ライフサイエンスコーパス: lung tumor

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

2 5% of cells isolated from the digested human lung tumors.

3 icantly decreased growth and angiogenesis of lung tumors.

4 skipping of an exon overexpressed in primary lung tumors.

5 II epithelial cells before the formation of lung tumors.

6 ated selective accumulation and retention in lung tumors.

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

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

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

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

11 r, SIRT4 knockout mice spontaneously develop lung tumors.

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

13 Interestingly, citrate regressed Ras-driven lung tumors.

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

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

16 hemical testing of SIRT1 activity in patient lung tumors.

17 susceptibility to spontaneous lymphomas and lung tumors.

18 leolar RNA 42 (SNORA42) was overexpressed in lung tumors.

19 tiation program in HBECs and also in primary lung tumors.

20 in chemo-radiotherapy to effectively reduce lung tumors.

21 brain metastases relative to paired primary lung tumors.

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

23 n unexpected cancers, including sarcomas and lung tumors.

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

25 to smoking-related transversion mutations in lung tumors.

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

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

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

29 ay the progression of RASSF1-hypermethylated lung tumors.

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

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

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

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

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

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

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

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

38 nd H1993, which are derived from the primary lung tumor and a metastasis, respectively, from the same

39 nsgenic mice are prone to carcinogen-induced lung tumors and a broad spectrum of spontaneous tumors.

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

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

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

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

44 tribbles homolog 2 (TRIB2) in primary human lung tumors and in non-small cell lung cancer cells that

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

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

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

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

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

50 y analyses in mice bearing subcutaneous A549 lung tumors and orthotopic Lewis lung carcinoma models s

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

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

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

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

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

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

57 ary Akt isoform activated by mutant K-ras in lung tumors, and that Akt3 may oppose Akt1 in lung tumor

58 70H) -specific sensitivity to simvastatin in lung tumors, and the transcriptional signature that unde

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

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

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

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

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

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

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

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

67 e develop chronic pulmonary inflammation and lung tumors at a high frequency.

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

69 howed that ADM and AHR were coupregulated in lung tumor biopsies from smoker patients.

70 p65/RelA reduces the number of K-Ras-induced lung tumors both in the presence and in the absence of t

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

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

73 NK cells, which resulted in an overwhelming lung tumor burden relative to that in animals receiving

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

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

76 f the systemic administration of poly I:C on lung tumor burden.

77 replication factor Ciz1 is present in 34/35 lung tumors but not in adjacent tissue, giving rise to s

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

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

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

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

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

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

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

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

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

87 Lung tumors catabolize circulating branched chain amino

88 Our results demonstrate that human lung tumor cell fate decisions may be regulated during t

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

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

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

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

93 IL-6 secretion unleashed previously addicted lung tumor cells from their EGFR dependency.

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

95 Immunophenotypic analysis of lung tumor cells intravenously injected or spontaneously

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

97 A549 lung tumor cells were orthotopically and metastatically

98 enograft model the preemptive cotreatment of lung tumor cells with an EGFR inhibitor and a BH3 mimeti

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

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

101 ased proliferation and induced senescence in lung tumor cells.

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

103 sufficient to eradicate the early-resistant lung-tumor-cells evading targeted inhibitors.

104 of the 64Cu-DOTA-knottin 2.5F tracer in the lung tumors combined with a low background in the thorax

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

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

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

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

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

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

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

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

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

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

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

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

117 Moreover, JNK is required for lung tumor development caused by mutational activation o

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

119 Lung tumor development was preceded by aberrant expansio

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

121 or studying the role of the immune system in lung tumor development.

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

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

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

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

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

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

128 Moreover, Klf5 is not required for lung tumor formation in an inducible oncogenic K-Ras(G12

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

130 with defective antitumor immunity to promote lung tumor formation, representing a unique system for s

131 with TNF-alpha inhibited the progression of lung tumors formed from MDA-MB-231 breast cancer cells (

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

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

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

135 By surveying lung tumor genomes for genes concomitantly inactivated w

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

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

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

139 mor-associated inflammatory cells may modify lung tumor growth and invasiveness.

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

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

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

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

144 stimulated in vivo conditions, and promoted lung tumor growth following i.v. injection of MADB106 tu

145 pal-7 provided significant 75% inhibition of lung tumor growth in nude mice.

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

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

148 aN cooperated with activated K-Ras to induce lung tumor growth in vivo.

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

150 Lung tumor growth was arrested after a single administra

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

152 n the respiratory epithelium and accelerated lung tumor growth, indicating that precise regulation of

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

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

155 ruitment of macrophages into tumor sites and lung tumor growth.

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

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

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

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

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

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

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

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

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

165 6), we found significantly fewer and smaller lung tumors in both groups compared with controls.

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

167 n macrophages reduced the number and size of lung tumors in macFoxm1(-/-) mice.

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

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

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

171 owth of SULF2M-ISG15H, but not SULF2U-ISG15L lung tumors in nude mice (P<0.002).

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

173 determined that K-Ras activates NF-kappaB in lung tumors in situ.

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

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

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

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

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

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

180 y C, group 5, member a (Gprc5a) gene develop lung tumors, indicating that Gprc5a is a tumor suppresso

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

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

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

184 We show that lung tumors initially respond to cisplatin by sensing DN

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

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

187 ng tumorigenesis allow careful evaluation of lung tumor initiation, progression, and response to ther

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

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

190 ancer program is active in breast, colon and lung tumors isolated directly from human patients and is

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

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

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

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

195 In this study, we assess the variability of lung tumor measurement using repeat CT scans performed w

196 ediate) (Gr-1(int)) myeloid cells within the lung tumor microenvironment of NLRP3(-/-) mice was coinc

197 mary lung cancer cells isolated from patient lung tumors migrated at a 10- to 40-fold higher rate tha

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

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

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

201 In a chemically-induced lung tumor model, macrophages expressed argI(high)iNOS(l

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

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

204 14 and increased anti-tumor activity against lung tumor models.

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

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

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

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

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

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

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

212 Notably, lung tumor number and size were increased in enFoxm1(-/-

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

214 -17F, resulted in a significant reduction in lung tumor numbers in CCSP(cre)/K-ras(G12D) mice and als

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

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

217 mbers suppresses the neutrophil response and lung tumor outgrowth.

218 Lung tumors predicted to be independent primary tumors b

219 These data support the use of miR-34 as a lung tumor-preventative and tumor-static agent.

220 mt3a may act like a tumor-suppressor gene in lung tumor progression and may be a critical determinant

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

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

223 utive HIF-2alpha activity can promote murine lung tumor progression, suggesting that HIF proteins may

224 ulin deficiency resulted in markedly delayed lung tumor progression.

225 t3 may oppose Akt1 in lung tumorigenesis and lung tumor progression.

226 ucidate an important role for macrophages in lung tumor promotion and indicate that these cells have

227 astasis, but information about their role in lung tumor promotion is limited.

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

229 g chemically and genetically-induced primary lung tumors, prostate tumors, colon xenografts, and lung

230 Here, lung tumors revealed decreased levels of both zyxin and

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

232 Lung tumor samples with corresponding microarray and cli

233 c analyses in mice bearing subcutaneous A549 lung tumors showed prolonged blood circulation (t(1/2),

234 nscription-PCR (RT-PCR) performed on patient lung tumors showed that ID1 levels were elevated in adva

235 on supported by recent studies in Ras-driven lung tumors showing that inhibiting endogenous Myc trigg

236 Lung tumor size, malignancy and associated morbidity wer

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

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

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

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

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

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

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

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

245 pose it as an 8p21.3 haploinsufficient human lung tumor suppressor.

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

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

248 ancer, mice expressing the transgene develop lung tumors that regress rapidly when the transgene is s

249 , we investigate the ability to characterize lung tumors that spontaneously arise in a transgenic mou

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

251 ough mutations in Kras are present in 21% of lung tumors, there is a high level of heterogeneity in p

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

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

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

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

256 Lung tumor tissue samples from patients demonstrated a s

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

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

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

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

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

262 also determined that the percentage of human lung tumor tissues positive for Brachyury expression inc

263 00152 expression in an independent cohort of lung tumor tissues using quantitative RT-PCR.

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

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

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

267 PET/CT for response assessment in malignant lung tumors treated with radiofrequency ablation (RFA) a

268 or 623 candidate genes in 188 non-small cell lung tumors using the new method.

269 4 expression signature in a panel of primary lung tumors, validating their specific response by a com

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

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

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

273 The incidence of urethane-induced lung tumors was decreased by 69% in PKCdelta-deficient k

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

275 e of both BRAF(V600E)- or KRAS(G12D)-induced lung tumors was dependent on MEK-->ERK signaling.

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

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

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

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

280 real-time imaging in viable slices of human lung tumors, we revealed that the density and the orient

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

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

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

284 olycomb-group complexes repress the locus in lung tumors, whereas the SWI/SNF family member Snf5 acts

285 ce, K-ras mutations are sufficient to induce lung tumors, which require phosphoinoside-3-kinase (PI3K

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

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

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

289 Lung tumors with loss of p65/RelA have higher numbers of

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

291 The inhibition of ALK in lung tumors with the ALK rearrangement resulted in tumor

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

293 37 significantly decreased tumor growth in a lung tumor xenograft mouse model, suppressed tumor phosp

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

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

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

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

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

299 sues and inhibits growth of human breast and lung tumor xenografts.

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