ライフサイエンスコーパス: NSCLC

1 NSCLC molecular subtypes have therapeutic implications a

2 NSCLC patients identified as high-risk groups exhibited

3 copy, and RNA and protein expression), 1023 NSCLC cases-519 from TCGA adenocarcinoma (AD) project an

4 squamous (N = 272) or nonsquamous (N = 582) NSCLC and disease progression during or after prior plat

5 Using simulations and a NSCLC application, we demonstrate that the forward selec

6 ne (DA) receptors in CD133+ve adenocarcinoma NSCLC cells.

7 d South Korea) with newly diagnosed advanced NSCLC and one EGFR mutation (exon 19 deletion or Leu858A

8 ndard of care for PD-L1-expressing, advanced NSCLC.

9 oxib in addition to chemotherapy in advanced NSCLC improved progression-free and overall survival in

10 D-CRT and IMRT outcomes for locally advanced NSCLC in a large prospective clinical trial.

11 ded 10% among patients with locally advanced NSCLC treated with definitive radiation.

12 rts routine use of IMRT for locally advanced NSCLC.

13 Of 3323 patients with advanced NSCLC and disease progression following first-line antic

14 with radiotherapy in patients with advanced NSCLC results in longer progression-free survival and ov

15 We assessed patients with advanced NSCLC treated on the phase 1 KEYNOTE-001 trial at a sing

16 with chemotherapy in patients with advanced NSCLC who are EGFR FISH-positive.

17 Of the 119 patients with advanced NSCLC, 27.7% (33/119) were suitable for treatment with N

18 in chemotherapy-naive patients with advanced NSCLC, we recruited all those who underwent (18)F-FDG PE

19 in previously treated patients with advanced NSCLC.

20 reatment strategy for patients with advanced NSCLC.

21 pressed tumour growth in a highly aggressive NSCLC circulating tumour cell (CTC) patient derived expl

22 these findings, we used afatinib to treat an NSCLC patient whose tumor harbored the HER2 V777_G778ins

23 cacy of pharmacological ascorbate in GBM and NSCLC therapy.

24 6% (71/107) and 39% (41/105) of melanoma and NSCLC patients, respectively.

25 O80 in promoting oncogenic transcription and NSCLC tumorigenesis, and reveals a potential treatment s

26 ranscribed uc.339 is upregulated in archival NSCLC samples, functioning as a decoy RNA for miR-339-3p

27 Methods The ASCO NSCLC Expert Panel made recommendations based on a syste

28 olism, including regional variation, between NSCLC histologic subtypes.

29 y-stage I and II non-small cell lung cancer (NSCLC) after resection.

30 nant subtypes of non-small cell lung cancer (NSCLC) and are distinct in their histological, molecular

31 or patients with non-small-cell lung cancer (NSCLC) and brain metastases.

32 vely sensitizing non-small-cell lung cancer (NSCLC) and glioblastoma (GBM) cells to ascorbate through

33 was observed in Non-Small Cell Lung Cancer (NSCLC) and Head and Neck Squamous Cell Carcinoma (HNSCC)

34 mutated genes in non-small cell lung cancer (NSCLC) and is commonly comutated with oncogenic KRAS mut

35 plified in human non-small cell lung cancer (NSCLC) and is required for cancer cell growth and surviv

36 or (EGFR)-mutant non-small-cell lung cancer (NSCLC) are associated with poor prognosis.

37 ROS1)-rearranged non-small-cell lung cancer (NSCLC) are sensitive to tyrosine kinase inhibitor (TKI)

38 ainst HuR, using non-small cell lung cancer (NSCLC) as a model.

39 radiotherapy for non-small-cell lung cancer (NSCLC) before receiving pembrolizumab.

40 in patients with non-small cell lung cancer (NSCLC) can facilitate the selection of subsequent manage

41 DSC curve of non-small cellular lung cancer (NSCLC) case is similar to the those of the healthy indiv

42 01) that induces non-small cell lung cancer (NSCLC) cell cycle arrest and apoptosis via restoring p53

43 y upregulated in non-small-cell lung cancer (NSCLC) cells and is associated with poor patient prognos

44 K-Ras-dependent non-small-cell lung cancer (NSCLC) cells.

45 - or EGFR-mutant non-small cell lung cancer (NSCLC) cells.

46 ur frequently in non-small cell lung cancer (NSCLC) cells.

47 es measured from non-small cell lung cancer (NSCLC) change during therapy and whether those features

48 Non-small-cell lung cancer (NSCLC) demonstrates remarkable molecular diversity.

49 roenvironment in non-small cell lung cancer (NSCLC) has not yet been adequately studied.

50 nts for advanced non-small-cell lung cancer (NSCLC) have been approved in the past decade, but little

51 itor therapy for non-small-cell lung cancer (NSCLC) is just 20%.

52 (ALK)-rearranged non-small-cell lung cancer (NSCLC) is not known.

53 ion screens in a non-small cell lung cancer (NSCLC) model.

54 m advanced stage non-small cell lung cancer (NSCLC) patients (n = 29) receiving PD-1-targeted therapi

55 n ALK-rearranged non-small cell lung cancer (NSCLC) patients treated with crizotinib, although all pa

56 ival in resected non-small cell lung cancer (NSCLC) patients.

57 survival in 210 non-small cell lung cancer (NSCLC) patients.

58 ment of advanced non-small-cell lung cancer (NSCLC) previously treated with chemotherapy.

59 cted early-stage non-small-cell lung cancer (NSCLC) provides a modest survival benefit.

60 r delineation in non-small cell lung cancer (NSCLC) radiation therapy planning by using pathology vol

61 48 patients with non-small cell lung cancer (NSCLC) to detect EGFR mutations.

62 significance in non-small-cell lung cancer (NSCLC) was investigated.

63 with early stage non-small cell lung cancer (NSCLC) with high risk of recurrence could help identify

64 locally advanced non-small cell lung cancer (NSCLC), but long-term prospective data are lacking.

65 ng patients with non-small-cell lung cancer (NSCLC), data on intratumor heterogeneity and cancer geno

66 locally advanced non-small-cell lung cancer (NSCLC), IMRT and three-dimensional conformal external be

67 pletely resected non-small-cell lung cancer (NSCLC), it remains uncertain whether this approach is su

68 efined subset of non-small cell lung cancer (NSCLC), KRAS-mutant lung cancer.

69 ts with advanced non-small-cell lung cancer (NSCLC), particularly with squamous cell histology.

70 ment outcomes in non-small cell lung cancer (NSCLC), preclinical models that can better predict indiv

71 the treatment of non-small-cell lung cancer (NSCLC), supporting the premise that evasion of immune de

72 nostic genes for non-small cell lung cancer (NSCLC), we had previously proposed the Cox-filter method

73 of patients with non-small-cell lung cancer (NSCLC), yet cardiac injury after treatment is a signific

74 the treatment of non-small cell lung cancer (NSCLC).

75 ommonly found in non-small cell lung cancer (NSCLC).

76 platinum-treated non-small-cell lung cancer (NSCLC).

77 worse outcome in non-small-cell lung cancer (NSCLC).

78 of patients with non-small cell lung cancer (NSCLC).

79 is important for non-small-cell lung cancer (NSCLC).

80 ts with stage IV non-small-cell lung cancer (NSCLC).

81 ugates (ADCs) in non-small-cell lung cancer (NSCLC).

82 tumorigenesis in non-small cell lung cancer (NSCLC).

83 isease outcome of nonsmall cell lung cancer (NSCLC).

84 s or nonsquamous non-small-cell lung cancer (NSCLC).

85 es in RT-treated non-small cell lung cancer (NSCLC).

86 utant metastatic non-small-cell lung cancer (NSCLC).

87 locally advanced non-small-cell lung cancer (NSCLC).

88 and survival in non-small-cell lung cancer (NSCLC).

89 the treatment of non-small cell lung cancer (NSCLC).

90 ts with advanced non-small cell lung cancer (NSCLC).

91 ently mutated in non-small-cell lung cancer (NSCLC).

92 or patients with non-small cell lung cancer (NSCLC).

93 helioma (MPM) or non-small-cell lung cancer (NSCLC).

94 eviously treated non-small-cell lung cancer (NSCLC).

95 tumor growth in non-small-cell lung cancer (NSCLC).

96 with EGFR-mutant non-small-cell lung cancer (NSCLC).

97 utation-positive non-small-cell lung cancer (NSCLC).

98 RAS, and EGFR in non-small-cell lung cancer (NSCLC).

99 tumor effect for non-small-cell lung cancer (NSCLC).

100 for KRAS mutant non-small cell lung cancers (NSCLC) and colorectal carcinomas that harbor wild-type T

101 ccurs in 40% of non-small-cell lung cancers (NSCLCs) and is associated with a high subclonal neoantig

102 rted that human non-small-cell lung cancers (NSCLCs) oxidize glucose in the tricarboxylic acid (TCA)

103 ly occurring in non-small cell lung cancers (NSCLCs), is a predominant caution of NSCLC initiation an

104 t study using non-small-cell lung carcinoma (NSCLC) cell lines, animal models, and clinical specimens

105 lied to human non-small cell lung carcinoma (NSCLC) cell lines, embedded as spheroids in a collagen g

106 this cancer, non-small cell lung carcinoma (NSCLC) comprises the majority of cases.

107 with advanced non-small cell lung carcinoma (NSCLC), especially in those whose cancer tissues are una

108 patients with non-small cell lung carcinoma (NSCLC).

109 es (including non-small-cell lung carcinoma [NSCLC], colorectal carcinoma, and melanoma) were sequenc

110 esectable IIIA/IIIB histologically confirmed NSCLC, Karnofsky performance status 70 to 100, and 6-mon

111 hirty patients with pathologically confirmed NSCLC were included.

112 and increases the apoptotic rate of cultured NSCLC cells in a STAT3-dependent manner.

113 izotinib in a patient with METDelta14-driven NSCLC, only to observe new missense mutations in the MET

114 rican Joint Committee on Cancer 6th edition) NSCLC.

115 Engineered single CLCb-expressing NSCLC cells, as well as "switched" cells that predominan

116 herapeutic strategies targeting TGF-beta for NSCLC.

117 ates a transcriptional program essential for NSCLC tumorigenesis.

118 images are not superior to static images for NSCLC delineation.

119 n of immune destruction is of importance for NSCLC progression.

120 intensity-modulated radiotherapy (IMRT) for NSCLC delivering conventionally fractionated radiotherap

121 values of (18)F-FMISO kinetic parameters for NSCLC lesions as well as for normal lung and muscle.

122 rognostic multigene expression signature for NSCLC.

123 actate is also a TCA cycle carbon source for NSCLC.

124 omarker and potential therapeutic target for NSCLC treatment, which warrants further study.

125 VMAT seemed to be the optimal technique for NSCLC.

126 ab plus ipilimumab as first-line therapy for NSCLC.

127 enhancement of immune checkpoint therapy for NSCLC.

128 ith pathology volume and could be useful for NSCLC autocontouring.

129 efflux of (18)F-IRS were performed with four NSCLC cell lines including HCC827, H1975, H358 and H520.

130 Within the study time, 36 patients died from NSCLC and 26 patients from other causes.

131 FR and HER2 exon 20 insertion mutations from NSCLC patients that had clinically achieved a partial re

132 n vitro using H1299, A549, HCC827, and H1975 NSCLC cells and MRC-9 and CCD-16 normal human fibroblast

133 icate that tumors, including bona fide human NSCLC, can use lactate as a fuel in vivo.

134 RNAi-mediated attenuation of SMPD1 in human NSCLC cells rendered them resistant to serum starvation-

135 In human NSCLC, evidence of lactate utilization was most apparent

136 Infusing human NSCLC patients with (13)C-lactate revealed extensive lab

137 we perform an integrative analysis of human NSCLC tumour samples, patient-derived xenografts, murine

138 tandard operative risk patients with stage I NSCLC, SBRT is not recommended outside of a clinical tri

139 90M mutation, osimertinib is recommended; if NSCLC lacks the T790M mutation, then chemotherapy is rec

140 without prior immune checkpoint therapy, if NSCLC tumor is positive for PD-L1 expression, clinicians

141 ld be used for risk assessment in stage I-II NSCLC.

142 om 1996 to 2009, 127 patients with stage III NSCLC (Eastern Cooperative Oncology Group performance st

143 erable or unresectable stage II to stage III NSCLC enrolled from November 2008, to May 2012.

144 ardiac toxicity after treatment of stage III NSCLC may occur earlier than historically understood, an

145 nt blood serum were determined for stage III NSCLC patients at times before, during, and after RT adm

146 raphy images for 107 patients with stage III NSCLC.

147 igh-dose PBT to treat unresectable stage III NSCLC.

148 teria included patients with stage II to III NSCLC treated on one of four prospective radiation thera

149 In NSCLC alterations in PDGF receptors are markers of worst

150 therapeutic strategy by targeting miR-218 in NSCLC.

151 rategy via specific activation of p53-72R in NSCLC.

152 d expression of PDGFR-alpha or PDGFR-beta in NSCLC cells.

153 cert with these results, targeting MUC1-C in NSCLC tumors suppresses PD-L1 and induces these effector

154 t accumulate during standard chemotherapy in NSCLC and HNSCC.

155 d enhanced cytotoxic effects of cisplatin in NSCLC cells.

156 peptide also demonstrates PD-L1 detection in NSCLC, breast, squamous cell carcinoma, and melanoma.

157 reverse acquired resistance to erlotinib in NSCLC through mediating its direct target gene LHX6 expr

158 We identify AURKA activity as essential in NSCLC cells lacking SMARCA4/BRG1.

159 hanced cell motility and colony formation in NSCLC cells, and these activities were inhibited by SU11

160 ound that CCT6A suppresses SMAD2 function in NSCLC cells and promotes metastasis.

161 ssion significantly enhanced tumor growth in NSCLC xenograft mouse models, while exogenous TRIM14 exp

162 y accurate parametric (18)F-FLT VT images in NSCLC patients before and during therapy.

163 emonstrates that apoptosis can be induced in NSCLC cells with acquired Erlotinib resistance by direct

164 INTERPRETATION: In NSCLC, first-line nivolumab plus ipilimumab had a tolera

165 als responsible for upregulation of PD-L1 in NSCLC cells and whether they are integrated with the reg

166 Clinically, AURKA displays high levels in NSCLC patients, and correlates with poor outcome of pati

167 ts of AZD1775 in the context of KRAS/LKB1 in NSCLC.

168 ults showed that inhibiting LKB1 or MARK1 in NSCLC increases the collagen fiber alignment and capture

169 ucin 1 (MUC1) is aberrantly overexpressed in NSCLC, activates the nuclear factor-kappaB (NF-kappaB) p

170 anism underlying LINC00152 overexpression in NSCLC.

171 the oncogenic Wnt/FZD signaling pathways in NSCLC.

172 show that perivascular-like cells present in NSCLC retain functional abnormalities in vitro.

173 knowledge of the immune landscape present in NSCLC.

174 r reactive T cells are frequently present in NSCLC.

175 stance, aggressiveness and poor prognosis in NSCLC patients.

176 uppressed in vitro cellular proliferation in NSCLC cancer cells.

177 omprising an erlotinib response signature in NSCLC.

178 that RT alters IDO-mediated immune status in NSCLC patients and that changes in this serum biomarker

179 significantly influence overall survival in NSCLC patients by specifically interacting with miR-204

180 d physicians' ability to predict survival in NSCLC with brain metastases has improved significantly.

181 ude that BCL6 is a new therapeutic target in NSCLC and combination therapy that targets multiple vuln

182 vascular-like cells as an eventual target in NSCLC warrants further investigation.

183 e indicator for MET-targeted therapeutics in NSCLC.

184 a novel tumor suppressive role for TRIM14 in NSCLC progression.

185 functional and prognostic role of TRIM14 in NSCLC using in vitro and in vivo perturbation model syst

186 hways and main effectors of tumorigenesis in NSCLC.

187 (18)F-FMISO uptake in NSCLC patients is strongly associated with poor prognosi

188 o-metastatic protein levels are validated in NSCLC patient specimens.

189 metabolic signatures specific to individual NSCLC subtypes remain unknown.

190 analysis may provide valuable insights into NSCLC patients' responses to PD-1-targeted therapies.

191 ible patients had confirmed stage IIIB or IV NSCLC with squamous or non-squamous histology, measurabl

192 ited patients with treatment-naive, stage IV NSCLC in 102 sites in 16 countries.

193 gible patients with treatment-naive stage IV NSCLC to receive paclitaxel (200 mg/m(2); every 21 days)

194 ZD1775 with DNA-damaging agents in KRAS/LKB1 NSCLC.

195 eness rather than tumor burden in metastatic NSCLC.

196 patients with BRAF(V600E)-mutant metastatic NSCLC.

197 trial in patients with pretreated metastatic NSCLC who received either 8 or 10 mg/kg on days 1 and 8

198 pt study, in which patients with EGFR-mutant NSCLC were treated with the combination of erlotinib and

199 imal management of patients with EGFR-mutant NSCLC who develop brain metastases and have not received

200 ith inferior OS in patients with EGFR-mutant NSCLC who develop brain metastases.

201 cacy of AZD3759 in patients with EGFR-mutant NSCLC with brain and leptomeningeal metastases.

202 cally confirmed, advanced-stage, EGFR-mutant NSCLC.

203 at are selectively expressed in KEAP1-mutant NSCLC cells.

204 e the transcriptional output of KEAP1-mutant NSCLC cells.

205 MDM2 inhibitors for treatment of KRAS mutant NSCLC and colorectal cancers.

206 usly untreated metastatic BRAF(V600E)-mutant NSCLC were enrolled into cohort C from 19 centres in eig

207 with previously untreated BRAF(V600E)-mutant NSCLC.

208 t stage IIIb or stage IV, chemotherapy-naive NSCLC.

209 of 119 patients with advanced EGFR-TKI-naive NSCLC and 15 EGFR-TKI-resistant patients to identify som

210 as well as noninferiority for ERCC1-negative NSCLC.

211 d two cohorts of patients with nonmetastatic NSCLC who had received at least a lobectomy followed by

212 In 25 patients with advanced nonsquamous NSCLC, (18)F-FDG PET/CT was performed before treatment a

213 izumab in patients with advanced nonsquamous NSCLC.

214 carboplatin plus pemetrexed for nonsquamous NSCLC and carboplatin plus gemcitabine for squamous hist

215 rsus 16% (95% CI, 12% to 20%) in nonsquamous NSCLC; relative reductions in the risk of death with niv

216 us NSCLC and 19 (34%) of 56 with nonsquamous NSCLC had ongoing responses after 2 years' minimum follo

217 t-derived xenografts, murine model of NSCLC, NSCLC cell lines and The Cancer Genome Atlas (TCGA) and

218 To accomplish this, we studied 186 cases of NSCLC with preoperative thin-slice CT scans.

219 ancers (NSCLCs), is a predominant caution of NSCLC initiation and progression.

220 , widens their application in the context of NSCLC.

221 , and increased the metastatic efficiency of NSCLC cells in vivo.

222 ng axis, in turn leading to the elevation of NSCLC cell proliferation, invasion and migration.

223 model that enables concurrent evaluation of NSCLC response to therapy while maintaining the tumor mi

224 d PDW is an unfavorable predictive factor of NSCLC patient survival.

225 directed toward METDelta14 in a fraction of NSCLC patients, confirm second-site mutations for furthe

226 Furthermore, recurrence and metastasis of NSCLC correlate well with CD133+ve tumor cells, a small

227 patient-derived xenografts, murine model of NSCLC, NSCLC cell lines and The Cancer Genome Atlas (TCG

228 bination treatment schema in mouse models of NSCLC reverses tumor immune evasion and modulates T cell

229 STAT3 and BCL6 inhibitors across a panel of NSCLC cell lines and in xenografted tumors significantly

230 d higher miR-214 expression in the plasma of NSCLC patients with acquired EGFR-TKI resistance than pr

231 notable changes occur in the DSC profile of NSCLC patient's blood serum.

232 ffectively inhibit cellular proliferation of NSCLC cells in a dose-dependent manner.

233 e clinical decision making in the staging of NSCLC.

234 Nine genomic subtypes of NSCLC were identified, three within SQCC and six within

235 ceived any radiotherapy for the treatment of NSCLC before the first cycle of pembrolizumab.

236 Treatment of NSCLC cells with CMLD-2 produced dose-dependent cytotoxi

237 cally enhance tumor regression in orthotopic NSCLC mouse model.

238 utic strategy for patients with ALK-positive NSCLC who have become resistant to currently available T

239 platinum doublet therapy for ERCC1-positive NSCLC as well as noninferiority for ERCC1-negative NSCLC

240 ratio (HR) for patients with ERCC1-positive NSCLC was </= 0.78.

241 h programmed death ligand 1 (PD-L1)-positive NSCLC.

242 ment of patients with EGFR-mutation-positive NSCLC and should be considered as a new treatment option

243 s had advanced ALK-positive or ROS1-positive NSCLC and were older than 18 years, with an Eastern Coop

244 with advanced ALK-positive or ROS1-positive NSCLC, most of whom had CNS metastases and had previousl

245 ALK-positive and 12 (23%) with ROS1-positive NSCLC; one patient had unconfirmed ALK and ROS1 status.

246 xpanded mesenchymal cells from human primary NSCLC samples based on co-expression of CD73 and CD90 wh

247 We found that approximately 70% of primary NSCLC specimens were amenable to explant culture with ti

248 Thirty-nine ALK-rearranged NSCLC patients treated with crizotinib as first ALK inhi

249 er for crizotinib efficacy in ALK-rearranged NSCLC patients.

250 apy in patients with advanced ALK-rearranged NSCLC.

251 atients with untreated stage IV or recurrent NSCLC and a PD-L1 tumor-expression level of 1% or more t

252 were performed in 35 patients (36 resectable NSCLCs) between 2009 and 2014.

253 ndent risk factor for TFS and OS in resected NSCLC patients.

254 djuvant chemotherapy in early-stage resected NSCLC.

255 secutive stage I-IIIA patients with resected NSCLC.

256 f chemoresistance and metastasis in residual NSCLC cells having survived repeated chemotherapy and co

257 /15) of the patients with EGFR-TKI-resistant NSCLC, suggesting that the NGS-based ctDNA assay might b

258 proliferative activity on EGFR TKI-resistant NSCLC.

259 ents with progressive or treatment-resistant NSCLC, providing a rationale for further studies of avel

260 %) versus 8% (95% CI, 4% to 13%) in squamous NSCLC and 29% (95% CI, 24% to 34%) versus 16% (95% CI, 1

261 chemotherapy in advanced-stage non-squamous NSCLC.

262 7%) of 27 confirmed responders with squamous NSCLC and 19 (34%) of 56 with nonsquamous NSCLC had ongo

263 ients with a new diagnosis of advanced-stage NSCLC and were treated with antineoplastic agents betwee

264 le shifts in the treatment of advanced-stage NSCLC occurred along with modest gains in survival and t

265 based treatment decisions for advanced-stage NSCLC.

266 to predict disease recurrence in early stage NSCLC from digitized H&E tissue microarray (TMA) slides.

267 Using a retrospective cohort of early stage NSCLC patients (Cohort #1, n = 70), we constructed a sup

268 dated on two independent sets of early stage NSCLC patients, Cohort #2 (n = 119) and Cohort #3 (n = 1

269 with decreased risk of death in early stage NSCLC patients.

270 on whole-exome sequencing on 100 early-stage NSCLC tumors that had been resected before systemic ther

271 erapy for patients with resected early-stage NSCLC.

272 atients with surgically resected early-stage NSCLC.

273 ts and evolutionary processes in early-stage NSCLC.

274 y for systematic analyses of the entire TCGA NSCLC cohort, including comparisons and contrasts betwee

275 Patterns from TCGA NSCLC subsets were examined in independent external data

276 Ten NSCLC patients underwent dynamic (18)F-FLT PET/CT at bas

277 avels an anti-metastatic role of AKT1 in the NSCLC cells with KRAS or EGFR mutations, and establishes

278 omarker-driven clinical studies to treat the NSCLCs harbouring SMARCA4/BRG1-inactivating mutations.

279 ways in Evaluation of Cancers of the Thorax) NSCLC data set.

280 d lend support to a personalized approach to NSCLC management based on molecular characterization.

281 ely suppresses tumor growth in p53 wild-type NSCLC harboring Arg72 homozygous alleles (p53-72R) throu

282 apy for patients with stage III unresectable NSCLC.

283 t chemotherapy and PBT to treat unresectable NSCLC afford promising clinical outcomes and rates of to

284 ion was preferential in the tumor, which was NSCLC with responsive EGFR exon 19 deleted.

285 otal of 270 patients who were diagnosed with NSCLC between January 2009 and December 2009 were retros

286 Sixteen patients diagnosed with NSCLC underwent 2 PET/CT scans (1-3 d apart) before radi

287 Chemonaive patients with NSCLC (stage IIIB and IV) were eligible.

288 Patients and Methods Patients with NSCLC (stage IIIB with pleural effusion or stage IV acco

289 sed on 4 factors found in 1833 patients with NSCLC and brain metastases diagnosed between 1985 and 20

290 a tolerable safety profile in patients with NSCLC and CNS metastases who had either never received a

291 ls and Methods A cohort of 113 patients with NSCLC diagnosed between April 2008 and September 2014 wh

292 f erlotinib and bevacizumab in patients with NSCLC harbouring activating EGFR mutations.

293 Conclusion Patients with NSCLC who undergo R0 resection and are found to have pN2

294 ducation) registry to identify patients with NSCLC with clinical radiographic stage T1-3, N0-3, M0 di

295 Results Of 3,533 patients with NSCLC, 1,181 (557 deaths) and 404 (170 deaths) were used

296 with anti-PD-1 monotherapy in patients with NSCLC, supporting further assessment of this combination

297 )F-IRS PET/CT imaging of three patients with NSCLC.

298 GFR mutations in the plasma of patients with NSCLC.

299 be used to estimate prN2/3 in patients with NSCLC.

300 present study was 12 months, and those with NSCLC-adenocarcinoma and Lung-molGPA scores of 3.5 to 4.