ライフサイエンスコーパス: tumor cell

1 fined as nuclear staining in more than 5% of tumor cells).

2 ression by immunohistochemistry on >/= 5% of tumor cells.

3 llowed by lethal regrowth of more aggressive tumor cells.

4 of HuR-regulated proteins (Bcl2 and p27) in tumor cells.

5 heir functional activities toward autologous tumor cells.

6 -6) cytokine secreted from EGFRvIII-positive tumor cells.

7 oproteinases in ACM reversed ACM's effect on tumor cells.

8 mTORC2 kinase activity and invasion in colon tumor cells.

9 d with temozolomide to increase apoptosis of tumor cells.

10 pecific innate killing of virus-infected and tumor cells.

11 more significant cell cycle G0/G1 arrest of tumor cells.

12 s in neurons, is directed to mitochondria of tumor cells.

13 h their ability to degrade the ECM in breast tumor cells.

14 y in tumors and analyzing single circulating tumor cells.

15 he hallmark of hematogenous dissemination of tumor cells.

16 pithelial mesenchymal transition pathways in tumor cells.

17 pro-metastatic proteins is a feature of many tumor cells.

18 ted with the STAT3 phosphorylation status of tumor cells.

19 ent infection was established in a subset of tumor cells.

20 f a labeled plasma receptor overexpressed on tumor cells.

21 ulating glycolysis and hypoxic adaptation in tumor cells.

22 reduction in labeling of PD-L1 expression in tumor cells.

23 fibroblasts (CAFs) when co-cultured with the tumor cells.

24 PGBD5-induced DNA rearrangements in rhabdoid tumor cells.

25 racteristics in primary MECs and spontaneous tumor cells.

26 enetically engineered mouse models and human tumor cells.

27 performed to confirm SSTR2 expression of the tumor cells.

28 anomalous cancer-associated antigens by the tumor cells.

29 lls or accumulate intracellularly in certain tumor cells.

30 ect on bone metastasis of Jagged1-expressing tumor cells, 15D11 dramatically sensitizes bone metastas

31 Under conditions of hypomethylation (e.g. in tumor cells), a window of opportunity for L1 derepressio

32 chanism known as lineage plasticity, whereby tumor cells acquire phenotypic characteristics of a cell

33 croenvironment that mediate intravasation of tumor cells across an intact endothelium.

34 al link between intracellular annexin A2 and tumor cell adhesion, migration and in vivo grafting.

35 We found that tumor cells adjacent to bundled collagen had a preferent

36 n of the CCSC population was observed in the tumor cells after OGT knockdown, whereas tumor cells tre

37 deletion of PD-L1 on highly immunogenic MC38 tumor cells allows effective antitumor immunity.

38 essing migratory and stem-like properties of tumor cells, also inhibit endothelial phenotypes of brea

39 cal that the NPs establish interactions with tumor cells and avoid removal from the tumors.

40 tudied genomic alterations in single primary tumor cells and circulating tumor cells (CTCs) from the

41 oncogene, promote invasion and metastasis of tumor cells and have been considered potential targets f

42 n in tumors and act at the interface between tumor cells and host cells.

43 urther increased uPA expression in TSC2-null tumor cells and immortalized TSC2-null angiomyolipoma ce

44 ected significantly less PD-L1 expression in tumor cells and immune cells.

45 e suppressed in a similar manner in vitro in tumor cells and in vivo but only in tumor tissue.

46 al and reduced tumor growth both directly on tumor cells and indirectly by promoting an antitumor bra

47 on due to their natural cytotoxicity against tumor cells and safety upon adoptive transfer to patient

48 ortantly, the omentum collects metastasizing tumor cells and supports tumor growth by immunological a

49 the genomic landscape of alterations within tumor cells and the composition of the microenvironment.

50 ic reaction that alters interactions between tumor cells and the stroma to promote tumor progression.

51 h-resolution imaging, we directly visualized tumor cells and their interactions with macrophages in z

52 Reciprocal interactions between tumor cells and their microenvironment drive cancer prog

53 Percentage of tumor cells and tumor-infiltrating lymphocytes (TILs) wi

54 s initially described to induce apoptosis of tumor cells and/or virally infected cells, although spar

55 stem cells (as well as hematologic and solid tumor cells) and their protective microenvironment.

56 f 138) were positive for PD-L1 expression in tumor cells, and 94.9% (131 of 138) were positive for PD

57 hese cells have reduced cytotoxicity against tumor cells, and mice with NFATc1-deficient T cells are

58 tumor blood vessels, spreads secondarily to tumor cells, and produces widespread CD8(+) T-cell-depen

59 igration and morphology of metastatic breast tumor cells, and this effect depends on the cells' mecha

60 PMP targeting was associated with tumor cell apoptosis in vivo.

61 We demonstrate here that mammary tumor cells arising from more epithelial carcinoma cell

62 all stages of metastatic seeding, including: tumor cell arrival; extravasation; growth and progressio

63 higher in the presence of metastatic breast tumor cells as compared to non-metastatic ones.

64 for the survival of non-EGFRvIII-expressing tumor cells as well as for evading molecularly targeted

65 36, inhibited proliferation of 4T1.2 mammary tumor cells as well as MDA-MB-231 breast cancer cells.

66 breast cancer MDA-MB-231 cells, where these tumor cells autocrinely produce angiotensin II by a chym

67 te-dependent metabolite labeling, confirming tumor-cell-autonomous lactate uptake.

68 Hypoxic stress has a strong impact on tumor cell biology.

69 lass I or LILRB1 potentiated phagocytosis of tumor cells both in vitro and in vivo, which defines the

70 expressed on prostate tissue and circulating tumor cells but also found in serum.

71 AK/SRC signaling is activated in mesenchymal tumor cells by crosslinked collagen in the ECM.

72 uggest strategies for eliminating refractory tumor cells by targeting epigenetic and developmental pa

73 Although migrating tumor cells can also change how they migrate in response

74 to the skin, but in later-stage disease, the tumor cells can escape into the blood, the lymph nodes,

75 CSF1 produced by tumor cells caused HDAC2-mediated downregulation of gran

76 e found that NRP1 shRNA expressing KRAS (mt) tumor cells caused increased cell viability by decreasin

77 was evaluated and compared with circulating tumor cells (CellSearch).

78 ed the growth of tumors following subsequent tumor cell challenge.

79 urrent medical and surgical therapies, whose tumor cells characteristically show a high level of aneu

80 ion and resulted in more compactly clustered tumor-cell colonies in coculture with PC3 cells, which m

81 of caspase-9 and -3 and cleavage of PARP in tumor cells compared to normal cells.

82 macrophages exposed to bevacizumab-resistant tumor cell conditioned media increased glioma cell proli

83 In a significant fraction of DLBCL patients, tumor cells constitutively produced the ELC-CXC chemokin

84 Thus, we present a model in which macrophage/tumor cell contact allows for the transfer of cytoplasmi

85 of cytoplasmic molecules from macrophages to tumor cells corresponding to increased tumor cell motili

86 state-specific antigen level and circulating tumor cell count (r = 0.63 [95% CI: 0.27, 0.83] and r =

87 individual patient data, week 13 circulating tumor cell (CTC) and prostate-specific antigen (PSA) res

88 fit from early taxane switch and circulating tumor cell (CTC) biomarkers to interrogate mechanisms of

89 expression was also observed in circulating tumor cells (CTC) during prostate cancer metastasis.

90 on of metastasis can be aided by circulating tumor cells (CTC), which also show potential to predict

91 static chemoprevention targeting circulating tumor cells (CTC).

92 splice variant-7 (AR-V7) mRNA in circulating tumor cells (CTCs) correlated with poor outcomes from th

93 Circulating tumor cells (CTCs) detection, enumeration and characteri

94 opy-number aberrations (CNAs) in circulating tumor cells (CTCs) from pretreatment SCLC blood samples.

95 n single primary tumor cells and circulating tumor cells (CTCs) from the same patient.

96 We tested the hypothesis that circulating tumor cells (CTCs) in preoperative peripheral blood (PPB

97 The detection of circulating tumor cells (CTCs) in the blood of cancer patients is a

98 c disease, through the spread of circulating tumor cells (CTCs), is responsible for the majority of t

99 asily accessible in the blood as circulating tumor cells (CTCs), making them ideal targets to noninva

100 ll analysis platforms focused on circulating tumor cells (CTCs).

101 d at high viability and suitable for primary tumor cell culture, are comprehensively characterized by

102 Similar to the primary tumor, tumor cell cultures expressed very high levels of the My

103 and sensitivity for detecting low levels of tumor cell death (2%-5%).

104 ression is a major susceptibility factor for tumor cell death and, as such, constitutes a potential b

105 osphatidylserine-binding agent for detecting tumor cell death in vivo based on the C2A domain of syna

106 lar nucleotide accumulation during regulated tumor cell death involves interplay between ATP/AMP effl

107 The MMP12 CTD initiates TRAIL-mediated tumor cell death through its conserved SR20 peptide.

108 trate that enhancing endogenous clearance of tumor cell debris is a new therapeutic target that may c

109 Taken together, our results illuminate how tumor cell deposition of tenascin-C in the tumor microen

110 rgets in VS, archived tumor specimens, fresh tumor cells derived from patients with sporadic VS, and

111 Finally, the ectopic expression of HD5 in tumor cells diminished the in vivo oncolytic activity of

112 Tumor cells display on their surface several molecular c

113 results suggest that skeletal sites prone to tumor cell dissemination contain less-mature HA (i.e., s

114 to-mesenchymal transition (EMT) and enhanced tumor cell dissemination in adjacent brain parenchyma af

115 rexpressing colorectal cancer cells promoted tumor cell dissemination in the bone marrow and enhanced

116 oikis, epithelial-to-mesenchymal transition, tumor cell dormancy and escape from immune surveillance,

117 LOXL2 ablation in mammary tumor cells dramatically decreased lung metastasis, wher

118 nology is a promising tool for understanding tumor cell-drug interactions in patient-derived samples

119 cells, indicating a reduced proliferation of tumor cells due to inhibition of OGT expression.

120 ng monocarboxylate transporter-1 (MCT1) from tumor cells eliminated lactate-dependent metabolite labe

121 of the two drugs can significantly increase tumor cell eradication.

122 e levels of phosphorylated MEK1/2 in various tumor cells expressing B-Raf(V600E) or K-Ras(G12C/D) Int

123 d that perivascular cells similarly regulate tumor cell fate at metastatic sites.

124 er (BC) is often used to eradicate remaining tumor cells following surgery with the goal of maximizin

125 amplification confers a growth advantage to tumor cells for clonal expansion.

126 Fibrotic tumors contain abundant FN, and tumor cells frequently up-regulate the FN receptor alpha

127 developed to isolate individual circulating tumor cells from blood, these devices are ineffective at

128 w that ENb-TRAIL has therapeutic efficacy in tumor cells from different cancer types which do not res

129 p phenotypic characterization of circulating tumor cells from peripheral venous blood in clinical pra

130 cosylation-dependent mechanism that protects tumor cells from serum growth factor withdrawal.

131 oreover, miR-26a overexpression inhibits the tumor cell growth both in vitro and in vivo.

132 ockout mice displayed striking impairment of tumor cell growth compared with wild-type mice, along wi

133 Trametinib effectively inhibited tumor cell growth in vitro, but the combination of trame

134 se inhibitor of EphA2 effectively suppressed tumor cell growth in vivo, including TNBC patient-derive

135 echanism underlying the effect of ILT3.Fc on tumor cell growth involves inhibition of the p70S6K sign

136 ly distinct resistance mechanisms, inhibited tumor cell growth, and increased cell death.

137 erocycles which were screened for effects on tumor cell growth, inhibition of tubulin polymerization,

138 The up-regulation of these aggressive tumor cell growth, migration, and invasion phenotypes is

139 Tumor cells have to overcome challenges in the host tiss

140 Since drug resistance is rooted mainly in tumor cell heterogeneity, we examined the drug effect in

141 to aneuploidy and chromosome instability in tumor cells, how untransformed ECs respond to excess cen

142 egarding the molecular mechanisms induced by tumor cell hypoxia with a special emphasis on therapeuti

143 TRAIL-R suppression in tumor cells impaired CCL2 production and diminished both

144 but also heterologous C51 or CT26 colorectal tumor cells in a CD8(+) T-cell-dependent process.

145 applications (e.g., working with circulating tumor cells in blood), only a limited number of cells ar

146 elopment and the potential of SOCS1-silenced tumor cells in raising an effective anti-melanoma immune

147 le activation TGF-beta receptor signaling in tumor cells in response to TGF-beta from the TME.

148 ng tumor size, PTX increased the circulating tumor cells in the blood and enhanced the metastatic bur

149 e of HIF-1 In addition, LOX was expressed by tumor cells in the bone marrow from colorectal cancer pa

150 ion augmented CAR T cell mediated killing of tumor cells in vitro and enhanced clearance of PD-L1+ tu

151 b synergistically inhibited proliferation of tumor cells in vitro and led to tumor growth regression

152 These findings indicate that, in contrast to tumor cells in which autophagy promotes caspase-independ

153 found that macrophages transfer cytoplasm to tumor cells in zebrafish and mouse models.

154 conditioned medium (ACM) applied directly to tumor cells increased tumor cell velocity, induced elong

155 nd BCC location, PD-L1 staining intensity in tumor cells increased with the number of distinct prior

156 sion, specifically depleting these stem-like tumor cells; increases their sensitivity to apoptosis; a

157 Functionally, tumor cells incubated with LGRFYAASG-pen showed disrupti

158 Thus, our findings have demonstrated how tumor cells inhibit innate sensing in DCs and suggested

159 n advanced breast cancer patients, depend on tumor cell interactions with the mineralized bone extrac

160 step of metastasis is the local invasion of tumor cells into the surrounding tissue.

161 e injection of 2 x 10(6) human ovarian SKOV3 tumors cells into 14 female nude mice, treatment with ve

162 test the combined inhibition of RAGE in both tumor cell-intrinsic and non-tumor cells of the microenv

163 of recurrent disease, which can result from tumor cell-intrinsic mechanisms in addition to tumor mic

164 Mechanistically, miR-520f inhibited tumor cell invasion by directly targeting ADAM9, the TGF

165 epression and overexpression of NNMT blocked tumor cell invasion in vitro.

166 Tumor cell invasion involves targeted localization of pr

167 Therefore, inhibition of tumor cell invasion may provide an effective therapy for

168 essed tumor cell proliferation but increased tumor cell invasion via greater mitochondrial traffickin

169 Tumor cell invasion was studied using organotypic raft c

170 al effects on cell proliferation but blocked tumor cell invasion.

171 nclear how Stx4 function is regulated during tumor cell invasion.

172 filing identified candidate ATOH1 targets in tumor cells involved in development and tumorigenesis.

173 Although the role of 5-LO in tumor cells is beginning to emerge, with the notion that

174 lysis of the mechanisms that limit effective tumor cell killing and the identification of apoptotic v

175 damage and replicative stress and increased tumor cell killing and tumor control by DNA damage thera

176 leotides in activating macrophages to induce tumor cell killing in mice.

177 produces widespread CD8(+) T-cell-dependent tumor cell killing in primary tumors and metastases, and

178 c-MPL signaling also enables sequential tumor cell killing, enhances the formation of effective

179 ses in tumor-infiltrating CD8(+) T cells and tumor cell killing.

180 quently, USP7 inhibition induces significant tumor-cell killing independently of ATM and p53 through

181 we used a stochastic Moran process model of tumor cell kinetics coupled with a prisoner's dilemma ga

182 identified MAT2A as an anticancer target in tumor cells lacking expression of 5'-methylthioadenosine

183 Mechanistic analyses revealed that each tumor cell line presented AH1, a common endogenous retro

184 ed efficiency in inhibiting proliferation in tumor cell lines and a rat xenograft model.

185 increases CD20 levels in established B-cell tumor cell lines and primary malignant cells.

186 ker for AsiDNA treatment was validated in 43 tumor cell lines from various tissues and 15 models of c

187 Further in vitro screen in 328 tumor cell lines revealed that tumor cells with KRAS, NR

188 nificant cell death in a wide range of human tumor cell lines, including glioblastoma, astrocytoma, n

189 ular uptake of 4-7-[(18)F]FTrps in different tumor cell lines.

190 glioblastoma and atypical teratoid rhabdoid tumor cell lines.

191 ht the heterogeneity of drug activity within tumor cells located in different tissue compartments.

192 Triggering of the complement cascade induces tumor cell lysis via complement-dependent cytotoxicity (

193 ent via a multistep process including direct tumor cell lysis, induction of cytotoxic or apoptosis-se

194 tif chemokine receptor 4 (CXCR4) on invading tumor cells, macrophage/microglial cells (MGCs), and gli

195 at aberrant signaling pathways in pancreatic tumor cells may improve the poor outcome of pancreatic d

196 acrophages exposed to bevacizumab-responsive tumor cell media, suggesting that macrophage polarizatio

197 ference for vesicles that mimic bacterial or tumor cell membranes.

198 subcutaneously for the study of spontaneous tumor cell metastasis, the rate of LLC metastasis to the

199 egulate immune function or cell adhesion and tumor cell metastasis.

200 However, following intravenous injection of tumor cells, mice lacking PITPalpha develop fewer lung m

201 To test the non-tumor cell microenvironment role of RAGE, we performed s

202 During metastasis to distant sites, tumor cells migrate to blood vessels.

203 f these genes, involved in proliferation and tumor cell migration like REPIN1/AP4, ST3GAL6, TRNAU1AP

204 ckdown significantly decreased IL-6-mediated tumor cell migration, tumorsphere formation and ALDH-pos

205 ntiation and pathological conditions such as tumor cell migration.

206 ecrete TNF-alpha in response to a variety of tumor cells more efficiently than their corresponding ac

207 that high Parkin activity levels could make tumor cells more sensitive to sorafenib's actions, provi

208 mental alteration by CSF-1R blockade renders tumor cells more susceptible to receptor tyrosine kinase

209 es to tumor cells corresponding to increased tumor cell motility and dissemination.

210 has been shown to be involved in modulating tumor cell motility and invasion, cancer stem cell viabi

211 is a tumor-secreted cytokine that stimulates tumor cell motility in vitro and metastasis in vivo.

212 AK1-T(423) signaling pathway, thus increased tumor cell motility.

213 Knockdown of TGF-beta1 expression in the tumor cells negatively affected matrix metalloproteinase

214 r, BIRC3 protein was highly expressed in the tumor cell niches compared to the perivascular niche acr

215 The accessibility of tumor cells obtained from peripheral blood or through bo

216 Telomere maintenance in STAG2 mutant tumor cells occurred by either telomere recombination or

217 ravascular cells clearly distinct and allows tumor cells of interest to be identified quickly as comp

218 of RAGE in both tumor cell-intrinsic and non-tumor cells of the microenvironment, we performed in viv

219 Despite this nutritional environment that tumor cells often experience, the effect of glutamine de

220 g LDL, and LDL receptor (LDLR) expression in tumor cells, on the growth of breast cancer using mouse

221 mean [SD] age, 51 [9.9] years) demonstrated tumor cell PD-L1 expression, regardless of HIV status.

222 Evolution of tumor cell phenotypes promotes heterogeneity and therapy

223 lso reveals the impact of such cross-talk on tumor cell phenotypes that are critical for cancer initi

224 idrug transporter gene, thus contributing to tumor cell proliferation and chemoresistance.

225 ncy enhances the ability of ECs to stimulate tumor cell proliferation and metastasis through stimulat

226 protein or SHH pathway inhibitors decreased tumor cell proliferation and suppressed metastatic tumor

227 s of cyclin D1 is associated with normal and tumor cell proliferation and survival.

228 and some K-Ras effectors, leading to reduced tumor cell proliferation and viability.

229 In turn, this suppressed tumor cell proliferation but increased tumor cell invasi

230 ited a significant decrease in bone-residing tumor cell proliferation compared with free docetaxel.

231 g the unfolded protein response and inducing tumor cell proliferation through a TF-dependent mechanis

232 hairpin RNA (shRNA) significantly inhibited tumor cell proliferation, colony formation and anchorage

233 owth, and metastasis, largely by stimulating tumor cell proliferation, migration, adhesion, and trans

234 ist to modulate MEK/ERK activity in favor of tumor cell proliferation.

235 not the mutant p53, significantly inhibited tumor cell proliferation.

236 Chimeric antigen receptors (CARs) direct tumor cell recognition of adoptively transferred T cells

237 livery of drug molecules to various types of tumor cells remains a major challenge in precision medic

238 ting genomic rearrangements and mutations in tumor cells remains an elusive goal in cancer therapy.

239 eduction of fibrin formation surrounding the tumor cells, rendering the metastases susceptible to muc

240 th patient-derived cells such as circulating tumor cells requires manipulating small sample volumes w

241 The tumor cells retain high-quality intact RNA suitable for

242 xpression of NICD1 or HES1 in STRAP-depleted tumor cells reversed the CSC phenotype.

243 ively studied, little is known regarding how tumor cell rolling on selectins facilitates adhesion to

244 owed high concordance between antibodies for tumor cell scoring (0.813; 95% CI, 0.815-0.839) and lowe

245 ations in EGFR drive tumor growth but render tumor cells sensitive to treatment with EGFR tyrosine ki

246 ast cancer related mRNA markers, with single tumor cell sensitivity.

247 terassay variability for PD-L1 expression in tumor cells showed high concordance between antibodies f

248 ts showed excellent concordance when scoring tumor cells stained with any antibody but poor concordan

249 or samples with more than 10% and 1% nuclear tumor cell staining were considered, respectively, AR- a

250 IL) expressing PD-1 can recognize autologous tumor cells, suggesting that cells derived from PD-1(+)

251 effect of the IL-32gamma isoform, leading to tumor cell survival and thus favoring tumor progression.

252 This promoted neutrophil infiltration, tumor cell (TC) adhesion to the endothelium, intravasati

253 ptor-ligand bonds regulate the rate by which tumor cells tether, roll, and adhere to vascular walls.

254 Accordingly, tumor cells that acquired the ability to metastasize in

255 ollectively, forming clusters of circulating tumor cells that are key tumor-initiating agents.

256 ere is negative feedback from differentiated tumor cells that inhibits the rate of tumor stem cell di

257 hil elastase (NE) can be rapidly taken up by tumor cells that lack endogenous NE expression, includin

258 e arrest, leaving a significant reservoir of tumor cells that may acquire or exhibit resistance.

259 e new insights into the genomic landscape of tumor cells that survive and initiate tumor recurrence.

260 rearrangements, such as those that occur in tumor cells, that can confound analysis using short read

261 plified in osimertinib-resistant EGFR-mutant tumor cells, the effects of which were overcome by combi

262 fferently to excess centrosomes than do most tumor cells-they undergo senescence in vascular sprouts

263 n GBM induces migration and proliferation of tumor cells through chemokine (C-C motif) ligand 2 (CCL-

264 delineate AR function in mitotically active tumor cells, thus providing critical insight into the mo

265 ng at the plasma membrane and thereby primes tumor cells to caspase-mediated apoptosis.

266 of p62 or inhibition of NF-kappaB sensitized tumor cells to CQ, resulting in increased apoptotic cell

267 mRNA expression predicts the sensitivity of tumor cells to cytotoxic treatments can play an importan

268 changes can promote the spreading of primary tumor cells to distant tissues.

269 ueous chamber of liposomes and taken up into tumor cells to enhance the photothermal therapeutic effe

270 hat shape the cHL microenvironment and allow tumor cells to evade immune surveillance.

271 Moreover, TMs are also used by some tumor cells to interconnect to one large, resistant mult

272 ors show that USP21 regulates the ability of tumor cells to repair damaged DNA by regulating BRCA2 st

273 ppressed EC-mediated stimulation of in vitro tumor cell transmigration, proliferation, and migration

274 the tumor cells after OGT knockdown, whereas tumor cells treated with the O-GlcNAcase inhibitor showe

275 differential selective pressures on the two tumor cell types.

276 l-free DNA (cfDNA) is shed into the blood by tumor cells undergoing apoptosis and can be used as sour

277 found that macrophages transfer cytoplasm to tumor cells upon cell contact in vitro.

278 mor accumulation and 46-fold increase in per-tumor-cell uptake in a mouse orthotopic model of human t

279 xpression of particular ectonucleotidases in tumor cell variants will determine whether chemotherapy-

280 M) applied directly to tumor cells increased tumor cell velocity, induced elongation, and promoted ac

281 anation for the different calcium content in tumor cells versus normal tissues.

282 tiproliferative activity of all compounds in tumor cells was evaluated along with kinase inhibition o

283 stress activates protein kinase D1 (PKD1) in tumor cells, we investigated the effect of excitotoxicit

284 pread were measured serially and circulating tumor cells were detected via fluorescence measurements.

285 Compression and tissue infiltration by tumor cells were the leading mechanisms resulting in org

286 Data show that invading mammary tumor cells, when cultured in a stiffened three-dimensio

287 ses interleukin (IL)-33 released from breast tumor cells, which is crucial for the induction of IL-13

288 induced expression of pro-apoptotic genes in tumor cells, which was partially reversed by overexpress

289 vivo primary chronic B-lymphocytic leukemia tumor cells while sparing healthy B cells.

290 ndent growth events and the proliferation of tumor cells with aberrant activation of the Hh pathway,

291 In tumor cells with activated beta -catenin, expression of

292 nd correlation of the level of expression on tumor cells with adverse clinical and pathologic feature

293 sitivity by immunohistochemistry (>/= 25% of tumor cells with at least 2+ staining intensity).

294 Co-implantation of CAFs and tumor cells with either intact TGF-beta1 expression or d

295 screen in 328 tumor cell lines revealed that tumor cells with KRAS, NRAS or BRAF mutation, or cyclin

296 Xenograft tumors from colon tumor cells with O-linked N-acetylglucosamine transferas

297 s showed an increased expression of MYBL1 in tumor cells with OGT knockdown.

298 lin D activation are more sensitive, whereas tumor cells with PTEN, PIK3CA, PIK3R1 or retinoblastoma

299 ole of cancer stem cells (CSCs), a subset of tumor cells with the self-renewal and differentiation ca

300 is-inducing ligand (TRAIL) selectively kills tumor cells, without damaging normal cells.