ライフサイエンスコーパス: lung adenocarcinoma

1 athways that are frequently altered in human lung adenocarcinoma.

2 tes of invasiveness and tumor progression to lung adenocarcinoma.

3 loci associated with EGFR mutation-positive lung adenocarcinoma.

4 utic target for the treatment of KRAS-driven lung adenocarcinoma.

5 y and helped differentiate among subtypes of lung adenocarcinoma.

6 by suppressing Wnt/beta-catenin signaling in lung adenocarcinoma.

7 ions for newly diagnosed stage IV (T2aN2M1b) lung adenocarcinoma.

8 eonine kinase and a commonly mutated gene in lung adenocarcinoma.

9 in two fully immunocompetent mouse models of lung adenocarcinoma.

10 fication of clinically-relevant mutations in lung adenocarcinoma.

11 rby CT-ncRNA have a role in tumorigenesis in lung adenocarcinoma.

12 Oncogenic KRAS mutations occur frequently in lung adenocarcinoma.

13 her susceptibility to EGFR mutation-positive lung adenocarcinoma.

14 ignificantly associated with poor outcome in lung adenocarcinoma.

15 l response in preclinical models of EML4-ALK lung adenocarcinoma.

16 in the external controls and the cohort with lung adenocarcinoma.

17 ding small RNAs in an induced mouse model of lung adenocarcinoma.

18 pants without cancer and 1,312 patients with lung adenocarcinoma.

19 e most common malignant finding is a primary lung adenocarcinoma.

20 orrelates with poor outcome of patients with lung adenocarcinoma.

21 presentative of the genomic heterogeneity in lung adenocarcinoma.

22 of the key findings from genomic studies of lung adenocarcinoma.

23 t also novel targets in breast carcinoma and lung adenocarcinoma.

24 bitors in individuals with EML4-ALK-positive lung adenocarcinoma.

25 gnificantly different between populations in lung adenocarcinoma.

26 termining if a pulmonary nodule is a primary lung adenocarcinoma.

27 linical subgroups, as well as within stage I lung adenocarcinoma.

28 BT-1) may be a potential antitumor agent for lung adenocarcinoma.

29 ute to the pro-oncogenic activity of CDK5 in lung adenocarcinoma.

30 n important therapeutic target in metastatic lung adenocarcinoma.

31 s have a strong negative prognostic value in lung adenocarcinoma.

32 cancer overall and six loci associated with lung adenocarcinoma.

33 ificantly overexpressed in SCLC, compared to lung adenocarcinoma.

34 mor grade and poor survival in patients with lung adenocarcinoma.

35 KRAS gene mutation causes lung adenocarcinoma.

36 ificantly higher levels in SCLC, compared to lung adenocarcinoma.

37 r the racial groups in five cancers, such as lung adenocarcinoma.

38 MT) has been linked to the TKI resistance in lung adenocarcinoma.

39 ity as a biomarker and therapeutic target in lung adenocarcinoma.

40 mutation and transcript were most common in lung adenocarcinoma.

41 lncRNAs and their potential target genes in lung adenocarcinoma.

42 t are selectively upregulated in KRAS-mutant lung adenocarcinomas.

43 nt mesothelioma and pancreatic, ovarian, and lung adenocarcinomas.

44 mutational frequency than observed in human lung adenocarcinomas.

45 favorable prognosis associated with TTF-1(+) lung adenocarcinomas.

46 3 activity promotes the progression of human lung adenocarcinomas.

47 erapeutic target for the treatment of deadly lung adenocarcinomas.

48 tigen burden and overall survival in primary lung adenocarcinomas.

49 e accurate than frozen section in diagnosing lung adenocarcinomas.

50 alue for intraoperative diagnosis of primary lung adenocarcinomas.

51 orescent contrast agent specific for primary lung adenocarcinomas.

52 rid EMT phenotype and invasive properties of lung adenocarcinomas.

53 rs and potentially targetable alterations in lung adenocarcinomas.

54 ctive of survival in independent datasets of lung adenocarcinomas.

55 anagement of incidentally or screen-detected lung adenocarcinomas.

56 r diverse solid tumors, including breast and lung adenocarcinomas.

57 of known cancer gene mutations in localized lung adenocarcinomas.

58 tsurgical relapse in patients with localized lung adenocarcinomas.

59 Actionable drivers were detected in 64% of lung adenocarcinomas.

60 between miR-34 and full-length HDM4 in human lung adenocarcinomas.

61 d the location of Thy-1(+) CAFs within human lung adenocarcinomas.

62 features in CT images of 258 non-small cell lung adenocarcinomas.

63 tumor phenotype in patients with KRAS mutant lung adenocarcinomas.

64 umour progression when activated in advanced lung adenocarcinomas.

65 quently occur in pancreatic, colorectal, and lung adenocarcinomas.

66 neck cancer (1.0%), low-grade glioma (1.5%), lung adenocarcinoma (1.6%), lung squamous cell carcinoma

67 agnosis of cancer in 8 (6.9%) individuals (2 lung adenocarcinomas, 1 osteosarcoma, 1 sarcoma, 1 astro

68 ohort included 316 consecutive patients with lung adenocarcinoma (225 men; 258 smokers) studied from

69 Lung adenocarcinoma, a major form of non-small cell lung

70 m to profile differential splicing events in lung adenocarcinoma A549 cells after downregulation of t

71 -lethal phenotype of ADAR1 deletion in human lung adenocarcinoma A549 cells is rescued by CRISPR/Cas9

72 cluding human hepatocarcinoma (Huh-7), human lung adenocarcinoma (A549), and human fibrosarcoma (HT10

73 gh level of expression of miR-155 in a human lung adenocarcinoma A549R cell line that is highly resis

74 Lung adenocarcinoma accounts for approximately 40% of lu

75 To compare lung adenocarcinoma (ADC) and lung squamous cell carcino

76 tial reactive oxygen species (ROS) levels in lung adenocarcinoma (ADC) and squamous cell carcinoma (S

77 The mechanisms by which TGF-beta promotes lung adenocarcinoma (ADC) metastasis are largely unknown

78 e, we demonstrate lineage switching of KRAS+ lung adenocarcinomas (ADC) to squamous cell carcinoma (S

79 ular mobility, migration, and invasion using lung adenocarcinoma (AdCA) cells with modified HIP1 expr

80 show that small cell lung cancer (SCLC) and lung adenocarcinoma (ADCA) exhibit unique immune cell co

81 evels in approximately half of Keap1-mutated lung adenocarcinomas (ADs).

82 und in both lung squamous cell carcinoma and lung adenocarcinoma, although mouse models of FGFR-drive

83 n white patients for all cancer types except lung (adenocarcinoma and squamous cell carcinoma) and co

84 apanese patients with EGFR mutation-positive lung adenocarcinoma and 15,158 controls.

85 ar the exon 14 splice sites are recurrent in lung adenocarcinoma and cause exon skipping (METDelta14)

86 ass cytometry to study immune infiltrates in lung adenocarcinoma and clear cell renal cell carcinoma,

87 The novel method was evaluated on lung adenocarcinoma and endocrine receptor positive brea

88 n in a genetically engineered mouse model of lung adenocarcinoma and found that Treg cells suppressed

89 th reduced overall survival of patients with lung adenocarcinoma and glioblastoma.

90 ZIKV infection in two human cell lines: A549 lung adenocarcinoma and HuH-7 hepatoma cells, and for pr

91 a region of genomic amplification present in lung adenocarcinoma and is most highly expressed in well

92 AS-MAPK dependence as a hallmark of EML4-ALK lung adenocarcinoma and provide a rationale for the upfr

93 stained histopathology whole-slide images of lung adenocarcinoma and squamous cell carcinoma patients

94 dy investigated the pattern of recurrence of lung adenocarcinoma and the predictive value of histolog

95 rmined that miR-31 is overexpressed in human lung adenocarcinoma and this overexpression independentl

96 METTL3 expression is elevated in lung adenocarcinoma and using both loss- and gain-of-fun

97 gulated lncRNAs in lung cancer utilizing 461 lung adenocarcinomas and 156 normal lung tissues from 3

98 at the protein level in approximately 20% of lung adenocarcinomas and 35% of squamous cell carcinomas

99 BRAF(V600E) mutation occurs in 1-2% of lung adenocarcinomas and acts as an oncogenic driver.

100 put microfluidic platform, to assess primary lung adenocarcinomas and human fibroblasts undergoing re

101 this study we analyse genomic profiles of 15 lung adenocarcinomas and one regional lymph node metasta

102 important therapeutic target in KRAS-mutant lung adenocarcinomas and pinpoint new potential targets.

103 complexity of the immune infiltrate in human lung adenocarcinomas and renal cell carcinomas can be re

104 In human lung adenocarcinomas and squamous cell carcinomas, membr

105 to the cytosol in U251 (glioblastoma), A549 (lung adenocarcinoma) and MDA-MB-231(breast cancer).

106 ng glioblastoma, astrocytoma, neuroblastoma, lung adenocarcinoma, and breast cancer.

107 ies including respiratory distress syndrome, lung adenocarcinoma, and debilitating fibrotic diseases,

108 tifies Setd2 as a potent tumor suppressor in lung adenocarcinoma, and establishes model systems to fa

109 t Ipo11 loss results in degradation of Pten, lung adenocarcinoma, and neoplasia in mouse prostate wit

110 pression correlates with worse prognosis for lung adenocarcinoma, and that a three-gene expression si

111 function and dominant-negative activity) in lung adenocarcinoma are unclear.

112 Approximately 1% of lung adenocarcinomas are driven by oncogenic ROS1 rearra

113 ll composition is fundamentally different in lung adenocarcinoma as compared with lung squamous cell

114 In a murine model of lung adenocarcinoma, ASM deficiency reduced tumor develo

115 at levels of S1PR3 are up-regulated in human lung adenocarcinomas, at least in part due to the TGF-be

116 DNA damage response kinase ATM are common in lung adenocarcinoma but directly targeting these with dr

117 In cultured lung adenocarcinoma but not in normal lung epithelial ce

118 ifying genes are frequently mutated in human lung adenocarcinoma, but the functional impact of these

119 type Braf allele prevents the development of lung adenocarcinoma by inducing a further increase in MA

120 The classification for invasive lung adenocarcinoma by the International Association for

121 rrelated with poor survival in patients with lung adenocarcinoma cancer (ADC).

122 Here we investigated lung adenocarcinoma cancer cells (344SQ) and endothelial

123 e been reported in only approximately 55% of lung adenocarcinoma cases in the United States, suggesti

124 mall GTPase gene RIT1 in approximately 2% of lung adenocarcinoma cases that cluster in a hotspot near

125 To qualify the device, we used a human lung adenocarcinoma cell line (A549) that was cultivated

126 d invasion and replication assays with human lung adenocarcinoma cell line A549.

127 patients with non-small cell lung cancer and lung adenocarcinoma cell lines, and SMARCD1 and miR-7 ex

128 ) are increased in a panel of cultured human lung adenocarcinoma cell lines, and that S1PR3-mediated

129 hibited proliferation of erlotinib-resistant lung adenocarcinoma cells (H1975) bearing the T790M EGFR

130 induced dose-dependent cytotoxicity in A549 lung adenocarcinoma cells and MA148 ovarian cancer cells

131 in treatment in a xenograft model using A549 lung adenocarcinoma cells did not result in a statistica

132 D1067V) and in NIH-3T3 and human EGFR-mutant lung adenocarcinoma cells engineered to express this mut

133 ession of S1PR3 promotes the growth of human lung adenocarcinoma cells in animals.

134 ion, soft agar growth, and invasion of human lung adenocarcinoma cells in vitro In the present study,

135 ne treatment in a xenograft model using A549 lung adenocarcinoma cells resulted in decreased tumor vo

136 nhibition of H2S-producing enzymes sensitize lung adenocarcinoma cells to chemotherapeutic agents via

137 ne the role of miR-378 in the sensitivity of lung adenocarcinoma cells to cisplatin (cDDP) and its wo

138 VGF silencing resensitized EGFR-mutated lung adenocarcinoma cells to TKI.

139 ant processes, and designate macrophages and lung adenocarcinoma cells, as potential sources of PGE2.

140 In the EGFR-mutant lung adenocarcinoma cells, expression of PIK3Cbeta(D1067

141 ne, enhanced the metastatic dissemination of lung adenocarcinoma cells.

142 EMT, and cancer dissemination in a subset of lung adenocarcinoma cells.

143 presses critical bioenergetics parameters in lung adenocarcinoma cells.

144 ble the chemoresistance against cisplatin in lung adenocarcinoma cells.

145 -stressed human and mouse melanoma and human lung adenocarcinoma cells.

146 n a CD63/PI3K/AKT/HIF-1-dependent pathway in lung adenocarcinoma cells.

147 latin-sensitive and cisplatin-resistant A549-lung adenocarcinoma cells.

148 human and murine SCLC cell lines, but not in lung adenocarcinoma cells.

149 ions in primary alveolar epithelium and A549 lung adenocarcinoma cells.

150 The new lung adenocarcinoma classification based on predominant

151 By studying lung adenocarcinoma clinical specimens and preclinical m

152 carrier frequency was 1.1% in patients with lung adenocarcinoma compared with 0.18% in controls (P =

153 a (Kras(LA1)), here we postulated that human lung adenocarcinomas containing Thy-1(+) CAFs have a wor

154 io (OR) = 2.78] is interpreted as the OR for lung adenocarcinoma corresponding to a 1000 bp increase

155 processing of The Cancer Genome Atlas (TCGA) Lung Adenocarcinoma dataset called known driver mutation

156 e proposed method to The Cancer Genome Atlas lung adenocarcinoma dataset to jointly explore associati

157 Here we show that mouse and human lung adenocarcinomas display hierarchical features with

158 Atm deletion in mouse models of Kras-mutant lung adenocarcinoma does not affect cisplatin responses.

159 ome sequencing of tumors from three GEMMs of lung adenocarcinoma driven by mutant epidermal growth fa

160 Lung adenocarcinoma driven by somatic EGFR mutations is

161 d in activation of the PI3K pathway in human lung adenocarcinomas driven by EGFR mutations.

162 are mutually exclusive with all other known lung adenocarcinoma driver mutations.

163 at peptic ulcers, would be effective against lung adenocarcinoma (Figure 4C and D).

164 ens the spectrum of CT antigens expressed in lung adenocarcinomas for clinical applications.

165 gene expression data in breast carcinoma and lung adenocarcinoma from The Cancer Genome Atlas (TCGA).

166 expression is dramatically down-regulated in lung adenocarcinomas from lung cancer patients, both at

167 Lung adenocarcinomas from never smokers account for appr

168 ned mutation status in 10 oncogenes among 89 lung adenocarcinomas from never smokers.

169 Thus, lung adenocarcinoma functions as a potent endogenous cir

170 Eligible patients had stage IV lung adenocarcinoma, had ROS1 rearrangement according to

171 Approximately half of lung adenocarcinomas harbor mutations in TP53 (p53), mak

172 Here we demonstrate in models of lung adenocarcinoma harboring the oncogenic fusion of AL

173 The Cancer Genome Atlas analysis of lung adenocarcinoma has identified a large number of pre

174 e enriched in genes that predict outcomes in lung adenocarcinoma, implicating these subpopulations as

175 sion of the orthologous mouse allele induced lung adenocarcinoma in a novel, immunocompetent mouse mo

176 end the catalogue of regions associated with lung adenocarcinoma in non-smoking Asian women and highl

177 to the human BRAF(D594A) mutation) triggers lung adenocarcinoma in vivo, indicating that BRAF-inacti

178 loyed an orthotopic immunocompetent model of lung adenocarcinoma in which murine lung cancer cells ar

179 d to express an oncogenic Kras(G12D) develop lung adenocarcinomas in a manner analogous to humans.

180 n the nonmetastatic and metastatic states in lung adenocarcinoma, including up-regulated expression o

181 ow in mice and cancer patients (n = 70) that lung adenocarcinomas increase bone stromal activity in t

182 rca4 (Brg1) or Arid1a had complex effects on lung adenocarcinoma initiation and progression.

183 llows the noninvasive risk stratification of lung adenocarcinomas into three groups with distinct pos

184 These data clearly suggest that lung adenocarcinoma is associated with distinct genomic

185 covered that poor patient prognosis in human lung adenocarcinoma is associated with low miR-26 and hi

186 Lung adenocarcinoma is comprised of distinct mutational

187 ting oncogenic event in almost half of human lung adenocarcinomas is still unknown, a fact that compl

188 asion in a murine model of Kras(G12D)-driven lung adenocarcinoma (Kras(LA1)), here we postulated that

189 tions in BRAF occur in approximately 2-7% of lung adenocarcinoma (LA), BRAF-mutant LA is the most fre

190 Several lung adenocarcinoma (LAD) cell lines were screened to ch

191 , a key driver of stemness, in KRAS-mediated lung adenocarcinoma (LADC).

192 We show that stage I lung adenocarcinoma lesions already harbor significantly

193 trategy to map the immune landscape of early lung adenocarcinoma lesions to search for tumor-driven i

194 In clinical specimens of lung adenocarcinoma, low KLF10 expression associated wit

195 the model using EGFR-gefitinib treatment for Lung Adenocarcinoma (LUAD) and Lung Squamous Cell Cancer

196 omatic gene mutation rate difference between lung adenocarcinoma (LUAD) and lung squamous cell carcin

197 their trends in predicting poor prognosis in lung adenocarcinoma (LUAD) but not in lung squamous cell

198 Lung adenocarcinoma (LUAD) is the most common histologic

199 Treating KRAS-mutant lung adenocarcinoma (LUAD) remains a major challenge in

200 chanisms underlying the propensity of latent lung adenocarcinoma (LUAD) to relapse are poorly underst

201 that the ion channel TRPA1 is implicated in lung adenocarcinoma (LUAD), where its role and mechanism

202 ng cancer, we analyzed RNA-Seq data from 461 lung adenocarcinomas (LUAD) and 156 normal lung tissues.

203 Human lung adenocarcinomas (LUAD) contain mutations in EGFR in

204 ial impact of 19 well-defined DCAFs in human lung adenocarcinomas (LuADCs) using integrative omics an

205 promoting cancer cell invasive phenotypes in lung adenocarcinoma, lung squamous cell carcinoma and br

206 found that PCBP4-deficient mice are prone to lung adenocarcinoma, lymphoma, and kidney tumor and that

207 A myriad of genetic changes accompany lung adenocarcinomas, many of which are poorly understoo

208 cell migration and metastasis in EMT-driven lung adenocarcinoma models.

209 Here, using lung adenocarcinoma mouse models, including genetic mode

210 plifications of super-enhancers 3' to MYC in lung adenocarcinoma (MYC-LASE) and endometrial carcinoma

211 Pathologically classified resected lung adenocarcinomas (n = 41) with thin-section CT data

212 n=1]); and four patients (8%) receiving BAT (lung adenocarcinoma [n=1], myelofibrosis [n=1], and seps

213 their parametric CANARY signatures, all the lung adenocarcinoma nodules were risk stratified into th

214 s are no more similar to each other than are lung adenocarcinomas of different patients from TCGA coh

215 Here, we show that lung adenocarcinoma operates as an endogenous reorganize

216 rwhelmingly higher frequencies of developing lung adenocarcinoma or ground-glass opacity lung lesions

217 ncreased significantly in human specimens of lung adenocarcinoma or patient serum.

218 nificantly associated with increased risk of lung adenocarcinoma (P = 6.3 x 10(-15)), even after excl

219 here may shed light into normal biology and lung adenocarcinoma pathogenesis, and be valuable for di

220 in the pancreatic ductal adenocarcinoma and lung adenocarcinoma patient cohorts from The Cancer Geno

221 he transcription factor ARNTL2 predicts poor lung adenocarcinoma patient outcome.

222 t-derived xenograft (PDX) tumor cells from a lung adenocarcinoma patient tumor xenograft.

223 d a large cohort of resected tumors from 442 lung adenocarcinoma patients with data including annotat

224 CL2 are co-regulated with MDSC/M2 markers in lung adenocarcinoma patients.

225 d a risk score representing expression of 69 lung adenocarcinoma-prognostic genes, classified PDX cel

226 cant correlation of LSD1 overexpression with lung adenocarcinoma progression and metastasis.

227 lar states that stochastically evolve during lung adenocarcinoma progression.

228 Expression profiling of 182 cases of lung adenocarcinoma proved a significant correlation of

229 N may be a unique target for KRAS-associated lung adenocarcinoma remediation.

230 an syndrome (NS), and drive proliferation of lung adenocarcinomas, respectively, akin to RAS mutation

231 Specifically, we found that KRAS/LKB1-mutant lung adenocarcinomas responded strongly to phenformin +

232 Whole-genome sequencing analysis of lung adenocarcinomas revealed noncoding somatic mutation

233 ate associations by EGFR mutation status for lung adenocarcinoma risk among never-smoking Asian women

234 hat genetic determinants of long TL increase lung adenocarcinoma risk avoids issues with reverse caus

235 shown to be strongly associated with overall lung adenocarcinoma risk in East Asians, were re-discove

236 mely, rs7216064 (17q24.3, BPTF), for overall lung adenocarcinoma risk, and rs3817963 (6p21.3, BTNL2)

237 cing telomere biology are also implicated in lung adenocarcinoma risk.

238 ur finding suggests that longer TL increases lung adenocarcinoma risk.

239 two large-scale NGS benchmark datasets: 183 lung adenocarcinoma samples and 121 melanoma samples.

240 o findings, immunohistochemistry analysis of lung adenocarcinoma samples showed that expression level

241 By analysing 3668 breast cancer and 1692 lung adenocarcinoma samples, we further demonstrate that

242 enome Atlas (TCGA) whole-exome sequencing of lung adenocarcinoma samples.

243 sted tumors and 2/64 additional never smoker lung adenocarcinoma samples.

244 was also found in vivo in a large dataset of lung adenocarcinoma samples.

245 Therefore, lung adenocarcinomas select for expression of a pathway

246 rearrangement, suggesting that patients with lung adenocarcinomas should be tested for ROS1.

247 egrin beta3 axis, was also detected in human lung adenocarcinoma specimens.

248 sent study, we examine S1PR3 levels in human lung adenocarcinoma specimens.

249 pective 294 eligible patients diagnosed with lung adenocarcinoma spectrum lesions in the low-dose CT

250 riptome analysis of 153 samples representing lung adenocarcinomas, squamous cell carcinomas, large ce

251 egmentation techniques to help differentiate lung adenocarcinoma subtypes.

252 ciates with clonal TCA/T-biased mutations in lung adenocarcinoma suggesting this enzyme makes broader

253 In a mouse xenograft model of lung adenocarcinoma, suppressing VGF expression was suff

254 and antioxidant enzyme levels are higher in lung adenocarcinoma than in normal tissues.

255 ribe a transgenic mouse model of KRAS-driven lung adenocarcinoma that affords reversible activation o

256 astasis in a mouse model of Kras/Tp53-mutant lung adenocarcinoma that develops metastatic disease due

257 show, using primary cell cultures from human lung adenocarcinoma, that the effectors of the Hippo pat

258 CAF-enriched tumors in a compendium of 1,586 lung adenocarcinomas, the presence of the 425-gene signa

259 ival of patients with EGFR mutation-positive lung adenocarcinoma through an analysis of data from two

260 Here we show that human lung adenocarcinoma tissue expresses high levels of hydr

261 umors with reduced IRS-1 staining in a human lung adenocarcinoma tissue microarray displayed a signif

262 lso observed in genetically engineered mouse lung adenocarcinoma tissues (Kras(G12D); Trp53(R172H/+);

263 we confirmed that GPC5 was downregulated in lung adenocarcinoma tissues compared with adjacent norma

264 Analysis of human lung adenocarcinoma tissues revealed that the cDDP sensi

265 that loss or reduced expression of IL-37 in lung adenocarcinoma tissues was significantly associated

266 nes in two Kras(G12D)-driven mouse models of lung adenocarcinoma to characterize the impact of their

267 For example, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and myocardial

268 nscripts including the metastasis associated lung adenocarcinoma transcript 1 (Malat1) and several sm

269 d long non-coding RNA, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in OSCC.

270 Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a broadly e

271 6)A site in the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was recently s

272 Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a cancer-prom

273 Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-co

274 oncoding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (Malat1), in ischemic s

275 Malat1 (metastasis-associated lung adenocarcinoma transcript 1) is among the most abun

276 anscript 1) or MALAT1 (metastasis associated lung adenocarcinoma transcript 1), long noncoding RNAs (

277 d-type, and TLR7-deficient mice grafted with lung adenocarcinoma tumor cells leads to increased tumor

278 ed, alone or in combination, in about 80% of lung adenocarcinoma tumors.

279 lue of histologic classification in resected lung adenocarcinoma using the new International Associat

280 on, and therapeutic response of EGFR-induced lung adenocarcinomas using tetracycline- and tamoxifen-i

281 ast low-dose CT scan before the diagnosis of lung adenocarcinoma was analyzed using CANARY blinded to

282 ion of 573 patients undergoing resection for lung adenocarcinoma was determined according to the IASL

283 cancer types and single-cell RNA-seq data of lung adenocarcinoma, we confirmed an anticorrelation bet

284 els for pancreatic ductal adenocarcinoma and lung adenocarcinoma, we found that abrogating SMYD3 cata

285 dates in 242 patients with oncogene-negative lung adenocarcinomas, we find that two (AKT2 and TFDP2)

286 post-transcriptional changes that accompany lung adenocarcinomas, we took an omics approach in profi

287 with EGFR mutation-positive stage IIIB or IV lung adenocarcinoma were enrolled in LUX-Lung 3 (n=345)

288 il 30, 2016, 26 patients with RET-rearranged lung adenocarcinomas were enrolled and given cabozantini

289 inhibitors, while Kras (G12D) -driven murine lung adenocarcinomas were resistant against these compou

290 f S1PR3 are significantly increased in human lung adenocarcinomas when compared with normal lung epit

291 600Glu) mutations are found in about 1-2% of lung adenocarcinomas, which might provide an opportunity

292 R mutation-positive advanced (stage IIIb-IV) lung adenocarcinomas who were given afatinib in a single

293 One patient with advanced-stage lung adenocarcinoma, who was treated with oral sorafenib

294 hologically confirmed stage IIIB or stage IV lung adenocarcinoma with a confirmed, activating EGFR mu

295 r a family with an unusually high density of lung adenocarcinoma with available DNA from the affected

296 ated YAP1 R331W as an allele predisposed for lung adenocarcinoma with high familial penetrance.

297 Treatment of mice bearing the LP07 lung adenocarcinoma with IND inhibited the suppressive a

298 ed tumor barcoding in a mouse model of human lung adenocarcinoma with unbiased genomic approaches to

299 ultiple genetic factors underlie the risk of lung adenocarcinomas with EGFR mutations.

300 nd 13 reduced the growth rates of A549 human lung adenocarcinoma xenografts with no evidence of syste

301 nodeficiency mice bearing H2009 tumor (human lung adenocarcinoma) xenografts.