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 Dysplastic adenomas accumulate beta-catenin and lose het

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

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

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

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

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

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

10 %, and 96.3%, respectively, for detection of dysplastic and cancerous esophageal lesions).

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

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

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

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

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

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

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

18 The dual dysplastic and proliferative features in these stem cell

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

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

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

22 n activated form of KRAS, become hypoxic and dysplastic, and are refractory to chemo and radiation th

23 Granulocytes were consistently increased, dysplastic, and hypofunctional.

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

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

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

27 mutation for synchronous tumors and multiple dysplastic areas.

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

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

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

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

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

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

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

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

36 ng endoscopies of patients with BORN and non-dysplastic Barrett's esophagus.

37 1%) of 6834 participants were diagnosed with dysplastic Barrett's oesophagus (n=4) or stage I oesopha

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

39 whereas no participants were diagnosed with dysplastic Barrett's oesophagus or stage I gastro-oesoph

40 Treatment of dysplastic Barrett's oesophagus prevents progression to

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

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

43 In particular, dysplastic basal ganglia are part of the malformative sp

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

45 Human EAC (FLO-1 and EsoAd1), dysplastic BE (CP-B, CP-C, CP-D), and nondysplastic BE (

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

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

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

49 wing evidence that genomic assessment of non-dysplastic BE samples can identify patients at greatest

50 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.

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

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

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

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

55 hese pathways to be overexpressed in EAC and dysplastic BE.

56 y were overexpressed specifically in EAC and dysplastic BE.

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

58 asts could be viewed as an overlap between a dysplastic bone marrow failure syndrome and an oligoblas

59 es in myeloid and erythroid precursor cells, dysplastic bone marrow, neutrophilic cutaneous and pulmo

60 t, present as somatic mosaicism at ~15.1% in dysplastic brain tissue and ~11% in blood, and the MTOR

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

62 n BE cell lines reduced the proliferation of dysplastic, but not nondysplastic, cells.

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

64 ight contribute to cellular heterogeneity in dysplastic cell lineages.

65 reveals loss of gallbladder and formation of dysplastic cell masses expressing biliary markers, sugge

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

67 ed genes, and clearance of virus-transformed dysplastic cells by the action of the CCR6/CCL20 axis.IM

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

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

70 ell (DSC) populations are also identified in dysplastic cells, which exhibited different clonogenic p

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

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

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

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

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

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

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

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

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

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

81 These MDS HSCs demonstrated dysplastic clonogenic activity.

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

83 The mice developed a hypoplastic dysplastic collecting system.

84 orescence spectroscopy in 15 patients with a dysplastic colorectal adenoma.

85 ed a transgenic mouse model that exhibited a dysplastic coronoid process and LF morphology.

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

87 The percentage of mice possessing dysplastic crypt in the recovery protocol among WT and C

88 g regenerative crypts in WT DSS Recovery and dysplastic crypts in Cld-1 Tg Recovery.

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

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

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

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

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

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

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

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

97 1 individuals with LSTV, 41.72% were type I (dysplastic enlarged transverse process), 41.4% were type

98 Although human dysplastic epithelia accumulated KLF5, KLF5 expression w

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

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

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

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

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

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

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

106 delayed craniofacial and tooth development, dysplastic facial features and delayed development of th

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

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

109 s in patients with deletions and predominant dysplastic features.

110 w subcategories of LGD with inflammatory and dysplastic features.

111 Entire dysplastic fields contained a founder mutation from whic

112 the unscheduled activation of EPAS1 in early dysplastic foci.

113 nce in our cohort, the size and grade of the dysplastic focus at the margin were significantly correl

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

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

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

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

118 Co-deletion of Cdkn2a and Trp53 in dysplastic gastric organoids promoted cancer phenotypes

119 ally showed a highly localized expression in dysplastic glands and indian file-like cells infiltratin

120 Metaplastic and dysplastic glands can be genetically related, indicating

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

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

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

124 n PIK3CA-related brain overgrowth, epilepsy, dysplastic gyrification and hydrocephalus (Roy et al., 2

125 However, the incidence and sequelae of dysplastic hematopoiesis at diagnosis are unknown.

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

127 the biological and clinical significance of dysplastic hematopoiesis in newly diagnosed MM, which ca

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

129 harness treatment of stable but sonographic dysplastic hips has no effect on acetabular development.

130 ct of bracing over natural history of stable dysplastic hips is not well known.

131 observation rather than treatment for stable dysplastic hips.

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

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

134 rotopia in the posterior frontal region, and dysplastic in-folding of the mesial occipital cortex.

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

136 Adult D673V homozygotes exhibit dysplastic isthmus and reduced bone volume of the dorsal

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

138 sts), affect a whole kidney (eg, multicystic dysplastic kidney or cystic dysplasia), or manifest as b

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

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

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

142 alities, and frequently display multicystic, dysplastic kidneys.

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

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

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

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

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

148 Cervical dysplastic lesions called cervical intraepithelial neopl

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

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

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

152 Organoid derivation from dysplastic lesions facilitated genomic, transcriptional

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

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

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

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

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

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

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

160 istep carcinogenesis process, from low-grade dysplastic lesions to carcinoma in situ and eventually t

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

162 formation in organoid assays, comprise early dysplastic lesions, and constitute up to 30% of all neop

163 99%), and detected 95% of malignant/severely dysplastic lesions, compared with 35% and 50% for carcin

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

165 opy lacks molecular information and can miss dysplastic lesions.

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

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

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

169 ntly mutated genes in CD34+ progenitors (and dysplastic lineages) from 67 patients revealed clonal he

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

171 ced nonalcoholic steatohepatitis with highly dysplastic liver nodules.

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

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

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

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

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

177 Consistently, we present evidence that a dysplastic mandibular coronoid process was also seen in

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

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

180 Severe thrombocytopenia, characterized by dysplastic megakaryocytes and intracranial bleeding, was

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

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

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

184 enhances beta1 integrin signaling leading to dysplastic MKs with severely impaired demarcation system

185 Analysis of sav1 mutant zebrafish revealed dysplastic morphology and expansion of both intrahepatic

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

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

188 derived xenografts (PDX) reproduce patients' dysplastic morphology with multi-lineage representation,

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

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

191 el, with significant c-Met overexpression in dysplastic mucosa.

192 and consequent apoptosis in both normal and dysplastic mucosa.

193 En-bloc resection of large, flat dysplastic mucosal lesions of the luminal GI tract can b

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

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

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

197 Neoplastic or dysplastic neuronal tissue in the brain stem and cerebel

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 In dysplastic nevi cases, the rate of clinically significan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 ze the role of keratinocyte dysplasia within dysplastic nevi.

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

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

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

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

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

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

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

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

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

242 ith multiple cutaneous melanomas and classic dysplastic nevus syndrome.

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

244 rate and characteristics of association with dysplastic nevus.

245 and precursor for cutaneous melanoma is the dysplastic nevus.

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

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

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

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

257 ral lichen planus were unlikely to be either dysplastic or malignant.

258 We have established metaplastic and dysplastic organoid lines, derived from Mist1-Kras(G12D)

259 Here, we report that dysplastic organoids die or show altered cellular behavi

260 viors and characteristics of metaplastic and dysplastic organoids.

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

262 Papillomas included lesions with benign and dysplastic pathological features.

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

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

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

266 operating genetic event that potentiates the dysplastic phenotype.

267 tion toward an exacerbated and proliferative dysplastic phenotype.

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

269 ther characterize mechanisms involved in the dysplastic progression of SSA, we investigated different

270 ement of the WNT/beta-catenin pathway in the dysplastic progression of SSAs with different genes bein

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

272 steoblast differentiation and prevents their dysplastic proliferation.

273 patients without any recurrence and without dysplastic recurrence.

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

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

276 otoreceptor degeneration was associated with dysplastic regions.

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

278 ncapg2, which resulted in significantly more dysplastic renal tubules in zebrafish larvae.

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

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

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

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

283 gnature was already activated in the earlier dysplastic stage.

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

285 Two dysplastic stem cell (DSC) populations are also identifi

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

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

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

289 nd quantitatively distinguish between tumor, dysplastic tissue, and healthy tissue would be of great

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

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

292 ferentially activated in EAC vs nonmalignant dysplastic tissues; pathway activities were confirmed wi

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

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

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

296 -associated dysplasia, and CAC as well as in dysplastic tumors of C57BL/6 mice treated with azoxymeth

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).