ライフサイエンスコーパス: lung carcinoma

1 ent response in patients with non-small cell lung carcinoma.

2 s and the higher expression of RHOA in human lung carcinoma.

3 istinguishing small-cell from non-small-cell lung carcinoma.

4 n Basal-like breast cancer and squamous cell lung carcinoma.

5 rames new directions with early detection of lung carcinoma.

6 ults emerging in sarcomas, breast cancer and lung carcinoma.

7 ociated macrophages and aggressive growth of lung carcinoma.

8 xpressed in prostate, breast, and small-cell lung carcinoma.

9 mined on an orthotopic murine model of human lung carcinoma.

10 t mutagens and heme iron are associated with lung carcinoma.

11 ric/autonomic) usually related to small-cell lung carcinoma.

12 ide strong evidence of a recent diagnosis of lung carcinoma.

13 amage associated apoptosis in non-small cell lung carcinoma.

14 o tumor formation in a K-Ras murine model of lung carcinoma.

15 is present in murine models of melanoma and lung carcinoma.

16 eneic metastatic murine models 4T1 and Lewis lung carcinoma.

17 d cancers, including colorectal, breast, and lung carcinomas.

18 nducing signaling pathways in neuroendocrine lung carcinomas.

19 various types of cancer including breast and lung carcinomas.

20 was found to be highly upregulated in human lung carcinomas.

21 cinomas, metastatic melanomas and small cell lung carcinomas.

22 oxygen-induced retinopathy (OIR), and Lewis lung carcinomas.

23 the treatment of human ovarian, breast, and lung carcinomas.

24 on in clinical samples of primary breast and lung carcinomas.

25 ween physical activity and smoking for total lung carcinomas = 0.002).

26 nteresting anticancer capacity against human lung carcinoma (A-549) and colon adenocarcinoma (DLD-1)

27 muM) cell lines; human glioblastoma U-87 and lung carcinoma A549 are less sensitive.

28 cells and the unaltered appearance of human lung carcinoma A549 cells.

29 bronchial epithelial Beas-2B cells and human lung carcinoma A549 cells.

30 duced a significant increase of ROS in human lung carcinoma A549 cells.

31 erative effects in breast cancer (MCF-7) and lung carcinoma (A549) cell lines.

32 contrast, physical activity was unrelated to lung carcinoma among never smokers (P(interaction) betwe

33 esults are also seen in mice bearing a Lewis lung carcinoma and a C26 colon adenocarcinoma.

34 ant Kras-driven GEMMs--one of non-small-cell lung carcinoma and another of pancreatic adenocarcinoma-

35 ong evidence of recent clinical diagnosis of lung carcinoma and are regarded as positive cases in our

36 pression of the folate receptor and EpCAM on lung carcinoma and breast adenocarcinoma cells, respecti

37 n animals, but promote tumor growth of human lung carcinoma and CNT-transformed lung epithelial cells

38 eficient macrophages against syngeneic Lewis lung carcinoma and ID8 ovarian carcinoma cells, a defect

39 the compounds were able to inhibit both A549 lung carcinoma and MCF-7 breast carcinoma cell growth in

40 in cancer, such as those between prostate or lung carcinoma and more aggressive tumors with neuroendo

41 ally, we show that the brain metastases from lung carcinoma and other carcinomas in patients contain

42 dely used in the treatment of non-small cell lung carcinoma and other late-stage tumors.

43 tivity at inhibiting proliferation of DMS-53 lung carcinoma and SK-N-MC neuroepithelioma cell lines c

44 ls, and diminished progression of both Lewis lung carcinoma and spontaneous mammary carcinomas.

45 Two patients had cancer (1 lung carcinoma and the other thymic carcinoma).

46 enic MR1(-/-) clonal derivatives of the A549 lung carcinoma and THP-1 monocytic cell lines and used t

47 cancer cells, including B16 melanoma, Lewis lung carcinoma and transgenic mouse prostate cancer-C2 c

48 hypermethylated CpG islands in primary human lung carcinomas and lung cancer cell lines.

49 f the four PAR family members to motility of lung carcinomas and primary tumor samples from patients.

50 l systems: an ectopic syngeneic tumor (Lewis lung carcinoma) and an orthotopically xenografted human

51 eatment inhibited A549 (human non-small cell lung carcinoma) and H358 (human bronchioloalveolar non-s

52 LLC1 (Lewis lung carcinoma) and primary mouse melanoma cells harbori

53 ncies, including distinct types of lymphoma, lung carcinoma, and neuroblastoma.

54 box P3 expression, in normal mice and Lewis lung carcinoma-bearing mice.

55 -dependent cancers, including pancreatic and lung carcinomas but its role in breast cancer has not be

56 oma), MCF-7 (breast carcinoma) and NCI-H460 (lung carcinoma) by 4-34%, respectively.

57 y 2% of all tumor cells in established Lewis lung carcinomas, caused rapid hypoxic necrosis of both c

58 l mechanism by which nicotine promotes human lung carcinoma cell growth.

59 culated subcutaneously with a non-small cell lung carcinoma cell line and treated with paclitaxel for

60 he Na(+) pump) has been studied in the human lung carcinoma cell line H1299 that expresses YFP-tagged

61 n PIC3611 rendered the strain cytotoxic to a lung carcinoma cell line; however, only prtS induction w

62 horylated-EGFR (p-EGFR) and miR-21 levels in lung carcinoma cell lines and the suppression of miR-21

63 y, viability, and cellular ATP levels of the lung carcinoma cell lines H1299 and A549.

64 A-mediated TRPC1 depletion in non small cell lung carcinoma cell lines induced G(0)/G(1) cell cycle a

65 rrelated with the 256 variants in the NCI-60 lung carcinoma cell lines, valine with high expression a

66 variant was enriched to MAF = 0.64 in NCI-60 lung carcinoma cell lines, whereas the TOP1MT R525W was

67 totoxicity of meayamycin B in non-small cell lung carcinoma cell lines.

68 parent diazeniumdiolate toward nonsmall cell lung carcinoma cells (A549), but they were not appreciab

69 idney epithelial cells (LLC-MK(2)) and human lung carcinoma cells (A549).

70 allowed for preferable elimination of human lung carcinoma cells (capital A, Cyrillic549) as compare

71 ta1 transcripts following culture with human lung carcinoma cells (LCCs).

72 tumor growth in nude mice using mouse Lewis lung carcinoma cells (LLCs).

73 In human colon carcinoma cells (HCT-8) and lung carcinoma cells (NCI-H460), small-interfering RNA-i

74 as shown to increase MUC2 expression in A549 lung carcinoma cells and both MUC6 and MUC5AC expression

75 K inhibits the proliferation of melanoma and lung carcinoma cells and induces apoptosis in vitro.

76 AMPK by ZMP in pemetrexed-treated colon and lung carcinoma cells and the downstream consequences of

77 of these mutants failed to replicate in A549 lung carcinoma cells and Wi38 normal lung cells.

78 5-LO in the TME using a model in which Lewis lung carcinoma cells are directly implanted into the lun

79 trasplenic injection of MC38 colon and Lewis lung carcinoma cells before depleting myeloid cells with

80 ent vinorelbine increased apoptosis of human lung carcinoma cells by inducing FBXL2 expression and cy

81 H2 expression is regulated in non-small cell lung carcinoma cells by oncogenic KRAS.

82 Liver metastasis of Lewis lung carcinoma cells followed this pattern but this mech

83 Subcutaneous implantation of Lewis lung carcinoma cells in IRAK-M(-/-) mice resulted in a f

84 nsplanted syngeneic B16F10 melanoma or Lewis lung carcinoma cells is slowed in Adora2a(f/f)-LysMCre(+

85 rived from long-term cultures of mouse Lewis lung carcinoma cells Matrigel plugs taken from morphine-

86 p-regulated by conditioned medium from Lewis lung carcinoma cells or C26 colon adenocarcinoma cells,

87 sion plasmid prior to inoculation with Lewis lung carcinoma cells or the induction of sepsis.

88 Silencing of PAR1 expression in the lung carcinoma cells phenocopied stromal Mmp1a-deficienc

89 -/-) endothelial cells exposed to M27 murine lung carcinoma cells reveal that Gas6 increases prostagl

90 Human lung carcinoma cells served as a heterologous expression

91 rdance, cultured SCLC but not non-small cell lung carcinoma cells showed no or extremely low levels o

92 In this study, we used non-small lung carcinoma cells to characterize the mechanism of a

93 Cytotoxicity was evaluated in A549 human lung carcinoma cells using 3-(4,5-dimethylthiazol-2-yl)-

94 The viability of A549 lung carcinoma cells was reduced by 2, and it increased

95 TCF binding to mucin gene expression, Calu-3 lung carcinoma cells were exposed to lipopolysaccharide

96 re exposed to cigarette smoke (CS) and Lewis lung carcinoma cells were injected to initiate the growt

97 rived from long-term cultures of mouse Lewis lung carcinoma cells when compared with placebo.

98 ring Gal-1-deficient mice as hosts for Lewis lung carcinoma cells where Gal-1 levels were preserved o

99 By treating A549 lung carcinoma cells with a novel small molecule that pr

100 oup H or haplogroup T in cultured A549 human lung carcinoma cells with identical nuclear backgrounds.

101 ition and consequent trapping of circulating lung carcinoma cells within DNA webs.

102 Mouse lung cancer cells (CMT167 and Lewis lung carcinoma cells) injected directly into lungs of sy

103 358 (human bronchioloalveolar non-small cell lung carcinoma cells) xenograft tumor growth in immunode

104 e superoxide dismutase (MnSOD) mRNA in human lung carcinoma cells, A549, mediated by a protein kinase

105 er progression, (ii) drug treatment in human lung carcinoma cells, and (iii) diagnosis of type 2 diab

106 nocarcinoma metastasis driven by ZEB1, human lung carcinoma cells, and human breast carcinoma cells.

107 hemic retinas and, to a lesser extent, Lewis lung carcinoma cells, whereas B16 melanomas showed littl

108 FMS) induce antibodies against murine Lewis lung carcinoma cells, with increased antibody-mediated c

109 rived from long-term cultures of mouse Lewis lung carcinoma cells.

110 inhibition of migration and invasion of A549 lung carcinoma cells.

111 n mark, a specific target of LSD1, in Calu-6 lung carcinoma cells.

112 educe NCAM polysialylation in SW2 small cell lung carcinoma cells.

113 din impeded migration and induced anoikis in lung carcinoma cells.

114 s are activated in mice implanted with Lewis lung carcinoma cells.

115 n mark, a specific target of LSD1, in Calu-6 lung carcinoma cells.

116 ve and pro-apoptotic effects on murine Lewis lung carcinoma cells.

117 o immunodeficient mice using human non-small lung carcinoma cells.

118 gration and invasion of MC38 colon and Lewis lung carcinoma cells.

119 tumor burden when inoculated s.c. with Lewis lung carcinoma cells.

120 lly, the seal H3N8 virus replicated in human lung carcinoma cells.

121 H localize in the mitochondria of H292 human lung carcinoma cells.

122 between MTOR and ponatinib in non-small cell lung carcinoma cells.

123 splayed sub-micromolar activity against H292 lung carcinoma cells.

124 ith the genomic profile of 178 squamous cell lung carcinomas characterized by The Cancer Genome Atlas

125 1, 2006, there were 10,227 incident cases of lung carcinoma, classified as adenocarcinoma (n = 4,036)

126 the lack of CBX7 protein expression in human lung carcinomas correlated with CCNE1 overexpression.

127 s, the B16F10.9 melanoma (B16) and the Lewis lung carcinoma (D122) in the NCR1 knockout mouse that wa

128 dicts the appearance of strong evidence of a lung carcinoma diagnosis via analysis of large-scale ano

129 rs who later input queries consistent with a lung carcinoma diagnosis, with a true-positive rate rang

130 relationship between alcohol consumption and lung carcinoma differs by histological subtype.

131 In human breast and lung carcinomas, ERK8 expression is reduced while ER O-g

132 Human non-small cell lung carcinoma expressed varying levels of both soluble

133 as the benefits of Gal-1 expression to Lewis lung carcinoma growth were abolished in immunodeficient

134 Rag1(-/-) mice inhibited melanoma as well as lung carcinoma growth.

135 ormation, but promoted tumor growth of human lung carcinoma H460 cells, suggesting the tumor-promotin

136 ecent advances in therapy for non-small cell lung carcinoma have shown that a personalized approach t

137 on strategy was effective in eradicating 3LL lung carcinoma in 100% of mice.

138 relationship between alcohol consumption and lung carcinoma in 492,902 persons from the National Inst

139 in both MTG8 and MTG16 in colon, breast, and lung carcinoma in addition to functioning as negative re

140 eat was associated with an increased risk of lung carcinoma in both men (HR(Q5vsQ1): 1.22; 95% CI: 1.

141 Heme iron intake increased the risk of lung carcinoma in both men (HR(Q5vsQ1): 1.25; 95% CI: 1.

142 efficiency of liver metastasis by colon and lung carcinoma in mice that are genetically deficient fo

143 n of S1PR3 profoundly inhibits the growth of lung carcinoma in mice.

144 ociated with increased risk of squamous cell lung carcinoma in the International Lung Cancer Consorti

145 rmation of a niche that supports ingrowth of lung carcinoma in vivo via activation of TGFbeta product

146 single KRAS mutation and form adenosquamous lung carcinomas in mice.

147 ted mortality worldwide, with non-small-cell lung carcinomas in smokers being the predominant form of

148 ese searchers and on the correlation between lung carcinoma incidence rates and our log-based statist

149 mutation E64D, which was detected in a human lung carcinoma, increases the lung cancer incidence in m

150 shown a decreased susceptibility to develop lung carcinomas induced by chemical carcinogens in Mmp1a

151 In mice bearing 4T1 breast tumor or Lewis lung carcinoma, intratumoral Tconv cells expressing elev

152 Lung carcinoma is the leading cause of cancer-related de

153 is by two cell lines, B16F1 melanoma and 3LL lung carcinoma, is greatly reduced in transgenic mice th

154 a variety of cancer cell lines such as A549 (lung carcinoma), KB (epidermal carcinoma), MCF-7 (breast

155 highly activated in skeletal muscle of Lewis lung carcinoma (LLC) and Apc(Min/+) mouse models of canc

156 ced growth of subcutaneously implanted Lewis lung carcinoma (LLC) and B16-F10 melanoma tumors, respec

157 A murine model of Lewis lung carcinoma (LLC) cell metastasis revealed that COX-2

158 vitro cytotoxicity data collected with Lewis Lung Carcinoma (LLC) cells are consistent with this rele

159 R) plasmid DNA (pDNA) was evaluated in Lewis lung carcinoma (LLC) cells cultured in vitro or in vivo

160 mice bearing subcutaneously implanted Lewis lung carcinoma (LLC) cells exhibited significantly short

161 ion of control monocytes together with Lewis lung carcinoma (LLC) cells into Hpa-KO mice resulted in

162 le mass induced in mice engrafted with Lewis lung carcinoma (LLC) cells or in Apc(Min) (/+) mice, an

163 Murine Lewis lung carcinoma (LLC) cells that overexpress or underexpr

164 Lewis lung carcinoma (LLC) cells were injected into 8-wk-old s

165 Sca1-positive stromal cells, and mouse Lewis lung carcinoma (LLC) cells, we found that adenosine rece

166 novel signalling pathway through which Lewis lung carcinoma (LLC) induces atrogin1/MAFbx upregulation

167 complex 1 was validated in the murine Lewis Lung Carcinoma (LLC) model.

168 Lewis lung carcinoma (LLC) or B16 melanoma grafted in KOR knoc

169 s of C57BL/6 mice bearing a metastatic Lewis lung carcinoma (LLC) variant.

170 w that, among the cell lines screened, Lewis lung carcinoma (LLC) were the most potent macrophage act

171 In the case of Lewis lung carcinoma (LLC), an additional defect in tumor cell

172 innate immune response in mice bearing Lewis lung carcinoma (LLC), and targeting TLR4 alone effective

173 ell lung cancer (SCLC) cells and mouse Lewis lung carcinoma (LLC), which display aggressive metastati

174 e to minimal expression in contrast to Lewis lung carcinoma (LLC).

175 vironment (TME) promoted the growth of Lewis lung carcinoma (LLC).

176 By contrast, in Lewis lung carcinomas (LLC), inhibition of VEGF or PDGF reduce

177 Coculturing of MPhi with mouse Lewis lung carcinoma (LLC1) and 10 different human lung cancer

178 Growth of mouse Lewis lung carcinoma (LLC1) and/or mouse melanoma B16 cell was

179 bitor in a murine model of OSA bearing Lewis lung carcinoma (LLC1) tumors.

180 ro by human embryonic kidney (HEK293), Lewis lung carcinoma (LLC1), and A549 cells and are devoid of

181 our KrasTgfbr2(-/-) mouse model of invasive lung carcinoma mirrors the genomic response and clinical

182 -4-1BBL/SVN subunit vaccine formulation in a lung carcinoma model and demonstrate the robust therapeu

183 eal instillation of a single dose in a Lewis lung carcinoma model in mice.

184 ral CD11b(+)Gr1(high) cells in a mouse Lewis lung carcinoma model in vivo and demonstrated that these

185 Here, using a Lewis lung carcinoma model of cancer cachexia, we show that tu

186 not seen in the LSL-Kras(G12D) nonsmall cell lung carcinoma model, down-regulation of PLCepsilon was

187 he mice were cured in both the 4T1 and Lewis lung carcinoma models compared to 20% treated with free

188 aneous A549 lung tumors and orthotopic Lewis lung carcinoma models showed significant tumor growth de

189 T generation is also observed in mammary and lung carcinoma models, suggesting that cancers, through

190 (-/-) BMDCs eliminate established s.c. Lewis Lung Carcinoma more efficiently than their WT counterpar

191 Using a Kras-driven non-small cell lung carcinoma mouse model, we found that either RALA or

192 cervical cancer and survivin-expressing 3LL lung carcinoma mouse models.

193 his association was strongest for small-cell lung carcinomas (multivariate RR = 1.56, 95% CI: 0.99, 2

194 Stable reexpression of Arkadia in lung carcinoma NCI-H460 cells, which we show contain a h

195 Non-small-cell lung carcinoma (NSCLC) accounts for 85% of malignant lun

196 ignificantly overexpressed in non-small cell lung carcinoma (NSCLC) as compared to normal tissues and

197 array data from cell lines of Non-Small Cell Lung Carcinoma (NSCLC) can be used to look for differenc

198 mic and proteomic analysis of non-small cell lung carcinoma (NSCLC) cell lines revealed significantly

199 or PF2341066 in MET-amplified non-small cell lung carcinoma (NSCLC) cell lines to identify drug resis

200 protein expression identifies non-small cell lung carcinoma (NSCLC) cell lines whose growth and invas

201 Our current study using non-small-cell lung carcinoma (NSCLC) cell lines, animal models, and cl

202 s method was applied to human non-small cell lung carcinoma (NSCLC) cell lines, embedded as spheroids

203 owed that nicotine stimulates non-small cell lung carcinoma (NSCLC) cell proliferation through nicoti

204 silencing of which sensitized non-small cell lung carcinoma (NSCLC) cells to the cytotoxic effects of

205 ors and restores autophagy in non-small-cell lung carcinoma (NSCLC) cells with a TKI-sensitive EGFR m

206 ential for PML degradation in non-small cell lung carcinoma (NSCLC) cells, and PML and PIAS1 were inv

207 In studies performed in non-small cell lung carcinoma (NSCLC) cells, we found that PGE(2) stimu

208 dwide, and among this cancer, non-small cell lung carcinoma (NSCLC) comprises the majority of cases.

209 PKCvarepsilon is required for non-small cell lung carcinoma (NSCLC) growth in vitro as well as tumor

210 demonstrate that HH-dependent non-small cell lung carcinoma (NSCLC) growth is sensitive to blockade o

211 mes of patients with advanced non-small-cell lung carcinoma (NSCLC) harbouring epidermal growth facto

212 ance of TIL subpopulations in non-small cell lung carcinoma (NSCLC) have thus far not been systematic

213 and parametric PET images of non-small cell lung carcinoma (NSCLC) in order to provide insight on th

214 Non-small-cell lung carcinoma (NSCLC) is among the deadliest of human c

215 Non-small cell lung carcinoma (NSCLC) is the leading cause of cancer-re

216 ressor is a frequent event in non-small cell lung carcinoma (NSCLC) leading to the activation of mTOR

217 (EGFR)-targeted therapies in non-small cell lung carcinoma (NSCLC) led to investigation of novel com

218 iven pro-malignant traits in a nonsmall cell lung carcinoma (NSCLC) model.

219 ted level of EAPII protein in non-small-cell lung carcinoma (NSCLC) patients and NSCLC cell lines in

220 (EGFR) are effective in most non-small cell lung carcinoma (NSCLC) patients whose tumors harbor acti

221 )F-FLT) PET in advanced-stage non-small cell lung carcinoma (NSCLC) patients with an activating epide

222 to overcome the resistance of non-small cell lung carcinoma (NSCLC) to the AKT inhibitor MK2206, whic

223 t inoperable locally-advanced non-small cell lung carcinoma (NSCLC), a disease poorly controlled by s

224 nes in patients with advanced non-small cell lung carcinoma (NSCLC), especially in those whose cancer

225 ic of many cancers, including non-small cell lung carcinoma (NSCLC), head and neck squamous cell carc

226 uctal adenocarinoma (PDAC) or non-small cell lung carcinoma (NSCLC), respectively, but despite the sa

227 val in never smokers who have non-small cell lung carcinoma (NSCLC), we conducted a consistency meta-

228 NK is frequently activated in non-small cell lung carcinoma (NSCLC), we investigated the role of the

229 arge-cell lymphoma (ALCL) and non-small cell lung carcinoma (NSCLC).

230 rs from Chinese patients with non-small cell lung carcinoma (NSCLC).

231 lial cancers, particularly in non-small cell lung carcinoma (NSCLC).

232 MISO) uptake in patients with non-small cell lung carcinoma (NSCLC).

233 prognosis and progression of non-small cell lung carcinoma (NSCLC).

234 samples from 17 patients with non-small cell lung carcinoma (NSCLC).

235 ients with radically resected non-small cell lung carcinoma (NSCLC).

236 erapeutic agents for treating non-small cell lung carcinoma (NSCLC).

237 d histopathologic response in non-small cell lung carcinoma (NSCLC).

238 ome in patients with resected non-small-cell lung carcinoma (NSCLC; n = 248).

239 expressed in the majority of non-small cell lung carcinomas (NSCLC) but not in normal lung tissue or

240 mical analysis of a cohort of non-small-cell lung carcinomas (NSCLC) indicated that 15.5% (16 of 103)

241 development and progression of nonsmall cell lung carcinomas (NSCLC) is widely recognized.

242 ound in approximately 3-7% of non-small cell lung carcinomas (NSCLC).

243 lid tumour samples (including non-small-cell lung carcinoma [NSCLC], colorectal carcinoma, and melano

244 e protumorigenic functions in non-small cell lung carcinomas (NSCLCs) but have AMPK-activating proper

245 was also prevalent in squamous nonsmall cell lung carcinomas (NSCLCs), and selective PAK1 inhibition

246 Non-small-cell lung carcinomas (NSCLCs), which represent around 80% of

247 ntenance of Kras(G12V)-driven non-small cell lung carcinomas (NSCLCs).

248 human cancers, but rarely in non-small cell lung carcinomas (NSCLCs).

249 oma, the two major classes of non-small-cell lung carcinomas (NSCLCs).

250 During follow-up to 2003, 6,745 lung carcinomas occurred (14.8% small cell, 40.3% adenoc

251 tal lung metastasis after injection of Lewis lung carcinoma or B16F10 melanoma cells.

252 ry and efficacy of cyclophosphamide in Lewis lung carcinomas or RIP-Tag2 tumors.

253 Non-small cell lung carcinoma patients are frequently treated with cisp

254 isolated from peripheral blood of small cell lung carcinoma patients given chemotherapy.

255 ymphoma kinase (ALK)-positive non-small-cell lung carcinoma patients, progression during treatment ev

256 patients with ROS1-rearranged non-small-cell lung carcinoma, recently emerging clinical evidence sugg

257 d with a modest nonlinear reduction in total lung carcinoma risk at lower levels of consumption (for

258 en NSCLC (14 adenocarcinoma, 9 squamous cell lung carcinoma [SCC], and 1 mixed adenocarcinoma and SCC

259 Small cell lung carcinoma (SCLC) is a highly lethal, smoking-associ

260 Small-cell lung carcinoma (SCLC) is a neuroendocrine subtype of lun

261 Small cell lung carcinoma (SCLC) is extremely aggressive and freque

262 ber of tumor types indicated that small cell lung carcinoma (SCLC) is sensitive to LSD1 inhibition.

263 Small cell lung carcinoma (SCLC) often features the upregulation of

264 In a human small-cell lung carcinoma (SCLC) primary xenograft model, ME and CM

265 Cancer (majority small-cell lung carcinoma [SCLC]) was detected in 66 of 84 evaluate

266 ice injected with galectin-1 knockdown Lewis lung carcinoma showed decreased expression and ectodomai

267 earchers who queried for symptoms related to lung carcinoma, some (n = 5443 of 4813985) later issued

268 was commonly downregulated in non-small cell lung carcinomas, suggesting that PPP2R2A status may serv

269 t gastric adenocarcinomas and non-small cell lung carcinomas, targets vascular endothelial growth fac

270 the prognosis of patients with squamous cell lung carcinomas than mRNA-based signatures.

271 Strikingly, patients with non-small cell lung carcinoma that had received WGP treatment for 10-14

272 Finally, we found that non-small-cell lung carcinoma that presented a cytonuclear ZO-1 pattern

273 mouse epithelial ovarian carcinoma and mouse lung carcinoma, the interaction between tumor-infiltrati

274 Using non-small cell lung carcinoma to illustrate this approach, we show a co

275 evels of CD73 expression were found on Lewis lung carcinoma tumor cells (DeltaMFI of 3.2 +/- 0.2).

276 ckade reduced TGF-beta signaling and limited lung carcinoma tumor progression.

277 PDGF-B blockade in Lewis lung carcinoma tumors by the DNA aptamer AX102 for 14 da

278 we show that the myeloid infiltrate in mouse lung carcinoma tumors encompasses two morphologically di

279 eutic efficacy against TC-1 cervical and 3LL lung carcinoma tumors, respectively.

280 uppressor cells (MDSC) in mice bearing Lewis lung carcinoma tumors.

281 We transplanted B16F0 and Lewis lung carcinoma tumour cells into Tc1 mice and showed tha

282 chemotherapy in patients with non-small cell lung carcinoma using functional diffusion maps (fDMs).

283 In the metastatic model of Lewis lung carcinoma, vaccination of the TAA survivin with SA-

284 feasibility of screening patients at risk of lung carcinoma via analysis of signals from online searc

285 on of tertiles 3 and 1 (T3vsT1), the risk of lung carcinoma was associated with intake of well-/very-

286 Small cell lung carcinoma was diagnosed in the patient with antibod

287 nical trials for the treatment of small cell lung carcinoma, was synthesized using this strategy.

288 as the growth of other tumors, such as Lewis lung carcinoma, was unaltered.

289 Twenty-one of the twenty-four non-small-cell-lung carcinomas we analyzed express IWS1.

290 Using a s.c. murine model of Lewis Lung Carcinoma, we found that HPK1(-/-) BMDCs eliminate

291 penetrates about 1 mm into xenografted A549 lung carcinoma, which is about four times penetration de

292 parameters in cell lines from squamous cell lung carcinoma, which is standardly treated by radiother

293 ate association between meat consumption and lung carcinoma, which might be explained by heme iron in

294 r2) in a mouse model of mutant K-ras-induced lung carcinoma, which normally induces the formation of

295 nal antibodies that attenuate non-small cell lung carcinoma xenograft growth by downregulation of rec

296 d the role of BMDC recruitment in breast and lung carcinoma xenograft models after local irradiation

297 duced EC migration and tumor growth in human lung carcinoma xenografted in immunodeficient mice.

298 inally, 2cPE was also tested in vivo on A549 lung carcinoma xenografts generated in mice.

299 aging modalities to evaluate the response of lung carcinoma xenografts in mice after gemcitabine ther

300 ET and diffusion-weighted (DW) MR imaging in lung carcinoma xenografts.