ライフサイエンスコーパス: premalignant

1 The tumor was benign (52%), premalignant (18%), or malignant (30%).

2 ctice, conjunctival tumors are benign (52%), premalignant (18%), or malignant (30%).

3 y UV radiation and to reduce the rate of new premalignant actinic keratoses.

4 rge carcinomas in all AhR-/- mice but mostly premalignant adenomas in less than half of AhR+/+ mice.

5 cer is to detect patients carrying high-risk premalignant adenomas with minimally invasive testing.

6 e increasingly been used in the treatment of premalignant and early oesophageal tumours.

7 Plasma cells from premalignant and early stages of myeloma were characteri

8 The most consistent dietary risk factor for premalignant and invasive breast cancer is alcohol, whet

9 The iKnife discriminates healthy from premalignant and invasive cervical lesions with high acc

10 omponents in distinguishing between healthy, premalignant and malignant conditions related to the pan

11 Premalignant and malignant lesions from the gastric muco

12 lerated the development of H. pylori-induced premalignant and malignant lesions in a cagA-dependent m

13 ace, thereby facilitating the development of premalignant and malignant lesions in the stomach.

14 replication stress, and induced formation of premalignant and malignant lesions.

15 diagnostic methods cannot robustly identify premalignant and malignant pancreatic cystic lesions.

16 In sun-associated premalignant and malignant skin neoplasia, E-cadherin is

17 was discovered in approximately one-third of premalignant and malignant skin tumors.

18 g qualitative epigenetic differences between premalignant and malignant stages.

19 nd that elevated MCT1 levels are manifest in premalignant and neoplastic Emu-Myc transgenic B cells a

20 ed an explanation to variable role of ROS in premalignant and transformed melanocytic cells and sugge

21 ore, splenic and thymic T cells derived from premalignant Atm(-/-)Casp2(-/-) mice also showed increas

22 ung cancer resection specimens, including 89 premalignant atypical adenomatous hyperplasia lesions, 1

23 (miRNAs), can compensate for lack of IL-6 in premalignant B cell activation.

24 y an asymptomatic preclinical phase in which premalignant B cells carrying a t(14;18) chromosomal tra

25 nd MNT-MAX interactions in B cells shifts in premalignant B cells toward a MYC-driven transcriptional

26 gnalling and initiated the transformation of premalignant B cells.

27 enhancing apoptosis and markedly decreasing premalignant B lymphoid cell populations.

28 ; a childhood kidney cancer) develops from a premalignant background, we examined the phylogenetic re

29 The gradual progression from premalignant Barrett's esophagus to esophageal adenocarc

30 In skin, premalignant basal cell carcinomas form 'buds', while in

31 le bone marrow (WBM) microenvironment during premalignant, baseline, on treatment, and post-treatment

32 on of liver progenitor cells, development of premalignant biliary lesions, and progression to metasta

33 he development of stroma-rich tumors and the premalignant biliary lesions, intraductal papillary bili

34 amental rethinking and deep understanding of premalignant biology.

35 ErbB2 is frequently highly expressed in premalignant breast cancers, including ductal carcinoma

36 GF)-A is overexpressed in most malignant and premalignant breast lesions.

37 romes as prognostic markers, particularly in premalignant breast lesions.

38 In normal and premalignant cancer cells, the TGFbeta signaling pathway

39 Peripheral blood mononuclear cells from premalignant cases (1 year prediagnosis) had significant

40 ) exhibit a cyclin D1-dependent expansion of premalignant CD24(+) CD29(low) luminal progenitors with

41 Premalignant CD4(+)CD8(+) T cells show persistent catena

42 induce gene-expression changes that favour a premalignant cell fate, and, in an assay for nephrogenes

43 chromatin and gene expression that favour a premalignant cell fate.

44 ends, we found that initiating mutations and premalignant cell kinetics can explain the primary featu

45 e results suggest that stiffness exacerbates premalignant cell line of MCF10A.

46 ishes oncogenic signals, thereby attenuating premalignant cell transformation and tumor progression.

47 he presence of even about 5% distribution of premalignant cells among healthy breast tissue.

48 found that mCXCL1 blocks differentiation of premalignant cells and activates quiescence in tumor-ini

49 levels of HPV16 E6/E7 oncogene expression in premalignant cells are regulated epigenetically.

50 TGF-beta) functions as a tumor suppressor in premalignant cells but as a metastasis promoter in cance

51 ion likely constitutes one mechanism whereby premalignant cells can circumvent this DNA damage respon

52 eterogeneous population of non-proliferating premalignant cells in the pancreas, and the concomitant

53 pies targeting these mutations can eradicate premalignant cells is unclear.

54 strates that gaining a survival advantage of premalignant cells may delay or prevent leukemic progres

55 r-ductal metaplasia (ADM) can transform into premalignant cells that can eventually become cancerous.

56 rscored by evidence that autophagy can allow premalignant cells to escape the genotoxic stress and in

57 protein-dependent checkpoint override allows premalignant cells to evade oncogene stress barriers, pr

58 in Drosophila this mechanism is hijacked by premalignant cells to gain a competitive growth advantag

59 s induced pluripotent stem cells from single premalignant cells with a partial complement of mutation

60 ired the proliferation of both malignant and premalignant cells with early-stage oncogenic lesions.

61 ive mechanism that prevents the expansion of premalignant cells(3,4) and has a beneficial role in wou

62 e suppresses cancer by halting the growth of premalignant cells, yet the accumulation of senescent ce

63 ting that the effects of Mdm2 loss extend to premalignant cells.

64 may provide a selective growth advantage to premalignant cells.

65 cancer development are sometimes present in premalignant cells.

66 nd was cytotoxic to normal cells, but not to premalignant cells.

67 ng M2-state and enhance the proliferation of premalignant cells.

68 g mutations occur before clonal expansion of premalignant cells.

69 Screening and treating premalignant cervical lesions (cervical intraepithelial

70 While editing of HPV genomes in benign and premalignant cervical lesions has been demonstrated, it

71 evels alone can exert long-term control over premalignant changes and susceptibility to DNA damage in

72 lysis of RDEB patient samples suggested that premalignant changes to the dermal microenvironment driv

73 Measuring these premalignant changes using microultrasound provides a po

74 oxin- or ethanol-induced injury and manifest premalignant changes within weeks.

75 MR imaging cannot depict premalignant changes; therefore, the standard of care fo

76 about hidden processes of tumor initiation, premalignant clonal expansion, and malignant transformat

77 the age of 60 years that are associated with premalignant clonal expansion.

78 In 14 of 23 cases studied (61%), we found premalignant clonal expansions in morphologically normal

79 Adult cancers often arise from premalignant clonal expansions.

80 e zygote, without being preceded by a common premalignant clone.

81 en in their 50s, suggesting that potentially premalignant clones are ubiquitous.

82 epertoire selection and counter-selection of premalignant clones for leukemia suppression.

83 We observe the rapid spread of premalignant clones in Crainbow mice expressing oncogeni

84 ventions to prevent progression or eradicate premalignant clones prior to the development of overt MM

85 ed information on the mean sojourn times for premalignant clones until occurrence of either the first

86 ain the differential rates of progression of premalignant colonic lesions and differences in behaviou

87 There were 73 premalignant colonic lesions diagnosed in 56 cases (tubu

88 nts with premalignant or benign tumors had a premalignant condition (cryptochydism in two and Peutz-J

89 entify not only a malignancy but a treatable premalignant condition (such as a colon polyp) as well.

90 Multiple myeloma (MM) evolves from a premalignant condition known as monoclonal gammopathy of

91 evalence of monoclonal B cell lymphocytosis, premalignant condition poorly described in KT recipients

92 nflammatory disease, behaves as a well-known premalignant condition that contributes to PDAC developm

93 , but the patient was diagnosed with MGUS, a premalignant condition.

94 ng sensitivity of endoscopic surveillance of premalignant conditions in the gastrointestinal tract.

95 Gastric premalignant conditions, atrophic gastritis (AG) and int

96 and possibly other cancers that evolve from premalignant conditions, that may miss pre-existing rare

97 ystem for precursor lesions, new findings in premalignant cystic neoplasms, and recently updated stag

98 iptional programs that are characteristic of premalignant differentiation, and this effect can be par

99 of a large group of patients with multifocal premalignant disease by Krysan and colleagues in this is

100 that may improve diagnosis and prevention in premalignant diseases and in screening of high-risk indi

101 MGUS is a premalignant disorder frequently encountered in KT recip

102 pathy of undetermined significance (a mostly premalignant disorder) and active multiple myeloma (MM).

103 on did not affect the onset of inflammation, premalignant dKO livers showed reduced liver damage and

104 ene expression and cellular function between premalignant (dysplastic) epithelial cells and their nor

105 In premalignant Emu-Myc transgenic mice deficient in Smchd1

106 Increased HAND2 methylation was a feature of premalignant endometrial lesions and was seen to paralle

107 g an important role of liver fibrosis in the premalignant environment (PME) of the liver.

108 that this tumor suppressor can promote early premalignant epidermal lesion formation.

109 The residual tumor was composed only of premalignant epithelial cells and inflammatory cells.

110 ntercellular interactions between normal and premalignant epithelial cells and their functional relev

111 fy with a CD24(med)CD49f(hi) population from premalignant ErbB2-expressing mammary glands.

112 al down-regulation of Myc-activated genes in premalignant Eu-Myc cells.

113 Additionally, the premalignant events taking place between initial mutatio

114 years) contain mutations that may represent premalignant events that cause clonal hematopoietic expa

115 f chimeric human prostate grafts and induced premalignant events.

116 ch, we previously demonstrated that a dermal premalignant field characterized by inflammatory angioge

117 Premalignant foci were detected in three patients, two w

118 gastropathy resembling Menetrier disease, a premalignant gastric disorder with epithelial hyperplasi

119 associated with both high levels of CagA and premalignant gastric histology.

120 ic strategy for preventing transformation of premalignant gliomas.

121 ggested a novel mechanism for suppression of premalignant growth by topical antioxidants.

122 ike receptor (TLR) activation contributes to premalignant hematologic conditions, such as myelodyspla

123 LR pathways during an immune response and in premalignant hematologic diseases, such as MDS.

124 pecific c-Fos expression leads to reversible premalignant hepatocyte transformation and enhanced DEN-

125 ate pathway gene expression by p53 occurs in premalignant hepatocytes, when p53 is needed to actively

126 ammary glands lacking ErbB3, thus inhibiting premalignant HER2-induced hyperplasia.

127 loproteinase dysregulation in proliferative, premalignant Hi-Myc prostatic glands.

128 Clones of premalignant HTLV-1-infected cells bearing known driver

129 e microenvironment in the organoid models of premalignant human mammary cell lines.

130 hree-dimensional (3D) colony organization of premalignant human mammary epithelial cells (HMECs) is o

131 ry revealed that alone, Pik3caH1047R induced premalignant hyperplasia of the ovarian surface epitheli

132 g radiation exposure but are dispensable for premalignant hyperproliferation.

133 C and possibly other epithelial cancers with premalignant immune involvement.

134 esentative of benign lesions in seven cases, premalignant in 13, and malignant or suggestive of malig

135 Primary diagnosis of malignant or premalignant, infectious, and inflammatory disease.

136 sity-dependent repression of gamma2, whereas premalignant keratinocytes and SCC cells overexpressed g

137 ons, suggesting the prevalent existence of a premalignant landscape in women without clinical evidenc

138 eports over the past year have redefined the premalignant landscape remarkably identifying tiny clone

139 be present within the cells of a polyclonal premalignant lesion and the features that underpin clona

140 Knowledge of premalignant lesion composition and the associated micro

141 ic gastroesophageal reflux and constitutes a premalignant lesion leading to a 30- to 60-fold increase

142 te clones, derived from cells of a low-grade premalignant lesion naturally infected with the major HR

143 Esophageal adenocarcinoma (EA) and its premalignant lesion, Barrett's esophagus (BE), are chara

144 e possibility of reducing gastric atrophy, a premalignant lesion, using micronutrient-antioxidant sup

145 prostatic intraepithelial neoplasia (PIN), a premalignant lesion.

146 ting that FTH may have the potential to be a premalignant lesion.

147 ing tested in clinical trials, to treat oral premalignant lesions (OPLs) and prevent oral cancers.

148 ral cancer development in patients with oral premalignant lesions (OPLs) are lacking.

149 Bronchial premalignant lesions (PMLs) are precursors of lung squam

150 amous cell carcinomas HNSCC from potentially premalignant lesions (PPOLS) to malignancy and lymph nod

151 However, it was never established that premalignant lesions actually contain tumor progenitors

152 Premalignant lesions and early stage tumors contain immu

153 overexpression in the mammary gland leads to premalignant lesions and eventually mammary tumors.

154 nificant correlation between ZAK+ colorectal premalignant lesions and gene sets belonging to the MAPK

155 DAC development, with higher TIGAR levels in premalignant lesions and lower TIGAR levels in metastasi

156 ption factor required for the development of premalignant lesions and their progression into pancreat

157 nduced gastric injury and the development of premalignant lesions by suppressing M1 macrophage polari

158 Whereas regression of lesions was shown for premalignant lesions caused by HPV, clinical benefit in

159 We show that formation of acinar-derived premalignant lesions depends on ectopic induction of the

160 Several studies have shown premalignant lesions gastric atrophy (GA) and intestinal

161 tern of [18 F]FDG uptake, 98 % of those with premalignant lesions had focal [18 F]FDG uptake.

162 nducible factors (HIF) in the progression of premalignant lesions has not been critically examined.

163 auses of cancer-related death, develops from premalignant lesions in chronically damaged livers.

164 eloping malignancy postulated to evolve from premalignant lesions in chronically damaged livers.

165 estigated the bacteria's potential to induce premalignant lesions in mice and studied the kinetics of

166 hisms have been linked to the development of premalignant lesions in the stomach.

167 F4/80(+)CD11b(+) macrophages produce Gas6 in premalignant lesions in vivo, and that macrophage-derive

168 the different steps of the transformation of premalignant lesions into HCC on cirrhosis.

169 ew biomarker predictive of transformation of premalignant lesions into HCC.

170 However, surveillance of these premalignant lesions is recommended by some of the leadi

171 Progression of premalignant lesions is restrained by oncogene-induced s

172 uptake is highly sensitive for malignant and premalignant lesions of the GIT.

173 Radiotherapy is often used to treat early premalignant lesions regardless of ErbB2 status.

174 The presence of p53 mutations in premalignant lesions suggests that they represent early

175 reatest chance (42 %) of being malignant and premalignant lesions than in any other area.

176 eld of lung injury can give rise to distinct premalignant lesions that may bear unique genetic aberra

177 on of caveolin-1 expression to progress from premalignant lesions to cancer.

178 extract against the progression of prostate premalignant lesions to malignant tumors.

179 high endometrial HAND2 methylation in their premalignant lesions were less likely to respond to prog

180 s in traditional serrated adenomas, sporadic premalignant lesions with a hitherto unknown pathogenesi

181 requires deciphering molecular processes in premalignant lesions, and revealing the determinants of

182 rce for the surveillance of gastrointestinal premalignant lesions, focusing on the scientific article

183 d alterations, including a discrimination of premalignant lesions, represents a major challenge in la

184 process characterized by the development of premalignant lesions, such as low- or high-grade dysplas

185 T cells as well as upregulation of PD-L1 in premalignant lesions, suggesting the presence of an adap

186 conjunction with samples from patients with premalignant lesions, to define the effects of a carcino

187 creatic ductal adenocarcinoma (PDAC) and its premalignant lesions, we aim to investigate the multidru

188 In 81 patients with oral premalignant lesions, we found that Ebp1 expression is s

189 a) accumulate in aging tissues and appear in premalignant lesions, yet their physiologic effects are

190 te of gastric cancer for patients with these premalignant lesions.

191 ariation in annual incidence rate of GC from premalignant lesions.

192 after pancreaticoduodenectomy for benign and premalignant lesions.

193 scence stimuli, as well as in senescent skin premalignant lesions.

194 olorectal tissues and proliferation rates of premalignant lesions.

195 enign, Sertoli adenomas can sometimes harbor premalignant lesions.

196 gland level, the smallest unit of colorectal premalignant lesions.

197 thelium, resulting in increased formation of premalignant lesions.

198 ncogenic Kras, Sox9 accelerates formation of premalignant lesions.

199 th main-duct and branch-duct IPMNs represent premalignant lesions.

200 of the development and progression of these premalignant lesions.

201 immune surveillance in progression of these premalignant lesions.

202 ss (RS) that leads to genomic instability in premalignant lesions.

203 progression, with incomplete mitoses, and a premalignant-like transformation.

204 of HPX and CFH may serve as an indicator of premalignant liver disease.

205 or and signaling protein that accumulates in premalignant liver diseases and most hepatocellular carc

206 into highly metastatic liver cancer cells in premalignant liver tissue.

207 We previously established a model of premalignant lung cancer wherein we treated human bronch

208 iloprost reduces endobronchial dysplasia, a premalignant lung lesion.

209 in-5AC and mucin-2, which could discriminate premalignant/malignant lesions from benign with an accur

210 -3-3zeta destabilizes p53, a Smad partner in premalignant mammary epithelial cells, by downregulating

211 , and Wnt/beta-catenin signaling pathways in premalignant mammary tissues.

212 hypothesizes overexpression of ERBB2 in the premalignant MCF10A cell lines at a stiffness value that

213 F9-dependent ROS in BRAF(V600E) signaling in premalignant melanocytes, offered an explanation to vari

214 Klf9 deficiency inhibited premalignant melanocytic hyperplasia in Braf(CA) mice bu

215 els: Braf(CA) mice, where Braf(V600E) causes premalignant melanocytic hyperplasia, and Braf(CA)/Pten(

216 ent recurrence-free survival for superficial premalignant, minimally invasive, and small invasive lun

217 CD138(+) cells from 56 subjects representing premalignant (monoclonal gammopathy of uncertain signifi

218 irements for early cellular invasion using a premalignant mouse model of pancreatic cancer with condi

219 n any order, leading to a complex network of premalignant mutational genotypes on the way to colorect

220 provide a potential mechanism through which premalignant mutations accrue in HSCs.

221 The order of premalignant mutations and their impact on HPC self-rene

222 Reprogramming also informed the order of premalignant mutations in patients with complex karyotyp

223 We show that in mice, premalignant myeloid cells harboring a Kras(G12D) allele

224 by methylation in acute myeloid leukemia and premalignant myeloid disorders.

225 e is a relative paucity of such knowledge in premalignant neoplasia, which inherently limits the pote

226 m for tumor-suppressive senescent cells in a premalignant neoplasm.

227 hRNA-mediated knockdown of A2BP1 or Myt1L in premalignant neural stem cells compromised neuronal line

228 Five (83%) of six patients with premalignant or benign tumors had a premalignant conditi

229 The premalignant organoids also displayed significant downre

230 anced cell proliferation and survival in the premalignant organoids in a manner that recapitulated th

231 Despite expression of oncogenic KRAS, premalignant pancreatic intraepithelial neoplasia 1 (Pan

232 ia, a process associated with development of premalignant pancreatic intraepithelial neoplasia lesion

233 are upregulated in human PDAC tissues and in premalignant pancreatic intraepithelial neoplasia tissue

234 fibroblasts and promotes the development of premalignant pancreatic intraepithelial neoplasias (PanI

235 The premalignant pancreatic lesions that developed in KPC an

236 e possible to design immunotherapies against premalignant pancreatic lesions to slow or prevent progr

237 tress, frequently prompting cells to enter a premalignant period during which they mount a defense ag

238 ar defense against transformation during the premalignant period.

239 l for KSHV-associated B-cell malignancies or premalignant persistence in B cells.

240 SNAIL1 gene deletion either during the premalignant phase or after primary tumors have reached

241 , we then tracked these cells throughout the premalignant phase, which revealed a dynamic multistep t

242 ), a plasma cell malignancy, evolves through premalignant phases characterized by genomic abnormaliti

243 nition, prevalence, and progression of these premalignant phases of light-chain multiple myeloma have

244 developed a cell-based assay that utilizes a premalignant phenotype of normal mammary epithelial cell

245 mined significance (MGUS) is an asymptomatic premalignant plasma cell disorder.

246 us stimuli, they are also largely present in premalignant plasma cell dyscrasia such as monoclonal ga

247 thy of undetermined significance (MGUS) is a premalignant plasma cell dyscrasia that consistently pre

248 was significantly increased in lesions with premalignant potential compared with normal mucosa or no

249 Since the original polyp studies, premalignant potential of sessile serrated adenomas has

250 ding suggests a scenario in which the common premalignant precursor had acquired shared transforming

251 effective in the treatment of SCCs and their premalignant precursor lesions, actinic keratoses.

252 Claudin-4 is overexpressed in several premalignant precursor lesions, including those of cance

253 Barrett's oesophagus is the premalignant precursor of oesophageal adenocarcinoma.

254 evelopment of multiple colonic adenomas, the premalignant precursors of colorectal cancer (CRC), freq

255 rrow senses distant tissue transformation at premalignant/preinvasive stages, suggesting that circula

256 Field cancerization is a premalignant process marked by clones of oncogenic mutat

257 have elucidated genetic processes underlying premalignant progression and preventive targets.

258 n to repeated episodes of acute hypoxia in a premalignant progression model.

259 ll expression of ST6Gal-I is associated with premalignant progression.

260 w show that the restoration of p53 in murine premalignant proliferating pineal lesions resulted in ce

261 the SELECT supplements on benign (primary), premalignant ( RWPE-1) and malignant (LNCaP) prostate ep

262 SSLs, the most common premalignant serrated subtype, and are found in up to 15

263 Actinic keratosis is the most frequent premalignant skin disease in the white population.

264 f a signaling molecule, Pak1, in sun-induced premalignant skin lesions and indicates that increased P

265 high in clinical samples of sunlight-induced premalignant skin lesions assessed by immunohistochemist

266 tinic keratosis, are generally considered as premalignant skin lesions that can progress into squamou

267 ways that promote the progression of certain premalignant skin lesions to malignant lesions will perm

268 s of ceramides may underlie inflammatory and premalignant skin.

269 -suppressive role of DDR activity during the premalignant stage has been studied, and strong evidence

270 At a premalignant stage of tumorigenesis, we documented a def

271 Furthermore, at the premalignant stage we observed disturbance of cell adhes

272 At the premalignant stage, hemizygous deletion of Bif-1 resulte

273 these changes are ultimately proven to be a premalignant stage, this method may prove useful in scre

274 MYC, increases p27(kip1) expression during a premalignant stage.

275 a critical need to detect PDAC early or at a premalignant stage.

276 be timely pondered to allow tissue repair at premalignant stages or to reduce aggressiveness at the t

277 chanism that restrains cancer progression at premalignant stages, in part by causing telomere dysfunc

278 because this disease is often preceded by a premalignant state (clonal hematopoiesis or myelodysplas

279 that expression of oncogenic Kras induced a premalignant state accompanied with an arrest in T-cell

280 Our work identifies a distinct premalignant state and multiple tumorigenic pathways cau

281 gene-environment interactions in shaping the premalignant state.

282 our strategies for correctly managing B-cell premalignant states.

283 le-cell-targeted sequencing of wild-type and premalignant Tet2(-/-) Lin(-)c-Kit(+) cells shows higher

284 everal microRNAs upregulated specifically in premalignant thymocytes, including miR-146a, miR-146b, a

285 mmunoglobulin-containing immune complexes in premalignant tissue and Fcgamma receptor-dependent activ

286 h different H. pylori infection statuses and premalignant tissue changes.

287 ancer genes are being detected in normal and premalignant tissue, thus placing greater emphasis on ge

288 e esophageal adenocarcinoma from a number of premalignant tissues and unveils mechanisms of phospholi

289 t differentially with age between normal and premalignant tissues, such as Barrett's esophagus (BE),

290 ger acyl chains, with stepwise enrichment in premalignant tissues.

291 tures commonly associated with malignant and premalignant tissues.

292 eased 5hmC characterizes the transition from premalignant to de-differentiated malignant lesions that

293 a critical regulator of the transition from premalignant to invasive cancer, and may lead to the dev

294 vironment develops during the progression of premalignant to malignant disease and becomes less preva

295 their functional relevance in the context of premalignant to malignant progression in Barrett's esoph

296 n species (ROS) regulation by TIGAR supports premalignant tumor initiation while restricting metastas

297 normal cells to create and interact with the premalignant tumor microenvironment to promote oncogenes

298 Loxl2 levels in premalignant tumors negatively correlate with expression

299 of multilayered epithelia-function to shape premalignant tumour architectures and influence tumour p

300 of the p53 pathway has different effects in premalignant versus invasive pineal tumors, and that p53