ライフサイエンスコーパス: gastric cancer

1 patients responding to treatment in advanced gastric cancer.

2 nt data set of 30 patients with diffuse-type gastric cancer.

3 tures from human saliva for the detection of gastric cancer.

4 of H pylori eradication on the incidence of gastric cancer.

5 influence progression to hypochlorhydia and gastric cancer.

6 biomarkers for the non-invasive detection of gastric cancer.

7 elevated SMOX expression and a high risk for gastric cancer.

8 otent therapeutic agent for the treatment of gastric cancer.

9 liferation, and eventually peptic ulcers and gastric cancer.

10 tional; however, these models rarely develop gastric cancer.

11 hown to be upregulated in some patients with gastric cancer.

12 h the presence of gastric ulceration but not gastric cancer.

13 chronic gastritis, peptic ulcer disease, and gastric cancer.

14 frequently overexpressed variant of CD44 in gastric cancer.

15 be genetic traits greatly affect the risk of gastric cancer.

16 ents cytotoxicity of chemotherapies in human gastric cancer.

17 pylori infection with a reduced incidence of gastric cancer.

18 t the occurrence of peptic ulcer disease and gastric cancer.

19 ogen that causes persistent inflammation and gastric cancer.

20 romising strategy for the treatment of human gastric cancer.

21 hat LG is oncologically comparable to OG for gastric cancer.

22 recognized risk factor for peptic ulcers and gastric cancer.

23 e discover a network regulating Claudin-4 in gastric cancer.

24 mage in the etiology of H. pylori-associated gastric cancer.

25 nvestigation for prevention and treatment of gastric cancer.

26 dherin gene (CDH1) cause a predisposition to gastric cancer.

27 orylation and thereby increases the risk for gastric cancer.

28 pylori infection is the main risk factor for gastric cancer.

29 a 5-10% increase in cancer related death of gastric cancer.

30 at heterogeneity is common for biomarkers in gastric cancer.

31 into a genetic model of MMP7 deficiency and gastric cancer.

32 c ulcers and is an important risk factor for gastric cancer.

33 h H pylori contributes to the development of gastric cancer.

34 strongest risk factor for the development of gastric cancer.

35 antigens were associated with lower risk of gastric cancer.

36 e treatment approaches for H. pylori-induced gastric cancer.

37 had a personal or family history of diffuse gastric cancer.

38 One example is Helicobacter pylori and gastric cancer.

39 n of the gastric mucosa that may progress to gastric cancer.

40 s population, and is the main risk factor of gastric cancer.

41 gene in the development of H. pylori induced gastric cancer.

42 prolonged survival in patients with advanced gastric cancer.

43 ylori) infection is strongly associated with gastric cancer.

44 as associated with an improved prognostic in gastric cancer.

45 assay could improve diagnostic accuracy for gastric cancer.

46 ng, esophageal, and hepato-pancreato-biliary/gastric cancer.

47 nd worse outcomes in people with lung and/or gastric cancer.

48 ontributed to EMT, migration and invasion of gastric cancer.

49 e population of Asian patients with advanced gastric cancer.

50 val of patients diagnosed with esophageal or gastric cancer.

51 vate each other to promote the metastasis of gastric cancer.

52 n promise in treating ulcerative colitis and gastric cancer.

53 h previously treated, HER2-positive advanced gastric cancer.

54 fic mortality in patients with esophageal or gastric cancer.

55 verexpressing xenograft models of breast and gastric cancer.

56 ion, and may protect against oesophageal and gastric cancers.

57 ncer, and functions as a tumor suppressor in gastric cancers.

58 contributes to the pathogenesis of lung and gastric cancers.

59 ther cancer predisposition genes in familial gastric cancers.

60 even pancreatic carcinomas, as well as seven gastric cancers.

61 erified therapeutic biomarker for breast and gastric cancers.

62 strated in bladder, liver, lung, breast, and gastric cancers.

63 h carcinogenesis including breast, renal and gastric cancers.

64 and 49% vs 46% in Scotland, respectively) or gastric cancer (58% vs 57% in England and 59% vs 55% in

65 Gastric cancer, a leading cause of cancer-related deaths

66 the first-/second-line therapy for advanced gastric cancer (AGC).

67 tion has been reported to reduce the risk of gastric cancer among asymptomatic individuals in high-ri

68 included in our meta-analysis (715 incident gastric cancers among a total of 48,064 individuals/340,

69 cohorts, comprising 3858 probands (353 with gastric cancer and 89 with breast cancer).

70 Helicobacter pylori, the causative agent of gastric cancer and duodenal and gastric ulcers, was earl

71 Patients with gastric cancer and germline CDH1 mutations had shorter s

72 We observe that Claudin-4 is up-regulated in gastric cancer and is associated with poor prognosis.

73 -related protein 1 (sFRP1) overexpression in gastric cancer and its relationship with radiological fi

74 se of the high risk of invasive diffuse-type gastric cancer and lack of reliable surveillance options

75 statistically linked to patient survival in gastric cancer and metastasis status in primary tumors o

76 ted and stem cell functions are disrupted in gastric cancer and other disorders.

77 Eligible patients had HER2-positive advanced gastric cancer and progressed during or after first-line

78 that highlights the molecular complexity of gastric cancer and provides a road map to facilitate gen

79 tatus in a series of Brazilian patients with gastric cancer and to evaluate its association with clin

80 e the endoscopic frequency of esophageal and gastric cancers and the usefulness of alarm symptoms in

81 r consumption and the risk of esophageal and gastric cancers and their different subtypes.In this stu

82 estimate HRs and 95% CIs for esophageal and gastric cancers and their subtypes.We identified 966 inc

83 al and duodenal adenomas, colorectal cancer, gastric cancer, and an early-onset astrocytoma.

84 nct disease types, ranging from gastritis to gastric cancer, and geographic origins, covering most co

85 this Belgian population, the best markers of gastric cancer- and duodenal ulcer-associated strains ar

86 Peptic ulcer disease and gastric cancer are caused most often by Helicobacter pyl

87 bacter pylori infection and the incidence of gastric cancer are high in Bhutan.

88 r risk stratification and chemoprevention of gastric cancer are needed.

89 the staging evaluations of locally advanced gastric cancer are not uniform.

90 a useful staging tool in many cancers, some gastric cancers are not (18)F-FDG-avid and its clinical

91 hereas D58 and E62 were underrepresented, in gastric cancer-associated H. pylori isolates worldwide.

92 pylori CagL hypervariable motif (CagLHM) in gastric cancer-associated isolates.

93 2 is also served as prognostic biomarker for gastric cancer because HER2 over-expression is associate

94 stablished therapeutic targets in breast and gastric cancer but agents targeting Her2 have not yet de

95 ial cause for failure of targeted therapy in gastric cancer, but the extent of heterogeneity of estab

96 s with significantly different incidences of gastric cancer, but virtually identical prevalence of H.

97 discovered in primary leukemia/lymphoma and gastric cancer by human cancer genome sequencing efforts

98 Of 3321 gastric cancer cases, 42.3% had a minimum of 15 lymph no

99 By continuously exposing the gastric cancer cell line MKN45 to 5-FU for >100 passages

100 fully screened out as the most potent one on gastric cancer cell line(MGC803) through the investigati

101 the host transcriptional profile in the AGS gastric cancer cell line.

102 e metastatic models using the SGC-7901/sFRP1 gastric cancer cell line.

103 receptor quantitation of a panel of lung and gastric cancer cell lines expressing heterogeneous level

104 synergy to inhibit the viability of several gastric cancer cell lines, with combination index values

105 CR2 were highly expressed in a high invasive gastric cancer cell model and in gastric cancer tissues.

106 A highly invasive gastric cancer cell model was established.

107 that SOX9 was required for bacteria-induced gastric cancer cell proliferation, increased levels of b

108 ing its interaction with CDK9 and suppresses gastric cancer cell proliferation, migration and invasio

109 ong anti-proliferative activity on other two gastric cancer cells (HGC27 and SGC7901), but less cytot

110 antly enhances in vivo tumorigenicity of AGS gastric cancer cells and correlates with poor prognosis

111 AKT/mTOR signaling pathway both in cultured gastric cancer cells and in gastric cancer xenografts.

112 nstrated to affect its critical functions in gastric cancer cells by affecting E-cadherin cellular lo

113 We found that the up-regulation of hTERT in gastric cancer cells could inhibit the expression of miR

114 Functionally, SOX9 silencing in gastric cancer cells enhanced apoptosis and senescence,

115 dy demonstrates that sFRP1 overexpression in gastric cancer cells leads to increased cell proliferati

116 We found that co-injection of BMFs with gastric cancer cells markedly promoted tumorigenesis.

117 E-cadherin has in its defective function in gastric cancer cells needs to be determined.

118 PIN1-binding-defective BRD4-T204A mutant in gastric cancer cells reduces BRD4's stability, attenuate

119 In addition, the invasive capacity of gastric cancer cells was also highly increased after hTE

120 Apoptosis of gastric cancer cells was observed.

121 S17 potently killed gastric cancer cells with causing modulation of Bcl-2 fa

122 documented in non-small cell lung cancer and gastric cancer cells with MET amplification.

123 t the RNA nanoparticles specifically bind to gastric cancer cells, and knock-down the BRCAA1 gene.

124 Whether MLN4924 is effective against gastric cancer cells, however, remains elusive.

125 Here we showed that in gastric cancer cells, MLN4924 rapidly inhibited cullin 1

126 a1 mediate the interactions between BMFs and gastric cancer cells, which regulate cancer stemness and

127 f DARPP-32 in regulating splicing factors in gastric cancer cells.

128 cobacter pylori infection in macrophages and gastric cancer cells.

129 tively regulated by prolyl isomerase PIN1 in gastric cancer cells.

130 ay suppress disease relapse after 5-FU-based gastric cancer chemotherapy.

131 2000 and 2012 from 7 institutions of the US Gastric Cancer Collaborative were analyzed, excluding 30

132 pression was associated with intestinal-type gastric cancer compared to matched non-neoplastic gastri

133 nd in assciation with atrophic gastritis and gastric cancer consistent with Bhutanese strains having

134 sive generations should be weighed in future gastric cancer control programs.

135 A prospective gastric cancer database identified 41 patients with CDH1

136 or interaction); the incidence rate ratio of gastric cancer decreased in a nonlinear fashion with inc

137 ividuals after endoscopic resection of early gastric cancer), demographic characteristics of patients

138 lori is a bacterial pathogen associated with gastric cancer development that is known to target mitoc

139 major causative agent for ulcer disease and gastric cancer development.

140 viduals might affect disease progression and gastric cancer development.

141 study the role of CagA toxin polymorphism in gastric cancer development.

142 Gastric cancer develops in the context of parietal cell

143 th at least 1 patient diagnosed with diffuse gastric cancer (DGC) before age 50; families with 3 or m

144 sophageal adenocarcinoma, erosive gastritis, gastric cancer, diarrhea, colonic diverticular disease,

145 ciated protein diffusion dynamics in a human gastric cancer epithelial cell line.

146 hase 2 study in Asian patients with advanced gastric cancer, especially in those with ataxia-telangie

147 and determine the overall incidence rate of gastric cancer for patients with these premalignant lesi

148 Human tumors, including gastric cancer, frequently express high levels of epider

149 proliferation and apoptosis-related genes in gastric cancer (GC) and adjacent mucosa with atrophic ga

150 Enhanced ErbB-2 expression was also found in gastric cancer (GC) and has been correlated with poor cl

151 We sought to identify ASs involved in human gastric cancer (GC) and to elucidate their mechanisms of

152 mmation is associated with a greater risk of gastric cancer (GC) and, therefore, requires tight contr

153 Whole-genome sequencing was conducted on two gastric cancer (GC) cells, BGC823 and AGS, which do and

154 Gastric cancer (GC) has a poor prognosis with wide varia

155 sis of some cancers, but the role of FPR2 in gastric cancer (GC) has not yet been elucidated.

156 The molecular mechanism underlying gastric cancer (GC) invasion and metastasis is still poo

157 onstrate that the invasion and metastasis of gastric cancer (GC) is closely associated with a multi-s

158 Gastric cancer (GC) is globally the fifth most common ca

159 Gastric cancer (GC) is the second leading cause of cance

160 cular mechanism of hTERT in the promotion of gastric cancer (GC) metastasis.

161 but relevant role in the adjuvant therapy of gastric cancer (GC) patients.

162 The risk of gastric cancer (GC) remains even after H. pylori eradica

163 the gastric mucosa associated with increased gastric cancer (GC) risk.

164 valence of HP, HP CagA+ and EBV infection in gastric cancer (GC) samples from adults and in gastric t

165 T signaling is crucial to the development of gastric cancer (GC), its effects on epigenetic alteratio

166 e (ARID1A), frequently mutates inactively in gastric cancer (GC).

167 hosphate-guanidine) island (CGI) promoter in gastric cancer (GC).

168 ons, it is currently unknown for its role in gastric cancer (GC).

169 So far, stomach-specific biomarkers, gastric cancer(GC)-related environmental factors, and ca

170 phisms (SNPs) in the AKT promoter region and gastric cancer (GCa) risk in a case-control study of 1,1

171 Although postoperative chemoradiotherapy for gastric cancer has been an accepted treatment option for

172 Improved cure rates for esophageal and gastric cancer have increased focus on health-related qu

173 Our results suggest that 7-12% of gastric cancers have defective double-strand DNA break r

174 internationally accepted hereditary diffuse gastric cancer (HDGC) criteria to identify individuals w

175 eeting clinically defined hereditary diffuse gastric cancer (HDGC).

176 itution for patients with hereditary diffuse gastric cancer (HDGC).

177 ood groups was associated with lower risk of gastric cancer, heart disease and stroke mortality in a

178 Deaths from esophageal and gastric cancer, heart disease and stroke were identified

179 Gastric cancer, highly dependent on tumor angiogenesis,

180 To extend these findings into a model of gastric cancer, hypergastrinemic WT INS-GAS or MMP7(-/-)

181 patients newly diagnosed with esophageal or gastric cancer, identified from cancer registries in Eng

182 , the main cause of peptic ulcer disease and gastric cancer in adult populations, is generally acquir

183 , delivery, gene silencing and regression of gastric cancer in animal models.

184 H. pylori cag(+) strain 7.13 rapidly induces gastric cancer in Mongolian gerbils.

185 H. pylori cag(+) strain 7.13 rapidly induces gastric cancer in Mongolian gerbils.

186 e usefulness of alarm symptoms in diagnosing gastric cancer in subjects undergoing endoscopy in north

187 r more foci of intramucosal signet ring cell gastric cancer in the examined specimen.

188 ese RNA nanoparticles could be used to image gastric cancer in vivo, while showing little accumulatio

189 tomach, providing a new conditional model of gastric cancer in which to investigate candidate therape

190 r in the evaluation of the aggressiveness of gastric cancer, in addition to clinical and surgical var

191 Baseline gastric cancer incidence modified the benefit of H pylor

192 Gastric cancer incidence remains highest among Asian/Pac

193 e benefits of eradication vary with baseline gastric cancer incidence, but apply to all levels of bas

194 After adjustment for baseline gastric cancer incidence, individuals with eradication o

195 s, as well as their modification by baseline gastric cancer incidence, study design (randomized trial

196 due to correlation between age and baseline gastric cancer incidence.

197 Standard pretreatment staging for gastric cancer includes CT of the chest, abdomen, and pe

198 ith esophageal cancer and 3833 patients with gastric cancer, including 3240 and 2392 cancer-specific

199 nresectable, locally advanced, or metastatic gastric cancer, including adenocarcinoma of the gastro-o

200 n to breast, ovarian and pancreatic cancers, gastric cancer is another cancer type that exhibits this

201 Helicobacter pylori and its role in causing gastric cancer is one of the richest examples of a compl

202 s in AG and IM in gastric mucosa adjacent to gastric cancer is still unclear.

203 Gastric cancer is the second leading cause of cancer-rel

204 Gastric cancer is usually diagnosed in an advanced stage

205 e the roles of CXCR4 and CXCR2 signalings in gastric cancer metastasis.

206 XCR4 and CXCR2 is more effective in reducing gastric cancer metastasis.

207 n of a mutant Kras gene in an in vivo murine gastric cancer model.

208 the main driving force behind the declining gastric cancer mortality in Japan.

209 hage (n=1), myocardial infarction (n=1), and gastric cancer (n=1).

210 ently infected epithelial cells derived from gastric cancers, nasopharyngeal carcinomas, and normal o

211 In a xenograft mouse model of gastric cancer (NCI-N87) or an ado-trastuzumab emtansine

212 This feedforward ACh-NGF axis activates the gastric cancer niche and offers a compelling target for

213 l biomarkers and therapeutic targets against gastric cancer.Non-coding RNAs can modify the expression

214 o the varied prevalence of H. pylori-related gastric cancer observed in diverse populations.

215 erin gene (CDH1), renders a lifetime risk of gastric cancer of up to 70%, prompting a recommendation

216 cores from 9 different areas of the primary gastric cancers of 113 patients and matched lymph node m

217 rostate, colorectal, bladder, pancreatic, or gastric cancer or non-Hodgkin lymphoma from 2002 to 2011

218 lies whose members developed intestinal-type gastric cancer, or in the 22 families whose families dev

219 ashion with increasing baseline incidence of gastric cancer (P = .018, in comparison with the linear

220 ndings establish the significance of SOX9 in gastric cancer pathobiology and heterogeneity, with impl

221 Similar experiments performed in 4 different gastric cancer patient-derived xenograft models showed l

222 proteins were analyzed and compared between gastric cancer patients and matched control subjects by

223 All three proteins could differentiate gastric cancer patients from normal control subjects, dr

224 terminal loop of pri-mir-30c-1 in breast and gastric cancer patients had been previously described to

225 The increased incidence of the tnpA gene in gastric cancer patients suggests a role of the tnpA gene

226 The majority of gastric cancer patients underwent gastrectomy at providi

227 Gastric cancer patients who underwent staging (18)F-FDG

228 ssion (p < 0.05) between normal controls and gastric cancer patients, including 7 up-regulated protei

229 luation, in particular for NSCLC, liver, and gastric cancer patients.

230 cells and correlates with poor prognosis in gastric cancer patients.

231 This includes 10 esophageal and 27 gastric cancer patients.

232 with recurrent or metastatic PD-L1-positive gastric cancer, pembrolizumab had a manageable toxicity

233 nces a potential tumor suppressor, NR4A3, in gastric cancer, plausibly representing a reliable biomar

234 led adjusted HR, 0.98; 95% CI, 0.89-1.09) or gastric cancer (pooled adjusted HR, 0.96; 95% CI, 0.85-1

235 led adjusted HR, 1.03; 95% CI, 0.85-1.25) or gastric cancer (pooled adjusted HR, 1.06; 95% CI, 0.85-1

236 nd individuals after endoscopic resection of gastric cancers (pooled incidence rate ratio, 0.46; 95%

237 The study considered the gastric cancer population under age 46, which included 9

238 usibly representing a reliable biomarker for gastric cancer prognosis.

239 improved outcomes and has been endorsed as a gastric cancer quality measure.

240 d from patients with peptic ulcer disease or gastric cancer, rather than asymptomatic colonization.

241 monly in strains that cause peptic ulcers or gastric cancer, rather than asymptomatic infection.

242 chance of developing severe diseases such as gastric cancer, rather than the current regime that is g

243 No patients have developed gastric cancer recurrence after resections.

244 hat regulate CD44 splicing and expression in gastric cancer remain unknown.

245 Gastric cancer remains one of the leading causes of glob

246 For surgically resectable gastric cancer, removal of 15 or more lymph nodes has be

247 relationships and affected the direction of gastric cancer research.

248 -1beta alleles are associated with increased gastric cancer risk among H. pylori-infected persons.

249 amine-driven oxidative stress is a marker of gastric cancer risk and a target for chemoprevention.

250 tion in populations with different levels of gastric cancer risk and in different clinical scenarios

251 e assessed the role of SMOX in the increased gastric cancer risk in Colombia associated with the Ande

252 7 promoter activity and its association with gastric cancer risk in eastern Indian case-control cohor

253 lysis showed that tobacco addiction enhanced gastric cancer risk in GG subjects when compared with AA

254 ation and expression are directly related to gastric cancer risk in human populations.

255 ggest that antibiotic treatment only reduces gastric cancer risk in patients with non-atrophic gastri

256 ns that harbor the oncoprotein CagA increase gastric cancer risk, and this risk is augmented under ir

257 GA) and intestinal metaplasia (IM) influence gastric cancer risk.

258 lence factors associated with an increase in gastric cancer risk.

259 een the intake of dietary micronutrients and gastric cancer risk.

260 = 1.9, 95% confidence interval = 1.1-3.3) to gastric cancer risk.

261 R-27a gene exhibited a significant effect on gastric cancer risk.

262 eal cancer increased by 32 % per decade, but gastric cancer rose only in patients under 60 years of a

263 tein expression was significantly reduced in gastric cancer samples compared to matched non-neoplasti

264 of CXCR4 and CXCR2 expression was studied in gastric cancer samples.

265 rin gene in patients with hereditary diffuse gastric cancer selectively affect the mechanism of insid

266 Expression of NOD1 differs in human gastric cancer specimens compared with noncancer samples

267 decrease was observed in the esophageal and gastric cancer subgroups.

268 The high incidence of atrophic gastritis and gastric cancer suggest the phylogeographic origin of an

269 ecutive patients who underwent esophageal or gastric cancer surgery between 2010 and 2012 in France w

270 ective analysis of a prospectively collected gastric cancer surgery database at a single National Can

271 To improve POM, esophageal and gastric cancer surgery should be centralized, irrespecti

272 e POM in esophageal and, to a lesser extent, gastric cancer surgery; however, the benefit of centrali

273 odification and CRL E3 ligase are attractive gastric cancer targets, and MLN4924 might be further dev

274 olombian Andes have a 25-fold higher risk of gastric cancer than inhabitants of the coastal town Tuma

275 H pylori infection had a lower incidence of gastric cancer than those who did not receive eradicatio

276 lder (>/=20 years if Japanese) with advanced gastric cancer that had progressed following, or during,

277 For gastric cancer, the highest mortality rate was "agricult

278 Helicobacter pylori infection causes gastric cancer, the third leading cause of cancer death

279 is the strongest identified risk factor for gastric cancer, the third most common cause of cancer-re

280 effect of nut consumption on esophageal and gastric cancers.The objective was to evaluate the associ

281 patient should have access to best available gastric cancer therapy.

282 rst-line treatment of HER2-positive advanced gastric cancer, there is no established therapy in the s

283 eradication of H pylori infection on risk of gastric cancer, through May 2015.

284 HGF overexpression in stromal cells in human gastric cancer tissues.

285 gh invasive gastric cancer cell model and in gastric cancer tissues.

286 ods are urgently needed for the screening of gastric cancer to reduce its high mortality.

287 ffect of MMRD and MSI in curatively resected gastric cancer treated with perioperative chemotherapy i

288 reviously treated for HER2-positive advanced gastric cancer (unresectable, locally advanced, or metas

289 f tumor cells by immunohistochemistry) TNBC, gastric cancer, urothelial cancer, and head and neck can

290 In Turkey, the incidence of gastric cancer varies widely among regions due to the di

291 l (UGI) cancers, and especially the rate for gastric cancer, varies from country to country and from

292 age of 80 years, the cumulative incidence of gastric cancer was 70% (95% CI, 59%-80%) for males and 5

293 d cancer (28 esophagogastric junction and 71 gastric cancers) were examined with a 1.5-T MR imaging s

294 e the authors reveal a regulatory network in gastric cancer whereby claudin-4 expression is reduced b

295 ity and 80% specificity for the detection of gastric cancer with accuracy of 0.93.

296 cal cohorts revealed elevated SOX9 levels in gastric cancer with advanced tumor stage and poor patien

297 as follows: families with 2 or more cases of gastric cancer, with at least 1 patient diagnosed with d

298 ortance given the incidence and lethality of gastric cancer worldwide.

299 Importantly, in a preclinical gastric cancer xenograft mouse model, drug co-treatments

300 both in cultured gastric cancer cells and in gastric cancer xenografts.