ライフサイエンスコーパス: premalignant lesion

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

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

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

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

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

6 ediated esophageal epithelial hyperplasia, a premalignant lesion.

7 ped to distinguish malignant from benign and premalignant lesions.

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

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

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

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

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

13 nal expansion and propagation of metaplastic premalignant lesions.

14 uggests that most cancers arise from certain premalignant lesions.

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

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

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

18 autoimmunity and lymphocytic infiltration of premalignant lesions.

19 ot produce the dramatic inflammation seen in premalignant lesions.

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

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

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

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

24 enign, Sertoli adenomas can sometimes harbor premalignant lesions.

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

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

27 thelium, resulting in increased formation of premalignant lesions.

28 ncogenic Kras, Sox9 accelerates formation of premalignant lesions.

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

30 of the development and progression of these premalignant lesions.

31 ells in the airway epithelium in potentially premalignant lesions.

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

33 ulate the growth of existing malignancies or premalignant lesions.

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

35 after pancreaticoduodenectomy for benign and premalignant lesions.

36 frequently lost in various cancers and their premalignant lesions.

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

38 sk of breast cancer developing from specific premalignant lesions.

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

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

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

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

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

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

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

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

47 Premalignant lesions and early stage tumors contain immu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 Premalignant lesions are currently defined by their hist

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 Premalignant lesions in the colon would have developed b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 Reviews of premalignant lesions of the conjunctiva, including diagn

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

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

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

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

123 The premalignant lesions of the pancreas were accompanied by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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