofrequency ablation

48 ll-cause mortality is similar to surgery for dysplastic Barrett's esophagus.

49 s controls [n=20], non-dysplastic [n=24] and dysplastic Barrett's oesophagus [n=23], and oesophageal

50 d role of different endoscopic therapies for dysplastic Barrett's oesophagus.

51 th a median interval of 37 months in 195 non-dysplastic Barrett's patients, and a third time point in

52 s and had endoscopic evidence of non-nodular dysplastic BE </=8 cm in length.

53 d resection is highly effective for treating dysplastic BE and early EAC, whereas esophagectomy is in

54 mean age, 56 +/- 17 years) found to have non-dysplastic BE at the index endoscopy and after 1 year or

55 nal metaplasia in the tubular esophagus) and dysplastic BE recurrence among patients who achieved CEI

56 a value was 0.22 (95% CI, 0.11-0.29) for non-dysplastic BE, 0.11 (95% CI, 0.004-0.15) for LGD, and 0.

57 des from patients with BE (23 samples of non-dysplastic BE, 22 samples of LGD, and 34 samples of high

58 In subjects with dysplastic BE, RFA therapy has an acceptable safety prof

59 as 33%; 22% of all recurrences observed were dysplastic BE.

60 gression, and safety of RFA in patients with dysplastic BE.

61 rmed a randomized trial of 127 subjects with dysplastic BE; after cross-over subjects were included,

62 Not only could normal hips appear dysplastic, but dysplastic hips also could have normal a

63 igh-risk group (8% of the cohort) had no non-dysplastic cases and five patients with high-grade dyspl

64 in the presence of normal epithelial cells, dysplastic cells but not normal cells, exhibit marked do

65 rious tissues consisting of undifferentiated dysplastic cells exhibiting global changes in DNA methyl

66 on a neuronal-glial spectrum, and that these dysplastic cells express glutamate receptor (GluR) patte

67 ML with multilineage dysplasia (MLD; >/= 50% dysplastic cells in 2-3 lineages) remains to be clarifie

68 We hypothesized that the dysplastic cells in TSC tubers are heterogeneous, includ

69 are distinct from the patterns seen in tuber dysplastic cells.

70 y but also for the treatment of HPV-positive dysplastic cervical lesions.

71 aman spectral differences between normal and dysplastic cervical tissue are observed at ~854, 937, 10

72 However, the mechanisms underlying these dysplastic changes are poorly understood.

73 itudinally monitor disease status, or detect dysplastic changes in patients with inflammatory bowel d

74 signaling reduces inflammation and inhibits dysplastic changes in the gastric mucosa after infection

75 hich is a clonal malignancy characterized by dysplastic changes of developing blood cell progenitors,

76 disorders of haematopoiesis characterised by dysplastic changes of major myeloid cell lines.

77 Lesions displaying a variety of dysplastic changes precede invasive oral and epidermal s

78 three different stages: common nevi without dysplastic changes, dysplastic nevi with structural and

79 way mutant embryos, and these mice exhibit a dysplastic circumvallate papilla with disrupted Shh expr

80 These MDS HSCs demonstrated dysplastic clonogenic activity.

81 Frequency of detection of atypical (dysplastic) CNS neuronal elements in ovarian teratomas r

82 The mice developed a hypoplastic dysplastic collecting system.

83 in-conjugated peptide bound more strongly to dysplastic colonocytes than to adjacent normal cells wit

84 children who underwent surgical resection of dysplastic cortex for the treatment of intractable epile

85 ncerous colonocytes within the epithelium of dysplastic crypts in mouse colon.

86 ificantly higher in cancerous and high-grade dysplastic cysts compared to benign mucinous cysts.

87 The presentations of a dysplastic disc and colobomatous microphthalmia are rare

88 detection of the lesion and the treatment of dysplastic disease.

89 n almost one third of patients with baseline dysplastic disease; most recurrences occurred during the

90 sis of chronic inflammatory, autoimmune, and dysplastic disorders.

91 mouse enamel organ morphology is noticeably dysplastic during late-stage development, when MMP20 is

92 as high-risk; the probability of having non-dysplastic endoscopic biopsies was 13% (5-27), whereas t

93 1 individuals with LSTV, 41.72% were type I (dysplastic enlarged transverse process), 41.4% were type

94 Although human dysplastic epithelia accumulated KLF5, KLF5 expression w

95 reased nuclear beta-catenin translocation in dysplastic epithelial cells.

96 and cellular function between premalignant (dysplastic) epithelial cells and their normal counterpar

97 ulture system, the cells formed a high-grade dysplastic epithelium with malignant cells invading into

98 Notably, cystatin A is upregulated in dysplastic epithelium, prompting us to hypothesize that

99 also present in nontumor, nondysplastic, and dysplastic epithelium.

100 T cells and was not expressed in persistent dysplastic epithelium.

101 tt's esophagus progression, including in non-dysplastic epithelium.

102 rentiation impairment, but not apoptosis, in dysplastic erythroblasts.

103 In addition, the megakaryocytes had dysplastic features, and they were abnormally distribute

104 chondria induces MDS progressing to AML with dysplastic features, we studied the therapeutic potentia

105 s in patients with deletions and predominant dysplastic features.

106 w subcategories of LGD with inflammatory and dysplastic features.

107 Entire dysplastic fields contained a founder mutation from whic

108 Dysplastic foci were also observed in Pofut1-deficient s

109 Dysplastic foci were observed less frequently but were a

110 the unscheduled activation of EPAS1 in early dysplastic foci.

111 ously were found to cause the spondylocheiro dysplastic form of Ehlers-Danlos syndrome (SCD-EDS), a h

112 he a/LCI nuclear size measurements separated dysplastic from nondysplastic tissue at a statistically

113 zed to evaluate its ability to differentiate dysplastic from nondysplastic tissue.

114 e loss of global DNA methylation both in the dysplastic gastric epithelial cells and in gastric strom

115 Metaplastic and dysplastic glands can be genetically related, indicating

116 tion, PSA slope, digital rectal examination, dysplastic glands or prostatitis on biopsy, ultrasound g

117 plicate the Atm gene product as a barrier to dysplastic growth in the early stages of intestinal tumo

118 P1 share molecular aspects with YAP1-induced dysplastic growth in the mouse.

119 d insight into pathogenic pathways governing dysplastic growth of hematopoietic progenitors.

120 xpression was associated with a cancer-like, dysplastic growth pattern, whereas GALNT6 knockout cells

121 he development of GI tumors, probably before dysplastic growth.

122 l expansion in the absence of cytopenias and dysplastic hematopoiesis can be considered clonal hemato

123 nly could normal hips appear dysplastic, but dysplastic hips also could have normal alpha angles.

124 teric, stromal, and mesenchymal cells within dysplastic human kidney tissue.

125 with tubule-specific deletion of VHL led to dysplastic hyperproliferation of tubular epithelial cell

126 and hippocampal neurons are enlarged and/or dysplastic in the Tsc1 mutant mice, strongly express pho

127 cells, and that their depletion in mice with dysplastic inflammation blocks the development of invasi

128 Infants with a multicystic dysplastic kidney and a normal contralateral kidney on r

129 ltrasound diagnosis and also revealed a left dysplastic kidney with a dilated, tortuous ureter.

130 Ultrasound and kidney biopsy revealed small dysplastic kidneys with cysts and tubular atrophy with s

131 ions, identified in a fetus with multicystic dysplastic kidneys, encompasses the TCF2 gene on 17q12,

132 NPC(Mdm)2(-/-) neonates have hypo-dysplastic kidneys, patchy depletion of the nephrogenic

133 a single clone can expand to form an entire dysplastic lesion.

134 patients (P = .016), females (P = .020), and dysplastic lesions (P = .040).

135 ic lesions and FVC identified a mean of 0.13 dysplastic lesions (P = .044).

136 In transgenic mice with high-grade cervical dysplastic lesions and cervical cancer, repressing the e

137 FUSE identified a mean of 0.37 dysplastic lesions and FVC identified a mean of 0.13 dys

138 o examined the clonal architecture of entire dysplastic lesions and the genetic changes associated wi

139 lished its onset at the stage of noninvasive dysplastic lesions by immunohistochemistry for anti-5-me

140 els of miR-196a were observed in EA, BE, and dysplastic lesions compared with normal squamous mucosa,

141 l-spectrum endoscopy increased the number of dysplastic lesions detected, compared with conventional

142 ed with normal mucosal resident T cells, and dysplastic lesions expressed transcripts for CCL19 and C

143 ort the concept of endoscopic elimination of dysplastic lesions in the esophagus by a mucosal ablatio

144 Nearly 25% of dysplastic lesions include cells that originate from the

145 ents with BE at high risk for cancer, detect dysplastic lesions more reliably, and uncover mechanisms

146 FVC missed 71.4% of dysplastic lesions per lesion whereas FUSE missed 25.0%

147 per lesion (P = .0001); FVC missed 75.0% of dysplastic lesions per subject and FUSE missed 25.0% per

148 ue acquisition identified significantly more dysplastic lesions than random biopsies (P < .0001).

149 Cells resembling HcPCs reside within dysplastic lesions that appear several months before HCC

150 Twenty-two percent of H pylori-induced dysplastic lesions were composed of glands that containe

151 99%), and detected 95% of malignant/severely dysplastic lesions, compared with 35% and 50% for carcin

152 ssful endoscopic visualization of high-grade dysplastic lesions, which were not detectable by convent

153 cancers and the vast majority of high-grade dysplastic lesions.

154 s rise to goblet cell IM and invasive fundic dysplastic lesions.

155 in animals caused regression of precancerous dysplastic lesions.

156 time point delayed the development of severe dysplastic lesions.

157 opy lacks molecular information and can miss dysplastic lesions.

158 ry cell accumulation, ductal hyperplasia, or dysplastic lesions/pancreatic intraepithelial neoplasia.

159 Overall, hepatocellular carcinomas or dysplastic liver lesions were observed in 69% of H. hepa

160 dition to inflammation, fibrosis, and highly dysplastic liver nodules.

161 ced nonalcoholic steatohepatitis with highly dysplastic liver nodules.

162 firmed significantly higher VEGFR2 levels in dysplastic livers (P = .02).

163 noVue and BR55 did not differ in healthy and dysplastic livers (SonoVue, P = .46; BR55, P = .43).

164 inutes, there was an accumulation of BR55 in dysplastic livers compared with healthy ones.

165 ue signal decreased similarly in healthy and dysplastic livers during the 4 minutes, there was an acc

166 , were upregulated in neoplastic relative to dysplastic livers.

167 e hyper-responsive to estrogen and developed dysplastic mammary lesions with adjacent stromal angioge

168 R mice decrease with age in association with dysplastic marrow changes.

169 omes (MDS) are characterized by abnormal and dysplastic maturation of all blood lineages.

170 d thrombocytosis, megakaryocyte hyperplasia, dysplastic megakaryocyte morphology, and myelofibrosis.

171 ated segmental overgrowth includes bilateral dysplastic megalencephaly, hemimegalencephaly and focal

172 ancer-associated hotspot PIK3CA mutations in dysplastic megalencephaly, hemimegalencephaly, and focal

173 determined expression of PEDF in common and dysplastic melanocytic nevi, melanoma in situ, invasive

174 reased incidence of visible colon tumors and dysplastic microadenomas in ER-deficient Min/+ relative

175 ular permeability accompanying diminution of dysplastic microvasculature by the antiangiogenic agent,

176 used to quantify leakage across premalignant dysplastic microvasculature.

177 f DOCK4 levels leads to erythroid cells with dysplastic morphology both in vivo and in vitro.

178 c syndromes (MDS) are defined by cytopenias, dysplastic morphology of blood and marrow cells, and clo

179 ificantly increased CHI3L1 expression in non-dysplastic mucosa from patients with inflammatory bowel

180 as expressed in 12 of 17 SCCHN, and 30 of 40 dysplastic mucosa samples, but not in normal mucosa.

181 T cells isolated from dysplastic mucosa were skewed toward a central memory ph

182 and consequent apoptosis in both normal and dysplastic mucosa.

183 oreover, use of FTIR to detect premalignant (dysplastic) mucosa results in a sensitivity, specificity

184 quence (normal squamous controls [n=20], non-dysplastic [n=24] and dysplastic Barrett's oesophagus [n

185 rogeneous disorder diagnosed by the triad of dysplastic nails, abnormal skin pigmentation, and oral l

186 ormations of cortical development containing dysplastic neuronal and glial elements, including hemime

187 However, dysplastic neuronal features persist, and there are only

188 defects, hippocampal heterotopias, enlarged dysplastic neurons and glia, abnormal myelination and an

189 tal lineage model in which balloon cells and dysplastic neurons are derived from radial glial progeni

190 2 expression suggests that balloon cells and dysplastic neurons derive from radial glial cells in the

191 GABA(A) R responses in dysplastic neurons from a single case of TSC were measur

192 Patch clamp recordings from dysplastic neurons in acute slices from TSC tubers demon

193 Balloon cells and large dysplastic neurons in all specimens expressed Otx1, phos

194 VGLUT expression argues that dysplastic neurons may be glutamatergic.

195 Most balloon cells and dysplastic neurons were VGLUT2 immunoreactive, whereas n

196 Dysplastic neurons, giant cells, and dysplastic astrogli

197 types including disoriented pyramidal cells, dysplastic neurons, giant neuroglial cells, dysplastic a

198 of myelodysplastic syndrome (MDS), including dysplastic neutrophils and multiple lineage cytopenia.

199 Indices corresponding to common nevi (0-1), dysplastic nevi (1-4), and melanoma (5-8) were significa

200 ing subtypes were more often associated with dysplastic nevi (20% and 18%, respectively) (P = .002),

201 The management of clinically atypical nevi/dysplastic nevi (CAN/DN) is controversial, with few data

202 Dysplastic nevi (DN) is a strong risk factor for cutaneo

203 ly excised, biopsy-proven, mild and moderate dysplastic nevi (DN).

204 Dysplastic nevi (DNs), also known as Clark's nevi or aty

205 quenced exomes of melanocytic nevi including dysplastic nevi (n = 19), followed by a targeted gene pa

206 rray analysis of NIK expression reveals that dysplastic nevi (n=22), primary (n=15) and metastatic me

207 Consecutive patient pathology samples of dysplastic nevi and cutaneous melanomas evaluated betwee

208 MPM images corresponding to dysplastic nevi and melanoma were compared with standard

209 Moderately-to-severely and severely dysplastic nevi are more often associated with melanoma,

210 from biopsy-diagnosed moderately-to-severely dysplastic nevi before excision to melanoma in situ afte

211 In dysplastic nevi cases, the rate of clinically significan

212 al. approach the problem of differentiating dysplastic nevi from common melanocytic nevi through a m

213 ults show that although melanocytic nevi and dysplastic nevi harbor stable genomes with relatively fe

214 Exome sequencing revealed that dysplastic nevi harbored a substantially lower mutationa

215 To portray the mutational repertoire of dysplastic nevi in patients with the dysplastic nevus sy

216 The incidence of moderately and severely dysplastic nevi increased from 1.0% to 7.2% and from 0.6

217 ion of biopsy-diagnosed mildly or moderately dysplastic nevi is unlikely to result in a clinically si

218 ear, then annually thereafter for moderately dysplastic nevi or atypical nevus syndrome; biannually f

219 years, then annually thereafter for severely dysplastic nevi or melanomas in situ; every 3 months for

220 Additionally, melanocytic nevi including dysplastic nevi showed a significantly lower frequency a

221 atistical effect of histologic subtype, age, dysplastic nevi syndrome, and associated cancers on muta

222 Gal-3 during the progression from benign to dysplastic nevi to melanoma and further to metastatic me

223 ges: common nevi without dysplastic changes, dysplastic nevi with structural and architectural atypia

224 tory profiles of melanocytic nevi (including dysplastic nevi) from melanoma, we sequenced exomes of m

225 Of dysplastic nevi, 196 of 580 (34%) showed a positive biop

226 ons, including melanomas, differently staged dysplastic nevi, and common nevi that were validated by

227 of melanomas arising in a nevus, Spitz nevi, dysplastic nevi, and misdiagnosed lesions.

228 that Gal-1 ligands were abundant in severely dysplastic nevi, as well as in primary and metastatic me

229 ents included in situ and invasive melanoma, dysplastic nevi, Spitz nevi, atypical nevus syndrome, fa

230 e following frequencies: annually for mildly dysplastic nevi, Spitz nevi, or solely family history of

231 ze the role of keratinocyte dysplasia within dysplastic nevi.

232 sue sections of melanoma arising in a nevus; dysplastic nevi; Spitz nevi; and misdiagnosed melanocyti

233 ved from an excisionally biopsied moderately dysplastic nevus 5 years later.

234 enotyping of a melanoma in situ arising in a dysplastic nevus revealed a phenotype-genotype paradox t

235 howed only BRAF wild-type results, while the dysplastic nevus showed both BRAF wild-type and BRAF V60

236 The coexistence of dysplastic nevus syndrome and a BAP1 germline mutation e

237 oire of dysplastic nevi in patients with the dysplastic nevus syndrome and to determine the discrimin

238 report of a patient with multiple melanomas, dysplastic nevus syndrome, and an inactivating germline

239 a who had a history of invasive melanoma and dysplastic nevus syndrome, history of invasive melanoma

240 -old man who was initially seen in 2003 with dysplastic nevus syndrome, multiple atypical melanocytic

241 ith multiple cutaneous melanomas and classic dysplastic nevus syndrome.

242 and precursor for cutaneous melanoma is the dysplastic nevus.

243 rate and characteristics of association with dysplastic nevus.

244 sis revealed a melanoma in situ arising in a dysplastic nevus.

245 tially expressed in early HCCs compared with dysplastic nodules (>2-fold change; area under the recei

246 cirrhotic nodules (CN), "attenuated" around dysplastic nodules (DN), and "absent" around HCC.

247 on profiling on cirrhotic (regenerative) and dysplastic nodules (DN), as well as eHCC.

248 ic examinations for the diagnosis of HCC and dysplastic nodules (DNs) and the role of biopsy.

249 lastic nodules (LGDNs; 32 cases), high-grade dysplastic nodules (HGDNs; 16 cases), early HCC (eHCC; 2

250 alignant lesions, such as low- or high-grade dysplastic nodules (LGDNs and HGDNs, respectively), in a

251 nging from benign to low-grade or high-grade dysplastic nodules (LGDNs/HGDNs) and hepatocellular carc

252 dules, 88 were firmly diagnosed as low-grade dysplastic nodules (LGDNs; 32 cases), high-grade dysplas

253 lidated in an independent set of 29 samples (dysplastic nodules [10] and small HCC [19; diameter, 20

254 91% of HH-HCC, 0% of HH-related cirrhotic or dysplastic nodules and 79% of mixed-aetiology HCC.

255 hologic features of regenerative nodules and dysplastic nodules and focus on HCC in the cirrhotic liv

256 ration, resulting in development of multiple dysplastic nodules in 100% of the PML-deficient livers a

257 otential role of cyclin D1 overexpression in dysplastic NPE cells in vitro.

258 ence of CA, HGD, and epithelia that were not dysplastic or cancerous but did contain evidence of prio

259 ditionally induces proliferation of immature dysplastic osteoblasts likely because of an ASC-sensitiv

260 gory and the probability of being a true non-dysplastic patient was 100% (99% CI 96-100) and the prob

261 k and others were thin, but all had the same dysplastic pattern.

262 is known about the molecular alterations in dysplastic peripheral blood cells.

263 of photoreceptor synaptic dysfunction and no dysplastic phenotype as in CRB1 (Crumbs homologue1) reti

264 operating genetic event that potentiates the dysplastic phenotype.

265 tion toward an exacerbated and proliferative dysplastic phenotype.

266 bition of AKT prevents the initiation of the dysplastic phenotype.

267 rs consistently showed an elevated number of dysplastic platelets with anisocytosis, degranulation, a

268 ters can regress over time, leaving behind a dysplastic pole ("segmental dysgenesis").

269 and that Notch promotes both initiation and dysplastic progression of these acinar-derived PanINs, a

270 g and spectroscopy microendoscope to monitor dysplastic progression within the oral cavity microenvir

271 steoblast differentiation and prevents their dysplastic proliferation.

272 patients without any recurrence and without dysplastic recurrence.

273 ently, the ventricular zone and lumen of the dysplastic region are lost, causing the left and right s

274 Furthermore, the dysplastic region lacks ephrinB3 expression at the midli

275 otoreceptor degeneration was associated with dysplastic regions.

276 stent with these findings, analysis of human dysplastic renal tissue demonstrates that undifferentiat

277 development and increased cell death in the dysplastic retina.

278 n mice results in thin brittle enamel with a dysplastic rod pattern.

279 We report that Irf6 cKO mice present with 1) dysplastic salivary glands due to disruptions of epithel

280 illous features or high-grade dysplasia, any dysplastic serrated lesion, or invasive cancer.

281 Chondrodystrophy in dogs is defined by dysplastic, shortened long bones and premature degenerat

282 features of human spina bifida, including a dysplastic spinal cord, open neural canal and disability

283 gnature was already activated in the earlier dysplastic stage.

284 alosome (CSN5) in early HCC as compared with dysplastic stage.

285 geneity was observed at the regenerative and dysplastic stages, overall, 460 differentially expressed

286 shorter population doubling times and formed dysplastic stratified epithelia in organotypic raft cult

287 Both cell lines formed large dysplastic structures in three-dimensional cultures that

288 increased proliferation and branching, with dysplastic terminal end buds (TEB) and ducts.

289 ntly higher site-specific binding of BR55 in dysplastic than healthy livers (P = .005).

290 s themselves but also in the surrounding pre-dysplastic tissue (so-called field cancerization), indic

291 validation cohort, the signature identified dysplastic tissues with an area under the curve value of

292 in the Mid-FT-IR spectra between normal and dysplastic tissues, especially regarding peak positions

293 ch arises through step-wise progression from dysplastic to invasive, to metastatic tumor.

294 these factors might be used as biomarkers of dysplastic transformation in the colon.

295 omolecules and their changes associated with dysplastic transformation in the tissue.

296 s with CS, including stromal alterations and dysplastic transformation to colorectal carcinoma.

297 r-associated progressive, proliferative, and dysplastic typhlocolitis in aging (18- to 24-month-old)

298 Furthermore, dysplastic ureteric tubules that were surrounded by high

299 ted for alternative age groups and high-risk dysplastic variants.

300 g low-risk, and the probability of being non-dysplastic was 96.0% (99% CI 73.80-99.99).