ライフサイエンスコーパス: gastric adenocarcinoma

1 strongest risk factor for the development of gastric adenocarcinoma.

2 is is the strongest singular risk factor for gastric adenocarcinoma.

3 o lower the threshold for the development of gastric adenocarcinoma.

4 is the strongest identified risk factor for gastric adenocarcinoma.

5 trophic gastritis, peptic ulcer disease, and gastric adenocarcinoma.

6 actor that contributes to the development of gastric adenocarcinoma.

7 in the pathogenesis of chronic gastritis and gastric adenocarcinoma.

8 take are risk factors for the development of gastric adenocarcinoma.

9 esence of cancer, as well as intestinal type gastric adenocarcinoma.

10 ith incurable locally advanced or metastatic gastric adenocarcinoma.

11 om an individual who progressed from ChAG to gastric adenocarcinoma.

12 that includes gastritis, peptic ulcers, and gastric adenocarcinoma.

13 cells and increased risk for development of gastric adenocarcinoma.

14 pylori and serum pepsinogen (PG) levels with gastric adenocarcinoma.

15 spanic ethnicity does not impact survival in gastric adenocarcinoma.

16 spital costs following total gastrectomy for gastric adenocarcinoma.

17 osa-associated lymphatic tissue lymphoma, or gastric adenocarcinoma.

18 potential etiologic role for DEGA/AMIGO-2 in gastric adenocarcinoma.

19 etimes progresses to peptic ulcer disease or gastric adenocarcinoma.

20 wth and cell death leads to the formation of gastric adenocarcinoma.

21 the pathogenesis of peptic ulcer disease and gastric adenocarcinoma.

22 tomatic gastritis, peptic ulcer disease, and gastric adenocarcinoma.

23 mucous neck cell hyperplasia, a precursor to gastric adenocarcinoma.

24 ng risk factor for the development of distal gastric adenocarcinoma.

25 al cell decrease, which is a key step toward gastric adenocarcinoma.

26 of survival following curative resection for gastric adenocarcinoma.

27 osa-associated lymphoid tissue lymphoma, and gastric adenocarcinoma.

28 d radiation therapy and died from metastatic gastric adenocarcinoma.

29 plausibly predisposing to ulcer disease and gastric adenocarcinoma.

30 er disease, mucosa-associated lymphomas, and gastric adenocarcinoma.

31 ion, and gastrin levels in a rodent model of gastric adenocarcinoma.

32 etecting metastatic disease in patients with gastric adenocarcinoma.

33 ter pylori infection prevents development of gastric adenocarcinoma.

34 resent at altered frequency in patients with gastric adenocarcinoma.

35 are associated with peptic ulcer disease and gastric adenocarcinoma.

36 edictors of recurrence after gastrectomy for gastric adenocarcinoma.

37 astern Iran, a population with high rates of gastric adenocarcinoma.

38 ry but not sufficient for the development of gastric adenocarcinoma.

39 licobacter pylori-associated intestinal-type gastric adenocarcinoma.

40 tcome following curative intent resection of gastric adenocarcinoma.

41 ociated lymphoid tissue (MALT) lymphoma, and gastric adenocarcinoma.

42 1) forms of VacA is strongly associated with gastric adenocarcinoma.

43 t of peptic ulceration, gastric atrophy, and gastric adenocarcinoma.

44 c inflammation, which increases the risk for gastric adenocarcinoma.

45 ach and contributes to peptic ulceration and gastric adenocarcinoma.

46 be a precursor to intestinal metaplasia and gastric adenocarcinoma.

47 gastric ulcers and an increased incidence of gastric adenocarcinoma.

48 type IV secretion system where it can cause gastric adenocarcinoma.

49 e leading cause for peptic ulcer disease and gastric adenocarcinoma.

50 ctively) are critical oncogenic mediators in gastric adenocarcinoma.

51 ies that may culminate in the development of gastric adenocarcinoma.

52 c gastritis; however, some develop ulcers or gastric adenocarcinoma.

53 2 receptors, for the treatment of metastatic gastric adenocarcinoma.

54 scopic detection, staging, and management of gastric adenocarcinoma.

55 nd development in the surgical management of gastric adenocarcinoma.

56 rproliferation, which increases the risk for gastric adenocarcinoma.

57 oesophageal junction (GEJ)/cardia and distal gastric adenocarcinomas.

58 of metaplasia, 80% of dysplasia, and 70% of gastric adenocarcinomas.

59 novel cDNA differentially expressed in human gastric adenocarcinomas.

60 geal squamous cell carcinomas (ESCCs) and 72 gastric adenocarcinomas.

61 or, and are precursors of intestinal-type of gastric adenocarcinomas.

62 contributes to carcinogenesis in a subset of gastric adenocarcinomas.

63 hat may underlie differences between BA+ and gastric adenocarcinomas.

64 mosome 18q has been noted in intestinal type gastric adenocarcinomas.

65 y, 11 showed no significant association with gastric adenocarcinomas.

66 cells and is up-regulated in human colon and gastric adenocarcinomas.

67 within the E2F-4 coding region in 16 primary gastric adenocarcinomas, 12 ulcerative colitis-associate

68 We included 272 cases of gastric adenocarcinoma (142 GCA, 103 GNCA, and 27 unspec

69 tions in these 3 genes in a panel of 25 MMP+ gastric adenocarcinomas: 64% in BAX and hMSH3, and 52% i

70 In total, 170 gastric adenocarcinomas, 68 esophageal squamous cell car

71 A subset of gastric adenocarcinomas (71%) also showed reduced trypsi

72 tion is a risk factor for the development of gastric adenocarcinoma, a disease that has a high incide

73 rphisms augment the risk for intestinal-type gastric adenocarcinoma, a malignancy that predominates i

74 k factor for peptic ulcer disease and distal gastric adenocarcinoma, a process for which adherence of

75 Cysteine had a U-shaped association with gastric adenocarcinomas; a model that included a linear

76 in presentation and outcomes between SRC and gastric adenocarcinoma (AC) in the United States.

77 d leukemia, two cervical malignancy, and one gastric adenocarcinoma after EMA/CO.

78 the GlcNAcalpha1-->4Gal epitope expressed in gastric adenocarcinoma AGS cells transfected with alpha1

79 synthesized, and their inhibitory effects on gastric adenocarcinoma (AGS) and esophageal squamous cel

80 ght hundred ninety-six patients (71.01%) had gastric adenocarcinoma and 774 (28.99%) had junctional t

81 underwent splenectomy for gastric carcinoid, gastric adenocarcinoma and cancer of the left adrenal gl

82 because of its epidemiologic relationship to gastric adenocarcinoma and gastric mucosa-associated lym

83 characteristics of six cases containing both gastric adenocarcinoma and GIST.

84 d with a significantly increased risk of all gastric adenocarcinoma and GNCA in multivariate models.

85 cause gastric outlet obstruction is primary gastric adenocarcinoma and it is followed by carcinoma o

86 elae is associated with an increased risk of gastric adenocarcinoma and lymphoma of the mucosa-associ

87 eptic ulcer, and is strongly associated with gastric adenocarcinoma and lymphoma.

88 peptic ulcers and is a major risk factor for gastric adenocarcinoma and mucosa-associated lymphoid ti

89 Patients with histologic proof of gastric adenocarcinoma and near-normal organ function we

90 Gastric adenocarcinoma and proximal polyposis of the sto

91 The reported associations with gastric adenocarcinoma and seropositivity to different H

92 ood and Drug Administration in 2014 to treat gastric adenocarcinomas and non-small cell lung carcinom

93 We catalogued the genes expressed in two gastric adenocarcinomas and normal stomach, using serial

94 veral Bcl-2 family proteins are expressed in gastric adenocarcinomas and suggest that the repertoire

95 ence of HPP1 silencing by DNA methylation in gastric adenocarcinomas and to define any association of

96 a adenocarcinoma, 67 patients with noncardia gastric adenocarcinoma, and 224 population controls.

97 the main cause of peptic ulceration, distal gastric adenocarcinoma, and gastric lymphoma.

98 vere gastric diseases such as peptic ulcers, gastric adenocarcinoma, and gastric lymphoma.

99 development of peptic ulceration, noncardia gastric adenocarcinoma, and gastric lymphoma.

100 risk factor for peptic ulceration, noncardia gastric adenocarcinoma, and gastric lymphoma.

101 ith Helicobacter pylori is a risk factor for gastric adenocarcinoma, and H. pylori-induced carcinogen

102 tis, which can lead to peptic ulcer disease, gastric adenocarcinoma, and mucosa-associated lymphoid t

103 t, increasing the risk of peptic ulceration, gastric adenocarcinoma, and possibly other diseases.

104 e risk of peptic ulcer disease and noncardia gastric adenocarcinoma, and potential benefits that H py

105 ylori is the strongest known risk factor for gastric adenocarcinoma, and strains that possess the cag

106 inal cancers such as hepatocellular cancers, gastric adenocarcinomas, and colonic adenocarcinomas.

107 is strongly associated with gastric ulcers, gastric adenocarcinomas, and mucosa-associated lymphoid

108 on from chronic atrophic gastritis (ChAG) to gastric adenocarcinoma-and defined the impact of these a

109 The outcomes of surgical treatment of gastric adenocarcinoma are improving due to several fact

110 The outcomes of surgical treatment of gastric adenocarcinoma are improving.

111 Recognized precursor lesions for gastric adenocarcinoma are intestinal metaplasia and spa

112 esectable gastroesophageal (GE) junction and gastric adenocarcinoma are limited.

113 We report the first definitive case of gastric adenocarcinoma arising from a hyperplastic polyp

114 There have been no previous case reports of gastric adenocarcinoma arising from the more commonly fo

115 urgical samples collected from patients with gastric adenocarcinoma as well as biopsy samples from pa

116 or all patients undergoing R0 resections for gastric adenocarcinoma at a tertiary center between 1985

117 A review of the prospective database for gastric adenocarcinoma at Memorial Sloan-Kettering Cance

118 atients who underwent curative resection for gastric adenocarcinoma between 2000 and 2012 from 7 inst

119 nt total gastrectomy for stage I through III gastric adenocarcinoma between 2009 and 2012.

120 nts who underwent surgery for stage I to III gastric adenocarcinoma between January 1, 2004, and Dece

121 rgoing curative-intent total gastrectomy for gastric adenocarcinoma between January 2009 and December

122 etic profile increases the risk of noncardia gastric adenocarcinoma but not other upper gastrointesti

123 agA+ strains, is a risk factor for noncardia gastric adenocarcinoma, but its relationship with gastri

124 Patients had intact, untreated, primary gastric adenocarcinoma cancer and were evaluated for eli

125 ing metastatic breast carcinoma from primary gastric adenocarcinoma cannot be done using histological

126 the villin promoter by H. pylori in a human gastric adenocarcinoma cell line (AGS) required activati

127 cagA gene positive, were cocultured with the gastric adenocarcinoma cell line AGS.

128 f the G(1)-specific marker cyclin D1, in the gastric adenocarcinoma cell line AGSE (expressing the ga

129 derived cell lines tested express CYR61, the gastric adenocarcinoma cell line RF-1 does not.

130 EGF receptor activation of AGS human gastric adenocarcinoma cell line stimulated gastrin gene

131 s detected in polarized HGT-1 cells (a human gastric adenocarcinoma cell line).

132 of a DEGA/AMIGO-2 antisense construct in the gastric adenocarcinoma cell line, AGS, led to altered mo

133 astic specimens from 33 patients and also in gastric adenocarcinoma cell lines.

134 iferation of HCT-116 and HT-29 colon and AGS gastric adenocarcinoma cells but not of mouse embryo fib

135 In gastric adenocarcinoma cells harboring highly methylated

136 g protein (CREB) overexpressed conditions in gastric adenocarcinoma cells.

137 ion followed by its nuclear translocation in gastric adenocarcinoma cells.

138 ation of the cytotoxin by HeLa or AGS (human gastric adenocarcinoma) cells were characterized by indi

139 obial composition in The Cancer Genome Atlas gastric adenocarcinoma cohort.

140 uent in HLA-DQB1*0301-positive patients with gastric adenocarcinoma compared with HLA-DQB1*0301-negat

141 Barrett adenocarcinoma (BA+) and gastric adenocarcinoma comprise a related group of neopl

142 as presented to our weekly Multidisciplinary Gastric Adenocarcinoma Conference, and the consensus was

143 nal dissection extent during gastrectomy for gastric adenocarcinoma continues to be debated.

144 d esophageal, gastroesophageal junction, and gastric adenocarcinomas, death as a result of these tumo

145 meni syndrome) are not at increased risk for gastric adenocarcinoma, despite the fact that they show

146 PPARdelta might contribute to gastric adenocarcinoma development in humans.

147 cinomas expressed Cldn7 whereas diffuse-type gastric adenocarcinomas did not (P < 0.001).

148 Thirty-two matched normal-gastric adenocarcinoma DNA pairs were studied for MSI st

149 efore and after his progression from ChAG to gastric adenocarcinoma during a 4-year interval.

150 cate that in properly selected patients with gastric adenocarcinoma, endoscopic submucosal dissection

151 Interestingly, 82% of human intestinal-type gastric adenocarcinomas expressed Cldn7 whereas diffuse-

152 ially curative resection for GE junction and gastric adenocarcinoma from 1998 to 2013.

153 can distinguish patients with esophageal and gastric adenocarcinoma from noncancer controls.

154 pectrometry could distinguish esophageal and gastric adenocarcinoma from noncancer controls.

155 nificant VOCs to discriminate esophageal and gastric adenocarcinoma from those with normal upper gast

156 sociated with an increased risk of noncardia gastric adenocarcinoma, gastric lymphoma, and peptic ulc

157 , and treating gastric neoplasms, especially gastric adenocarcinoma, gastrointestinal stromal tumors,

158 M GC-), and 18 patients with intestinal type gastric adenocarcinoma (GC) and AG or IM in the adjacent

159 vey the distal enhancer landscape of primary gastric adenocarcinoma (GC), a leading cause of global c

160 either ERCC1 or TS mRNA levels in a primary gastric adenocarcinoma has a statistically significant r

161 Because pathogenesis of gastric adenocarcinoma has been associated with abnormal

162 Gastric adenocarcinoma has been previously recognized as

163 show foveolar dysplasia, and rarely invasive gastric adenocarcinoma has been reported in patients wit

164 Although incidence rates for noncardia gastric adenocarcinoma have declined steadily, paralleli

165 non-Hodgkin lymphoma, Merkel cell carcinoma, gastric adenocarcinoma, hepatocellular carcinoma, thyroi

166 was observed only for intestinal-type distal gastric adenocarcinoma (HR = 0.66, 95% CI: 0.47, 0.95; P

167 ) = 0.01), as opposed to diffuse-type distal gastric adenocarcinoma (HR = 0.92, 95% CI: 0.53, 1.60; P

168 In gastric adenocarcinoma, hypermethylation frequently targ

169 H. pylori infection induces gastric adenocarcinoma in an experimental mouse model of

170 on pilot observations of unexpectedly early gastric adenocarcinoma in C57BL/6 x 129S6/SvEv (B6129) m

171 iated with gastritis, peptic ulceration, and gastric adenocarcinoma in humans, secretes a protein tox

172 vivo adapted H. pylori strain, 7.13, induces gastric adenocarcinoma in rodent models of gastritis.

173 cobacter pylori infection is associated with gastric adenocarcinoma in some humans, especially those

174 The majority of patients with gastric adenocarcinoma in the United States present with

175 Gastric adenocarcinoma is a leading cause of cancer mort

176 Minimal access approach to treat gastric adenocarcinoma is evolving and continuing to hav

177 The mechanism linking HLA-DQB1*0301 with gastric adenocarcinoma is not likely through increased s

178 Gastric adenocarcinoma is one of many cancers associated

179 Gastric adenocarcinoma is one of the leading causes of c

180 Gastric adenocarcinoma is strongly associated with Helic

181 Gastric adenocarcinoma is the most common malignancy of

182 Gastric adenocarcinoma is the third leading cause of can

183 from 81 patients with esophageal (N = 48) or gastric adenocarcinoma (N = 33) and 129 controls includi

184 Cases for this study consisted of incident gastric adenocarcinomas (n = 643) identified between 199

185 on past and future intestinal-type noncardia gastric adenocarcinoma (NCGA) incidence.

186 For patients with laparoscopic stage M1 gastric adenocarcinoma, no resection of the primary tumo

187 formation with altered lipid metabolism and gastric adenocarcinoma occurred in 96 and 54% of these m

188 role in gastric tumorigenesis by studying 35 gastric adenocarcinomas of all histopathological types a

189 of a high-salt diet (a known risk factor for gastric adenocarcinoma) on H. pylori diversification wit

190 rongest known risk factor for development of gastric adenocarcinoma, only a small proportion of infec

191 n use to be inversely associated with distal gastric adenocarcinoma, particularly of the intestinal t

192 A majority of US gastric adenocarcinoma patients are inadequately staged

193 Gastric adenocarcinoma patients from 2004-2012 were enro

194 Resected stage IB-III gastric adenocarcinoma patients receiving adjuvant CRT o

195 These results indicated that unmarried gastric adenocarcinoma patients were at greater risk of

196 ately 45% of tumor versus normal tissue from gastric adenocarcinoma patients.

197 obacter pylori increases the risk for distal gastric adenocarcinoma, possibly by altering gastric epi

198 In patients with resectable GE junction and gastric adenocarcinoma, pretreatment NLR independently p

199 We identified 3 subtypes of gastric adenocarcinoma: proliferative, metabolic, and me

200 to have multiple foci of T1 invasive diffuse gastric adenocarcinoma (pure signet-ring cell type).

201 te improvements in the surgical treatment of gastric adenocarcinoma, recurrence rates remain high in

202 ons affecting the promoter 1B are at risk of gastric adenocarcinoma, regardless of whether or not col

203 isk of POM; centralization of junctional and gastric adenocarcinoma resection is warranted.

204 Postoperative mortality after junctional and gastric adenocarcinoma resection remains a significant i

205 -induced gastritis and its relationship with gastric adenocarcinoma rests on the assumption that atro

206 scriptase-polymerase chain reaction of human gastric adenocarcinoma samples indicated that, of these

207 erial contact, is overexpressed within human gastric adenocarcinoma specimens and enhances tumor form

208 model offers a valuable tool to investigate gastric adenocarcinoma subtypes where RAS/MAPK pathway a

209 A-DQB1*0301 was more common in patients with gastric adenocarcinoma than controls (54% vs. 27%; bonfe

210 01 is more common in caucasian patients with gastric adenocarcinoma than noncancer controls.

211 ort study included all patients with curable gastric adenocarcinoma that underwent gastrectomy betwee

212 idylate synthase (TS) mRNA levels in primary gastric adenocarcinomas treated with fluorouracil (5-FU)

213 t of a genetically engineered mouse model of gastric adenocarcinoma tumorigenesis based on Kras(G12D)

214 Patients with gastric adenocarcinoma underwent extended HLA class II r

215 One hundred eleven patients with gastric adenocarcinoma underwent laparoscopy at Memorial

216 PC was detected in 7 (28%) of 25 informative gastric adenocarcinomas using two 5q dinucleotide repeat

217 Recurrence after complete resection of gastric adenocarcinoma usually occurs within 2 years and

218 At 4 months postinfection, gastric adenocarcinoma was detected in 100% of the WT-in

219 Hence, DNA from 30 primary sporadic gastric adenocarcinomas was obtained from patients livin

220 gen associated with peptic ulcer disease and gastric adenocarcinoma, we cloned a putative DNA methylt

221 Patients with localized gastric adenocarcinoma were eligible.

222 Operable patients with localized gastric adenocarcinoma were eligible.

223 Four cases of gastric adenocarcinoma were identified (1.4%), one witho

224 utive patients who underwent gastrectomy for gastric adenocarcinoma were identified and their relevan

225 patients who underwent surgical resection of gastric adenocarcinoma were identified from a multi-inst

226 three patients with pathologically confirmed gastric adenocarcinoma were treated with neoadjuvant che

227 f 220 patients with histologically confirmed gastric adenocarcinomas were interviewed.

228 can assist in the selection of patients with gastric adenocarcinoma when staging (18)F-FDG PET is bei

229 cter pylori is the strongest risk factor for gastric adenocarcinoma, which develops within a hypochlo

230 most important in both cases of synchronous gastric adenocarcinoma with GIST and GIST alone.

231 of extended resection for clinical stage T4b gastric adenocarcinoma with good long-term results.

232 CD117, CD34 and Dog1 in all six synchronous gastric adenocarcinomas with GIST, and in GIST alone.

233 We sought to identify subtypes of gastric adenocarcinomas with particular biological prope

234 Endoscopy and histology confirmed a gastric adenocarcinoma within a hiatus hernia, which had

235 ylori is the strongest known risk factor for gastric adenocarcinoma, yet only a fraction of infected

236 cter pylori is the strongest risk factor for gastric adenocarcinoma, yet only a minority of infected