ライフサイエンスコーパス: lung cancer

1 gression, in an autochthonous mouse model of lung cancer.

2 ng PIM1 to Drp1 and mitochondrial fission in lung cancer.

3 better therapies for squamous non-small-cell lung cancer.

4 s prognostic factors for overall survival in lung cancer.

5 mending physical activity would help prevent lung cancer.

6 ng cancer module, QLQ-LC29, in patients with lung cancer.

7 stoma, breast cancer, colorectal cancer, and lung cancer.

8 tool for staging patients with lymphoma and lung cancer.

9 ot confer additional increase in the risk of lung cancer.

10 744 with oesophageal cancer, and 29 305 with lung cancer.

11 llow-up procedures for results suggestive of lung cancer.

12 rt that HACE1 is frequently mutated in human lung cancer.

13 toperative complications after lobectomy for lung cancer.

14 t body composition analysis in patients with lung cancer.

15 imodal PET/MRI voxelwise-matched analyses in lung cancer.

16 new avenues for the therapeutic treatment of lung cancer.

17 gies for targeting HDAC10 as a treatment for lung cancer.

18 ty of RAC-family GTPases in human and murine lung cancer.

19 inhibitors targeting EGFR in non-small-cell lung cancer.

20 e to Myc-driven lymphoma and Eml4-Alk-driven lung cancer.

21 therapy questions in squamous non-small-cell lung cancer.

22 ip between physical activity and the risk of lung cancer.

23 hing need to identify the key biomarkers for lung cancer.

24 response to manual contouring variability in lung cancer.

25 ion of tumor-suppressive effects of Rig-G in lung cancer.

26 LC), the most common histological subtype of lung cancer.

27 s for testicular to over 1,000,000 cases for lung cancer.

28 origenesis in human breast and nonsmall cell lung cancer.

29 stage and can reduce the risk of dying from lung cancer.

30 cancer, colorectal cancer, or non-small cell lung cancer.

31 kpoint inhibitors in melanoma and small-cell lung cancer.

32 al responses in nearly half of patients with lung cancer.

33 noma, a pathologic subtype of non-small cell lung cancer.

34 k squamous cell carcinoma and non-small cell lung cancer.

35 d smoking information and miss many incident lung cancers.

36 on unmet needs in the treatment of advanced lung cancers.

37 Tobacco smoking causes lung cancer(1-3), a process that is driven by more than

38 Cancer (EORTC) Quality of Life Questionnaire-Lung Cancer 13 (QLQ-LC13) assesses quality of life (QOL)

39 -of-Life Questionnaire-Core 30 (QLQ-C30) and Lung Cancer 13 (QLQ-LC13) were administered at cycles 1-

40 okers (159 [81%] of 196), had non-small-cell lung cancer (151 [76%] of 200), and were on therapy at t

41 Methods: Patients suspected of relapse of lung cancer after definitive radiotherapy (conventional

42 second cause of cancer-related deaths (after lung cancer) among women.

43 types including hematologic malignancies and lung cancers, among others.

44 he study included 109 patients (61 men) with lung cancer and 197 controls (78 men).

45 Analysis of a dataset of lung cancer and another dataset of gastric cancer with F

46 of the most common driver mutations in human lung cancer and correlates with aggressive disease progr

47 nd nonsuspicious for cancer in patients with lung cancer and lymphoma by using a convolutional neural

48 ody (18)F-FDG PET/CT images in patients with lung cancer and lymphoma.

49 n the cell-free DNA (cfDNA) of patients with lung cancer and of risk-matched controls reflect clonal

50 quantitative exposure assessment to evaluate lung cancer and subtype risks associated with occupation

51 established relationship between smoking and lung cancer and suggest that smoking may also be a risk

52 Smoking is a well-established cause of lung cancer and there is strong evidence that smoking al

53 to all histological types of non-small-cell lung cancer and to add focus on immunotherapy combinatio

54 esses quality of life (QOL) in patients with lung cancer and was the first EORTC module developed for

55 ndicated the expression of PIERCE1 in 83% of lung cancers and its correlation with pAKT expression.

56 e novel mechanistic insight into BRG1-mutant lung cancers and suggest that their dependency on ATR ca

57 n influences the outcome of lung infections, lung cancer, and chronic inflammatory disease.

58 lates with patient outcomes in patients with lung cancer, and loss of carboxypeptidase D reduced tumo

59 q served as potential prognostic markers for lung cancer, and M2 predominance and juxtaposition of M2

60 in papillary thyroid cancer, non-small-cell lung cancer, and multiple other cancers.

61 V have high burdens of chronic lung disease, lung cancers, and pulmonary infections despite antiretro

62 tertumoral and intratumoral heterogeneity of lung cancers as well as incidences of subtype transdiffe

63 f SOX2 as a prognostic marker in EGFR-mutant lung cancer, as SOX2-mediated cell plasticity regulated

64 models of mammary tumours and of metastatic lung cancer, as well as during fluorescence-guided robot

65 The cumulative rate ratio for death from lung cancer at 10 years was 0.76 (95% confidence interva

66 onsecutive patients undergoing lobectomy for lung cancer at 3 centers from 2014 to 2017 were retrospe

67 g of high-risk patients enables detection of lung cancer at an early stage and can reduce the risk of

68 ts undergoing lobectomy or pneumonectomy for lung cancer at our institution from 2000 to 2018 were re

69 care were obtained from the English National Lung Cancer Audit, 2007 to 2011.

70 data until Dec 31, 2014, and diagnosed with lung cancer between Jan 1, 2012, and Dec 31, 2012, with

71 asis, which commonly arises in patients with lung cancer, breast cancer and melanoma, is associated w

72 many malignancies, including non-small cell lung cancer, but its benefits have not extended to pancr

73 stration for the treatment of non-small-cell lung cancers, but their efficacy can be compromised by a

74 ontrol analysis on diesel engine exhaust and lung cancer by including three additional studies and qu

75 and Main Results: Our study included 16,901 lung cancer cases and 20,965 control subjects.

76 The lung cancer cases diagnosed by screening were more likel

77 RNA-seq analysis in human lung cancer cell line H1299 reveals that downregulated g

78 ve-like B cells from NSCLC patients with two lung cancer cell lines demonstrate that the naive-like B

79 is, modulation of SASH1 levels in a panel of lung cancer cell lines mediated changes in cellular prol

80 It was discovered that some lung cancer cell lines release surfactants only when pla

81 R) by antibody or CRISPR knockout of IL37 in lung cancer cell lines repolarized TAMs, resulting in re

82 n human lung cancer tissues and immortalized lung cancer cell lines via indirect immunofluorescence a

83 an normal lung epithelial cell line and four lung cancer cell lines were treated with TGF-beta.

84 In lung cancer cell lines, SMURF2 overexpression increased

85 d MET or c-Src signaling, including in human lung cancer cell lines.

86 ltimately apoptotic cell death in breast and lung cancer cell lines.

87 k between SOX2 and TGFbeta signaling affects lung cancer cell plasticity and TKI tolerance.

88 reducing cell cycle pathways and inhibiting lung cancer cell proliferation and migration.

89 24 subfamily A member 1 (CYP24A1) increases lung cancer cell proliferation by activating RAS signali

90 ated A(2)B(2) porphyrins were carried out in lung cancer cells (A549) to test their photodynamic ther

91 nker (P2-6R), which killed NCI-H460 and A549 lung cancer cells 100 times more effectively than the S

92 on (EMT) and migration in both primary human lung cancer cells and cell lines.

93 d epithelial-mesenchymal transition (EMT) in lung cancer cells and promoted metastatic spreading.

94 ) acetate monohydrate (Ag-Phen), toward A549 lung cancer cells are presented.

95 stemness and adherence independent growth of lung cancer cells but these inhibitors could also effici

96 he naive-like B cells suppress the growth of lung cancer cells by secreting four factors negatively r

97 TKI treatment favored selection of lung cancer cells displaying mesenchymal morphology with

98 immune rejection and allows growth of human lung cancer cells in lal(-/-) mice.

99 red for survival and outgrowth by metastatic lung cancer cells in the brain parenchyma.

100 A 10-min exposure of A549 human lung cancer cells to sequential 50- and 385-Hz oscillati

101 strated that a senescence-like state enables lung cancer cells to survive dual inhibition of EGFR and

102 e discovered that a subset of non-small cell lung cancer cells underwent a gradually progressing epit

103 The treatment of lung cancer cells with chloropyramine, a compound that i

104 Coculturing lung cancer cells with Th9/Th17 cells or exposing them t

105 Preselection of EGFR-mutant lung cancer cells with the mesenchymal phenotype diminis

106 64%, and 8% of human colon, pancreatic, and lung cancer cells, respectively, overexpressed SHH at tr

107 lony formation in liver, but also breast and lung cancer cells.

108 epa1-GFP hepatoma cells or AHR-deficient LLC lung cancer cells.

109 inase in maintaining survival of KRAS-mutant lung cancer cells.

110 stem-like cells as well as therapy resistant lung cancer cells.

111 nes, mammalian fibroblast and pancreatic and lung cancer cells.

112 ased EGFR steady-state levels and sensitized lung cancer cells.

113 , the videos of labeled EVs uptake by living lung cancer cells.

114 tion induced by femoral inoculation of Lewis lung cancer cells.

115 uate the solution space of trees in a recent lung cancer cohort.

116 ated by 365,307 DNA methylations in the TCGA lung cancer cohort.

117 k reveals metabolic heterogeneity within the lung cancer collective invasion pack and provides ration

118 her odds of lung cancer in the International Lung Cancer Consortium (odds ratio [OR] 1.80; 95% confid

119 NF-kappaB is known to play a pivotal role in lung cancer, contributing to tumor growth, microenvironm

120 ne microenvironment plays a critical role in lung cancer control versus progression and metastasis.

121 although levels are very low in early-stage lung cancers, ctDNA is present prior to treatment in mos

122 In this study, in silico analysis of TCGA lung cancer data sets revealed a significant increase in

123 ata from both synthetic and real (breast and lung cancer) datasets comparing it also against several

124 with chest computed tomography (CT) reduces lung cancer death.

125 conjunction with Lung-RADS leads to improved lung cancer detection.Keywords: CT, Lung, Thorax(C) RSNA

126 Median time to lung cancer diagnosis in patients with (n = 29) versus w

127 signaling, trended toward a shorter time to lung cancer diagnosis.

128 immune checkpoint inhibitors for small cell lung cancer, discuss challenges faced by regulatory agen

129 in lung cancers to affect TKI tolerance and lung cancer dissemination has yet to be elucidated.

130 lly engineered mouse model of non-small cell lung cancer driven by K-Ras G12D and p53 deficiency, G6P

131 As), DNA methylation, and point mutations in lung cancer driver genes in 292 tumor samples from 84 pa

132 porting the potential of ERBB2DeltaEx16 as a lung cancer driver, its expression transformed immortali

133 cterization of CANTOS patients who developed lung cancer during the study, including circulating tumo

134 Moreover, we reveal a lung cancer epithelial cell-autonomous function for p38a

135 ort a causal role of pulmonary impairment in lung cancer etiology.

136 trials in adult patients with non-small-cell lung cancers evaluating a platinum-based doublet with or

137 ial cells can be reprogrammed toward diverse lung cancer fates when exposed to the appropriate set of

138 ket dose-expansion cohort (12 non-small-cell lung cancer, five gynaecological malignancy, four colore

139 Adults with non-small cell lung cancer followed from 30 days post-diagnosis in Engl

140 itate better stratification of patients with lung cancer for anticancer therapies.

141 stic characteristics of female patients with lung cancer harboring RET fusion gene for the first time

142 ine derivatives - was initially described in lung cancers harbouring an EGFR mutation, and was subseq

143 fort to raise public awareness screening for lung cancer has been ongoing.

144 atures derived from yeast were detectable in lung cancers, head and neck cancers and tumors from pati

145 d < 0.0001) and lower risk of both liver and lung cancers (highest vs. lowest quintile: for liver, HR

146 al outcomes for patients with advanced-stage lung cancer; however, this disease remains the leading c

147 herapy-naive individuals with non-small-cell lung cancer identified the transcription factor IRF4 as

148 rmance in determining the risk of developing lung cancer in a patient with a nodule found at screenin

149 physical activity with histologic types and lung cancer in ever and never smokers.

150 esponse relationship between EC exposure and lung cancer in men.

151 ith statistically significant higher odds of lung cancer in the International Lung Cancer Consortium

152 prenatal sex steroids exposure) and primary lung cancer in women and men.

153 reased public awareness of pollution-related lung cancer in XF might have led to early diagnosis and

154 CYP24A1 could be therapeutically targeted in lung cancers in which its expression is high.

155 was used to estimate hazard ratios (HRs) for lung cancer incidence by sex, tobacco smoking, asbestos

156 Up to 12-year lung cancer incidence predicted by CXR-LC.

157 In patients with lung cancer, increased expression of HACE1 correlated wi

158 Tissue microarrays of human lung cancers indicated the expression of PIERCE1 in 83%

159 nd KDELR2, as robust, independent drivers of lung cancer invasion and metastasis.

160 factor receptor (EGFR) mutant non-small-cell lung cancer is a persistent challenge in cancer therapy.

161 Lung cancer is a prevalent and lethal cancer type that l

162 stics of RET fusions in female patients with lung cancer is available, this study revealed the geneti

163 ype-specific regulation of tumor fibrosis in lung cancer is mediated through differential SMAD3 promo

164 Lung cancer is one of most common malignancies worldwide

165 Lung cancer is the world's leading cause of cancer death

166 ociations between PM2.5 and incidence of non-lung cancers is limited.

167 tly mutated version of RAS in non-small-cell lung cancer, KRAS(G12C), we have the opportunity to eval

168 The Lung Cancer Master Protocol (Lung-MAP; S1400) is a compl

169 n-small-cell lung cancer [NSCLC], small-cell lung cancer, mesothelioma, thymic epithelial tumours, an

170 ority of clinical trials are in melanoma and lung cancer, meta-analyses that pool multiple cancer typ

171 ells) as a typical normal host cell from the lung cancer microenvironment and found no effect of fiel

172 screening modalities for early detection of lung cancer might result in the discovery of thyroid inc

173 nfirmed in subcutaneous and orthotopic mouse lung cancer models.

174 e and psychometric properties of the updated lung cancer module, QLQ-LC29, in patients with lung canc

175 ciation, however, is based on research using lung cancer mortality, not incidence.

176 mputed tomographic (CT) screening can reduce lung-cancer mortality among male former and current smok

177 per 1000 person-years in the control group; lung-cancer mortality was 2.50 deaths per 1000 person-ye

178 In this trial involving high-risk persons, lung-cancer mortality was significantly lower among thos

179 tases analyzed ex vivo from an autochthonous lung cancer mouse model had lower mitochondrial membrane

180 ERCE1 depletion in the KRAS mutation-related lung cancer mouse models revealed the suppressive effect

181 rst compared the expression of Rig-G between lung cancer (n = 138) and normal tissues (n = 23), from

182 are no targeted therapies for this subset of lung cancers, nor is it known how mutations in BRG1 cont

183 ients with previously treated non-small cell lung cancer (NSCLC) are assigned to personalized therapy

184 ity of targeted therapies for non-small-cell lung cancer (NSCLC) are directed against oncogenic drive

185 osimertinib (AZD9291) in the non-small cell lung cancer (NSCLC) cell line H1975, which harbors two E

186 ed resynthesized compounds in non-small-cell lung cancer (NSCLC) cells showed that cytotoxicities var

187 ation data: One set of public non-small cell lung cancer (NSCLC) data.

188 inum at the cellular level in non-small cell lung cancer (NSCLC) explant models after treatment with

189 patients with advanced-stage non-small-cell lung cancer (NSCLC) in light of the ever-expanding toolb

190 KRAS-mutant non-small cell lung cancer (NSCLC) is a major lung cancer subtype that

191 Non-small cell lung cancer (NSCLC) is known to have poor patient outcom

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

193 Non-small cell lung cancer (NSCLC) is the deadliest form of cancer worl

194 embrolizumab in patients with non-small-cell lung cancer (NSCLC) or melanoma with untreated brain met

195 rsus distant recurrences in a non-small cell lung cancer (NSCLC) population with mutated EGFR receivi

196 chemistry (IHC) on 8 pairs of non-small cell lung cancer (NSCLC) primary tumors and matched distant m

197 miR-21-5p isolated from human non-small cell lung cancer (NSCLC) tissue possesses 3'-terminal 2'Ome.

198 monocytes from patients with non-small cell lung cancer (NSCLC) where c-MAF is overexpressed.

199 he treatment of patients with non-small cell lung cancer (NSCLC) with EGFR-mutant tumors, TKI resista

200 py for patients with stage IV non-small-cell lung cancer (NSCLC) without driver alterations.

201 In non-small cell lung cancer (NSCLC), accumulation of anti-inflammatory t

202 icantly advanced treatment of non-small cell lung cancer (NSCLC), but protein level quantitation of d

203 s an option for patients with non-small cell lung cancer (NSCLC), distinguishing between N0, N1, and

204 d and neck (SCCHN), melanoma, non-small-cell lung cancer (NSCLC), or urothelial cancer.

205 labor between YAP and TAZ in non-small cell lung cancer (NSCLC), the most common histological subtyp

206 pplied to advanced metastatic non-small cell lung cancer (NSCLC).

207 cy of cetuximab for stage III non-small-cell lung cancer (NSCLC).

208 inhibit the proliferation of non-small-cell lung cancer (NSCLC).

209 e to these agents in treating non-small cell lung cancer (NSCLC).

210 ole for proline catabolism in non-small cell lung cancer (NSCLC).

211 ram of de novo lipogenesis in non-small cell lung cancer (NSCLC).

212 ty during clonal evolution in non-small cell lung cancer (NSCLC).

213 sence of any thoracic cancer (non-small-cell lung cancer [NSCLC], small-cell lung cancer, mesotheliom

214 ions are oncogenic drivers of non-small-cell lung cancers (NSCLCs)(1).

215 atients' receipt of initial assessments by a lung cancer nurse specialist and according to trust-leve

216 Lung cancer nurse specialist assessments before/at diagn

217 r study provides initial measures of overall lung cancer nurse specialist working practices at trusts

218 among those who received an assessment by a lung cancer nurse specialist, compared with no assessmen

219 led studies with longitudinal measurement of lung cancer nurse specialist-patient interaction are nee

220 A national survey of lung cancer nurse specialists provided information on se

221 tic regression models were used to calculate lung cancer odds ratios and 95% confidence intervals (CI

222 ient assigned amiloride died from metastatic lung cancer, one patient assigned riluzole died from isc

223 ective analysis of consecutive patients with lung cancer or lymphoma referred to a single center from

224 ients with advanced melanoma, non-small cell lung cancer, or bladder cancer.

225 ta, we examine and directly compare modeling lung cancer overall survival using gene expressions vers

226 t data in cancer prognosis modeling and into lung cancer overall survival.

227 lume growth was associated with a history of lung cancer (P < .001), a baseline nodule volume less th

228 ction of postoperative pulmonary function in lung cancer patients before tumor resection is essential

229 thway from smoking to overall survival among lung cancer patients potentially mediated by 365,307 DNA

230 we evaluated the incidence of infections in lung cancer patients treated with CPIs plus conventional

231 omic signature in early-stage non-small cell lung cancer patients treated with stereotactic body radi

232 We examined 281 lung cancer patients with distant metastasis and found t

233 clinical significance of circulating LDN in lung cancer patients, and further assessed its diagnosti

234 In breast and lung cancer patients, CAR-T cells targeting the tumor-as

235 In renal and lung cancer patients, the presence of the enterococcal p

236 lines, and correlated with poor prognosis in lung cancer patients.

237 ents and detectable in blood and tumors from lung cancer patients.

238 to improve the management of IPNs.Methods: A Lung Cancer Prediction Convolutional Neural Network mode

239 with traditional risk prediction models, the Lung Cancer Prediction Convolutional Neural Network was

240 As one of the most common forms of cancer, lung cancers present as a collection of different histol

241 ithelial p38alpha promotes Kras(G12V)-driven lung cancer progression via maintenance of cellular self

242 it known how mutations in BRG1 contribute to lung cancer progression.

243 proinflammatory cytokine in the at-risk for lung cancer pulmonary and the lung tumor microenvironmen

244 rgeons who met minimum volume thresholds for lung cancer resection based on definitions provided by t

245 e stage at diagnosis occurred among men with lung cancer residing in currently privileged areas that

246 g CYP2A expression may alter smoking-related lung cancer risk and tissue damage from other inhaled to

247 romoter was identified to be associated with lung cancer risk in Chinese populations.

248 us genetic variants that are associated with lung cancer risk, but the biological mechanisms underlyi

249 ex-based differences in smoking behaviors or lung cancer risk.

250 e aimed to address current knowledge gaps in lung cancer risks associated with low levels of occupati

251 associated (P trend < 0.01) with increasing lung cancer risks in nonsilicotics and in current, forme

252 nt effects of smoking and silica exposure on lung cancer risks.Methods: Subjects from 14 case-control

253 Small cell lung cancer (SCLC) is a highly aggressive subtype of lun

254 Small cell lung cancer (SCLC) is a neuroendocrine tumor treated cli

255 on in adult solid tumors, such as small-cell lung cancer (SCLC), is unknown.

256 se A (PKA) as an active kinase in small cell lung cancer (SCLC).

257 focus on the current evidence on LDCT-based lung cancer screening and discuss the clinical developme

258 indings establish the potential of cfDNA for lung cancer screening and highlight the importance of ri

259 ic, it is appropriate to defer enrollment in lung cancer screening and modify the evaluation of lung

260 The VRC performs well in an urban, diverse lung cancer screening program.

261 were developed to guide clinicians managing lung cancer screening programs and patients with lung no

262 Validation in lung cancer screening trials and not a clinical setting.

263 ifications of solid lung nodules detected at lung cancer screening using manual measurements of avera

264 Lung cancer screening with chest computed tomography (CT

265 caid Services (CMS) eligibility criteria for lung cancer screening with CT require detailed smoking i

266 PET/CT scans of patients with non-small cell lung cancer served as model for three 3-dimensionally pr

267 lmonary nodules (PN) detection and secondary lung cancer (SLC) diagnosis.

268 -wide CRISPR screens in 2D monolayers and 3D lung-cancer spheroids.

269 on-small cell lung cancer (NSCLC) is a major lung cancer subtype that leads to many cancer-related de

270 l stratified analyses by smoking history and lung cancer subtypes were performed in men.Measurements

271 h different exposure subgroups and different lung cancer subtypes.Objectives: We expanded on a previo

272 rmed as part of routine 6-month postsurgical lung cancer surveillance follow-up (Figs 2, 3).

273 ing characteristic curve [AUC]) for incident lung cancer than CMS eligibility (PLCO AUC, 0.755 vs. 0.

274 cer (SCLC) is a highly aggressive subtype of lung cancer that remains among the most lethal of solid

275 , which remain concentrated in patients with lung cancers that are associated with minimal exposure t

276 p represents around 20% of all patients with lung cancer, the discovery of stratified medicine option

277 Lung cancer, the leading cause of cancer mortality, exhi

278 of Th9 and Th17 cells was detected in human lung cancer tissue and correlated with poor survival.

279 d that Rig-G was frequently downregulated in lung cancer tissues and cell lines, and correlated with

280 ssion, which was later corroborated in human lung cancer tissues and immortalized lung cancer cell li

281 Remarkably, human lung cancer tissues can only be distinguished from adjac

282 ness and differentiation signaling emerge in lung cancers to affect TKI tolerance and lung cancer dis

283 te ratio (NLR) and survival in patients with lung cancer, treated with radiotherapy.

284 ocal control in patients with non-small cell lung cancer undergoing SBRT and could be combined in an

285 is developed to identify biomarker genes for lung cancer using gene expression profiles.

286 prognostic value of SASH1 in non-small cell lung cancers using publicly available datasets.

287 At 10 years of follow-up, the incidence of lung cancer was 5.58 cases per 1000 person-years in the

288 Lung cancer was detected in 44/87 (51%) LEMS patients.

289 cation on the association between asthma and lung cancer was identified for the variables of sex, smo

290 In men, exposure response between EC and lung cancer was observed: odds ratios ranged from 1.09 (

291 The association between ACR and lung cancer was uniquely robust, warranting future studi

292 sequencing in human and mouse non-small-cell lung cancers, we identify a cluster of dendritic cells (

293 The incidences of all cancer and lung cancer were consistently associated with PM2.5.

294 were excluded; patients with non-small-cell lung cancer were later excluded in an amendment.

295 year in patients with stage I-III small-cell lung cancer who have undergone curative-intent treatment

296 udy of patients with advanced non-small cell lung cancer who received CPIs combined with CC and those

297 age 18 years or older with breast, colon, or lung cancer who were prescribed cancer drug regimens by

298 ified, EGFR mutation-positive non-small-cell lung cancer, who had progressed on EGFR TKIs.

299 met need for targeted therapy in people with lung cancers with MET exon 14 alterations and adds to an

300 ossible treatment for EGFR mutation-positive lung cancers with MET-driven acquired resistance.