ライフサイエンスコーパス: normal cell

1 tively inhibit the cancer cells, but not the normal cell.

2 centrations-a condition that generally kills normal cells.

3 However, chimeric RNAs can also be found in normal cells.

4 or samples would always be contaminated with normal cells.

5 re epigenetically repressed in virtually all normal cells.

6 rowth, thereby distinguishing them from most normal cells.

7 cytotoxic mechanism against cancer cells vs. normal cells.

8 t, and pancreatic cancers, but is limited in normal cells.

9 neoplastic cells without similarly affecting normal cells.

10 PS synthesis and reduced PS levels by 50% in normal cells.

11 expressed metabolic enzyme in cancer versus normal cells.

12 cancer cells of different origins as well as normal cells.

13 in myeloma cell lines with little effect on normal cells.

14 d ATP depletion in melanoma cells but not in normal cells.

15 thus more sensitive to MPS1 inhibition than normal cells.

16 ressed at different levels by neoplastic and normal cells.

17 s of various cancer cell lines while sparing normal cells.

18 the non-metastatic MCF-7 cancer cells or in normal cells.

19 280 nM, while they had negligible effects on normal cells.

20 es drive the separation of RasV12 cells from normal cells.

21 growth and invasion with minimal toxicity to normal cells.

22 tients with advanced cancers without harming normal cells.

23 cancer cells and with lower toxicity toward normal cells.

24 ncer cells specifically but had no effect on normal cells.

25 lenge to eradicate tumor cells while sparing normal cells.

26 selectively kills cancer cells while sparing normal cells.

27 ce on arginine is diverse for both tumor and normal cells.

28 sus mutated cells and were only genotoxic to normal cells.

29 n turnover in HGPS-derived cells compared to normal cells.

30 t is not required for division in almost all normal cells.

31 found the doubling time to be twice that of normal cells.

32 pigenetic signature for tumor suppressors in normal cells.

33 ) LT and was unable to promote the growth of normal cells.

34 hown to be more acidic compared with that of normal cells.

35 lls without inducing significant toxicity in normal cells.

36 ould preferentially eliminate malignant over normal cells.

37 er gene expression that is otherwise seen in normal cells.

38 ansformed cells but does not induce death of normal cells.

39 cleavage of PARP in tumor cells compared to normal cells.

40 ing present at low or undetectable levels in normal cells.

41 mechanism of action also may be occurring in normal cells.

42 2 protein, was the most common aberration in normal cells.

43 downregulated in primary tumors compared to normal cells.

44 n in these strains while it strongly affects normal cells.

45 against tumor cell lines when compared with normal cells.

46 regions of the non-junctional SR compared to normal cells.

47 her in the cancer cells or in the associated normal cells.

48 cells, while being transiently expressed in normal cells.

49 to potential for deleterious recognition of normal cells.

50 oxicity in some types of cancer cell but not normal cells.

51 l lymphoma types and low cytotoxicity toward normal cells.

52 ntly more DNA damage in cancer cells than in normal cells.

53 ectively kills tumor cells, without damaging normal cells.

54 trigger cancer cell apoptosis while sparing normal cells.

55 g indiscriminate IKK/NF-kappaB inhibition in normal cells.

56 y that is required for cell proliferation of normal cells.

57 fferently compared with unselected tumor and normal cells.

58 hibits proliferation in cancer cells but not normal cells.

59 l settings are always mixtures of cancer and normal cells.

60 over tumor cells and minimize toxicity over normal cells.

61 y of cancer cell lines but have no effect on normal cells.

62 without modeling the effect of the drugs on normal cells.

63 neoantigens that distinguish malignant from normal cells.

64 ivery in lung cancer cells and its impact on normal cells.

65 ree proteins without causing toxicity toward normal cells.

66 t were more extreme than those observed with normal cells.

67 ee of aberrant CpG island DNA methylation in normal cells.

68 umour type, but it was almost never found in normal cells.

69 antly more DNA damage in the cancer cells vs normal cells.

70 ctively kills cancer cells, while protecting normal cells.

71 In normal cells, A20 constitutively associates with caspase

72 t DKC1 mRNA levels were elevated relative to normal cells across a panel of 15 neuroblastoma cell lin

73 sia mutated (ATM) DNA repair pathway that in normal cells acts to repair double-strand DNA breaks.

74 Visually normal cells adjacent to, and extending from, tumors of

75 f metastatic cells and that the induction of normal cells affected the metastatic velocity of each ca

76 ve effects against cancer cells, but protect normal cells against DNA damage.

77 utant behaved as an oncogene and transformed normal cells, an activity that was enhanced by PTEN depl

78 could constitute a "stemness marker" of the normal cell and a possible target for immunotherapeutic

79 e length of primary cilia is associated with normal cell and organ function.

80 s, neurotransmitter synthesis, modulation of normal cell and tumor growth, and many others.

81 A-EphA2 signals, RasV12 cells integrate with normal cells and adopt a pro-invasive morphology.

82 uman embryonic kidney 293 cells (HEK 293) as normal cells and Au/Fc-PAMAM(G2)/FA electrode showed two

83 ds AGS cancer cells when compared to HEK 293 normal cells and bone marrow mesenchymal stem cells (BM-

84 omain of PI3K, resulting in proliferation of normal cells and cancer cells.

85 -Myc is essential for rapid proliferation of normal cells and has causal relationship with many cance

86 induced by small electrical perturbations in normal cells and in cells with simulated long QT syndrom

87 where and when genes are expressed, both in normal cells and in the context of diseases.

88 mes occurs once every cell division cycle in normal cells and is a tightly controlled process that en

89 hibitor with dual selectivity: leukemia over normal cells and NOTCH1 mutants over wild-type receptors

90 D47, which is a protein broadly expressed on normal cells and often overexpressed on cancer cells, an

91 cule with pleiotropic physiological roles in normal cells and pathophysiological roles in cancer.

92 eracting pathways restrains proliferation in normal cells and prevents tumor initiation is still poor

93 by exons 1-6 was expressed as an isoform in normal cells and promoted cell death, a truncated splice

94 Cell-cell interactions between normal cells and RasV12 cells trigger ephrin-A-EphA2 sig

95 TGFbeta receptor abundance and signaling in normal cells and supplementation of recombinant LTBP4 en

96 intracellular environments of cancerous and normal cells and the particular characteristics of tumor

97 rapeutics to stomach cancer without damaging normal cells and tissues, reduce the toxicity and side e

98 eactivity against fully-glycosylated MUC1 on normal cells and tissues.

99 dual modeling of drug responses to tumor and normal cells and utilize them to design targeted combina

100 /or virally infected cells, although sparing normal cells, and has been implicated in the pathogenesi

101 nucleus has a smooth, regular appearance in normal cells, and its shape is greatly altered in human

102 based activity, selectivity for cancer over normal cells, and oral bioavailability.

103 was more selective toward cancer cells than normal cells, and was >10 times more potent than 5-FU, t

104 In normal cells, apoptin exists in filamentous networks in

105 er cells undergo apoptosis or necrosis while normal cells are not adversely affected.

106 de that transformed cells engage surrounding normal cells as active and essential microenvironmental

107 Apaf-1 exists in normal cells as an autoinhibited monomer.

108 ed proliferation of cancer cells, but not of normal cells, as well as to attenuated tumour growth in

109 To determine smoking effect on FSTL1, normal cell BEAS2B and lung cancer cell lines was treate

110 romosome instability (CIN) is deleterious to normal cells because of the burden of aneuploidy.

111 tes epigenetic and metabolic homeostasis and normal cell behavior.

112 and low levels of BZR1 are required for the normal cell behaviors in the elongation zone and quiesce

113 indicate the nature of VKORC1v2 function in normal cell biology.

114 In addition to a good compatibility with the normal cells, Bmattacin2 loaded nanofibrous membranes de

115 yosin Tm5NM1, regulates the proliferation of normal cells both in vitro and in vivo.

116 n not only the development and maturation of normal cells, but also the development and progression o

117 in is dispensable for V(D)J recombination in normal cells, but because of functional redundancy, it i

118 valent promoters is only lowly methylated in normal cells, but frequently shows elevated methylation

119 exhibit shorter telomere length compared to normal cells, but it is not fully understood how WRN def

120 regulating miR-148a/152 feedback circuit in normal cells, but not in cancer cells because of the DNA

121 pressor protein p53 is tightly controlled in normal cells by its two negative regulators--the E3 ubiq

122 n by a131 causes reversible growth arrest in normal cells by transcriptionally upregulating PIK3IP1,

123 Therapy-induced damage of normal cells can alter the tumor microenvironment, causi

124 In contrast to normal cells, cancer cells coopt this pathway to propaga

125 Compared to normal cells, cancer cells have an increased antioxidant

126 cells to survive nutrient deprivation, which normal cells cannot do.

127 sed susceptibility to CD40 killing, while in normal cells CD40 signalling is cytoprotective.

128 and 80%, respectively, reflecting a loss of normal cell-cell adhesion and signalling between axons a

129 ALDH(+)/CD49f(+)/EpCAM(+) tumor and normal cells clustered differently compared with unselec

130 in selectivity toward neoplastic relative to normal cells compared to its parent thiosemicarbazone.

131 NNs targeting Plk1 generate less toxicity in normal cells compared to the small molecule Plk1 inhibit

132 V-induced mutation frequencies compared with normal cells, consistent with their GGR deficiency.

133 ples containing a mixture of subtypes and/or normal cell contamination.

134 wards skin and colon cancer cells over their normal cell counterparts.

135 loop was formed by CTCF self-dimerisation in normal cells (CTCF binds to both unmethylated CTCF-BS3 a

136 Jurkat and K562 cells were examined under normal cell culture conditions and during exposure to cu

137 of Rad51 requires TCTP in MCF-7 cells under normal cell culture conditions.

138 t kinase that maintains dNTP levels during a normal cell cycle and up-regulates dNTP synthesis upon c

139 in LF differentiation despite maintenance of normal cell cycle exit.

140 K20) and its function has been implicated in normal cell cycle progression and cancer metastasis.

141 kdown of EPHB3 partially restores growth and normal cell cycle progression of TCF7L1-Null cells.

142 RGPs inhibited in basal INM still showed normal cell cycle progression, although neurogenic divis

143 global histone acetylation patterns and for normal cell cycle progression.

144 rom inhibition of proliferation and restored normal cell cycle progression.

145 regulatory proteins, leading to the loss of normal cell-cycle control, are a hallmark of many cancer

146 egion contains several residues required for normal cell-cycle regulation and cytokinesis, this trans

147 tion of TEL-AML1 in different populations of normal cells demonstrate the molecular model.

148 Epithelial-mesenchymal transition (EMT) is a normal cell differentiation event during development and

149 unctions of defined transcription factors in normal cell differentiation.

150 se-seq to pools of tumour cells and pools of normal cells, dissected from formalin-fixed paraffin-emb

151 illion bases in the human genome each time a normal cell divides.

152 ntioxidant-treated NAFLD hepatocytes resumed normal cell division and returned to a physiological sta

153 FgCDC14 is required for normal cell division and septum formation and FgCdc14 po

154 t were arrested at the membrane of HBEC30-KT normal cells during the initial transfection period.

155 damental gaps remain in our knowledge of how normal cells evolve into cancer cells.

156 l epithelial cells, dysplastic cells but not normal cells, exhibit marked down-regulation of a number

157 eport that A20-deficient macrophages, unlike normal cells, exhibit spontaneous NLRP3 inflammasome act

158 In normal cells exposed to stress, the central transcriptio

159 (-)) CML cells, in contrast to corresponding normal cells, express a functional interleukin-1 (IL-1)

160 y similar to high-affinity cells, but spared normal cells expressing physiologic target levels.

161 are histone demethylases that both regulate normal cell fates during development and contribute to t

162 d, individual cells rapidly canalize towards normal cell fates.

163 In normal cells, following DNA damage the acetyltransferase

164 We analyzed 420 tumor cells and 284 adjacent normal cells for expression of 93 genes that included a

165 We demonstrate that analysis of normal cells from cancer patients leads to identificatio

166 Amifostine protects normal cells from DNA damage induction by ionizing radia

167 ostine may not only protect in multiple ways normal cells from radiation-induced DNA damage but also

168 Oncogene-induced senescence (OIS) protects normal cells from transformation by Ras, whereas cells l

169 Adequate protein folding is necessary for normal cell function and a tightly regulated process tha

170 itin ligases are deemed to play key roles in normal cell function and homeostasis, whether their alte

171 or PI3K catalytic and regulatory subunits in normal cell function and in disease.

172 es (ROS) family of molecules produced during normal cell function and in response to various stimuli,

173 es in specific SGs are sufficient to disrupt normal cell function and point to a possible role for SG

174 moderate levels of ROS/RNS are essential for normal cell function and take part in numerous cellular

175 ce because of the critical role of folate in normal cell function and the wide range of disorders, in

176 al response, which has implications for both normal cell function as well as disease.

177 tals, and proteins is required to understand normal cell function, and ultimately, elucidate the mech

178 active oxygen species (ROS) is important for normal cell function, but excessive production of ROS ca

179 ification of proteins or SUMOylation ensures normal cell function.

180 ion, is crucial for cellular homeostasis and normal cell function.

181 ed proteins, which ultimately interfere with normal cell function.

182 etermine cell- and tissue-specific features, normal cell functioning, and responses of eukaryotic cel

183 iated flanking sequences, we reveal that, in normal cells, genomic repair rates display a distinctive

184 The initial loss of normal cell geometry can be explained by a failure to ma

185 multiple cancer cell lines without affecting normal cell growth and survival.

186 6 is expressed latently and is essential for normal cell growth and viability.

187 ncing them resulted in dramatic reduction in normal cell growth and/or motility.

188 d to decreased neuronal marker staining, and normal cell growth as judged by phosphohistone H3 staini

189 cle fusion kinetics, diffusion could support normal cell growth rates.

190 ed growth would be significantly slower than normal cell growth.

191 s increase the frequency of apoptosis during normal cell growth.

192 urgery, chemo- and radiotherapy also inhibit normal cells growth.

193 Our circuit analysis showed that while normal cells have an oxidative state and a glycolytic st

194 CMLD-2-treated normal cells, HuR-regulated mRNAs and proteins albeit sh

195 3.59 microM, but they are less cytotoxic on normal cells (IC50 > 100 microM).

196 Centrosome loss irreversibly arrested normal cells in a senescence-like G1 state by a p53-depe

197 Cancer cells differ from normal cells in both gain of functions (i.e., upregulati

198 e proteomes of virus-infected and uninfected normal cells in response to cell-intrinsic dsDNA sensing

199 g a role in the cross-talk between tumor and normal cells in the early steps of neuroblastoma develop

200 sociated mutations fundamentally differ from normal cells in their response to centrosome loss.

201 rotein 1) that acts to supress apoptosis in "normal" cells in the fly.

202 mediated killing of cancer cells, but not of normal cells, in vitro.

203 er cells have altered metabolism compared to normal cells, including dependence on glutamine (GLN) fo

204 tize tumors to chemotherapy while protecting normal cells, including hematopoietic stem and immune ce

205 We show that RCC1 overexpression in normal cells increased cellular RanGTP levels and accele

206 for GM-CSF-induced STAT5 phosphorylation in normal cells incubated with either patient or normal pla

207 The oncogenic transformation of normal cells into malignant, rapidly proliferating cells

208 plex, a component of the spliceosome that in normal cells is found in the cell.

209 The proliferation of normal cells is inhibited at confluence, but the molecul

210 eric regions are sensitive to DSBs, which in normal cells is responsible for ionizing radiation-induc

211 hey are resistant to tumorigenesis, and most normal cells isolated from them grow slowly in culture.

212 While EXO1 plays a minimal role in normal cells, its loss strongly influences DNA replicati

213 In normal cells, Ki-67 was a late marker of cell-cycle entr

214 r NAD+ preferentially in cancer cells versus normal cells, leading to depletion of ATP and robustly i

215 agues show that augmenting oxidant stress in normal cells limits tumor initiation and progression.

216 tides with several cancer cell lines and one normal cell line, the unphosphorylated D-tetrapeptides a

217 MBD1-deficient stem cells may interfere with normal cell lineage commitment and cause the accumulatio

218 Normal cell lines and tissue were unstained by mAb-A4.

219 lso 4a was found to be less cytotoxic toward normal cell lines as compared to cancer cell lines.

220 screening on a unique pair of matched cancer/normal cell lines obtained from a single patient.

221 ic standpoint, selectivity for cancer versus normal cells may be enhanced by pairing VSV with IFN-alp

222 es with broad H3K4me3 peaks conserved across normal cells may represent pan-cancer tumor suppressors,

223 llenged by the DNA damage that arises during normal cell metabolism.

224 d RRM2B, were predicted to be dispensable in normal cell metabolism.

225 or of MMP activity was sufficient to restore normal cell migration, thus providing a potential approa

226 structurally and functionally different from normal cell mitochondria.

227 intaining sensitivity below a threshold over normal cell models.

228 equired for neuronal differentiation and for normal cell morphology, cytoskeletal organization, proli

229 small molecule inhibitors and disruption of normal cell morphology.

230 ressed on malignant cells, but expression on normal cells must be absent or limited.

231 Compared with normal cells, neoplastic cells have been shown to requir

232 that neither discriminate between cancer and normal cells nor eliminate the risk of cancer recurrence

233 a cell depends is typically consistent among normal cells of a particular phenotype, Bcl-2 family dep

234 nergistically conspire to greatly outperform normal cells or any extracellular guidance cues in isola

235 in animals and patients, but recognition of normal cells or excessive activation can result in signi

236 tients with advanced cancers without harming normal cells or tissues.

237 maining cells represent either non-aberrant "normal" cells or "aberrant cells of unknown origin" that

238 mutant mice do not accumulate mutant p53 in normal cells, our study on a mutant p53 mouse model of L

239 ed property of any radioprotector to protect normal cells over cancerous cells.

240 As a result, normal cells overexpressing RCC1 evaded DNA damage-induc

241 In normal cells, p53 is activated by DNA damage checkpoint

242 Forced-expression of MICU1 in normal cells phenocopies the metabolic aberrations of ma

243 impede advances in our deep understanding of normal cell physiology and disease pathogenesis.

244 ite their well-known function in maintaining normal cell physiology, how inorganic elements are relev

245 CpG methylation status in normal cells points to locally active regulatory sites a

246 are initially present at low frequencies in normal cells preferentially expand in the altered tumor

247 ining distinct sub-populations of cancer and normal cells present challenges in the development of re

248 n tumor and other stressed cells, but not on normal cells, prevents NK cell activation via NKp30.

249 r regulation of this switch is important for normal cell processes; aberrations could result in a num

250 ike USP22, USP51 and USP27X are required for normal cell proliferation, and their depletion suppresse

251 and which, we hypothesize, is a hallmark of normal cell proliferation.

252 -cell genomics of breast tumors and adjacent normal cells propagated for a short duration under growt

253 During G1-phase of the cell cycle, normal cells respond first to growth factors that indica

254 C revealed that Glu-229 is critical for both normal cell separation and the release of PG fragments b

255 er in sequence contamination (deviation from normal cell sequence) and in subclonality, an ensemble o

256 In normal cells, serum stimulation causes brief peaks of ex

257 e metabolic pathways is required to maintain normal cell shape in E. coli.

258 lack >90% anticoagulant activity but retain normal cell signaling.

259 APC-associated bleeding risk while retaining normal cell-signaling activity, have shown benefits in p

260 which may be transient in many situations in normal cells since they can be effectively resolved by h

261 roadly cytotoxic, causing cell death also in normal cells such as dermal fibroblasts and endometrial

262 In normal cells, such metabolic stress leads to inhibition

263 and Langerin on immune cells than that from normal cells, suggesting that the glycans on B7-H3 may a

264 ndocytic machinery necessary for maintaining normal cell-surface AMPAR levels.

265 icient ER export is not sufficient to enable normal cell-surface expression of TREM2.

266 repair activities and impairs tumour but not normal cell survival.

267 KB, MCF-7, Hep-G2, and U87) relative to HDF normal cells than that of the parent spiramycin.

268 ust also correctly detects a small number of normal cells that are mixed in a cancer cell population.

269 ons between mutant cells and the surrounding normal cells that make up the tumor microenvironment.

270 pressed at any level, including at levels in normal cells that were undetectable by flow cytometry.

271 Due to the infiltration of tumor surrounding normal cells, the expression data derived from tumor sam

272 readily infect transformed cells compared to normal cells, the former appearing to exhibit defective

273 well as between cancer and non-transformed (normal) cells, thereby impacting a number of aspects of

274 ive stress with increased levels of ROS than normal cells, these findings support the idea of exploit

275 rs resistance to TRAIL-induced cell death in normal cells through blockade of initiation of the extri

276 MENs distinguish cancer cells from normal cells through the membrane's electric properties;

277 uit inflammatory cells and induce changes in normal cells to create and interact with the premalignan

278 Cancer cells utilize more glucose than normal cells to meet the energy demand arising due to th

279 llular mutations drive the transformation of normal cells to the cancerous state.

280 that causes the related gene instability and normal cells to transform into tumor cells.

281 We found that the ratio of viable normal cells to tumor cells was increased prominently af

282 In comparison with normal cells, TRAK1-deficient fibroblasts showed irregul

283 cts of normal brain architecture but without normal cell-type regionalization, these spheroids bore a

284 In contrast, a panel of normal cell types did not express MC2 mRNA, and similar

285 fically kill transformed cells while leaving normal cells unharmed in a manner that is independent of

286 ow nanomolar range (3-20 nM), but not affect normal cell viability.

287 perative to distinguish circulating DNA from normal cells vs mutation-bearing sequences originating f

288 cytoplasmic vesicles and it is required for normal cell wall composition and integrity, affecting ad

289 In normal cells, we found that ESE3/EHF bound and repressed

290 susceptible to MDA-5-mediated cytotoxicity, normal cells were highly resistant and instead developed

291 pipeline by detecting subtle alterations in normal cells when subjected to small mechano-chemical pe

292 g pathway that has been tightly regulated in normal cells, whereas its deregulation strongly correlat

293 nct cell killing outcomes between cancer and normal cells whereby cancer cells undergo apoptosis or n

294 d STAT3 cancer cells without cytotoxicity to normal cells with dormant STAT3.

295 r the clinical trial was that, although most normal cells with exception of Treg cells do not express

296 higher cytotoxicity against tumor cells over normal cells with greater water solubility than triptoli

297 ld reveal therapeutic targets that may spare normal cells with intact p53.

298 an alternating electric field on cancer and normal cells within an in vivo-like microenvironment wit

299 y for HNSCC by inhibiting VSV replication in normal cells without a corresponding inhibition in cance

300 An equivalent mass of normal cells would be highly heterogeneous as a result o