ライフサイエンスコーパス: lung tumor

1 ng EBUS-TBNI of cisplatin into the patient's lung tumor.

2 in chemo-radiotherapy to effectively reduce lung tumors.

3 partially reduced progression of Hace1(-/-) lung tumors.

4 n unexpected cancers, including sarcomas and lung tumors.

5 ce results in the formation of more abundant lung tumors.

6 to smoking-related transversion mutations in lung tumors.

7 for prevention and treatment of K-ras-mutant lung tumors.

8 autophagy-deficient (Atg7(-/-)) Kras-driven lung tumors.

9 ay the progression of RASSF1-hypermethylated lung tumors.

10 r growth of established EGFR(L858R)-mediated lung tumors.

11 in adults constituting less than 1% of adult lung tumors.

12 reshly resected human primary non-small-cell lung tumors.

13 ths of age, with 94% of mice also developing lung tumors.

14 n is observed at the invasive front of human lung tumors.

15 5% of cells isolated from the digested human lung tumors.

16 icantly decreased growth and angiogenesis of lung tumors.

17 skipping of an exon overexpressed in primary lung tumors.

18 II epithelial cells before the formation of lung tumors.

19 ated selective accumulation and retention in lung tumors.

20 e endothelium to enter mammary, prostate and lung tumors.

21 of the human RBL2 gene has been reported in lung tumors.

22 cond hit" in the etiology of smoking-related lung tumors.

23 data and DNA sequencing data for ovarian and lung tumors.

24 r, SIRT4 knockout mice spontaneously develop lung tumors.

25 CLC) but not in normal lung tissue or benign lung tumors.

26 igh activity of crizotinib in this subset of lung tumors.

27 hemical testing of SIRT1 activity in patient lung tumors.

28 o enhanced progression of KRas(G12D) -driven lung tumors.

29 +) T cell subpopulations in murine and human lung tumors.

30 2020 from patients undergoing lobectomy for lung tumors.

31 a critical role in shaping the phenotypes of lung tumors.

32 block formation or proliferation of primary lung tumors.

33 identify novel molecular features unique to lung tumors.

34 nant, minimally invasive, and small invasive lung tumors.

35 h results in recurrence of highly aggressive lung tumors.

36 , acts as an oncogenic driver in a subset of lung tumors.

37 ld be a strategy for treating LKB1-deficient lung tumors.

38 enografts (PDXs) from primary pancreatic and lung tumors.

39 Interestingly, citrate regressed Ras-driven lung tumors.

40 vation is found in non-KRAS-associated human lung tumors.

41 rovide a detailed immune cell atlas of early lung tumors.

42 ween loss of IPO11 and PTEN protein in human lung tumors.

43 hain reaction analyses of 102 non-small cell lung tumors, 61 ovarian tumors, 70 liver tumors, 156 gli

44 ion of PKCvarepsilon in breast, prostate and lung tumors above that of normal adjacent tissue.

45 mice, IL6-deficient mice developed much more lung tumors after an activating mutant of K-Ras was indu

46 shown to survive KRAS mutations and to form lung tumors after tobacco carcinogen exposure.

47 ssues and, because Ipo11 mutant mice develop lung tumors, also implicates Importin-11 as a novel tumo

48 observe an excess loss of heterozygosity in lung tumors among ATM L2307F allele carriers.

49 ogenesis, is frequently expressed in primary lung tumors, an active RANK pathway correlates with decr

50 Consequences on multimodal PET/MRI voxelwise lung tumor analyses were evaluated.

51 distortion for multimodal PET/MRI voxelwise lung tumor analyses.

52 Fibronectin and Tenascin-C (Tnc), in primary lung tumors and associated lymph node metastases compare

53 Ablation of club cells prevents chemical lung tumors and causes alveolar destruction in adult mic

54 D cells diminished their ability to initiate lung tumors and distant metastases.

55 nd hematopoietic tumors, K-Ras(G12V) induced lung tumors and gastric lesions.

56 nd deletions of exon 16 in a subset of these lung tumors and in a number of other carcinomas.

57 e, expression of miR-4423 is reduced in most lung tumors and in cytologically normal epithelium of th

58 Fzd9 expression was low in human lung tumors and in progressive dysplasias.

59 of mutations in the TP53 gene of nonsmokers' lung tumors and in the cII transgene of lung cellular DN

60 s (HPV) 16/18 E6 oncoprotein is expressed in lung tumors and is associated with p53 inactivation.

61 cinoma (NSCLC) accounts for 85% of malignant lung tumors and is the leading cause of cancer deaths.

62 g aggressive cancers, such as non-small-cell lung tumors and metastatic melanoma.

63 he cellular origins of environmental-induced lung tumors and of the dysfunctional airway and alveolar

64 at 20q11.21 were differentially expressed in lung tumors and paired normal tissues.

65 G is overexpressed in murine KrasG12D-driven lung tumors and that Sag deletion suppressed lung tumori

66 ess of the advancement made in understanding lung tumor, and its multimodal treatment, in general the

67 t mice developed fewer and smaller TSC2-null lung tumors, and introduction of uPA shRNA in tumor cell

68 ) composition of normal lung, fibrotic lung, lung tumors, and metastases.

69 (PSC) are present in tumor cell lines, mouse lung tumors, and mouse embryonic fibroblasts undergoing

70 multiforme, prostate tumors, non-small cell lung tumors, and ovarian tumors, but not nontumor prosta

71 70H) -specific sensitivity to simvastatin in lung tumors, and the transcriptional signature that unde

72 igarette smoking; it simultaneously inhibits lung tumor angiogenesis and metastasis by catalyzing the

73 Smoking-related lung tumors are characterized by profound epigenetic cha

74 showed the greatest reduction in metastatic lung tumors as a result of increased apoptotic resistanc

75 d that LINC00152 was highly overexpressed in lung tumors as compared to their adjacent normal tissues

76 er harboring KRAS/KEAP1- or KRAS/NRF2-mutant lung tumors as likely to respond to glutaminase inhibiti

77 a CD8(+)/CD103(-) T cell clone specific of a lung tumor-associated Ag, we demonstrated that the trans

78 Using human CD8(+) T cells specific to a lung tumor-associated Ag, we show in this article that C

79 Human lung tumor-associated CD8+ T lymphocytes also harbored s

80 Our data demonstrate that lung tumor-associated pDCs are responsive to the activat

81 anscriptomes of genetically engineered mouse lung tumors at seven stages, from pre-neoplastic hyperpl

82 tion was demonstrated in D54 glioma and A549 lung tumor bearing mice.

83 Lung tumor burden additionally correlated (r(2) = 0.714;

84 ntrast, high-dose LPS (10 mug/mouse) reduced lung tumor burden and was associated with a greater infl

85 MALT1-deficient mice show significantly less lung tumor burden when compared with its heterozygous co

86 e LPS administration resulted in a decreased lung tumor burden.

87 tain a more accurate estimation of the total lung tumor burden.

88 increased the number of mutant Kras-induced lung tumors, but decreased the number of mutant Hras-ind

89 sential effector of oncogenic KRAS in murine lung tumors, but it is unknown whether p110alpha contrib

90 notated to CpGs differentially methylated in lung tumors, but not blood, were enriched for RNA proces

91 inhibitor rapamycin in breast-cancer-derived lung tumors, but not in primary breast tumors.

92 zation of BCAA nitrogen limits the growth of lung tumors, but not pancreatic tumors.

93 eld significant efficacy against KRAS-driven lung tumors, but the combination of Torin2 with mitogen-

94 rted to increase the incidence of spleen and lung tumors, but to suppress tumors in three other conte

95 to demonstrate that combination therapy of a lung tumor by using radiofrequency ablation (RFA) with l

96 iting for the promotion of KRAS(G12D)-driven lung tumors by inducing the expression of KRAS(G12D) in

97 e monitored glycolysis in mouse lymphoma and lung tumors by measuring the conversion of hyperpolarize

98 se required to kill all cancerous cells in a lung tumor can be reduced by roughly 3 orders of magnitu

99 diversity of somatic lesions detected among lung tumors can confound efforts to identify these targe

100 Lung tumors catabolize circulating branched chain amino

101 Heterozygous deletion of NMNAT1 in lung tumor cell lines correlates with low expression lev

102 ive Src, both within the human tumors and in lung tumor cell lines exposed to hypoxia.

103 addition, the in vitro proliferation of the lung tumor cell lines was not affected by either CD22 an

104 Recombinant TTR stimulated lung tumor cell proliferation and growth, which were med

105 e developed a MALAT1 knockout model in human lung tumor cells by genomically integrating RNA destabil

106 survival, whereas re-expression of LZTFL1 in lung tumor cells inhibited extravasation/colonization of

107 Immunophenotypic analysis of lung tumor cells intravenously injected or spontaneously

108 eek mythology) confers anoikis resistance in lung tumor cells through repression of cell adhesion-rel

109 A549 lung tumor cells were orthotopically and metastatically

110 Interestingly, Ptges-knockout in mouse lung tumor cells, although reduced their stemness and EM

111 s the tumorigenicity of NF-kappaB1-deficient lung tumor cells.

112 he mesenchymal changes triggered by PREP1 in lung tumor cells.

113 dependent growth, and survival of anoikis of lung tumor cells.

114 ased proliferation and induced senescence in lung tumor cells.

115 strate that EphB4 is overexpressed 3-fold in lung tumors compared to paired normal tissues and freque

116 he tumor number, size, and histopathology of lung tumors compared to the control and bexarotene group

117 tors) in crizotinib-resistant ALK-rearranged lung tumors compared to treatment-naive controls, suppor

118 s study, higher endocan levels were found in lung tumors compared with cancer-free tissues and correl

119 ternative splicing in primary non-small cell lung tumors compared with normal lung tissue.

120 expression level was significantly lower in lung tumors compared with their corresponding normal tis

121 vival of SCID beige mice carrying A549 human lung tumors compared with treatment with antibodies targ

122 lium of adult mice initially elicited benign lung tumors comprising cuboidal epithelial cells express

123 ld increase in the susceptibility to develop lung tumors, confirming the role of ADAMTS12 as a tumor

124 -cell proteomic profiling of treatment-naive lung tumors, coupled with ex vivo testing of PDOs, ident

125 ung lesions yielded similar results (primary lung tumors: CT, 3.71; STIR short inversion time inversi

126 d and underexpressed in multiple independent lung tumor data sets, in both major NSCLC subtypes and i

127 FcepsilonRI signaling was observed in lung tumors derived from B16F10 cells.

128 of mice significantly reduced the weights of lung tumors derived from H1650 SP cells and tumor burden

129 d SOX2 in promoting a resistant phenotype of lung tumors derived from H1650 SP cells.

130 However, lung tumors developed in IL6-deficient mice were signifi

131 Mito-LND blocks lung tumor development and brain metastasis by inhibitin

132 ly link local microbiota-immune crosstalk to lung tumor development and thereby define key cellular a

133 Here we describe a new mouse model for lung tumor development to investigate the role of B-RAF

134 Lung tumor development was preceded by aberrant expansio

135 esis such that fibroblast transformation and lung tumor development were more reminiscent of that dri

136 e recombinase and sgRNAs, which caused rapid lung tumor development.

137 utic regimens were available 10 years ago, a lung tumor diagnosed today requires extensive pathologic

138 we demonstrate elevated ASM activity in the lung tumor environment and blood serum of patients with

139 In addition, collagen fibers in metastatic lung tumors exhibit greater linearity and organization a

140 Human lung tumors exhibit robust and complex mitochondrial met

141 g cancer gene expression data, immunostained lung tumors for MMP19, and performed in vitro assays to

142 a single lamin B1 allele induced spontaneous lung tumor formation and RET activation.

143 et al. demonstrate that SOX2 not only drives lung tumor formation but also restricts tumor lineage to

144 erence-mediated depletion of KIF23 inhibited lung tumor formation in vivo and induced apoptosis in lu

145 ool for lipidomic profiling of MYC-dependent lung tumors formed in this model.

146 mary human lung cancers, it inhibits primary lung tumors from metastasizing in a mouse model system.

147 SN2-type alkylation signature were higher in lung tumors from smokers than never-smokers, pointing to

148 uman lung cancer specimens and in orthotopic lung tumors generated by injection of a LH2-expressing h

149 By surveying lung tumor genomes for genes concomitantly inactivated w

150 X9 correlated negatively and positively with lung tumor grade, respectively.

151 The population model suggests that lung tumors grow faster and shed a significant number of

152 and mithramycin A (MMA) treatment inhibited lung tumor growth and down-regulated Sp1 protein express

153 dicates LINC00152 plays an important role in lung tumor growth and is potentially a diagnostic/progno

154 ndings therefore indicate that ACEE inhibits lung tumor growth and metastasis by inducing apoptosis a

155 e were used to evaluate the role of ALCAM in lung tumor growth and metastasis.

156 of concept that silencing of HOIL-1L impairs lung tumor growth and that HOIL-1L expression predicts s

157 essed from myeloid cells promotes CS-induced lung tumor growth by further recruitment of inflammatory

158 ed to CGPUs also exhibited the inhibition of lung tumor growth compared to animals administered with

159 hat a single 15 Gy radiation dose eliminated lung tumor growth in mice when ATM was deleted in cancer

160 drug carboplatin, ND-646 markedly suppressed lung tumor growth in the Kras;Trp53(-/-) (also known as

161 l tumor microenvironment profoundly affected lung tumor growth in three different i.v. metastasis mod

162 Lung tumor growth increased at 3 and 7 d after the admin

163 Lung tumor growth was arrested after a single administra

164 g bioluminescent imaging and showed that the lung tumor growth was suppressed but not eradicated by (

165 ibutions of each of the two circulations for lung tumor growth.

166 he proliferation of tumor cells and promotes lung tumor growth.

167 rophages and reduces CD8+ T cells to promote lung tumor growth.

168 Patients with lung tumors harboring activating mutations in the EGF re

169 nical rationale to improve the management of lung tumors harboring KRAS mutations with NRF2 pathway i

170 fortunately, attempts to target K-ras-mutant lung tumors have thus far failed, clearly indicating the

171 In early stage lung tumors high Trim28 correlates with increased overal

172 of lung cancer risk in smokers, progress in lung tumor immunotherapy, and implementation of populati

173 In conclusion, IMT is a rare lung tumor in adults and may simulate malignancy.

174 Although it is the most common lung tumor in children, it is seen rarely in adults cons

175 pletion in human breast cancer cells reduced lung tumors in a mouse xenograft model and clinical data

176 is upregulated in a significant fraction of lung tumors in correlation with mutational status of K-r

177 increased progression of KRas(G12D) -driven lung tumors in Hace1(-/-) mice.

178 Histological sections of lung tumors in mice treated with MSU-42011 exhibited red

179 Using transplantable models of lung tumors in mice, we found that amphiregulin, a membe

180 d onset and multiplicity of urethane-induced lung tumors in mice.

181 d induced apoptosis in lung cancer cells and lung tumors in murine orthotopic and metastatic models,

182 flammation and markedly increased numbers of lung tumors in response to urethane, even when transgene

183 believed to contribute to the development of lung tumors in smokers.

184 bility of porphysomes for in vivo imaging of lung tumors in the mucosal/submucosal layers, providing

185 or the first time, the role of C/EBPalpha in lung tumors in vivo using transgenic mice with lung epit

186 atory epithelium prevented the initiation of lung tumors in vivo.

187 significantly increased the proliferation of lung tumors in wild-type mice, but not in CRAMP-deficien

188 ss or inhibition in established SCLC primary lung tumors, in liver metastases, and in chemotherapy-re

189 Myc inhibition not only contains Ras-driven lung tumors indefinitely, but also leads to their progre

190 s this sensitivity was also present in human lung tumors, indicating that this therapeutic approach m

191 y demonstrated the role of CD103 integrin on lung tumor-infiltrating lymphocyte (TIL) clones in promo

192 preading of freshly isolated CD8(+)/CD103(+) lung tumor-infiltrating lymphocytes and CD103(+) tumor-s

193 sociation of the cardinal events involved in lung tumor initiation and cancer progression.

194 mation and aggressiveness in mouse models of lung tumor initiation and progression.

195 emphasize a role for PI3K signaling, not in lung tumor initiation per se, but in both the rate of tu

196 F ablation after SPACE to treat unresectable lung tumors is technically feasible, safe, and effective

197 hich is frequently co-amplified with KRAS in lung tumors, is essential for microtubule polymerization

198 eed serve a unique and nondegenerate role in lung tumor maintenance that cannot be complemented by an

199 edical domains, we propose a novel model for lung tumor malignancy prediction.

200 ytoid dendritic cells (pDCs) highly populate lung tumor masses and are strictly correlated to bad pro

201 In lung tumors, mature dendritic cells (DC) present in tumo

202 phorylation observed in cell lines and human lung tumors may explain how the CDCP1/SFK complex regula

203 nimally invasive adenocarcinoma, or invasive lung tumors measuring less than 1 cm.

204 ole of nonclassical, patrolling monocytes in lung tumor metastasis and their functional relationships

205 monocytes play a critical role in preventing lung tumor metastasis via NK cell recruitment and activa

206 ling, epithelial-mesenchymal transition, and lung tumor metastasis.

207 omes modulate the immune response to promote lung tumor metastasis.

208 m Lewis lung carcinoma (LLC) s.c. tumors and lung tumor metastasis.

209 ypes to generate a novel resource called the Lung Tumor Microenvironment Interactome (LTMI).

210 ne evasion in the context of a heterogeneous lung tumor microenvironment is vital for the development

211 he at-risk for lung cancer pulmonary and the lung tumor microenvironments.

212 Nkx2-1-negative murine lung tumors mimic mucinous human lung adenocarcinomas, w

213 diopharmaceutical on NSCLC using a xenograft lung tumor model and the reporter gene imaging technique

214 An orthotopic A549 lung tumor model was used to monitor the in vivo distrib

215 Anti-tumor activity was carried out in H1650 lung tumor model.

216 ha(Delta/Delta) mice) and a urethane-induced lung tumor model.

217 growth rate of 5.9) in mouse xenograft A549 lung tumor models within 14 days.

218 14 and increased anti-tumor activity against lung tumor models.

219 r mouse-tail IV injections in xenograft A549 lung tumor models.

220 database of 150 patients to characterize the lung tumor motion.

221 loid cells of the CCSP-rtTA/(tetO)(7)-Stat3C lung tumor mouse model.

222 linking overexpression of CHI3L1 to various lung tumor mouse models.

223 D-fed mice exhibited significantly decreased lung tumor multiplicity and attenuated pulmonary inflamm

224 prospective and retrospective human primary lung tumors (n = 458).

225 In patient tumor samples, overall lung tumor NF-kappaB activity was strongly associated wi

226 s and a resulting reduction in the number of lung tumor nodules were observed.

227 the airway field of the most common type of lung tumors, non-small cell lung cancer (NSCLC).

228 y pyrosequencing in an independent set of 48 lung tumor/normal paired.

229 Calpha resulted in a significant increase in lung tumor number, size, burden and grade, bypass of onc

230 -17F, resulted in a significant reduction in lung tumor numbers in CCSP(cre)/K-ras(G12D) mice and als

231 microenvironments and spontaneous liver and lung tumors occurring with increased incidence in carcin

232 ically heterogeneous disease, giving rise to lung tumors of varying histologies that include adenocar

233 mbers suppresses the neutrophil response and lung tumor outgrowth.

234 Lung tumors predicted to be independent primary tumors b

235 d that FAM83H-AS1 plays an important role in lung tumor progression and may be potentially used as di

236 itutively active Yap was sufficient to drive lung tumor progression in vivo.

237 IKK2/NF-kappaB-driven primary-to-metastatic lung tumor progression.

238 ulin deficiency resulted in markedly delayed lung tumor progression.

239 dependent and Yap/Taz-dependent pathways, in lung tumor propagation and metastasis.

240 total injected dose per gram tissue) in the lung tumor regions after mouse-tail IV injections in xen

241 ly expanded stromal progenitors from patient lung tumor resections without complex sorting methods or

242 rofiling reveal increased collagen levels in lung tumors resistant to PD-1/PD-L1 blockade.

243 In tyrosine kinase inhibitor-resistant lung tumors, rociletinib and AZD9291 are highly active w

244 Lung tumor size, malignancy and associated morbidity wer

245 Here, we used viable human lung tumor slices and autologous tumor antigen-specific

246 suppressor miRNA, restored miR-34a levels in lung tumors, specifically down-regulated miR-34a target

247 Here we show that low DAB2 levels in lung tumor specimens are significantly correlated with p

248 necessary for proliferation and survival in lung tumor spheroids.

249 Herein, we stratified lung tumor subpopulations based on AXL signaling as a po

250 Notably, both the lung tumor-suppressing and -promoting functions of IL6 i

251 ent but Tpl2-depenednt role of NF-kappaB1 in lung tumor suppression.

252 role in the cell cycle and is implicated in lung tumor suppression.

253 These findings indicate that KMT2D is a lung tumor suppressor and that KMT2D deficiency confers

254 Lung tumor suppressor gene Gprc5a-knockout (ko) mice are

255 In conclusion, the role of C/EBPalpha as a lung tumor suppressor was demonstrated for the first tim

256 suggests a possible role of C/EBPalpha as a lung tumor suppressor, there is no direct proof for this

257 wn cells were less efficient in establishing lung tumors than BRMS1(KD) cells.

258 Particularly, the M109 lung tumors that did not respond to doxorubicin treatmen

259 i.v.) injection into live mice bearing human lung tumors that were sensitive and resistant to cisplat

260 inhibited the formation of KrasG12D-induced lung tumors through a similar mechanism involving inacti

261 and metastasis in aggressive neuroendocrine lung tumors through regulation of the receptor tyrosine

262 hibited the growth and viability of squamous lung tumors, thus providing an effective strategy to ove

263 re distinctly expressed at a higher level in lung tumor tissue and the testes compared with other non

264 Lung tumor tissue microarrays from 104 patient samples w

265 SNORA42 expression in lung tumor tissue specimens is inversely correlated with

266 inversely correlated with that of ARHGAP5 in lung tumor tissues (P=0.0156).

267 l lines (9/9) and 70.83% (85/120) of primary lung tumor tissues compared with none (0/20) of normal a

268 of histone deacetylase 11 (HDAC11) in human lung tumor tissues correlate with poor patient outcome a

269 ulated in lung cancer cell lines and primary lung tumor tissues harboring a hypermethylated SOX30.

270 vel of SNORA42 on frozen surgically resected lung tumor tissues of 64 patients with stage I NSCLC by

271 00152 expression in an independent cohort of lung tumor tissues using quantitative RT-PCR.

272 D11b (a macrophage marker) expression in the lung tumor tissues.

273 ion or SHP-1 inhibition sensitizes resistant lung tumors to anti-PD-1.

274 of tumor growth and the propensity of benign lung tumors to progress to a malignant phenotype.

275 DAPT6 provided significantly higher tumor-to-lung, tumor-to-liver, tumor-to-spleen, and tumor-to-musc

276 A greater decrease in lung tumor volume (-37.2% vs. -27.6%) was associated wit

277 Baseline lung tumor volume addressed with (68)Ga-DOTA-E-[c(RGDfK)

278 nsmokers and patients with a higher baseline lung tumor volume were more likely to have a higher prog

279 Targeting of xenograft and orthotopic lung tumors was demonstrated with fluorescent (DiR) CLG

280 pha in the maintenance of mutant Kras-driven lung tumors was explored using an inducible mouse model.

281 apy strategies for patients with early stage lung tumors, we developed a multiscale immune profiling

282 To investigate NF-kappaB function in human lung tumors, we identified a gene expression signature i

283 rmational), and -p53(R270H) (contact) mutant lung tumors, we identified genotype-independent and geno

284 the interactions between cells within human lung tumors, we perform RNA-seq profiling of flow-sorted

285 Although nearly 10% of the lung tumors were positive for any HPV DNA (7% for HPV16

286 ember of the MMP family, is overexpressed in lung tumors when compared with control subjects.

287 ng to the lipoproteinated NC accumulation in lung tumors, where they exert a significant therapeutic

288 e transcription factor STAT3 in K-ras-mutant lung tumors, which was further amplified by the tumor-en

289 pression of SMARCA4 observed in some primary lung tumors, whose mechanism was largely unknown, can be

290 that target alternative mechanisms to treat lung tumors with acquired resistance to first-line EGFR

291 ally administered porphysomes accumulated in lung tumors with significantly enhanced disease-to-norma

292 In mouse models that develop lung tumors with well precise boundaries, the method tha

293 Hk2 deletion is therapeutic in mice bearing lung tumors without adverse physiological consequences.

294 of targeted radiotherapy on human orthotopic lung tumors without influencing acute DNA damage or a la

295 so effectively inhibited the growth of human lung tumor xenografts (A549) harboring aberrantly active

296 Applying this approach to patient-derived lung tumor xenografts (PDTX), we show that the liver sup

297 genation during an oxygen challenge in H1299 lung tumor xenografts grown in a murine model as indepen

298 Subcutaneous and lung tumor xenografts were used to compare lesion detect

299 al levels dramatically reduced the growth of lung tumor xenografts.

300 s and survival in highly vascularized murine lung tumor xenografts.