ライフサイエンスコーパス: lung cancer

1 cer and the death rate was second to that of lung cancer.

2 an ARE-BP, is robustly up-regulated in human lung cancer.

3 2012, 16,641 patients underwent surgery for lung cancer.

4 mous epithelial cells of smokers, but not in lung cancer.

5 xenograft and Kras(LSL/G12D) mouse models of lung cancer.

6 in patients with advanced-stage EGFR-mutant lung cancer.

7 umber of staging scenarios in non-small-cell lung cancer.

8 f local recurrence and distant metastasis in lung cancer.

9 ributing factors for smoking and non-smoking lung cancer.

10 ates their prognostic value in patients with lung cancer.

11 to provide new insights into the etiology of lung cancer.

12 adversely impacts clinical outcome in human lung cancer.

13 registry data to identify incident cases of lung cancer.

14 and evolution in early-stage non-small cell lung cancer.

15 ultiple immunocompetent orthotopic models of lung cancer.

16 lular signaling have been widely observed in lung cancer.

17 for patients with early-stage non-small-cell lung cancer.

18 ns may provide a novel therapeutic target of lung cancer.

19 -small cell lung cancer (NSCLC), KRAS-mutant lung cancer.

20 r for detection of patients with gastric and lung cancer.

21 and pro-metastatic signals in LKB1-deficient lung cancer.

22 er, glioblastoma multiforme, colon, skin and lung cancer.

23 history of pneumonia, and family history of lung cancer.

24 ions as disseminated brain metastases due to lung cancer.

25 aromatic hydrocarbon, is the major cause of lung cancer.

26 c has been consistently associated only with lung cancer.

27 d risk factor in various cancers, especially lung cancer.

28 antification in patients with non-small cell lung cancer.

29 motherapy in select patients with small-cell lung cancer.

30 rrest and increased radiochemosensitivity in lung cancer.

31 ery likely to experience recurrence of their lung cancer.

32 in more than 80% of patients with small-cell lung cancer.

33 ine dependence, heavy smoking and consequent lung cancer.

34 is a novel, promising therapeutic target for lung cancer.

35 h advanced-stage tumors, such as melanoma or lung cancer.

36 or ER-positive breast cancer and KRAS mutant lung cancer.

37 tive and chemoresistant models of small cell lung cancer.

38 of mRNA splicing genes in the development of lung cancer.

39 tive agents for the treatment of EGFR-mutant lung cancer.

40 trategy to target KRAS mutant colorectal and lung cancers.

41 adjuvant therapy in resected non-small-cell lung cancers.

42 to optimize MK-1775 treatment efficiency in lung cancers.

43 le for inclusion, 42 (39%) in non-small-cell lung cancer, 36 (33%) in breast cancer, 25 (23%) in colo

44 ans), melanoma (69 patients, 271 scans), and lung cancer (84 patients, 286 scans).

45 models to estimate the 2-year probability of lung cancer, accounting for the competing risk of death.

46 er patients, most especially with small cell lung cancer, although the long-term survival is hardly s

47 owever, this study strengthens evidence that lung cancer, anal cancer, and myeloma are diagnosed at m

48 -depth (579x+/-315) nextgen sequencing of 30 lung cancer and 89 control samples, resulting in sensiti

49 fficacy in pancreatic cancer, non-small cell lung cancer and breast cancer.

50 olled, including 74 patients with small-cell lung cancer and eight with large-cell neuroendocrine car

51 retrotransposable element insertion bias in lung cancer and found a significant pairwise association

52 ditive interaction between family history of lung cancer and HL treatment was shown ( P = .03).

53 tumour cells in a mouse model of small-cell lung cancer and in human tumours.

54 These data uncover a direct role for RANK in lung cancer and may explain why female sex hormones acce

55 ased pancreatic and testicular but decreased lung cancer and melanoma risk, and exhibited preferred p

56 trials investigating checkpoint blockade in lung cancer and mesothelioma is provided.

57 fic TFs become preferentially inactivated in lung cancer and precursor lung cancer lesions and furthe

58 following primary surgery for non-small-cell lung cancer and the characterization of emerging subclon

59 sed outcomes in patients with non-small-cell lung cancer and the EGFR Thr790Met mutation who were tre

60 discuss existing treatment for patients with lung cancer and the promise of precision medicine, with

61 (prostate cancer), NIH3T3 (fibroblast), H23 (lung cancer), and A-172 (glioblastoma multiforme) cell l

62 ncreased mortality from respiratory disease, lung cancer, and cardiovascular disease.

63 s were associated with non-Hodgkin lymphoma, lung cancer, and liver cancer.

64 ease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epide

65 es of small cell lung cancer, non-small cell lung cancer, and non-lung cancer patients all dropped be

66 s predictive of a better survival outcome in lung cancer, and this effect was independent of that con

67 ient samples obtained from breast, prostate, lung cancers, and melanoma.

68 Although most lung cancers are still diagnosed at a late stage, there

69 a highly sensitive biomarker for Small Cell Lung Cancer, as a model.

70 It occupies enhancer regions near lung cancer-associated genes, and its occupancy correlat

71 gnosed with breast, prostate, colorectal, or lung cancer between 2000 and 2013 for each racial/ethnic

72 e survival differences in KRas(G12D) -driven lung cancer between male and female mice, and we show th

73 ted with specific types of cancer other than lung cancer by examining associations of ambient air pol

74 the relationship between animal farming and lung cancer by investigating the types of animals, tasks

75 We evaluated use of 43 pesticides and 654 lung cancer cases after 10 years of additional follow-up

76 y (initiated in 1985)-involving 807 incident lung cancer cases and 807 smoking-matched controls.

77 g Screening Trial (NLST) participants (1,925 lung cancer cases and 884 lung cancer deaths) and 80,672

78 rial (PLCO) ever-smoking participants (1,463 lung cancer cases and 915 lung cancer deaths).

79 ography-mass spectrometry (LC-MS) data, with lung cancer cases at the time of BAL collection.

80 The thirteen new lung cancer cases diagnosed during the follow up time pe

81 tion in non-tumor lung (NTL) tissue from 237 lung cancer cases in the Environment And Genetics in Lun

82 C), as a proportion, makes up only 15-17% of lung cancer cases.

83 KRAS-mutated lung cancer cell clones were stably silenced for LSD1 ex

84 TGF-beta and IL-6 in myofibroblasts (MFs) - lung cancer cell interactions, lung cancer cells (Lewis

85 We have analyzed a panel of 17 KRAS mutant lung cancer cell lines classified as K-Ras-dependent or

86 -67 intensity and clonogenicity and promoted lung cancer cell migration.

87 to delineate their effects on non-small cell lung cancer cell proliferation and apoptosis.

88 ues and its expression level is critical for lung cancer cell proliferation, which may serve as a pro

89 CNTD2 overexpression increased lung cancer cell viability, Ki-67 intensity and clonogen

90 lasts (MFs) - lung cancer cell interactions, lung cancer cells (Lewis and CTM-167 cell lines) were st

91 aling and triggered apoptosis in KRAS-mutant lung cancer cells and inhibited tumor growth in murine m

92 wires energy homeostasis in human and murine lung cancer cells and promotes expansion of lung cancer

93 Non-neuroendocrine Notch-active small-cell lung cancer cells are slow growing, consistent with a tu

94 pithelial-to-mesenchymal transition (EMT) of lung cancer cells by directly repressing the expression

95 Metastatic lung cancer cells can undergo an epithelial-to-mesenchym

96 Together, our data suggest that lung cancer cells escape oncogene-induced premature sene

97 Lung cancer cells expressing oncogenic K-Ras have bypass

98 , secreted peptide by epithelial ovarian and lung cancer cells in situ This finding prompted us to st

99 s the migratory and invasive capabilities of lung cancer cells in vitro and in vivo.

100 Breast and lung cancer cells of murine and human origin induced IL-

101 ition, depletion of SMYD5 in human colon and lung cancer cells results in increased tumor growth and

102 kappaB and Akt signaling pathways sensitizes lung cancer cells to cisplatin-induced apoptosis, we for

103 serve enhanced sensitivity of STK11-silenced lung cancer cells to the FDA-approved CDK4 inhibitor pal

104 ne tumor models, in primary human breast and lung cancer cells, and in deposited expression data.

105 acilitates CK2alpha binding to histone H4 in lung cancer cells, resulting in increased H4S1ph and epi

106 at mediated the interactions between MFs and lung cancer cells.

107 n BRAF-, NRAS-, KRAS-, EGFR-, and ALK-mutant lung cancer cells.

108 ced growth inhibition and apoptosis in human lung cancer cells.

109 ene expression in ZEB1-activated mesenchymal lung cancer cells.

110 ich increased cisplatin-induced apoptosis in lung cancer cells.

111 eration in vitro and tumor growth in vivo of lung cancer cells.

112 ed, CNTD2 was significantly overexpressed in lung cancer compared to adjacent normal tissue, and exhi

113 ous cell lung carcinoma in the International Lung Cancer Consortium (N=60,586, meta-analysis P=0.0095

114 [AUC]) between individuals with and without lung cancer (death), and (3) clinical usefulness (net be

115 articipants (1,925 lung cancer cases and 884 lung cancer deaths) and 80,672 Prostate, Lung, Colorecta

116 articipants (1,463 lung cancer cases and 915 lung cancer deaths).

117 a molecular biomarker, used to support early lung cancer detection, is appropriate for clinical use.

118 ential to improve the current state of early lung cancer detection.

119 y explain why female sex hormones accelerate lung cancer development.

120 up of 1,469,518 person-years, there were 738 lung cancer diagnoses.

121 logically confirmed limited-stage small-cell lung cancer, Eastern Cooperative Oncology Group performa

122 or polymetastatic extensive stage small-cell lung cancer (ES-SCLC) to the overall survival (OS).

123 cer cases in the Environment And Genetics in Lung cancer Etiology study, using the Infinium HumanMeth

124 73 patients with advanced non-small cell lung cancer from the prospective multicenter trials ACRI

125 These results demonstrate that lung cancers from black patients are similar to cancers

126 predicted clinical outcome in breast cancer, lung cancer, glioblastoma, and pancreatic cancer.

127 d that citrate administration inhibited A549 lung cancer growth and additional benefit accrued in com

128 ciation studies on genetic susceptibility to lung cancer have been published over the last two decade

129 e, the authors sequence multiple synchronous lung cancers, highlighting the evolutionary pressures th

130 ey element of cell migration and invasion in lung cancer; however, the underlying mechanisms are not

131 t neoplasms (HR = 1.06, 95% CI: 1.03, 1.09), lung cancer (HR = 1.08, 95% CI: 1.02, 1.14), ischemic he

132 We identified 277 cases of incident lung cancer in 21 666 participants with HIV.

133 me-wide association study (GWAS) analysis of lung cancer in 29,266 cases and 56,450 controls.

134 19-gene signature identified previously from lung cancer in a collection of 4,801 breast tumor gene e

135 tion of EMT-related traits and metastasis of lung cancer in part by modulation of Slug/ZEB2 signaling

136 ccupational pesticide use is associated with lung cancer in some, but not all, epidemiologic studies.

137 tients diagnosed with stage 1 non-small cell lung cancer in the NLST to a nationally representative c

138 revention, early detection, and treatment of lung cancer in the years ahead.

139 l studies have linked female sex hormones to lung cancer in women; however, the underlying mechanisms

140 ed as a prognostic marker for non-small cell lung cancer, in cerebrovascular pathogenesis of ischemic

141 Six-year lung cancer incidence and mortality risk predictions wer

142 nsitivity and specificity for predicting 6-y lung cancer incidence in the PLCO chest radiography arm,

143 ing pesticides evaluated was associated with lung cancer incidence.

144 iagnostic approaches to address mortality of lung cancer include improved early detection and stratif

145 nslated our findings to two murine models of lung cancer, including orthotopic human xenograft and Kr

146 rine models of small-cell and non-small cell lung cancers, including patient-derived xenograft and th

147 ar features in which mesenchymal, Ras-mutant lung cancer is acutely dependent on TBK1-mediated suppor

148 Small cell lung cancer is initially highly responsive to cisplatin

149 The pathobiology of early squamous lung cancer is poorly understood.

150 Lung cancer is the leading cause of cancer death in the

151 Lung cancer is the leading cause of cancer death in the

152 Lung cancer is the leading cause of cancer-related death

153 Lung cancer is the most frequent cause of cancer-related

154 This article reviews the major shifts in the lung cancer landscape over the past 100 years.

155 lly inactivated in lung cancer and precursor lung cancer lesions and further demonstrate that these r

156 As systemic therapies improve, patients with lung cancer live longer and thus are at increased risk f

157 orm MLNR when screen-diagnosed nonsmall cell lung cancer manifests as a subsolid nodule.

158 s utility in the treatment of non-small cell lung cancer metastases in the brain.

159 gh the development of an in vivo spontaneous lung cancer metastasis model, we show that the developme

160 ogically targetable effector of CD109-driven lung cancer metastasis.

161 he genetically engineered mutant KRAS-driven lung cancer models, CYD-2-11 suppressed malignant growth

162 ration, invasion, and metastasis in multiple lung cancer models.

163 ne kinase inhibitor-resistant non-small-cell lung cancer models.

164 2.5 mum (PM2.5)) on respiratory disease and lung cancer mortality is poorly understood.

165 ence a unique cohort of multiple synchronous lung cancers (MSLCs) to determine the relative diversity

166 ET done for IS or FOM in 81.0% and 73.5% for lung cancer (n = 148 and 136) and 69.4% and 67.5% for ot

167 Incident, primary, invasive lung cancers (n = 808) were ascertained by prospectively

168 ince the 1-year survival rates of small cell lung cancer, non-small cell lung cancer, and non-lung ca

169 e two predominant subtypes of non-small cell lung cancer (NSCLC) and are distinct in their histologic

170 t frequently mutated genes in non-small cell lung cancer (NSCLC) and is commonly comutated with oncog

171 is highly amplified in human non-small cell lung cancer (NSCLC) and is required for cancer cell grow

172 factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) are associated with poor prognosis.

173 r directed against HuR, using non-small cell lung cancer (NSCLC) as a model.

174 sly received radiotherapy for non-small-cell lung cancer (NSCLC) before receiving pembrolizumab.

175 (EBUS-TBNA) in patients with non-small cell lung cancer (NSCLC) can facilitate the selection of subs

176 rum proteins DSC curve of non-small cellular lung cancer (NSCLC) case is similar to the those of the

177 in (BRG1) occur frequently in non-small cell lung cancer (NSCLC) cells.

178 Non-small-cell lung cancer (NSCLC) demonstrates remarkable molecular di

179 the tumor microenvironment in non-small cell lung cancer (NSCLC) has not yet been adequately studied.

180 Multiple agents for advanced non-small-cell lung cancer (NSCLC) have been approved in the past decad

181 ckpoint inhibitor therapy for non-small-cell lung cancer (NSCLC) is just 20%.

182 d samples from advanced stage non-small cell lung cancer (NSCLC) patients (n = 29) receiving PD-1-tar

183 ong-term survival in resected non-small cell lung cancer (NSCLC) patients.

184 es with lower survival in 210 non-small cell lung cancer (NSCLC) patients.

185 in the treatment of advanced non-small-cell lung cancer (NSCLC) previously treated with chemotherapy

186 rapy for resected early-stage non-small-cell lung cancer (NSCLC) provides a modest survival benefit.

187 he plasma of 48 patients with non-small cell lung cancer (NSCLC) to detect EGFR mutations.

188 Among patients with non-small-cell lung cancer (NSCLC), data on intratumor heterogeneity an

189 sed to treat locally advanced non-small-cell lung cancer (NSCLC), IMRT and three-dimensional conforma

190 nced or incompletely resected non-small-cell lung cancer (NSCLC), it remains uncertain whether this a

191 genomically defined subset of non-small cell lung cancer (NSCLC), KRAS-mutant lung cancer.

192 ise in patients with advanced non-small-cell lung cancer (NSCLC), particularly with squamous cell his

193 ave improved the treatment of non-small-cell lung cancer (NSCLC), supporting the premise that evasion

194 specific prognostic genes for non-small cell lung cancer (NSCLC), we had previously proposed the Cox-

195 in the care of patients with non-small-cell lung cancer (NSCLC), yet cardiac injury after treatment

196 in patients with EGFR-mutant non-small-cell lung cancer (NSCLC).

197 vanced EGFR-mutation-positive non-small-cell lung cancer (NSCLC).

198 es of TP53, KRAS, and EGFR in non-small-cell lung cancer (NSCLC).

199 scription and tumor growth in non-small-cell lung cancer (NSCLC).

200 robust anti-tumor effect for non-small-cell lung cancer (NSCLC).

201 ic change in the treatment of non-small cell lung cancer (NSCLC).

202 alterations commonly found in non-small cell lung cancer (NSCLC).

203 th advanced, platinum-treated non-small-cell lung cancer (NSCLC).

204 ociated with worse outcome in non-small-cell lung cancer (NSCLC).

205 blood serum of patients with non-small cell lung cancer (NSCLC).

206 e have shown is important for non-small-cell lung cancer (NSCLC).

207 py for patients with stage IV non-small-cell lung cancer (NSCLC).

208 ment in the disease outcome of nonsmall cell lung cancer (NSCLC).

209 sequencing for patients with non-small cell lung cancer (NSCLC).

210 ients with previously treated non-small-cell lung cancer (NSCLC).

211 reviously reported that human non-small-cell lung cancers (NSCLCs) oxidize glucose in the tricarboxyl

212 Late-stage diagnosis of lung cancer occurs 95% of the time due to late manifest

213 may heighten immunotherapeutic responses in lung cancer, offering findings with immediate implicatio

214 ment inhibited tumor growth in 11/11 PDXs of lung cancer or melanoma without apparent toxicity in mic

215 lung cancer, with four loci associated with lung cancer overall and six loci associated with lung ad

216 ation of DNMT1 or KIT has been implicated in lung cancer pathogenesis, whether and how DNMT1 and KIT

217 cancer, non-small cell lung cancer, and non-lung cancer patients all dropped below 20%.

218 py combined with radiation in Non-Small Cell Lung Cancer patients for use in clinical trial design.

219 burden following treatment of ALK or ROS1(+) lung cancer patients with oncogene-targeted therapy ulti

220 down-regulated in lung adenocarcinomas from lung cancer patients, both at the mRNA and protein level

221 ntify radiosensitivity in 134 non-small-cell lung cancer patients, by using K-Means clustering to gro

222 atively correlates with disease prognosis in lung cancer patients.

223 ering AZD9291 and selumetinib to EGFR-mutant lung cancer patients.

224 , which may serve as a prognostic marker for lung cancer patients.

225 of erlotinib treatment in 50 non-small cell lung cancer patients.

226 s of CNTD2 and decreased overall survival in lung cancer patients.

227 nd dosimetry of (18)F-FAZA in non-small cell lung cancer patients.

228 CT scan in erlotinib-treated non-small cell lung cancer patients.

229 we show that female sex hormones can promote lung cancer progression via the RANK pathway.

230 tion serves as a critical immunomodulator in lung cancer progression, acting to drive immune escape v

231 AD, we examined the effects of Keap1 loss in lung cancer progression.

232 ed States (colon cancer: R = 0.61; P < .001; lung cancer: R = 0.73; P < .001; lymphoma: R = 0.51; P <

233 nd Fuyuan counties in China have the highest lung cancer rates in the world due to household air poll

234 cetaxel in previously treated non-small-cell lung cancer, regardless of PD-L1 expression or histology

235 r, its cause and mechanistic relationship to lung cancer remain unclear.

236 g cancer (SCLC), the most aggressive form of lung cancer, remain urgently needed.

237 to the time interval between non-small-cell lung cancer resection and the initiation of postoperativ

238 gulation of genes overexpressed in colon and lung cancers, respectively.

239 mpairs the progression of KRas(G12D) -driven lung cancer, resulting in a significant survival advanta

240 was associated with a 30% to 40% increase in lung cancer risk among men.

241 ations were used to estimate odds ratios for lung cancer risk associated with concentrations of inter

242 SNPs) in 43 genes of this TCPTP pathway with lung cancer risk by using summary data of six published

243 Purpose Several lung cancer risk prediction models have been developed,

244 Lung cancer risk was inversely related to duration of ex

245 847282 may be potential susceptible loci for lung cancer risk.

246 s been observed in blood cells and linked to lung cancer risk.

247 ations between proinflammatory cytokines and lung cancer risk.

248 n between an index of vitamin B6 levels with lung cancer risk.

249 ed/unmethylated DNA and in DNA from clinical lung cancer samples and matched normal tissue.

250 Small cell lung cancer (SCLC) is a devastating disease due to its p

251 es and xenografts of melanoma and small cell lung cancer (SCLC) origin.

252 Purpose Treating small-cell lung cancer (SCLC) remains a therapeutic challenge.

253 Small cell lung cancer (SCLC), as a proportion, makes up only 15-17

254 Effective targeted therapies for small-cell lung cancer (SCLC), the most aggressive form of lung can

255 are frequent oncogenic events in small cell lung cancer (SCLC).

256 Selection of candidates for lung cancer screening based on individual risk has been

257 pplying risk-based eligibility would improve lung cancer screening efficacy.

258 odel had better discrimination than standard lung cancer screening eligibility criteria (c-statistic

259 ion with low-dose computed tomography (LDCT) lung cancer screening is recommended in multiple clinica

260 fits, harms, and feasibility of implementing lung cancer screening policies based on risk prediction

261 ions has primarily been reserved for certain lung cancer screening trials rather than clinical practi

262 Lung cancer screening with low-dose CT can save lives.

263 ries need to set a timeline for implementing lung cancer screening.

264 detection of lung cancer with an emphasis on lung cancer screening.

265 ntly associated with a higher risk of future lung cancer.Significance: This large cohort study firmly

266 Lung cancer-specific mortality, all-cause mortality, and

267 lung cancer cells and promotes expansion of lung cancer stem-like cells, which is blocked by inhibit

268 xture model to three microarray datasets for lung cancer studies.

269 ryngeal cancer conducted in 1998-2000; and a lung cancer study conducted in 1988-1993 (Jockel et al.,

270 Canada, implemented a policy to regionalize lung cancer surgery at 14 designated hospitals, enforced

271 tivated to reduce length of stay (LOS) after lung cancer surgery, yet it is unclear if a routine of e

272 042522) showed significant associations with lung cancer susceptibility with strong cumulative epidem

273 ouble-positive human NCI-H358 non-small cell lung cancer target tumors over single-positive, non-targ

274 titumor response in a model of E7-expressing lung cancer than its unconjugated components.

275 ovel approach for the long-term treatment of lung cancer through TIC elimination.

276 Here, using human lung cancer tissue microarrays and fresh frozen tissues,

277 eport that PIPKIgamma is highly expressed in lung cancer tissues and its expression level is critical

278 n levels were significantly downregulated in lung cancer tissues compared with adjacent non-cancerous

279 Lung cancer treatment remains a challenge for clinical p

280 xl-expressing cell lines, and suppress H1299 lung cancer tumor growth in a mouse xenograft NOD-SCIDga

281 Overall, 509 lung cancer tumors specimens (319 adenocarcinomas; 142 s

282 Thus, small-cell lung cancer tumours generate their own microenvironment

283 ortality from all causes, heart disease, and lung cancer using the parametric g-formula.

284 erage cumulative exposure, increased risk of lung cancer was associated with low CD4 cell count (p tr

285 Small cell lung cancer was identified as an independent predictor o

286 , cigarette smoke, a leading risk factor for lung cancer, was also identified to be an important cont

287 To target KRas in lung cancers we used a systems approach of integrating a

288 q profiles of CTCs from breast, prostate and lung cancers, we observe consistent induction of beta-gl

289 n or radiologically suspected non-small cell lung cancer were prospectively enrolled in the study.

290 Incident lung cancers were identified through linkage with cancer

291 le gene expression dataset of non-small cell lung cancer when combined with the existing prior knowle

292 of GDH1 on AMPK is evident in LKB1-deficient lung cancer, where AMPK activation predominantly depends

293 omenon occurs in ALK-positive non-small cell lung cancer, where targeted therapies are used to inhibi

294 AU) in patients with head and neck cancer or lung cancer who have psychological distress.

295 We discuss prevention and early detection of lung cancer with an emphasis on lung cancer screening.

296 h EGFR-mutant or ALK-positive non-small-cell lung cancer with brain metastases now have the potential

297 tibility across the histological subtypes of lung cancer, with four loci associated with lung cancer

298 27 induces cooperative antitumor activity in lung cancer xenograft model in vivo.

299 eous HER3 overexpressing H441 non-small cell lung cancer xenograft.

300 is the leading cause of death in people with lung cancer, yet the molecular effectors underlying tumo