ライフサイエンスコーパス: gastric adenocarcinoma

1 develop targeted risk reduction programs for gastric adenocarcinoma.

2 gastric ulcers and an increased incidence of gastric adenocarcinoma.

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

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

5 ctively) are critical oncogenic mediators in gastric adenocarcinoma.

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

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

8 2 receptors, for the treatment of metastatic gastric adenocarcinoma.

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

10 nd development in the surgical management of gastric adenocarcinoma.

11 d to gastric metaplasia and increase risk of gastric adenocarcinoma.

12 rproliferation, which increases the risk for gastric adenocarcinoma.

13 strongest risk factor for the development of gastric adenocarcinoma.

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

15 eptic ulcer disease, atrophic gastritis, and gastric adenocarcinoma.

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

17 is the strongest identified risk factor for gastric adenocarcinoma.

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

19 actor that contributes to the development of gastric adenocarcinoma.

20 in the pathogenesis of chronic gastritis and gastric adenocarcinoma.

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

22 ith incurable locally advanced or metastatic gastric adenocarcinoma.

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

24 cells and increased risk for development of gastric adenocarcinoma.

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

26 ature of perioperative care in patients with gastric adenocarcinoma.

27 spanic ethnicity does not impact survival in gastric adenocarcinoma.

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

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

30 etimes progresses to peptic ulcer disease or gastric adenocarcinoma.

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

32 the pathogenesis of peptic ulcer disease and gastric adenocarcinoma.

33 en, had a significantly lower risk of cardia gastric adenocarcinoma.

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

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

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

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

38 of survival following curative resection for gastric adenocarcinoma.

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

40 d radiation therapy and died from metastatic gastric adenocarcinoma.

41 plausibly predisposing to ulcer disease and gastric adenocarcinoma.

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

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

44 might progress to neuroendocrine tumours and gastric adenocarcinoma.

45 etecting metastatic disease in patients with gastric adenocarcinoma.

46 ter pylori infection prevents development of gastric adenocarcinoma.

47 resent at altered frequency in patients with gastric adenocarcinoma.

48 Helicobacter pylori is the primary cause of gastric adenocarcinoma.

49 ess tumor growth in peritoneal metastasis of gastric adenocarcinoma.

50 be a precursor to intestinal metaplasia and gastric adenocarcinoma.

51 ng to disease progression that may result in gastric adenocarcinoma.

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

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

54 spital costs following total gastrectomy for gastric adenocarcinoma.

55 are associated with peptic ulcer disease and gastric adenocarcinoma.

56 edictors of recurrence after gastrectomy for gastric adenocarcinoma.

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

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

59 licobacter pylori-associated intestinal-type gastric adenocarcinoma.

60 tcome following curative intent resection of gastric adenocarcinoma.

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

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

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

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

65 ach and contributes to peptic ulceration and gastric adenocarcinoma.

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

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

68 novel cDNA differentially expressed in human gastric adenocarcinomas.

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

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

71 contributes to carcinogenesis in a subset of gastric adenocarcinomas.

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

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

74 ologic conditions such as gastric ulcers and gastric adenocarcinomas.

75 stinal tract tumors including esophageal and gastric adenocarcinomas.

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

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

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

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

80 geal, 64% gastroesophageal junction, and 24% gastric adenocarcinoma), 26 of whom were also imaged wit

81 he primary outcome was a diagnosis of distal gastric adenocarcinoma 30 days or more after detection o

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

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

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

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

86 d gastritis is the strongest risk factor for gastric adenocarcinoma, a malignancy preceded by a serie

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

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

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

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

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

92 ncidence of and risk factors for nonproximal gastric adenocarcinomas after detection of H pylori.

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

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

95 ive activity in breast carcinoma (MCF-7) and gastric adenocarcinoma (AGS) cell lines.

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

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

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

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

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

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

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

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

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

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

106 Gastric adenocarcinoma and proximal polyposis of the sto

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

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

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

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

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

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

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

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

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

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

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

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

119 duals in each group (one cardiac arrest, one gastric adenocarcinoma, and one hypertensive heart disea

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

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

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

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

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

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

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

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

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

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

130 ons with the assumption that all early stage gastric adenocarcinomas are alike.

131 Gastric adenocarcinomas are staged using the American Jo

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

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

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

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

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

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

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

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

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

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

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

143 lore the male predominance in esophageal and gastric adenocarcinoma by evaluating the preventive pote

144 cid glycosphingolipids isolated from a human gastric adenocarcinoma by mass spectrometry, enzymatic h

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

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

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

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

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

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

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

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

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

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

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

156 In gastric adenocarcinoma cells harboring highly methylated

157 uce the adhesion of H. pylori 26695 to human gastric adenocarcinoma cells via AFM.

158 d promote the proliferation and migration of gastric adenocarcinoma cells.

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

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

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

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

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

164 Women had decreased risk of gastric adenocarcinoma compared with men (SHR, 0.52; 95%

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

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

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

168 aroscopic vs open gastrectomy for resectable gastric adenocarcinoma (cT1-4aN0-3bM0).

169 ts with locally advanced, clinically curable gastric adenocarcinoma ( cT3 and/or N+, M0 category base

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

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

172 PPARdelta might contribute to gastric adenocarcinoma development in humans.

173 Diffuse-type gastric adenocarcinoma (DGAC) is a deadly cancer often d

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

175 Intestinal and diffuse gastric adenocarcinomas differ in clinical, epidemiologi

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

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

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

179 Gastric adenocarcinoma, even when diagnosed at an early

180 s for patients with clinical stage II or III gastric adenocarcinoma, excluding gastric cardia tumors,

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

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

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

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

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

186 Gastric adenocarcinoma (GAC) is a lethal disease charact

187 metric analysis of circulating MDSCs from 20 gastric adenocarcinoma (GAC) patients found that >=80% A

188 n output to promote malignant progression of gastric adenocarcinoma (GAC) with lethal peritoneal asci

189 relevant biomarker in esophageal (EAC) -and gastric adenocarcinoma (GAC).

190 ntestinal metaplasia (GIM) is a precursor to gastric adenocarcinoma (GAC).

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

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

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

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

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

196 Because pathogenesis of gastric adenocarcinoma has been associated with abnormal

197 Gastric adenocarcinoma has been previously recognized as

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

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

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

201 rcinoma (HR 1.17 [95% CI 0.60-2.32]), cardia gastric adenocarcinoma (HR 0.99 [95% CI 0.40-2.46]), or

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

203 ) = 0.01), as opposed to diffuse-type distal gastric adenocarcinoma (HR = 0.92, 95% CI: 0.53, 1.60; P

204 In gastric adenocarcinoma, hypermethylation frequently targ

205 targeting the specific molecular subsets of gastric adenocarcinomas identified by genomic and/or mul

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

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

208 ted to the intestinal-type are translated to gastric adenocarcinoma in general; thus, the peculiariti

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

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

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

212 ed several-fold differences in incidences of gastric adenocarcinoma in specific anatomic sites among

213 2011 through 2015 to estimate incidences of gastric adenocarcinoma in specific anatomic sites for no

214 Nearly all studies of gastric adenocarcinoma in the United States have relied

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

216 , which covers more than 70% newly diagnosed gastric adenocarcinomas in the US, between 2006 and 2017

217 ted lymphomas, nasopharyngeal carcinoma, and gastric adenocarcinoma - in part by evading surveillance

218 We aimed to estimate the differences in gastric adenocarcinoma incidence in specific anatomic si

219 lack of precise, contemporary information on gastric adenocarcinoma incidence in specific anatomic si

220 y multimodality treatment regimens exist for gastric adenocarcinoma, including neoadjuvant vs adjuvan

221 Gastric adenocarcinoma is a leading cause of cancer mort

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

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

224 Gastric adenocarcinoma is one of many cancers associated

225 Gastric adenocarcinoma is one of the leading causes of c

226 Gastric adenocarcinoma is strongly associated with Helic

227 Gastric adenocarcinoma is the most common malignancy of

228 Gastric adenocarcinoma is the third leading cause of can

229 a decision analysis, screening for noncardia gastric adenocarcinoma might be cost-effective for non-W

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

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

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

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

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

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

236 /LP variant harbored occult signet ring cell gastric adenocarcinoma on final pathology (median age, 5

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

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

239 ag PAI) are associated with a higher risk of gastric adenocarcinoma or peptic ulcer disease than cag

240 e outcomes, including gastric ulcer disease, gastric adenocarcinoma, or gastric mucosa-associated lym

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

242 A majority of US gastric adenocarcinoma patients are inadequately staged

243 Gastric adenocarcinoma patients from 2004-2012 were enro

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

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

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

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

248 Here, we identify a role for a lncRNA-gastric adenocarcinoma predictive long intergenic noncod

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

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

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

252 t obstruction secondary to a newly diagnosed gastric adenocarcinoma, receiving neoadjuvant chemothera

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

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

255 nts undergoing gastrectomy for nonmetastatic gastric adenocarcinoma registered in the Population Regi

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

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

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

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

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

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

262 dge of the molecular and cellular biology of gastric adenocarcinomas, summarize the current approache

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

264 01 is more common in caucasian patients with gastric adenocarcinoma than noncancer controls.

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

266 Patients with gastric adenocarcinoma that was cT2-T4b, any N, and M0 a

267 significantly higher incidences of noncardia gastric adenocarcinoma; the incidence was highest among

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

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

270 Patients with gastric adenocarcinoma underwent extended HLA class II r

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

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

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

274 ts 50 years and older, the risk of noncardia gastric adenocarcinoma was 1.8-fold (95% CI, 1.37-2.31)

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

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

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

278 Patients with localized gastric adenocarcinoma were eligible.

279 Operable patients with localized gastric adenocarcinoma were eligible.

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

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

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

283 ds, patients with resectable (cT1-4aN0-3bM0) gastric adenocarcinoma were randomly assigned to either

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

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

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

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

288 One of these deaths was due to gastric adenocarcinoma, which was assessed by the invest

289 with survival among patients with resectable gastric adenocarcinoma who received PC.

290 (PC) is unclear in patients with resectable gastric adenocarcinoma who received preoperative chemoth

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

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

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

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

295 l response in patients with locally advanced gastric adenocarcinoma, with an acceptable safety profil

296 f PPARD mice developed spontaneous, invasive gastric adenocarcinomas, with severe chronic inflammatio

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

298 l and ethnic differences in the incidence of gastric adenocarcinoma worldwide and in the US.

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

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