ライフサイエンスコーパス: gastric cancer

1 apy in platinum-sensitive ovarian cancer and gastric cancer.

2 fection, the most well-known risk factor for gastric cancer.

3 x 10(-6) p=5 x 10(-7), and p=5 x 10(-8)) for gastric cancer.

4 ase has been found in multiple sclerosis and gastric cancer.

5 ibute to the pathogenesis and progression of gastric cancer.

6 e of these cells and PPARD in development of gastric cancer.

7 ered as one of the principal risk factors of gastric cancer.

8 g metaplasia (SPEM), a putative precursor of gastric cancer.

9 another 2 in patients undergoing surgery for gastric cancer.

10 tive therapeutic target for the treatment of gastric cancer.

11 he expression of miR-135b-5p and its role in gastric cancer.

12 morphology, similar to human intestinal-type gastric cancer.

13 le tumor types, including liver, breast, and gastric cancer.

14 isk in minorities could lessen the burden of gastric cancer.

15 s a major risk factor for the development of gastric cancer.

16 orphologic similarities to subtypes of human gastric cancer.

17 ognostic markers and therapeutic targets for gastric cancer.

18 ection is the main cause of peptic ulcer and gastric cancer.

19 (H. pylori) is the strongest known risk for gastric cancer.

20 differentiated thyroid, adenoid cystic, and gastric cancer.

21 ascade that is amenable for the treatment of gastric cancer.

22 miR-135b-5p promotes cisplatin resistance in gastric cancer.

23 pylori infection is a proven carcinogen for gastric cancer.

24 nd peritoneal dissemination of patients with gastric cancer.

25 a favorable environment for the evolution of gastric cancer.

26 GS-Wnt mice developed adenomatous tooth-like gastric cancer.

27 constitutive STAT3 serine phosphorylation in gastric cancer.

28 et ring cells, resembling human diffuse-type gastric cancer.

29 terize different molecular subtypes of human gastric cancer.

30 in mucosa physiology and pathology including gastric cancer.

31 y be of therapeutic benefit to patients with gastric cancer.

32 creased risk for gastric diseases, including gastric cancer.

33 be used to study different subtypes of human gastric cancer.

34 to the advancement of precision medicine in gastric cancer.

35 obacter pylori can lead to peptic ulcers and gastric cancer.

36 mulation in murine and human intestinal-type gastric cancer.

37 patients responding to treatment in advanced gastric cancer.

38 n promise in treating ulcerative colitis and gastric cancer.

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

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

41 nvestigation for prevention and treatment of gastric cancer.

42 al in patients with HER2-positive metastatic gastric cancer.

43 One example is Helicobacter pylori and 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 gnostic marker for the detection of lung and gastric cancer.

51 H. pylori is the main risk factor for distal gastric cancer.

52 a patient diagnosed with hereditary diffuse gastric cancer.

53 most important of them i.e. peptic ulcer and gastric cancer.

54 on of H. pylori-infected individuals develop gastric cancer.

55 substantially reduce their risk of incident gastric cancer.

56 perative treatment in patients with operable gastric cancer.

57 d cancers, such as nasopharyngeal cancer and gastric cancer.

58 y island is a risk factor for development of gastric cancer.

59 rapy and surgical resection in patients with gastric cancer.

60 [1.61-2.69], p<0.0001) had a greater risk of gastric cancer.

61 No consistent associations were observed for gastric cancer.

62 rs frequently in colorectal, endometrial and gastric cancers.

63 frequently overexpressed in early stages of gastric cancers.

64 with nuclear localization of STAT3 in human gastric cancers.

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

66 geal carcinomas, Burkitt lymphomas, and some gastric cancers.

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

68 ic target in many types of cancer, including gastric cancer - a major health threat of cancer related

69 odifiable risk factor for the development of gastric cancer, a leading cause of cancer-related deaths

70 nt increase in the relative risk of incident gastric cancer across the quintiles of the polygenic ris

71 signature, which was efficiently exported to gastric cancer, allowing the identification, among micro

72 Han Chinese individuals, of whom 10 254 had gastric cancer and 10 914 geographically matched control

73 as 2 L chemotherapy for advanced/metastatic gastric cancer and a third received doublets.

74 aimed to establish a genetic risk model for gastric cancer and assess the benefits of adhering to a

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

76 ing in preclinical models of intestinal-type gastric cancer and ex vivo organoid cultures.

77 Family history of gastric cancer and Helicobacter pylori treatment.

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

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

80 haracterised by a high prevalence of diffuse gastric cancer and lobular breast cancer.

81 so occurred in naturally infected epithelial gastric cancer and nasopharyngeal cancer cell lines.

82 lammatory drugs (NSAIDs) induce apoptosis in gastric cancer and normal mucosal cells is elusive becau

83 indomethacin that promotes apoptosis in both gastric cancer and normal mucosal cells, thereby contrib

84 tomach and contributes to the development of gastric cancer and peptic ulcer disease.

85 vitro and contributes to the pathogenesis of gastric cancer and peptic ulcer disease.

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

87 ACAM1) expression and malignant potential of gastric cancer and to address whether CEACAM1 cytoplasmi

88 that VPAC1 is significantly overexpressed in gastric cancer and VPAC1/TRPV4/Ca(2+) signaling axis cou

89 c/Latino patients have a higher incidence of gastric cancer and worse cancer-related outcomes compare

90 study, EBV-infected cell lines derived from gastric cancers and Burkitt lymphomas were incubated wit

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

92 n primary intestinal and diffuse subtypes of gastric cancer (and in metastases of these subtypes), an

93 ource for deciphering the early formation of gastric cancer, and for isolating and characterizing hum

94 regulated in several malignancies, including gastric cancer, and is an important biomarker in drug di

95 nancies, including nasopharyngeal carcinoma, gastric cancer, and lymphoma.

96 APC mutations in colorectal cancer, KRAS in gastric cancer, and pancreatic cancer were mostly associ

97 ia Helicobacter pylori, the primary cause of gastric cancer, and risk of colorectal cancer (CRC).

98 tial of targeting Wnt receptors for treating gastric cancer, and the specific Wnt receptor transmitti

99 linical outcomes in HER2-positive breast and gastric cancers, and are emerging as potential treatment

100 tated, metastatic ovarian cancer; metastatic gastric cancer; and relapsed small-cell lung cancer.

101 he genomically stable (GS) subtypes of human gastric cancer: Anxa10-CreER(T2);Kras(G12D/+);Tp53(R172H

102 al origin, such as nasopharyngeal cancer and gastric cancer, as well as multiple blood cell-based mal

103 The relative and absolute risk of incident gastric cancer associated with healthy lifestyle factors

104 , 2 228 966 in general population), lung and gastric cancer (both k=1; 420 with mental illness, none

105 In one gastric cancer, both aneuploid and euploid cells contain

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

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

108 ecognition of a potential hereditary diffuse gastric cancer can provide a substantial health benefit

109 ageal squamous cell carcinoma (n = 267), and gastric cancer (cardia: n = 603; noncardia: n = 631) amo

110 s Program 2000-2014 data for 77,881 incident gastric cancer cases (cardia, n = 23,651; non-cardia, n

111 that accounts for approximately 1-3% of all gastric cancer cases.

112 rtant function of TRPM2 in the modulation of gastric cancer cell invasion likely through controlling

113 yrosine kinase inhibition in a MET-amplified gastric cancer cell line by a single, high exposure of t

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

115 taneous gastric cancer mouse model and human gastric cancer cell line xenografts abrogated tumor grow

116 CEACAM1 transfected or knockdown gastric cancer cell line, NUGC3 and MKN7 cells, were exa

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

118 as investigated using exosomes isolated from gastric cancer cell lines MKN-28, MKN-45, and SGC-7901.

119 exposed to exosomes isolated from all three gastric cancer cell lines when the mice were injected wi

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

121 Results suggest that exosomes derived from gastric cancer cells (especially MKN-45 and MKN-28) chan

122 The reconstitution of TFF1 protein in human gastric cancer cells and 3D gastric glands organoids fro

123 ible for transmitting Wnt signaling in human gastric cancer cells and mouse models of gastric cancer,

124 y demonstrated the critical role of TRPM2 in gastric cancer cells bioenergetics and survival; however

125 s, specifically Fzd7, inhibits the growth of gastric cancer cells even in the presence of adenomatous

126 nd abolished the tumor growth ability of AGS gastric cancer cells in NOD/SCID mice.

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

128 Expression of CEACAM1 in gastric cancer cells modulates invasiveness, lumen forma

129 ed in vitro and in vivo studies with NCI-N87 gastric cancer cells to determine how HER2 endocytosis a

130 better understand the mechanisms that allow gastric cancer cells to evade the immune system.

131 The drug sensitivity of human BGC823 gastric cancer cells toward different drugs, paclitaxel

132 Treatment of gastric cancer cells with TNF-alpha induced miR-135b-5p

133 anced the expression and secretion of VIP in gastric cancer cells, enforcing a positive feedback regu

134 our different type of cells including BGC823 gastric cancer cells, erythrocytes, lymphocytes, and E.

135 bits the migration and invasion abilities of gastric cancer cells, with a significant reversion in th

136 nvasion, lumen formation and tumor growth of gastric cancer cells.

137 isoform balance modulates the properties of gastric cancer cells.

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

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

140 nce higher incidence of, and mortality from, gastric cancer compared to other U.S. populations(, ).

141 gher expression of VIP/VPAC1 was observed in gastric cancer compared to the adjacent normal tissues.

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

143 The increased expression of VIP/VPAC1 in gastric cancer correlated positively with invasion, tumo

144 individuals at an increased risk of incident gastric cancer could be identified by use of our newly d

145 A prospective gastric cancer database identified 41 patients with CDH1

146 l, this study provides new insights into how gastric cancer derived exosomes modulate the immune resp

147 t that glucocorticoid deficiency may lead to gastric cancer development.

148 viduals might affect disease progression and gastric cancer development.

149 in CDH1 are associated with risk for diffuse gastric cancer (DGC) and lobular breast cancer.

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

151 Anatomic subsite risk factors for gastric cancer differ substantially, and subsite-specifi

152 ction-NCD pairs with the largest burden were gastric cancer due to H pylori (14.6 million DALYs), cir

153 ontribution of pyloric LGR5(+) stem cells to gastric cancer following dysregulation of the WNT pathwa

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

155 ne (6%, 95% CI 0.2-30.2) of 16 patients with gastric cancer, four (25%, 7.3-52.4) of 16 patients with

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

157 otein on cancer cells are found in 10-26% of gastric cancer (GC) and esophagogastric junction cancer

158 Targeted treatments for advanced gastric cancer (GC) are needed, particularly for HER2-ne

159 anisms of UHMK1 in the pathogenesis of human gastric cancer (GC) are unclear.

160 The risk of gastric cancer (GC) declines after Helicobacter pylori (

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

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

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

164 Gastric cancer (GC) is a world health problem and it is

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

166 Gastric cancer (GC) is one of the most prevalent cancers

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

168 Gastric cancer (GC) is the third leading cause of cancer

169 Gastric cancer (GC) patients with metastasis had limited

170 ing and tumor-infiltrating MDSCs existing in gastric cancer (GC) patients, the phenotypic characteris

171 signaling pathway is critically involved in gastric cancer (GC) progression.

172 The poor prognosis of gastric cancer (GC) results largely from metastasis and

173 recancerous lesions are strategies to reduce gastric cancer (GC) risk.

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

175 s by affordable tools is crucial for guiding gastric cancer (GC) treatments especially at earlier sta

176 Gastric cancer (GC) with peritoneal metastases (PMs) is

177 s such as nasopharyngeal carcinoma (NPC) and gastric cancer (GC).

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

179 , prostate cancer (PC), lung cancer (LC) and gastric cancer (GC).

180 in gastric epithelial cells that can lead to gastric cancer (GC).

181 = 37), intestinal metaplasia (IM, N = 21) or gastric cancer (GC, N = 16) from Mexico and Colombia.

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

183 We report proteogenomic analysis of diffuse gastric cancers (GCs) in young populations.

184 any human epithelial malignancies, including gastric cancer, has invariably been associated with its

185 A subset of patients with gastric cancer have mutations in genes that participate

186 L) chemotherapies for advanced or metastatic gastric cancer have shown improved survival but there is

187 Hereditary diffuse gastric cancer (HDGC) is an autosomal dominant cancer sy

188 cademic institution, and it includes all the gastric cancer histologic and molecular types identified

189 Compared to the general U.S. population, gastric cancer in AN people occurs at a younger age, is

190 Gastric cancer in Hispanic/Latino patients has unique ge

191 To determine the genomic landscape of gastric cancer in Hispanic/Latino patients, we performed

192 ation of the WNT pathway-a frequent event in gastric cancer in humans(3)-is unknown.

193 tion, we found significantly higher risks of gastric cancer in racial and ethnic minorities and smoke

194 the association between genetic variants and gastric cancer in six independent genome-wide associatio

195 as to identify the best strategies to combat gastric cancer in the AN population through prevention a

196 l leaders together to evaluate issues around gastric cancer in the AN population.

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

198 ies (p(trend)<0.0001), with a higher risk of gastric cancer in those with an unfavourable lifestyle t

199 artment are a source of WNT-driven, invasive gastric cancer in vivo, using newly generated Aqp5-creER

200 e IL-11, which is required for the growth of gastric cancers in mice.

201 We examined differences in gastric cancer incidence by subsite, stratified by race

202 ne decarboxylase, reduces H. pylori-mediated gastric cancer incidence in Mongolian gerbils.

203 There was a uniform decrease in gastric cancer incidence, but an increasing incidence of

204 Targeted therapies licensed to treat gastric cancer include trastuzumab (HER2-positive patien

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

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

207 t transcription factor STAT3 is a feature of gastric cancer, including H. pylori-infected tissues, an

208 and accurate histopathological diagnosis of gastric cancer increase the chances of successful treatm

209 Hereditary diffuse gastric cancer is a rare condition that accounts for app

210 Gastric cancer is associated with chronic inflammation (

211 thogenesis of Helicobacter pylori-associated gastric cancer is dependent on delivery of CagA into hos

212 Gastric cancer is diagnosed histologically after endosco

213 The main treatment for early gastric cancer is endoscopic resection.

214 urgery, or to those whose risk of developing gastric cancer is not well defined.

215 Gastric cancer is one of the leading causes of cancer-re

216 clinical outcome for patients with advanced gastric cancer is poor; thus, the identification and val

217 complications revealed that gastrectomy for gastric cancer is still associated with heavy morbidity

218 Gastric cancer is the fifth most common cancer and the t

219 Gastric cancer is the world's third leading cause of can

220 Advanced gastric cancer is treated with sequential lines of chemo

221 Non-early operable gastric cancer is treated with surgery, which should inc

222 ptor transmitting oncogenic Wnt signaling in gastric cancer is unknown.

223 ter pylori (Hp) infection, a risk factor for gastric cancer, is high in AN people; however, high anti

224 e guidelines for HDGC from the International Gastric Cancer Linkage Consortium (IGCLC), which recogni

225 of signal transduction pathway mutations in gastric cancer, liver cancer, colorectal cancer, and pan

226 This immune suppressive environment promotes gastric cancer lung metastasis.

227 median survival of 11-14 months), 50-91% for gastric cancer (median survival of 8-15 months), 71-86%

228 nergetics and survival; however, its role in gastric cancer metastasis, the major cause of patient de

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

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

231 We generated a wide, multilevel platform of gastric cancer models, comprising 100 patient-derived xe

232 n of pS-STAT3 in the gp130 (F/F) spontaneous gastric cancer mouse model and human gastric cancer cell

233 ion is associated with a marked reduction in gastric cancer mutational load, as revealed by exomic se

234 rett's oesophagus (n=4) or stage I oesophago-gastric cancer (n=5) in the intervention group, whereas

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

236 Besides gastric cancer, no disease association has been describe

237 e, colorectal, bladder, uterine, pancreatic, gastric cancer, or non-Hodgkin lymphoma from 2005 throug

238 leavage of alpha2,6-linked sialic acids from gastric cancer organoid-derived monolayers restored susc

239 ing homeostatic epithelial cell apoptosis in gastric cancer pathogenesis, suggesting a mechanism for

240 protein, into gastric cells, contributing to gastric cancer pathogenesis.

241 and function of the Cag T4SS and its role in gastric cancer pathogenesis.

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

243 with poor overall survival (OS) for lung and gastric cancer patients and hence led to the conclusion

244 sociated with improved long-term survival in gastric cancer patients and merits further focus in surg

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

246 tumor and tumor nearby tissues (TNT) from 58 gastric cancer patients, enabling comparisons between tu

247 In conclusion, we generated a wide gastric cancer PDX platform, whose exploitation will hel

248 Moreover, transcriptomic analysis of gastric cancer PDXs allowed the identification of a canc

249 This study reports a multilevel platform of gastric cancer PDXs and identifies a MSI gastric signatu

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

251 Hispanic/Latino patients with gastric cancer possess unique genomic landscapes, includ

252 diated Ca(2+) entry, and eventually promoted gastric cancer progression in a Ca(2+) signaling-depende

253 ld enforce a positive feedback regulation in gastric cancer progression.

254 will be effective in treating patients with gastric cancer regardless of APC mutation status.

255 l, 4414 and 2943 patients with esophageal or gastric cancer, respectively, were included.

256 4%, and 71%, 56%, and 49% for esophageal and gastric cancer, respectively.

257 0(-5)) showed the strongest association with gastric cancer risk (p=7.56 x 10(-10)).

258 nise the emerging evidence of variability in gastric cancer risk between families with HDGC, the grow

259 tformin increases acid secretion and reduces gastric cancer risk in humans.

260 strectomy remains the recommended option for gastric cancer risk management in pathogenic CDH1 varian

261 lifestyle factors have been associated with gastric cancer risk, but the extent to which an increase

262 H(2)O(2), is associated with increased human gastric cancer risk.

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

264 e bacteria as a priority issue and designing gastric cancer screening policies are also recommended.

265 eradication after treatment reduced risk of gastric cancer (SHR, 0.24; 95% CI, 0.15-0.41; P < .001).

266 ori infection still had an increased risk of gastric cancer (SHR, 1.16; 95% CI, 0.74-1.83; P = .51) b

267 d with nontumor tissues, and associated with gastric cancer stage and grade.

268 ersely, epithelial monolayers generated from gastric cancer stem cells retained high levels of ST6Gal

269 findings emphasize the value of centralizing gastric cancer surgeries in the Western world.

270 The annual number of gastric cancer surgeries performed at the participating

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

272 rial, hospitals with a high annual volume of gastric cancer surgery were associated with higher overa

273 ormance and patient outcomes in laparoscopic gastric cancer surgery.

274 veness of such interventions in laparoscopic gastric cancer surgery.

275 bacter pylori eradication therapy to prevent gastric cancer: systematic review and meta-analysis.

276 d a favourable lifestyle had a lower risk of gastric cancer than those with a high genetic risk and a

277 ole and obligate requirement for pS-STAT3 in gastric cancer that could be extrapolated to other STAT3

278 the main risk factor for the development of gastric cancer, the third leading cause of cancer death

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

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

281 Analysis of human gastric cancer tissue microarrays, showed high levels of

282 e the overexpression of miR-135b-5p in human gastric cancer tissue samples compared with normal tissu

283 alculated based on CEACAM1 expression in the gastric cancer tissue.

284 Levels of PPARD were increased in human gastric cancer tissues, compared with nontumor tissues,

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

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

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

288 rative laparoscopy, locally advanced diffuse gastric cancer was diagnosed.

289 ar increase in the relative risk of incident gastric cancer was observed across the lifestyle categor

290 GI cancers combined, esophageal cancer, and gastric cancer were lower when biomass was burned using

291 the CRITICS trial, patients with resectable gastric cancer were randomized to receive preoperative c

292 man gastric cancer cells and mouse models of gastric cancer, whereby Fzd7-deficient cells were retain

293 he colorectal cancer, pancreatic cancer, and gastric cancer while they were beta-catenin and CTNNB1 i

294 CEACAM1 were performed in 235 patients with gastric cancer who underwent surgery.

295 investigated on a selection of cervical and gastric cancer whole genome sequences where Alphapapillo

296 However, in a second gastric cancer with aneuploid cells, no somatic L1 inser

297 ataset of lung cancer and another dataset of gastric cancer with FSSEM inferred differential GRNs in

298 Multivariate analysis demonstrated that gastric cancer without CEACAM1 is an independent prognos

299 acterium, is the most common risk factor for gastric cancer worldwide.

300 ab tumor uptake was also observed in NCI-N87 gastric cancer xenografts, allowing tumor detection as e