ライフサイエンスコーパス: premalignant lesion

1 ediated esophageal epithelial hyperplasia, a premalignant lesion.

2 made major strides in our knowledge of this premalignant lesion.

3 h infection can attenuate gastric atrophy, a premalignant lesion.

4 s a marker of increased risk, or is itself a premalignant lesion.

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

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

7 olorectal tissues and proliferation rates of premalignant lesions.

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

9 sk of breast cancer developing from specific premalignant lesions.

10 ped to distinguish malignant from benign and premalignant lesions.

11 the development of hepatitis B virus-induced premalignant lesions.

12 sis expressed in most human skin cancers and premalignant lesions.

13 uld explore not only frank cancers but other premalignant lesions.

14 be used as biomarkers for assessing risk of premalignant lesions.

15 ARF) remain poorly understood in oral cavity premalignant lesions.

16 nal expansion and propagation of metaplastic premalignant lesions.

17 uggests that most cancers arise from certain premalignant lesions.

18 , the loss of protein expression occurred in premalignant lesions.

19 se B coincides with the angiogenic switch in premalignant lesions.

20 of contiguous adjacent normal tissue and/or premalignant lesions.

21 autoimmunity and lymphocytic infiltration of premalignant lesions.

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

23 ot produce the dramatic inflammation seen in premalignant lesions.

24 n of at least one copy is quite high in some premalignant lesions.

25 d that loss of 9p21 is also frequent in oral premalignant lesions.

26 l-1,2-benzanthracene) for 6 weeks, producing premalignant lesions.

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

28 in complete regression of carcinogen-induced premalignant lesions.

29 esions or detect malignant transformation in premalignant lesions.

30 striking deviation in the trajectory of the premalignant lesions.

31 ibutable to skin biopsies and cryotherapy of premalignant lesions.

32 attributable to biopsies and destruction of premalignant lesions.

33 after pancreaticoduodenectomy for benign and premalignant lesions.

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

35 enign, Sertoli adenomas can sometimes harbor premalignant lesions.

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

37 thelium, resulting in increased formation of premalignant lesions.

38 immune surveillance in progression of these premalignant lesions.

39 ncogenic Kras, Sox9 accelerates formation of premalignant lesions.

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

41 of the development and progression of these premalignant lesions.

42 ells in the airway epithelium in potentially premalignant lesions.

43 months postinfection (mpi) for gastritis and premalignant lesions.

44 ulate the growth of existing malignancies or premalignant lesions.

45 marker indicating the presence of high-risk premalignant lesions.

46 frequently lost in various cancers and their premalignant lesions.

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

48 d cyclin D1 expression was also found in the premalignant lesions adjacent to all 16 amplified tumors

49 ic alterations have already occurred in oral premalignant lesions, allowing at least a focal clonal e

50 etable consumption and the incidence of oral premalignant lesions among 42,311 US men in the Health P

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

52 suppress carcinogenesis in individuals with premalignant lesions and a high risk to develop cancer o

53 tice excluding Mohs surgeons, destruction of premalignant lesions and biopsies were mediators for the

54 Moreover, high-grade premalignant lesions and cancers in humans and transgeni

55 ment-related morbidity, long latency between premalignant lesions and clinically evident cancer, and

56 Premalignant lesions and early stage tumors contain immu

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

58 CRBP1 methylation appeared in premalignant lesions and frequently occurred with RARbet

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

60 Therefore, early diagnosis of high-risk premalignant lesions and incipient cancers is important.

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

62 ditions, normal repair, aberrant repair with premalignant lesions and lung cancer, and their correlat

63 nically efficient for the early detection of premalignant lesions and lung cancer.

64 Pdx1 progenitors induced the development of premalignant lesions and malignant transformation in old

65 help treat patients suspected of harbouring premalignant lesions and minimally invasive non-small-ce

66 e data suggest that retinomas represent true premalignant lesions and not regressed retinoblastoma tu

67 as been shown to be effective in eradicating premalignant lesions and preventing second primary malig

68 n effective intervention for preventing oral premalignant lesions and second primary tumors.

69 ials to prevent malignant conversion of oral premalignant lesions and the development of second prima

70 Immune response during the progression of premalignant lesions and their molecular subtype to colo

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

72 We probed lymphatic vessels in premalignant lesions and tumors by in vivo screening of

73 lized with LGR5 in Lynch syndrome colorectal premalignant lesions and tumors.

74 healthy high-risk [eg, smokers]), secondary (premalignant lesions), and tertiary (prevention of secon

75 ed that Pten deficiency initiated widespread premalignant lesions, and a low tumor incidence that was

76 (RIP1-Tag2), an angiogenic switch occurs in premalignant lesions, and angiogenesis persists during p

77 rential incidence of tumors as compared with premalignant lesions, and dramatically abbreviated survi

78 samples, including normal colorectal mucosa, premalignant lesions, and early-stage colorectal cancers

79 2 are highly enriched in uninvolved tissues, premalignant lesions, and metastases, respectively.

80 evention in groups at high risk, reversal of premalignant lesions, and prevention of second primary t

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

82 pairing angiogenic switching, progression of premalignant lesions, and tumor growth.

83 all associated with higher odds of advanced premalignant lesions (APLs) and CRC.

84 Currently, the best-characterized premalignant lesions are atypical ductal hyperplasia, at

85 Premalignant lesions are currently defined by their hist

86 relevance to human pancreatic cancer because premalignant lesions are found specifically in ductal ce

87 tic mechanisms controlling its expression in premalignant lesions are poorly described.

88 of breast and ovarian cancers but is high in premalignant lesions, ARHI-induced autophagy could be ma

89 These epithelial cells are found within premalignant lesions as well as in fields of morphologic

90 he virus life cycle, and is expressed in all premalignant lesions as well as some cancers.

91 two-stage model allows for greater yield of premalignant lesions, as well as separation of the initi

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

93 leading to initiated cells that give rise to premalignant lesions because of abrogated growth/differe

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

95 ter AOM injections, rodents develop putative premalignant lesions called aberrant crypt foci (ACF) th

96 port the hypothesis that clonal expansion of premalignant lesions can be driven by agents, such as io

97 Gastric premalignant lesions can develop into cancer through mul

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

99 transgenic mice showed an elevated number of premalignant lesions characterized by dysplasia and mark

100 corroborated the early increment of Tregs in premalignant lesions compared with the associated normal

101 Knowledge of premalignant lesion composition and the associated micro

102 However, recent publications show that many premalignant lesions comprise multiple clones expressing

103 Accordingly, human cancers and some premalignant lesions contain multiple genetic abnormalit

104 sting of both adenocarcinomas and associated premalignant lesions corroborated the early increment of

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

106 estigation of the hypothesis that regions of premalignant lesions develop a substrate-limited environ

107 ed a higher incidence of inflammation and/or premalignant lesions, especially in the heart and prosta

108 iation analysis, biopsies and destruction of premalignant lesions explained 74.1% (95% CI, 69.6%-77.9

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

110 be great interest in Barrett esophagus, the premalignant lesion for adenocarcinoma of the esophagus

111 d morbidity, but the lack of knowledge about premalignant lesions for OPSCC poses a significant chall

112 Single-cell RNA sequencing (scRNA-seq) of premalignant lesions from mouse models and a patient wit

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

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

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

116 remain about the best treatment for managing premalignant lesions (high-grade squamous intraepithelia

117 edly elevated in several types of cancer and premalignant lesions, implicating its association with c

118 ated H3K79 in testicular seminoma and in the premalignant lesion in situ carcinoma.

119 m must include a chemopreventive arm to hold premalignant lesions in check, a role well-suited to ant

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

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

122 indicate that CagA variants are linked with premalignant lesions in distinct populations and that ep

123 hose biological abnormalities characterizing premalignant lesions in individuals without overt lung c

124 creatic ductal adenocarcinomas (PDAC) and in premalignant lesions in mice and humans.

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

126 l inflammation that facilitates outgrowth of premalignant lesions in skin after carcinogen exposure.

127 f CP in patients with symptomatic benign and premalignant lesions in the body and neck of the pancrea

128 Premalignant lesions in the colon would have developed b

129 pt foci (ACF) are grossly invisible putative premalignant lesions in the colon.

130 depletion in IKTA mice reduced the number of premalignant lesions in the lungs in association with an

131 MSC or MSC resulted in a lower prevalence of premalignant lesions in the mammary gland, and fewer mam

132 challenges that hinder the identification of premalignant lesions in the oropharynx and discuss poten

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

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

135 uggests a novel therapy for the treatment of premalignant lesions in vivo.

136 aimed at preventing the angiogenic switch in premalignant lesions, intervening in the rapid expansion

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

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

139 Clonal expansion of premalignant lesions is an important step in the progres

140 formation on the risk of developing CRC from premalignant lesions is essential.

141 l malignancy in which the early diagnosis of premalignant lesions is known to directly correlate with

142 The treatment of premalignant lesions is largely based on the utilization

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

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

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

146 suggest that the unique dependencies of each premalignant lesion may be exploited therapeutically or

147 Also, significantly more hyperplastic and premalignant lesions, most of which were found within th

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

149 ically or histopathologically diagnosed oral premalignant lesions occurring between 1986 and 2002.

150 ells develop tubular metaplasia, a potential premalignant lesion of the pancreatic ductal epithelium.

151 the number of infiltrating T lymphocytes in premalignant lesions of mouse basal-like breast cancer.

152 Here, we report that early premalignant lesions of nasopharyngeal epithelium overex

153 Reviews of premalignant lesions of the conjunctiva, including diagn

154 flammatory effect against the progression of premalignant lesions of the gastric corpus at 6 months p

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

156 ic mapping in tumors, cancer cell lines, and premalignant lesions of the lung and breast, including t

157 dysregulated expression was detected in the premalignant lesions of the non-amplified tumors.

158 The premalignant lesions of the pancreas were accompanied by

159 Especially in premalignant lesions of the skin and colon, rapid progre

160 including the frequency and growth rates of premalignant lesions, of nascent solid tumors, and of in

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

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

163 Oral premalignant lesions (OPLs) are related to tobacco use a

164 detected in most cancer biopsies, but not in premalignant lesions or in normal tissue samples with a

165 n accurately measure the cancer risk of oral premalignant lesions, or intraepithelial neoplasia (IEN)

166 lary mucinous neoplasms of the bile duct are premalignant lesions originating in the bile duct and pr

167 rotocols using immunotherapy to reverse oral premalignant lesions, particularly high-risk leukoplakia

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

169 ing our knowledge about the biology of these premalignant lesions (PMLs) is necessary to design new m

170 Bronchial premalignant lesions (PMLs) precede the development of i

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

172 cases showed cyclin D1 gene amplification in premalignant lesions prior to development of invasive ca

173 une response and their important role in CRC premalignant lesion progression and subtypes.

174 al maps of the molecular events driving lung premalignant lesion progression will refine our understa

175 re induction of macrophage infiltration into premalignant lesions promoted an early onset of the angi

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

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

178 ous cell carcinomas and were associated with premalignant lesions resembling actinic keratoses, where

179 ted risk factors and its known precursors or premalignant lesions, should lend itself well to chemopr

180 receptor-alpha (ER-alpha)-negative, although premalignant lesions such as atypical ductal hyperplasia

181 breast cancer risk may be the development of premalignant lesions such as atypical ductal hyperplasia

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

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

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

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

186 ntly, higher immune activity was observed in premalignant lesions than in CRCs of the CMS3 subtype.

187 nly available approach employed to eradicate premalignant lesions that carry the potential for cancer

188 granulosa cells results in the formation of premalignant lesions that develop into granulosa cell tu

189 model is characterized by ER-alpha-positive premalignant lesions that give rise to both ER-alpha-pos

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

191 lonal genetic alterations are common in oral premalignant lesions; that multiple genetic alterations

192 spectrum of melanocyte pathology from early premalignant lesions through distant metastases.

193 cell to move from the microenvironment of a premalignant lesion to adjacent normal tissue.

194 erge simultaneous with the transition from a premalignant lesion to an invasive cancer.

195 in that occurs during the progression from a premalignant lesion to invasive carcinoma.

196 vity consistently decreased from NLs through premalignant lesions to adenocarcinoma, more prominently

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

198 might be targeted to prevent progression of premalignant lesions to invasive cancer.

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

200 t of biomarkers to detect those incubating a premalignant lesion, to stratify risk for progression to

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

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

203 The risk of oral premalignant lesions was significantly reduced with high

204 ia (large cell change), long thought to be a premalignant lesion, was hypothesized to represent abnor

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

206 otential inactivation of p16(INK4a) in these premalignant lesions, we analysed 74 biopsies from 36 pa

207 etter understand genetic alterations in oral premalignant lesions, we examined 84 oral leukoplakia sa

208 Similar to human premalignant lesions, we find activated ATM and other ma

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

210 stages of disease, including normal tissue, premalignant lesions, well-differentiated cancer, and po

211 Premalignant lesions were identified within the Dutch CR

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

213 nducible nitric-oxide synthase in lungs with premalignant lesions, whereas macrophages in carcinoma-b

214 on characterizes the clinical emergence of a premalignant lesion which is carried forward to carcinom

215 rams in serrated- and conventional-initiated premalignant lesions, which is perpetuated in colorectal

216 etect a precancerous state or identify which premalignant lesions will develop into invasive breast c

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

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