ライフサイエンスコーパス: lung carcinoma

1 in targeting c-Myc for degradation in human lung carcinoma.

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

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

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

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

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

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

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

9 ociated macrophages and aggressive growth of lung carcinoma.

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

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

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

13 rames new directions with early detection of lung carcinoma.

14 O901317 in a murine model of syngeneic Lewis Lung carcinoma.

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

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

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

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

19 nducing signaling pathways in neuroendocrine lung carcinomas.

20 various types of cancer including breast and lung carcinomas.

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

22 cinomas, metastatic melanomas and small cell lung carcinomas.

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

24 ation, a DBD mutant found to be prevalent in lung carcinomas.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 enesis in multiple mouse models of melanoma, lung carcinoma and pancreatic B-cell insulinoma and prov

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

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

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

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

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

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

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

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

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

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

50 earing mouse models (A549 lung cancer, Lewis lung carcinoma, and MDMAMB 231 xenografts) with a high s

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

52 network is active in human HCC, breast, and lung carcinomas, as well as in 2 independent mouse liver

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

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

55 de CRISPR-Cas9-mediated screen using a human lung carcinoma cell line and identify semaphorin (SEMA)

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

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

58 entry into A549 cells, a highly transducible lung carcinoma cell line, in comparison to well-studied

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

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

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

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

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

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

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

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

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

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

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

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

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

72 cell targeting and magnetic transfection of lung carcinoma cells are demonstrated using gradient-fre

73 5-LO in the TME using a model in which Lewis lung carcinoma cells are directly implanted into the lun

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

75 1-mediated resistance, induced DNA damage in lung carcinoma cells but exerted DNA protective activity

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

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

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

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

80 tenuate LOX activity and metastasis of Lewis lung carcinoma cells in mice.

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

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

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

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

85 Likewise, restoration of Rig-G in Lewis lung carcinoma cells permitted development of fewer canc

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

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

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

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

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

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

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

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

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

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

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

97 358 (human bronchioloalveolar non-small cell lung carcinoma cells) xenograft tumor growth in immunode

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

99 In cultured A549 lung carcinoma cells, anakinra, PAS600-IL-1Ra, and PAS80

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 1, 2006, there were 10,227 incident cases of lung carcinoma, classified as adenocarcinoma (n = 4,036)

119 ive cancers, such as advanced non-small-cell lung carcinoma, combination immunotherapies have resulte

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

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

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

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

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

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

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

127 SIX2 protected RAS/P53-driven non-small-cell lung carcinomas from inflammatory cell death induced by

128 e murine models of high-grade neuroendocrine lung carcinomas generated by the loss of 4 tumor suppres

129 ors, including small-cell and non-small cell lung carcinomas, glioma, neuroblastoma, and pancreatic c

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

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

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

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

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

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

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

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

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

139 Lung carcinoma in situ (CIS) lesions are the pre-invasiv

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 es of adoptively transferred syngeneic Lewis lung carcinoma (LLC) cells are significantly reduced in

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

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

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

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

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

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

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

162 toxic effects and induced apoptosis in Lewis lung carcinoma (LLC) cells.

163 or one week in the presence of a CM of Lewis lung carcinoma (LLC) cells.

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

165 was increased in skeletal muscle in a Lewis lung carcinoma (LLC) model of cancer cachexia.

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

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

168 in regulating macrophage function from Lewis lung carcinoma (LLC) s.c. tumors and lung tumor metastas

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

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

171 C/EBPbeta with mutated Lys39 impaired Lewis lung carcinoma (LLC)-induced activation of the C/EBPbeta

172 all cell lung cancer: CMT167 (CMT) and Lewis lung carcinoma (LLC).

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

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

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

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

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

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

179 s (MDSC) and regulatory T cells in colon and lung carcinoma LM is TNFR2-dependent in female, but not

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

181 -4-1BBL/SVN subunit vaccine formulation in a lung carcinoma model and demonstrate the robust therapeu

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

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

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

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

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

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

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

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

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

191 pectively included 79 patients with stage IV lung carcinomas (n=24), renal carcinomas (n=11), or mela

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

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

194 ine drug for cancers, such as non-small cell lung carcinoma (NSCLC) and bladder cancer.

195 6 female, median age 73) with non-small cell lung carcinoma (NSCLC) and treated with ICI were prospec

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 ose crizotinib induces ICD in non-small cell lung carcinoma (NSCLC) cells and effectively controls th

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

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

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

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

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

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

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

214 Progression on therapy in non-small cell lung carcinoma (NSCLC) is often evaluated radiographical

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 atform to detect and quantify non-small cell lung carcinoma (NSCLC) rare genetic mutants (EGFR T790M)

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

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

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

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

227 d with Akt hyperactivation in non-small-cell lung carcinoma (NSCLC), promotes tumour development and

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

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

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

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

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

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

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

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

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

237 e first-line chemotherapy for non-small-cell lung carcinoma (NSCLC).

238 y, are often overexpressed in non-small cell lung carcinoma (NSCLC).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 nes and ceca, and B16-F10 melanoma and Lewis lung carcinoma progressed more quickly than in control m

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 ocrine cell carcinoma, LCNEC, and small-cell lung carcinoma, SCLC) are among the most deadly lung can

267 s), renal carcinoma (eight patients, 17.8%), lung carcinoma (seven patients, 15.6%), and bladder carc

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

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

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

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

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

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

274 ular carcinomas, and primary human liver and lung carcinomas that desaturate palmitate to the unusual

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

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

277 women; median age, 73 y) with non-small cell lung carcinoma treated with ICIs were prospectively coll

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

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

280 on of PERK increases muscle wasting in Lewis lung carcinoma tumor-bearing mice.

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

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

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

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

285 tration into subcutaneously implanted murine lung carcinoma tumors.

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

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

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

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

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

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

292 e expression studies, focusing on breast and lung carcinomas, we analyzed the correlation between TIM

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

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

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

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.