ライフサイエンスコーパス: NSCLC

1 unohistochemistry in tissue samples from 151 NSCLC patients who had curative resection.

2 Of the 2,289 NSCLC cases, 911 (39.8%) cases pertained to lower lobe c

3 ; SCCHN, 36% (8/22; 95% CI, 17.2% to 59.3%); NSCLC, 33% (7/21; 95% CI, 14.6% to 57.0%); and urothelia

4 The 42 NSCLC patients treated with palliative intent at Maria S

5 PMN-MDSCs in peripheral blood samples of 62 NSCLC patients before and after nivolumab treatment.

6 naive-like B cells are decreased in advanced NSCLC, and their lower level is associated with poor pro

7 -amplified, EGFR mutation-positive, advanced NSCLC, who had disease progression on a previous EGFR TK

8 immunotherapy in previously treated advanced NSCLC and suggest that continuing nivolumab beyond 1 yea

9 Patients with previously treated advanced NSCLC received nivolumab monotherapy (3 mg/kg every 2 we

10 I randomized trial in patients with advanced NSCLC harboring an EGFR-sensitizing mutation and a perfo

11 Methods: Seventy-two patients with advanced NSCLC were recruited in a single-institution ancillary t

12 b were assessed in 69 patients with advanced NSCLCs harboring MET exon 14 alterations.

13 ially effective therapeutic strategy against NSCLC with EGFR(WT).

14 y, the exosomes derived from normal lung and NSCLC cells can be effectively distinguished through pre

15 nt or ADORA1 antagonist-treated melanoma and NSCLC immune-competent mouse models.

16 ADORA1 antagonist treatment of melanoma and NSCLC xenografts.

17 activity of serum IgM in healthy persons and NSCLC patients at different cancer stages.

18 levels in primary tumor samples of TNBC and NSCLC patients.

19 fied medicine options for tobacco-associated NSCLC is a high priority.

20 e and challenges associated with ctDNA-based NSCLC genotyping and suggest a framework for the impleme

21 Cultured human non-small cell lung cancer (NSCLC) A549 cells take up the precursor, which is extend

22 diting can model non-small cell lung cancer (NSCLC) adenocarcinomas, enabling treatment studies to va

23 of NF-kappaB in non-small cell lung cancer (NSCLC) and discuss its contributing effect on cancer hal

24 In non-small cell lung cancer (NSCLC) and prostate cancers, lineage plasticity manifest

25 types, including non-small-cell lung cancer (NSCLC) and small-cell lung cancer (SCLC).

26 d the human A549 non-small cell lung cancer (NSCLC) and SW620 colorectal cancer cell lines to SRA737.

27 eviously treated non-small cell lung cancer (NSCLC) are assigned to personalized therapy based on the

28 ed therapies for non-small-cell lung cancer (NSCLC) are directed against oncogenic drivers that are m

29 d therapies with non-small cell lung cancer (NSCLC) being a paradigm for precision medicine in this s

30 ffective in some non-small cell lung cancer (NSCLC) but not in triple-negative breast cancer (TNBC),

31 aive EGFR-mutant non-small-cell lung cancer (NSCLC) by preventing or delaying resistance.

32 The majority of non-small-cell lung cancer (NSCLC) cases are diagnosed at advanced stages, primarily

33 (AZD9291) in the non-small cell lung cancer (NSCLC) cell line H1975, which harbors two EGFR mutations

34 a KRAS-dependent non-small cell lung cancer (NSCLC) cell line, H23-KRAS(G12C) Using a combination of

35 A large panel of non-small cell lung cancer (NSCLC) cell lines (73 of 77) were sensitive to 6-thio-dG

36 zed compounds in non-small-cell lung cancer (NSCLC) cells showed that cytotoxicities varied by more t

37 the nucleolus of non-small-cell lung cancer (NSCLC) cells, where it binds the transcription factor up

38 egulating CME in non-small-cell lung cancer (NSCLC) cells.

39 ne set of public non-small cell lung cancer (NSCLC) data.

40 ellular level in non-small cell lung cancer (NSCLC) explant models after treatment with clinically re

41 its function in non-small cell lung cancer (NSCLC) has not been established.

42 Non-small cell lung cancer (NSCLC) have been reported to secret a high concentration

43 er patients with non-small cell lung cancer (NSCLC) have poorer prognosis and survival than those wit

44 with EGFR-mutant non-small-cell lung cancer (NSCLC) have significantly benefited from the use of EGFR

45 h advanced-stage non-small-cell lung cancer (NSCLC) in light of the ever-expanding toolbox of targete

46 KRAS-mutant non-small cell lung cancer (NSCLC) is a major lung cancer subtype that leads to many

47 -mutant advanced non-small-cell lung cancer (NSCLC) is an epidermal growth factor receptor (EGFR)-dir

48 A subset of non-small cell lung cancer (NSCLC) is driven by amplification and overexpression or

49 Non-small cell lung cancer (NSCLC) is known to have poor patient outcomes due to dev

50 osimertinib, in non-small cell lung cancer (NSCLC) is limited by acquired resistance.

51 Non-small cell lung cancer (NSCLC) is often characterized by mutually exclusive muta

52 Non-small-cell lung cancer (NSCLC) is terminal in most patients with locally advance

53 Non-small cell lung cancer (NSCLC) is the deadliest form of cancer worldwide, due in

54 Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death worl

55 Non-small cell lung cancer (NSCLC) is the most frequent subtype of lung cancer and r

56 in patients with non-small-cell lung cancer (NSCLC) or melanoma with untreated brain metastases to de

57 lso tested using non-small cell lung cancer (NSCLC) patient samples, where anti-epidermal growth fact

58 3%) of stage III non-small cell lung cancer (NSCLC) patients are prescribed with chemo and/or radiati

59 EGFR-mutant non-small-cell lung cancer (NSCLC) patients inevitably develop drug resistance when

60 issue samples of non-small cell lung cancer (NSCLC) patients, and identify subtypes of tumor-infiltra

61 onse criteria in non-small cell lung cancer (NSCLC) patients.

62 onse criteria in non-small-cell lung cancer (NSCLC) patients.

63 recurrences in a non-small cell lung cancer (NSCLC) population with mutated EGFR receiving TKIs and C

64 C) on 8 pairs of non-small cell lung cancer (NSCLC) primary tumors and matched distant metastases.

65 involved in male non-small cell lung cancer (NSCLC) radiation sensitivity.

66 Non-small-cell lung cancer (NSCLC) represents approximately 80-85% of lung cancer di

67 lated from human non-small cell lung cancer (NSCLC) tissue possesses 3'-terminal 2'Ome.

68 of cisplatin in non-small cell lung cancer (NSCLC) treatment.

69 16) that targets non-small cell lung cancer (NSCLC) was previously identified through in vivo SELEX.

70 om patients with non-small cell lung cancer (NSCLC) where c-MAF is overexpressed.

71 of patients with non-small cell lung cancer (NSCLC) with EGFR-mutant tumors, TKI resistance often ret

72 ugh treatment of non-small cell lung cancer (NSCLC) with immune checkpoint inhibitors (ICIs) can prod

73 12 patients with nonsmall-cell lung cancer (NSCLC) with PD-1 gene-edited bulk autologous T cells, wi

74 ts with stage IV non-small-cell lung cancer (NSCLC) without driver alterations.

75 In non-small cell lung cancer (NSCLC), accumulation of anti-inflammatory tumor-associat

76 ets of melanoma, non-small cell lung cancer (NSCLC), and anaplastic thyroid cancer (ATC), making BRAF

77 r types, notably non-small cell lung cancer (NSCLC), and associated with reduced survival.

78 ced treatment of non-small cell lung cancer (NSCLC), but protein level quantitation of drug targets p

79 or patients with non-small cell lung cancer (NSCLC), distinguishing between N0, N1, and N2 or N3 (N2|

80 ns are common in non-small cell lung cancer (NSCLC), effective treatments are lacking.

81 CCHN), melanoma, non-small-cell lung cancer (NSCLC), or urothelial cancer.

82 n YAP and TAZ in non-small cell lung cancer (NSCLC), the most common histological subtype of lung can

83 ncers, including non-small cell lung cancer (NSCLC).

84 ful treatment of non-small-cell lung cancer (NSCLC).

85 y, including for non-small-cell lung cancer (NSCLC).

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

87 genic drivers of non-small cell lung cancer (NSCLC).

88 tumors including non-small cell lung cancer (NSCLC).

89 worse outcome of non-small cell lung cancer (NSCLC).

90 ancer (TNBC) and non-small cell lung cancer (NSCLC).

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

92 ncers, including non-small-cell lung cancer (NSCLC).

93 ced EGFR-mutant non -small cell lung cancer (NSCLC).

94 tro and in human non-small-cell lung cancer (NSCLC).

95 ing modality for non-small cell lung cancer (NSCLC).

96 e development of non-small-cell lung cancer (NSCLC).

97 in patients with non-small cell lung cancer (NSCLC).

98 ancer, including non-small cell lung cancer (NSCLC).

99 o lipogenesis in non-small cell lung cancer (NSCLC).

100 nal evolution in non-small cell lung cancer (NSCLC).

101 ne catabolism in non-small cell lung cancer (NSCLC).

102 anced metastatic non-small cell lung cancer (NSCLC).

103 ab for stage III non-small-cell lung cancer (NSCLC).

104 proliferation of non-small-cell lung cancer (NSCLC).

105 ents in treating non-small cell lung cancer (NSCLC).

106 thoracic cancer (non-small-cell lung cancer [NSCLC], small-cell lung cancer, mesothelioma, thymic epi

107 gies employed in non-small cell lung cancer, NSCLC, are tyrosine kinase inhibitors, TKIs, and immune

108 ty dynamics, exemplified by prostate cancer, NSCLC, and SCLC.

109 frequencies in non-small cell lung cancers (NSCLC).

110 enic drivers of non-small-cell lung cancers (NSCLCs)(1).

111 istic of nearby non-small cell lung cancers (NSCLCs).

112 aluating this approach in spontaneous canine NSCLC, tumor fluorescence was observed in 6 of 7 canines

113 age 73) with non-small cell lung carcinoma (NSCLC) and treated with ICI were prospectively collected

114 on therapy in non-small cell lung carcinoma (NSCLC) is often evaluated radiographically, however, ima

115 Clinically, NSCLC patients expressing high FCHSD2 exhibit elevated s

116 that HDAC11 is a potential target to combat NSCLC.

117 dynamics, particularly in PPP2R2A-deficient NSCLC cells.

118 th reported in PKCe-deficient KRAS-dependent NSCLC cells.

119 -dependent melanoma cells and MCL1-dependent NSCLC cells.

120 nd accurate methods to analyze the different NSCLC cells-derived exosomes.

121 is, but the impact of endocan on EGFR-driven NSCLC progression remains unknown.

122 before chemoradiotherapy in oncogene-driven NSCLC.

123 gh PD-L1-expressing and high IDO1-expressing NSCLC.

124 in formalin-fixed, paraffin-embedded (FFPE) NSCLC specimens.

125 of sensitive and non-invasive biomarkers for NSCLC's early-stage diagnosis.

126 astasis (BMs) is a major mortality cause for NSCLC; there is no drug specifically approved for the os

127 e clinical evaluation of immunotherapies for NSCLC.

128 Thus, CDO1 is a metabolic liability for NSCLC cells with high intracellular cysteine, particular

129 d early forecasting of ultimate outcomes for NSCLC patients receiving ICIs.

130 ve for massive high-throughput screening for NSCLC in clinical specimens.

131 offer an attractive therapeutic strategy for NSCLC.

132 ence and improved survival after surgery for NSCLC.

133 unotherapy and oncogene-directed therapy for NSCLC, focusing on the role of predictive biomarkers.

134 tic strategies for efficacious treatment for NSCLC.

135 f 77) were sensitive to 6-thio-dG; only four NSCLC lines were resistant to 6-thio-dG.

136 -culture of isolated naive-like B cells from NSCLC patients with two lung cancer cell lines demonstra

137 elf-renewal of cancer stem cells (CSCs) from NSCLC but also decreases Sox2 expression that is essenti

138 unotherapy in patients with CNS disease from NSCLC is warranted.

139 y isolate and release 76% more exosomes from NSCLC patients than from healthy donors.

140 izumab has activity in brain metastases from NSCLC with PD-L1 expression at least 1% and is safe in s

141 Among men, incidence-based mortality from NSCLC decreased 6.3% annually from 2013 through 2016, wh

142 Mortality from NSCLC decreased even faster than the incidence of this s

143 Population-level mortality from NSCLC in the United States fell sharply from 2013 to 201

144 d, normal lung tissue, and tumor tissue from NSCLC patients.

145 e now report an updated analysis of the full NSCLC cohort.

146 e overall survival of patients with stage IA NSCLC in the National Cancer Data Base from 2004 to 2015

147 recommended patients with operable stage IA NSCLC to consider delaying surgery by at least 3 months

148 ational analysis, for patients with stage IA NSCLC, extended delay of surgery was associated with imp

149 CLC patients, which is promising to identify NSCLC patients sensitive to EGFR-TKI or ICI-treatments.

150 used for routine surveillance in stage I-III NSCLC but may be used every 3 months for the first year

151 est reported in the literature for stage III NSCLC.

152 Joint Committee on Cancer-defined stage IIIA NSCLC that was deemed locally to be surgically resectabl

153 erapy in patients with resectable stage IIIA NSCLC.

154 chemoimmunotherapy for resectable stage IIIA NSCLC.

155 arrays and expression of linc-SPRY3-2/3/4 in NSCLC RNA-seq and microarray data revealed a negative co

156 d 6-month clinical benefit (AUROC = 0.83) in NSCLC.

157 at targeting LYCAT expression or activity in NSCLC may provide new avenues for the therapeutic treatm

158 infrequent genomic actionable alterations in NSCLC as well as the current and emerging therapeutic op

159 ise understanding of antigens and T cells in NSCLC is needed to improve therapeutic efficacy and redu

160 ombining PIM inhibition with chemotherapy in NSCLC.

161 Assessment of Y chromosome in NSCLC tissue microarrays and expression of linc-SPRY3-2/

162 ation between PIM1 and Drp1 was confirmed in NSCLC patient samples.

163 lts show that SOX9 expression is elevated in NSCLC cells after treatment with the chemotherapeutic ci

164 KCe, an oncogenic kinase highly expressed in NSCLC and other cancers, in KRAS-driven tumorigenesis.

165 POLA1, POLE, and POLE2 protein expression in NSCLC and colorectal cancer cells correlated with single

166 owth factor receptor 1 (FGFR1) expression in NSCLC cell lines H1975, HCC827, and YLR086, and knockdow

167 ted higher EGFR expression commonly found in NSCLC EVs.

168 ng tumorigenic functions and tumor growth in NSCLC.

169 and their potential clinical implications in NSCLC.

170 d immunotherapy-modified RECIST (iRECIST) in NSCLC patients.

171 e (GSH), which accumulates to high levels in NSCLC relative to normal lung.

172 prognostic role of primary tumor location in NSCLC.

173 Stable knockdown of LYCAT in NSCLC cell lines not only reduced CL and increased monol

174 y and ATR or CHK1 inhibition was observed in NSCLC in vitro and in vivo and was independent of p53 st

175 esent an important marker of radiotherapy in NSCLC.

176 s associated with autoantibody reactivity in NSCLC as a potential means for early detection.

177 of genes and biological pathways relevant in NSCLC, suggesting that a permissive role of PKCe in KRAS

178 apeutic targets to overcome CP resistance in NSCLC.

179 alternative target of EGFR-TKI resistance in NSCLC.

180 ed to predict anti-PD-1 therapy responses in NSCLC, its accuracy is relatively less.

181 paralogs YAP and TAZ have distinct roles in NSCLC and are associated with differential response to a

182 se quantification of EGFR mutation status in NSCLC patients, which is promising to identify NSCLC pat

183 GIAT4RA was linked with overall survival in NSCLC.

184 l metabolic pathway amenable to targeting in NSCLC.

185 has been approved as a first-line therapy in NSCLC, representing the most successful advance in molec

186 to EGFR Tyrosine kinase inhibitors (TKIs) in NSCLC with activating EGFR mutations is a critical limit

187 Matrix Trial, the largest umbrella trial in NSCLC.

188 while accounting for ITH-driven variance in NSCLC.

189 -1 at high frequency in multiple independent NSCLC cohorts, occurring both clonally and subclonally.

190 with histologically confirmed stage IIIB-IV NSCLC who were treated with immune checkpoint blockade b

191 were at least 18 years of age with stage IV NSCLC with at least one brain metastasis 5-20 mm in size

192 guideline update for patients with stage IV NSCLC with driver alterations will be published separate

193 BP1 on mitochondrial function in mutant KRAS NSCLC.

194 gm for treating BRCA-proficient cancers like NSCLC.

195 adiographic stage T1 to T3, N0 to N3, and M0 NSCLC who underwent endobronchial ultrasound-guided stag

196 comes of patients with clinical T1-2, N1, M0 NSCLC who underwent lobectomy without induction therapy

197 RNA regulators of radiation response in male NSCLC and show a correlation between loss of chromosome

198 hich was not observed in radioresistant male NSCLC cell lines.

199 hromosome Y (LOY) in the radioresistant male NSCLC cell lines.

200 Radiosensitive male NSCLC cell lines demonstrated a dose-dependent induction

201 tors in combination with EGFR-TKIs to manage NSCLC.

202 underlying BRAF driver mutations: melanoma, NSCLC, and ATC.

203 first-line treatment of advanced/metastatic NSCLC.

204 city, for palliative treatment of metastatic NSCLC.

205 interactors that are critical to metastatic NSCLC.

206 ic data from 4 autopsy cases with metastatic NSCLC and one metastatic lung cancer mouse model.

207 munotherapy-treated patients with metastatic NSCLC with a low extent of PD-1/PD-L1 interaction show s

208 be tailor-made therapeutics for EGFR mutant NSCLC; however, drug resistance mutations limit their su

209 ent and PD tumor samples from 54 EGFR-mutant NSCLC patients.

210 echanism inherent to a subset of EGFR-mutant NSCLC to attenuate tyrosine kinase inhibitor delivery to

211 Patients with EGFR-mutant NSCLC without prior treatment of advanced disease were e

212 outcomes in previously untreated EGFR-mutant NSCLC, despite recognized activity in the acquired resis

213 s a therapeutic strategy against KRAS-mutant NSCLC and propose the clinical benefit of PIERCE1.

214 cle-related protein, PIERCE1, in KRAS-mutant NSCLC.

215 Here, we report that half of KRAS-mutant NSCLCs aberrantly express the homeobox protein HOXC10, l

216 omising therapeutic strategy for KRAS-mutant NSCLCs, identify a predictive biomarker of response, and

217 uired for 3D spheroid growth of EGFR-mutated NSCLC cells.

218 mpact of a VATS approach to lobectomy for N1 NSCLC on short-term outcomes and survival.

219 6% (P = 0.01) in patients with node negative NSCLC established via routine lymphadenectomy alone (n =

220 ession, mixed progression was common (45% of NSCLC and 53% of MMRD) and associated with improved surv

221 pproved for the osimertinib-resistant BMs of NSCLC yet.

222 sensitive and multiplex characterizations of NSCLC-derived exosomes by bioaffinity interactions of an

223 And the multiplex characterizations of NSCLC-related exosomes are also achieved by anti-CD63, a

224 ovel mechanistic role of MBIP as a driver of NSCLC progression and metastasis.

225 ific helicase (LSH), an epigenetic driver of NSCLC.

226 arcinoma, the most common histologic form of NSCLC.

227 D2 loss correlates to higher tumor grades of NSCLC.

228 lar proliferation, migration and invasion of NSCLC cells in vitro and metastasis in vivo.

229 Here we investigated the immune landscape of NSCLC in the presence of protumoral TAMs expressing the

230 ted rDNA transcription for the management of NSCLC.

231 se in a highly drug-resistant mouse model of NSCLC.

232 alidated using multiple siRNAs in a panel of NSCLC and colorectal cancer cell lines.

233 f (18)F-FDG PET in the general population of NSCLC patients treated with ICIs, the findings suggest t

234 r interacting proteins in the progression of NSCLC are further validated by proteomics data.

235 heir diverse functions in the progression of NSCLC.

236 factor promotes the stem-like properties of NSCLC cells and increases their aldehyde dehydrogenase (

237 to be detected because a large proportion of NSCLC patients does not respond to currently used therap

238 TOR; this in turn reduces the sensitivity of NSCLC cells with wild-type EGFR (EGFR(WT)) to EGFR TKI b

239 bit cancer cell growth in the early stage of NSCLC, but promote cell growth in the advanced stage of

240 promote cell growth in the advanced stage of NSCLC.

241 ted ERBB2DeltaEx16 expression in a subset of NSCLC cases, as well as splicing site mutations facilita

242 ly driven therapies for oncogenic subsets of NSCLC.

243 derlie enhanced OXPHOS and tumorigenicity of NSCLC cells.

244 4 alteration defines a molecular subgroup of NSCLCs for which MET inhibition with crizotinib is activ

245 iomarker of response, and define a subset of NSCLCs with a targetable epigenetic vulnerability.

246 ogy and Ontario Health (Cancer Care Ontario) NSCLC Expert Panel made updated recommendations based on

247 Using an experimental model of ALK positive NSCLC, we explored the evolution of resistance to differ

248 to 36% of patients with ROS1 fusion-positive NSCLC have brain metastases at the diagnosis of advanced

249 luded all patients with ROS1 fusion-positive NSCLC in the three trials who received at least one dose

250 advanced or metastatic ROS1 fusion-positive NSCLC who received entrectinib at a dose of at least 600

251 ontrol in patients with ROS1 fusion-positive NSCLC, and is well tolerated with a manageable safety pr

252 tions for patients with ROS1 fusion-positive NSCLC.

253 advanced or metastatic ROS1 fusion-positive NSCLC.

254 vity in patients with advanced ROS1-positive NSCLC, including those with CNS metastases and those pre

255 e analyze published WES data from 35 primary NSCLC and metastasis pairs, and transcriptomic data from

256 those who experienced systemic progression (NSCLC hazard ratio [HR], 0.58; P = .001; MMRD HR, 0.40;

257 studies demonstrated that ERbeta can promote NSCLC VM formation and cell invasion via altering the ER

258 PRODH promotes NSCLC tumorigenesis by inducing epithelial to mesenchyma

259 onstrate a novel role for LYCAT in promoting NSCLC and suggest that targeting LYCAT expression or act

260 a novel role for LYCAT activity in promoting NSCLC.

261 Representative NSCLC cell lines as well as patient-derived data showed

262 g ICG in patients with surgically resectable NSCLC.

263 exhibited greater potency in drug-resistant NSCLC cells (IC(50) = 17 nM) and in mice with H1975 xeno

264 apeutic strategy in acquired EGFRi-resistant NSCLC.

265 In EGFR-mutant osimertinib-resistant NSCLC models with EGFR-dependent and EGFR-independent re

266 microarray and RNA sequencing, the resistant NSCLC cell lines clustered together, providing a molecul

267 inhibitor (TKI)-sensitive and TKI-resistant NSCLC cells (IC(50) = 77 nM) and in xenograft mice.

268 gulatory axis in patients with TKI-resistant NSCLC.

269 ARPi and DNMTi therapy to robustly sensitize NSCLC cells to ionizing radiation in vitro and in vivo.

270 ion of TNF receptor-1 (TNFR1) and sensitized NSCLC cells to cytokine-induced apoptosis.

271 Inhibition of PIM sensitized NSCLC cells to chemotherapy and produced a synergistic a

272 g in nearly all patients with advanced-stage NSCLC.

273 se correlates with recurrence in early stage NSCLC.

274 oire analysis in a cohort of 236 early-stage NSCLC patients.

275 V-CTCs) at surgical resection of early-stage NSCLC represent subclones responsible for subsequent dis

276 ls could represent a novel approach to treat NSCLC and warrant further study.

277 es from nonresponders among PD-1 mAb-treated NSCLC patients.

278 and potential utility of P2-6R for treating NSCLC and other solid tumors.

279 lthough numerous studies on KRAS-mutant type NSCLC have been conducted, new oncogenic or tumor suppre

280 r registry data were used to determine which NSCLC patients diagnosed in the years 2010 through 2012

281 aimed to identify novel loci associated with NSCLC risk, and generate a PRS and evaluate its utility

282 Patients newly diagnosed with NSCLC in a tertiary referral hospital from January 2011

283 ic survival improved from 26% among men with NSCLC that was diagnosed in 2001 to 35% among those in w

284 scans from 109 treatment-naive patients with NSCLC (21 EGFR-mutant and 88 EGFR-wild type) underwent r

285 related with poor prognosis in patients with NSCLC harboring mutant EGFR; circulating endocan levels

286 dentification, at baseline, of patients with NSCLC most likely to have irSAEs, treatment plans can be

287 facilitate decision-making in patients with NSCLC when stereotactic ablative radiotherapy is an opti

288 Methods: Seventy-two patients with NSCLC who were treated with nivolumab or pembrolizumab a

289 nvolvement in the treatment of patients with NSCLC with chemotherapy, targeted therapies, and immunot

290 Trx1+ NK cells were present in patients with NSCLC with elevated ROS levels in the tumor.

291 eight patients with HNSCC, 20 patients with NSCLC, and 23 patients with other tumour types] in the d

292 Among 4064 patients with NSCLC, exploratory associations between tumor genomics a

293 er all-cause mortality risk in patients with NSCLC, which is partly mediated by a lower proportion of

294 of N0, N1, and N2|3 disease in patients with NSCLC.

295 ely with sensitivity to TKI in patients with NSCLC.

296 d OS but increased toxicity in patients with NSCLC.

297 r for 6-thio-dG sensitivity in patients with NSCLC.

298 of the T cells in the lungs of patients with NSCLC.

299 predict EGFR TKI sensitivity in smokers with NSCLC carrying EGFR(WT) and that the combination of EGFR

300 Similar patterns were found among women with NSCLC.