ライフサイエンスコーパス: lung adenocarcinoma

1 nine SF3B1 wild-type tumors (including five lung adenocarcinomas).

2 ivo and in most individuals with EGFR-mutant lung adenocarcinoma.

3 s may cooperate in the pathogenesis of human lung adenocarcinoma.

4 KLK5 is similarly prognostic for outcome in lung adenocarcinoma.

5 ll cell lung cancer, particularly those with lung adenocarcinoma.

6 nd its role in the metastatic progression of lung adenocarcinoma.

7 adenocarcinoma are the pre-invasive forms of lung adenocarcinoma.

8 xpression correlates with a worse outcome in lung adenocarcinoma.

9 rities and differences between OPA and human lung adenocarcinoma.

10 emness and risk of metastatic progression in lung adenocarcinoma.

11 2 and PYCR1 levels are markedly increased in lung adenocarcinoma.

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

13 mutation and transcript were most common in lung adenocarcinoma.

14 fication of clinically-relevant mutations in lung adenocarcinoma.

15 orrelates with poor outcome of patients with lung adenocarcinoma.

16 gnificantly different between populations in lung adenocarcinoma.

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

18 cancer overall and six loci associated with lung adenocarcinoma.

19 ificantly overexpressed in SCLC, compared to lung adenocarcinoma.

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

21 KRAS gene mutation causes lung adenocarcinoma.

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

23 in tissue pathology images of patients with lung adenocarcinoma.

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

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

26 lncRNAs and their potential target genes in lung adenocarcinoma.

27 athways that are frequently altered in human lung adenocarcinoma.

28 tes of invasiveness and tumor progression to lung adenocarcinoma.

29 rly stage, predominantly female, non-smoking lung adenocarcinoma.

30 loci associated with EGFR mutation-positive lung adenocarcinoma.

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

32 y and helped differentiate among subtypes of lung adenocarcinoma.

33 vage therapy of patients with advanced-stage lung adenocarcinoma.

34 oxylin and eosin-stained pathology images in lung adenocarcinoma.

35 d lung epithelial cells to model early-stage lung adenocarcinoma.

36 tations of the metalloproteinase ADAMTS12 in lung adenocarcinoma.

37 esent nonmetastatic and metastatic states of lung adenocarcinoma.

38 s for management of early stage never-smoker lung adenocarcinoma.

39 e highest mutation frequency in BRAF gene in lung adenocarcinoma.

40 tumor growth in a mouse model of KRAS-mutant lung adenocarcinoma.

41 and antidepressants) and one attributable to lung adenocarcinoma.

42 e naturally occurring animal model for human lung adenocarcinoma.

43 umour progression when activated in advanced lung adenocarcinomas.

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

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

46 tumor phenotype in patients with KRAS mutant lung adenocarcinomas.

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

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

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

50 cancer-1 (ALAL-1) as frequently amplified in lung adenocarcinomas.

51 cians seeking to better understand and treat lung adenocarcinomas.

52 of the most common activating alterations in lung adenocarcinoma(1,2).

53 allmark of cancer and a prevalent feature of lung adenocarcinoma(1-3).

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

55 We analyzed 40 patients diagnosed with lung adenocarcinoma (20 short-term and 20 long-term surv

56 compared smoking-related DNA methylation in lung adenocarcinoma (61 never smokers, 91 current smoker

57 rently under evaluation for the treatment of lung adenocarcinoma(7-9).

58 that mice exposed to ECS for 54 wk developed lung adenocarcinomas (9 of 40 mice, 22.5%) and bladder u

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

60 ll lines: acute monocytic leukemia THP-1 and lung adenocarcinoma A549.

61 the synthesis of specific proteins in human lung adenocarcinoma (A549) cells in which eEF2K had been

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

63 Lung adenocarcinoma accounts for approximately 40% of lu

64 -based predictive model for the prognosis of lung adenocarcinoma (ADC) patients across multiple indep

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

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

67 er prevalence of PTPRT and JAK2 mutations in lung adenocarcinomas among African Americans compared wi

68 -cell RNA-seq profiles of cells derived from lung adenocarcinoma and breast cancer patients into a mu

69 hat MCL-1 gains occur with high frequency in lung adenocarcinoma and can be targeted therapeutically.

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

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

72 Using murine models of lung adenocarcinoma and coccidoidomycosis, we found that

73 OPA to previously published data from human lung adenocarcinoma and found a large degree of overlap

74 nsgenic mouse models of EGFR(L858R) -induced lung adenocarcinoma and found that it is mediated largel

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

76 pharmacologic approaches on syngeneic mouse lung adenocarcinoma and human lung adenocarcinoma xenogr

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

78 revealed loss of Mst1/2 promotes aggressive lung adenocarcinoma and large-scale proteomic analysis r

79 Lung adenocarcinoma and lung squamous cell carcinoma pat

80 rations of SUGP1 genocopy SF3B1 mutations in lung adenocarcinoma and other cancers.

81 o boost immune infiltration and responses in lung adenocarcinoma and potentially other aggressive can

82 we show that PINCH-1 is highly expressed in lung adenocarcinoma and promotes proline synthesis throu

83 transcriptional regulator Id1 in KRAS-mutant lung adenocarcinoma and provide mechanistic insight into

84 eatic islet cells, and (iii) metaanalysis of lung adenocarcinoma and renal transplant rejection trans

85 l PRSS3/mesotrypsin-KLK5 signaling module in lung adenocarcinoma and reveal the potential therapeutic

86 allenging due to the heterogeneous nature of lung adenocarcinoma and the subjective criteria for eval

87 iagnosed with a new right upper lobe stage I lung adenocarcinoma and underwent video-assisted thoraco

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

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

90 Current observations that ECS induces lung adenocarcinomas and bladder urothelial hyperplasia,

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

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

93 ting KRAS(G12C), a mutation found in ~13% of lung adenocarcinomas and, at a lower frequency, in other

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

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

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

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

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

99 including colon, breast, prostate, pancreas, lung adenocarcinoma, and squamous cell carcinoma) for th

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

101 rognostic for poor outcome for patients with lung adenocarcinoma, and that genetic or pharmacologic t

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

103 Here we show that human primary lung adenocarcinomas are characterized by the emergence

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

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

106 rly marked survival effects in patients with lung adenocarcinoma, bladder cancer, low-grade glioma, a

107 Brain metastases from lung adenocarcinoma (BM-LUAD) frequently cause patient m

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

109 gets for tyrosine kinase inhibitors (TKI) in lung adenocarcinoma, but acquired resistance to TKIs ine

110 In lung adenocarcinoma, but not lung squamous cell carcinom

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

112 robiota provoke inflammation associated with lung adenocarcinoma by activating lung-resident gammadel

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

114 ain, shows potential antitumor activities in lung adenocarcinoma by uniquely targeting a HIF1alpha/LE

115 ned in a subset of surgically resected human lung adenocarcinomas by multispectral imaging, which pro

116 n-Darby canine kidney subclone II, and human lung adenocarcinoma [Calu-3] cells).

117 logic targeting of PRSS3/mesotrypsin reduces lung adenocarcinoma cell invasiveness and proliferation.

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

119 Using a human lung adenocarcinoma cell line, we show pharmacologic inh

120 we show that knocking down the hGMPK gene in lung adenocarcinoma cell lines decreases cellular viabil

121 apoptotic responses across a panel of human lung adenocarcinoma cell lines.

122 The crucial role of hMATE1 was validated in lung adenocarcinoma cells (A549), which expresses high l

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

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

125 nd depletion of SOX9 in Hdac10 knockout (KO) lung adenocarcinoma cells inhibited growth of tumorspher

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

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

128 Highly tumorigenic and stem-like lung adenocarcinoma cells were increased in Hdac10-delet

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

130 nchronization and biochemical experiments in lung adenocarcinoma cells, revealing a link between CYP2

131 idermal growth factor receptor (EGFR)-mutant lung adenocarcinoma cells, we demonstrate that residual

132 uman hepatocarcinoma cells and HCC4006 human lung adenocarcinoma cells.

133 by fibroblasts on proliferation of malignant lung adenocarcinoma cells.

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

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

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

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

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

139 g contributed to SOX9 induction in Hdac10 KO lung adenocarcinoma cells.

140 By studying lung adenocarcinoma clinical specimens and preclinical m

141 vely correlated with high CCL2 expression in lung adenocarcinoma, conferring a worse overall patient

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

143 els (GEMMs) of KRAS-dependent pancreatic and lung adenocarcinomas converts preneoplastic lesions into

144 We applied our method to the lung adenocarcinoma dataset from TCGA and identified spl

145 C neuroblastoma dataset and the NIH/NCI TCGA lung adenocarcinoma dataset).

146 lidated the model in The Cancer Genome Atlas lung adenocarcinoma dataset, in which the predicted high

147 As expected, neoantigen expression during lung adenocarcinoma development leads to T cell-mediated

148 nic KRAS is the most common driving event in lung adenocarcinoma development.

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

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

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

152 In EGFR-mutated lung adenocarcinoma, EGFR-TKIs show enhanced efficacy in

153 ssion of protein kinase Calpha (PKCalpha) in lung adenocarcinomas, especially those with EGFR mutatio

154 Human lung adenocarcinoma exhibits a propensity for de-differe

155 , we analyzed the gene regulatory network in lung adenocarcinoma, finding a cofunctional module of ge

156 lly in the lung epithelium rapidly developed lung adenocarcinomas following transgene induction.

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

158 n-3 inhibitor GB1107 reduced human and mouse lung adenocarcinoma growth and blocked metastasis in the

159 as(G12D/+);Trp53(fl/fl) autochthonous murine lung adenocarcinoma had no effect on survival.

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

161 oming resistance to platinum chemotherapy in lung adenocarcinoma has previously been hampered by inap

162 rigger Treg expansion in inflammation-driven lung adenocarcinoma (IDLA).

163 s naturally occurring animal model for human lung adenocarcinoma.IMPORTANCE Ovine pulmonary adenocarc

164 y aggressive, immunocompetent mouse model of lung adenocarcinoma improves long-term survival and cisp

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

166 Finally, ablation of PINCH-1 from lung adenocarcinoma in mouse increases DRP1 expression a

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

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

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

170 deletion accelerated KRAS-driven early-onset lung adenocarcinomas, increased macrophage infiltration

171 Transcriptome analyses from lung adenocarcinomas indicate that the observed link bet

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

173 ts suggest that the metastatic cell state in lung adenocarcinoma is associated with a specifically al

174 Classification of histologic patterns in lung adenocarcinoma is critical for determining tumor gr

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

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

177 Mesylate (AM) against EGFR-TKI resistance in lung adenocarcinoma (LA) patients.

178 able diagnostics for some tumours, including lung adenocarcinoma (LA), are limited.

179 During the diagnostic workup of lung adenocarcinomas (LAC), pathologists evaluate distin

180 vasion, metastasis and anoikis resistance in lung adenocarcinoma (LAD).

181 se LSL-Kras(G12D);Trp53(fl/fl) (KP)-mediated lung adenocarcinoma (LADC) tumorigenesis can proceed thr

182 Mutational processes giving rise to lung adenocarcinomas (LADCs) in non-smokers remain elusi

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

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

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

186 COX6B2 is expressed in human lung adenocarcinoma (LUAD) and expression correlates wit

187 ic factor receptor (CNTFR) signaling axis in lung adenocarcinoma (LUAD) and generated a high-affinity

188 To explore the biology of lung adenocarcinoma (LUAD) and identify new therapeutic

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

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

191 CeRNA networks for four sequential stages of lung adenocarcinoma (LUAD) based on multi-omics data of

192 Combining profiling studies on early-stage lung adenocarcinoma (LUAD) biopsies and on A549 LUAD cel

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

194 this study, we profiled lncRNA expression in lung adenocarcinoma (LUAD) cell lines, compared their ex

195 model to two independent datasets from TCGA, Lung Adenocarcinoma (LUAD) dataset and Low Grade Glioma

196 Lung adenocarcinoma (LUAD) harboring EGFR mutations prev

197 The evolutionary trajectories of early lung adenocarcinoma (LUAD) have not been fully elucidate

198 large genomic and transcriptomic dataset of lung adenocarcinoma (LUAD) in individuals of East Asian

199 Lung adenocarcinoma (LUAD) is the most common histologic

200 odermal and pulmonary specifying TF GATA6 in lung adenocarcinoma (LUAD) progression.

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

202 ause of the refractory nature of mutant KRAS lung adenocarcinoma (LUAD) to current therapies, identif

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

204 Compared with pure lung adenocarcinoma (LUAD), adenocarcinoma component of

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

206 genomic alterations may impact prognosis of lung adenocarcinoma (LUAD).

207 omatin state transitions in a mouse model of lung adenocarcinoma (LUAD).

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

209 ata were compared with transcriptome data of lung adenocarcinomas (LUAD) and squamous cell carcinomas

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

211 The functional role of U2AF1 mutations in lung adenocarcinomas (LUADs) remains incompletely unders

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

213 By applying this pipeline to lung adenocarcinoma, lung squamous cell carcinoma, and g

214 and kallikrein-related peptidase 5 (KLK5) in lung adenocarcinoma malignancy.

215 Purpose To test whether the growth of lung adenocarcinomas manifesting as subsolid nodules at

216 Materials and Methods Patients with lung adenocarcinomas manifesting as subsolid nodules sur

217 ated by smoke exposure, we identified 296 in lung adenocarcinoma meeting a P < 10(-4) cutoff, while p

218 rom newborns and adults were enriched in the lung adenocarcinoma methylation signal.

219 ployed to characterize a novel aggregated 3D lung adenocarcinoma model, developed by the group to mim

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

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

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

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

224 In a mouse model of lung adenocarcinoma, NK cells localized to tumor stroma

225 ically classifies the histologic patterns of lung adenocarcinoma on surgical resection slides.

226 cell-specific MHCII (csMHCII) expression in lung adenocarcinoma on T cell recruitment to tumors and

227 an alternative treatment to chemotherapy in lung adenocarcinoma osimertinib-treated patients after d

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

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

230 EGFR-mutated lung adenocarcinoma patients treated with gefitinib and

231 of p38alpha correlate with poor survival in lung adenocarcinoma patients, and that genetic or chemic

232 ls in pleural effusions across a panel of 32 lung adenocarcinoma patients.

233 sion was correlated with overall survival in lung adenocarcinoma patients.

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

235 pathologists in improving classification of lung adenocarcinoma patterns by automatically pre-screen

236 RNA expression with poor patient survival in lung adenocarcinoma, potentially identifying plectin as

237 ort exome and transcriptome sequencing of 98 lung adenocarcinoma precursor lesions and 99 invasive ad

238 for assessing the invasiveness of individual lung adenocarcinomas presenting as subsolid nodules on c

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

240 Here we model RB loss during lung adenocarcinoma progression and pathway reactivation

241 Our study presents a novel role of HDAC11 in lung adenocarcinoma progression and the potential use of

242 ary, galectin-3 is an important regulator of lung adenocarcinoma progression.

243 lar states that stochastically evolve during lung adenocarcinoma progression.

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

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

246 e distinct for squamous cell lung cancer and lung adenocarcinoma, respectively.

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

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

249 e functional variant rs17079281C>T decreased lung adenocarcinoma risk by creating an YY1-binding site

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

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

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

253 Therefore, lung adenocarcinomas select for expression of a pathway

254 Galgo-generated colorectal and lung adenocarcinoma signatures were stronger predictors

255 used as a marker by pathologists to identify lung adenocarcinomas since TTF-1 is expressed in 60 ~ 70

256 expression and poor outcome in patients with lung adenocarcinoma specifically harboring KRAS mutation

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

258 d (P trend <= 0.01) with increasing risks of lung adenocarcinoma, squamous cell carcinoma, and small

259 Ablation of kindlin-2 in lung adenocarcinoma substantially reduces PYCR1 and prol

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

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

262 target uPAR extend the survival of mice with lung adenocarcinoma that are treated with a senescence-i

263 dentify highly plastic subpopulations within lung adenocarcinoma that may underlie intratumoral linea

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

265 requirement for two glucose transporters in lung adenocarcinoma, the dual blockade of which could re

266 t KRAS is the prevailing oncogenic driver of lung adenocarcinoma, the most common histologic form of

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

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

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

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

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

272 1 expression than those with C/C genotype in lung adenocarcinoma tissues.

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

274 (LSL-G12D/+);p53(f/f) autochthonous model of lung adenocarcinoma to express the CAR target ROR1.

275 n various cancers, ranging from prostate and lung adenocarcinoma to melanoma and basal cell carcinoma

276 sly showed that lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) acts as a prot

277 he long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been propo

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

279 Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long nonc

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

281 of the lncRNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) on atherosclerosis was

282 dent multisample cohort of 970 patients with lung adenocarcinoma, tumors with more than one immune co

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

284 d transplant models of murine pancreatic and lung adenocarcinoma, we found that tumor type, anatomica

285 In real data analysis on lung adenocarcinoma, we revealed a differential network

286 In a genetically-engineered mouse model of lung adenocarcinoma, we show that the deletion of only o

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

288 in adenomatous premalignancy and associated lung adenocarcinomas, we sequenced exomes from 41 lung c

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

290 /- 9 [standard deviation]; 48 women) with 74 lung adenocarcinomas were evaluated.

291 227 lung adenocarcinomas were included: 31 atypical adenomat

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

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

294 e first generated a KRAS-specific SigMap for lung adenocarcinoma, which recapitulated published KRAS

295 A 43-year-old female patient with metastatic lung adenocarcinoma, who harbored KIF5B-RET fusion and h

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

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

298 al for the growth of both cultured cells and lung adenocarcinoma xenografts, while a subset had clini

299 yngeneic mouse lung adenocarcinoma and human lung adenocarcinoma xenografts.

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