ライフサイエンスコーパス: MDA

1 MDA is a precursor to methylene diphenyl diisocyanate (M

2 MDA levels were higher in all experimental groups than i

3 MDA-9/Syntenin (SDCBP) provides a direct target for ther

4 MDA-9/Syntenin, a highly conserved double-PDZ domain-con

5 MDA-induced cytokine secretion in vitro was dependent on

6 TNBC cells (MDA-MB-157, MDA-MB-231, and Hs578T) were treated with bromodomain-co

7 G24-EGF to tumor cells (MDA-MB-231, SK-OV-3, MDA-MB-231/H2N, or TrR1) coexpressing HER2 and EGFR was

8 (MDA) 2-ring isomers (2,2'-, 2,4'-, and 4,4'-MDA) is reported using matrix assisted laser desorption/

9 ver the concentration range of 1-40 ppm 4,4'-MDA.

10 verexpressing Snail) and breast (MDA-MB-468, MDA-MB-231, and MCF-7 overexpressing Snail) cancer cells

11 Melanoma differentiation-associated gene 5 (MDA-5, IFIH1), a cytosolic innate pattern recognition re

12 melanoma differentiation-associated gene 9 [MDA-9/Syntenin; syndecan-binding protein (SDCBP)] as a d

13 d with breast (MDA-MB-231-ACKR3 [231-ACKR3], MDA-MB-231 [231], MCF7), lung (HCC95), or esophageal (KY

14 zures induced by maximal dentate activation (MDA) acute kindling.

15 (TT) 2 years after mass drug administration (MDA) activities have ceased.

16 The coverage of mass drug administration (MDA) for neglected tropical diseases, such as the soil-t

17 en described after mass drug administration (MDA) for the control of schistosomiasis, but they have n

18 Mass drug administration (MDA) is therefore considered a potent cause of antimalar

19 d proliferation of mass drug administration (MDA) programmes using the drug praziquantel is resulting

20 Mass drug administration (MDA) using dihydroartemisinin plus piperaquine (DHAp) re

21 Mass drug administration (MDA) with ivermectin is the cornerstone of efforts to el

22 Mass drug administration (MDA) with praziquantel is the cornerstone of schistosomi

23 Repeated mass drug administration (MDA) with preventive chemotherapies is the mainstay of m

24 individuals during mass drug administration (MDA).

25 nd 58% lower (0.42; .18-.98; P = .046) after MDA compared with control in lower- and higher-transmiss

26 ed to track 935 individuals before and after MDA.

27 was found to have selective activity against MDA-MB-453 cells, a model of the luminal androgen recept

28 ivo was significantly more effective against MDA-MB-231 tumors, whereas T-47D tumors showed no signif

29 d analogues showed promising results against MDA-MB-231 and HCT116 cancer cell lines.

30 prominent contrast enhancement in aggressive MDA-MB-231 triple negative breast cancer in mice at a lo

31 ated TRAF2 activation in the more aggressive MDA-MB-231 cells was TNFalpha independent but involved t

32 CSC-related genes are elevated across all MDA-MB-231 in vitro models following paclitaxel treatmen

33 droplet multiple displacement amplification (MDA), a method that uses commercially available liquid d

34 limited multiple-displacement amplification (MDA), low-input library preparation, DNA barcoding, targ

35 ethods, multiple displacement amplification (MDA-Qiagen REPLI-g kit) and the hybrid or modified PCR-b

36 umor effects of NT-7-16 were evaluated in an MDA-MB-435 xenograft model and it had excellent activity

37 Significant increase of LPS (p = 0.0002) and MDA (p = 0.005) concentration was observed in glaucomato

38 reduced growth of MCF-7 (-36%, P < 0.05) and MDA-MB-231 (-66%, P < 0.01) tumors and, for the MCF-7 tu

39 nding of 4-(11)C-MBZA to B16F1, MCF-10A, and MDA-MB-231 cells was 6.41% +/- 1.28%, 1.51% +/- 0.17%, a

40 reased upon drug treatment in MDA-MB-231 and MDA-MB-157 cells (P < 0.01-0.001).

41 In MDA-MB-231 and MDA-MB-157 TNBC cell lines, miR-9 and miR-200 promoted a

42 nd biodistribution studies in MDA-MB-231 and MDA-MB-157 xenografts and a patient-derived xenograft mo

43 ession in human breast cancer MDA-MB-231 and MDA-MB-468 cell lines.

44 curred partly via apoptosis in both PC-3 and MDA-MB-231 cells.

45 -125, we validated our findings in MCF-7 and MDA-MB-231 breast cancer cell lines, which harbor lower

46 inhibit the growth and survival of MCF-7 and MDA-MB-231 breast cancer cells.

47 +/- 0.1 and 0.80 +/- 0.19 kPa for MCF-7 and MDA-MB-231 cells).

48 on migration and proliferation of MCF-7 and MDA-MB-231 cells.

49 f p38delta in breast cancer cells, MCF-7 and MDA-MB-231 resulted in a reduced rate of cell proliferat

50 ce) function approaches in breast (MCF-7 and MDA-MB-231) and ovarian (SKOV3 and SKOV3ip) cancer cell

51 d nanoparticle (NP) formulation in MCF-7 and MDA-MB-231, two cell lines representative of different m

52 ed in two breast tumor cell lines, MCF-7 and MDA-MB-231.

53 ing human breast cancer cell lines MCF-7 and MDA-MB-453 also degraded recombinant IFN-gamma, but this

54 n did not change Rho-GTP loading in A549 and MDA-MB-231.

55 ed significant cell death in U251, A549, and MDA-MB-231.

56 lioblastoma), A549 (lung adenocarcinoma) and MDA-MB-231(breast cancer).

57 igh purity (81.8 and 82.5% for the ADSCs and MDA-MB-231 cells, respectively).

58 tion between the MCF-7 (less aggressive) and MDA-MB-231 (more aggressive) cell lines.

59 lls), MCF-10A (breast epithelial cells), and MDA-MB 231 (breast cancer cells).

60 tic breast cancer cells in 4T1.2 BALB/cJ and MDA-MB-231 nude mouse models.

61 ore or after adjustment for risk factors and MDA.

62 (ZMP) and growth inhibition in NCI-H460 and MDA-MB-231met2 cancer cell lines.

63 ome inhibitor PS-341 treatment, in HepG2 and MDA-MB-453 cells.

64 and severe cancer models by using HMEpiC and MDA-MB-231 cells to study cancer cell migration and anti

65 protein, which acts downstream of RIG-I and MDA-5 in the interferon induction pathway.

66 cant interaction between telomere length and MDA in their association with mammographic density.

67 ntitumor activity in the MV4;11 leukemia and MDA-MB-231 triple-negative breast cancer xenograft model

68 rosstalk in both MDA-MB-468 (basal-like) and MDA-MB-231 (mesenchymal-like) TNBC cell lines in which N

69 In an experimental tumor construct, MCF7 and MDA-MB-231 breast cancer cells were coinjected into the

70 Tumors derived from MCNeuA and MDA-MB-231 cells had high LDLR expression and formed lar

71 Using chemical probes and MDA-MB-231 breast cancer cells, we found here that the i

72 activity, free proline, soluble protein and MDA contents fluctuated in response to soil drying.

73 = 7) decreased MCF-7 (hormone-sensitive) and MDA-MB-231 (hormone-insensitive) breast cancer cell viab

74 two human breast cancer cell lines T47D and MDA-MB-231 are also evaluated.

75 DT over time was found between the U87MG and MDA-MB-435 tumors in both static and dynamic PET.

76 ion (MCF)-7 and triple negative-MD Anderson (MDA) metastatic breast (MB)-231 cells, or as an oncogeni

77 be ameliorated by administration of an anti-MDA antibody.

78 s the circumstances under which antimalarial MDA increases or decreases the risk of resistance.

79 ymatically generated lipid fragments such as MDA are recycled back into plastidic galactolipids that,

80 tion of 4T1.2 mammary tumor cells as well as MDA-MB-231 breast cancer cells.

81 The present study aims to assess MDA levels in the saliva of patients with chronic period

82 virus/phage (AAVP) particles in mice bearing MDA-PCa-118b, a patient-derived xenograft (PDX) of castr

83 ic LF elimination, while annual and biannual MDA options required significantly longer durations to a

84 ote feed-forward NOS2/COX2 crosstalk in both MDA-MB-468 (basal-like) and MDA-MB-231 (mesenchymal-like

85 cent cells by the presence of membrane-bound MDA-vimentin, presumably as part of a senescence eradica

86 reduce the viability of colon HT-29, breast MDA-MB231, and ovarian SKOV-3 cancer cell lines, thus re

87 tudies using mice carrying orthotopic breast MDA-MB-231 tumors showed that the cyclic peptide prefere

88 tate (DU-145), melanoma (SK-MEL-28), breast (MDA-MB-231), and ovarian (OVCAR-3) cancer cells revealed

89 rmone-insensitive prostate (PC3) and breast (MDA-MB-231 and BT-549) cancer cell lines the mTOR inhibi

90 nd ARCaP-E overexpressing Snail) and breast (MDA-MB-468, MDA-MB-231, and MCF-7 overexpressing Snail)

91 ion studies in mice xenografted with breast (MDA-MB-231-ACKR3 [231-ACKR3], MDA-MB-231 [231], MCF7), l

92 474, T47D, ZR-75-1, SKBR3, MDA-MB-468, BT20, MDA-MB-231); normal breast cells (MCF-10A); and cell lin

93 ding of hyaluronic acid to CD44 expressed by MDA-MB-231.

94 splicing of Bcl-x pre-mRNA was modulated by MDA-7/IL-24, which would suggest that specific NSCLC tum

95 i-unsaturated fatty acids incorporated (14)C-MDA into 18:2-16:2-MGDG.

96 rds at least two cancer cells, breast cancer MDA-MB-231 and human glioblastoma U87 cancer lines, was

97 and -beta1 expression in human breast cancer MDA-MB-231 and MDA-MB-468 cell lines.

98 r, whereas CG and MG inhibited breast cancer MDA-MB-231 cell growth.

99 ngeal carcinoma CNE2 cells and breast cancer MDA-MB-231 cells, where these tumor cells autocrinely pr

100 Among them, triple-negative breast cancer MDA-MB-231, which has the highest xCT messenger RNA leve

101 hotopic mouse models of human breast cancer, MDA-MB-231 and T-47D, which morphologically correlate to

102 roved HRV and LV function, decreased cardiac MDA, TNF-alpha and Bax levels, and improved cardiac mito

103 nsing to perform high-throughput single-cell MDA in nanoliter volumes.

104 rated whole-genome sequencing of single-cell MDA products with excellent coverage uniformity and mark

105 TNBC cells (MDA-MB-157, MDA-MB-231, and Hs578T) were treated with br

106 f (177)Lu-DOTA-Fab-PEG24-EGF to tumor cells (MDA-MB-231, SK-OV-3, MDA-MB-231/H2N, or TrR1) coexpressi

107 ately targeting the evolutionarily conserved MDA-5-IPS-1 antiviral pathway in tumors can provoke para

108 ), which was similar to the negative control MDA-MB-231 xenografts (percent ID per gram, 0.42 +/- 0.0

109 Cre)/Tgfbr2 knockout significantly decreased MDA-MB-231 bone lesion development in both the cardiac a

110 Adenovirus-delivered MDA-7/IL-24 (Ad.mda-7) reduced the viability of NSCLC ce

111 This, in turn, impacted three-dimensional MDA-MB-231 tumor cell migration behavior.

112 Droplet MDA provides an accessible and scalable method for perfo

113 The performance of droplet MDA is characterized using a large dataset of 129 normal

114 tection using targeted sequencing of droplet MDA product to achieve a median allelic dropout of 15%,

115 R tumors, nine mutant G521R ER tumors, eight MDA-MB-231 tumors, and four MCF-7 ER-positive tumors).

116 transient increases in levels of endogenous MDA in wounded Arabidopsis thaliana leaves, raising the

117 ines (NIH 3T3 fibroblasts, NMuMG epithelial, MDA-MB-231 and MCF-7 breast cancer cells).

118 mmunity-wide MDA and household-level (focal) MDA with DHAp compared with no mass treatment.

119 of intracellular PCCA detection 45-fold for MDA-MB-231 cells and 7-fold for MCF-7 cells, relative to

120 s in (18)F-FLT uptake were also observed for MDA-MB-231 xenografts (tumor-to-muscle ratio, 7.2 +/- 0.

121 method presented here has been validated for MDA quantification in industrial grease samples over the

122 ivo neutralization of endogenously generated MDA epitopes by intravenous injection of a specific MDA

123 cellent GFP gene silencing efficiency in GFP-MDA-MB-468 TNBC cells without any significant cytotoxici

124 was validated in solitary cells of GM14667, MDA-MB-231 and MCF-7 cell lines, achieving a DNA amplifi

125 group had significantly lower GSH and higher MDA concentration in the liver compared with the control

126 da-7/IL-24 or treatment with recombinant His-MDA-7 protein resulted in downregulation of miR-221 and

127 logy to ablate Kindlin-2 expression in human MDA-MB-231 and murine 4T1 breast cancer cells.

128 depleted or substituted cholesterol in human MDA-MB-231 epithelial cells with various alternative ste

129 ZDHHC3 ablation in human MDA-MB-231 mammary tumor cell xenografts reduced the siz

130 RNA by pattern-recognition receptors (RIG-I/MDA-5) and that NKG2D ligand up-regulation can be blocke

131 Knockdown of Spry1 impaired MDA-MB-231 cell migration, Matrigel invasion, and anchor

132 In MDA-MB-231 and MDA-MB-157 TNBC cell lines, miR-9 and miR

133 ptake was significantly greater (p<0.001) in MDA-MB-231 cells (93.0% internalization at MI=1.0, 79.5%

134 vity and synaptic plasticity in naive and in MDA-kindled anaesthetised rats.

135 sed proliferation and activated apoptosis in MDA-MB-231 breast cancer cells in vitro and in vivo.

136 idant responsive element luciferase assay in MDA-MB-231 cells.

137 e target enzymes legumain and cathepsin B in MDA-MB-435S, A375, and C8161 melanoma cells.

138 Syk expression induced phenotype changes in MDA-MB-231 cells.

139 231-stable clones or peritumoral delivery in MDA-MB-231 xenografted mice, strongly decreased the numb

140 st growth factor (bFGF) was downregulated in MDA-MB-231-injected tibiae from the LysM(Cre)/Tgfbr2 KO

141 differentiated extracellular matrix (ECM) in MDA-MB-231 tumors relative to T-47D tumors.

142 ations, iNPG-pDox shows enhanced efficacy in MDA-MB-231 and 4T1 mouse models of metastatic breast can

143 displayed remarkable anti-tumor efficacy in MDA-MB-436 xenograft model without apparent toxicities.

144 ors and demonstrated that SNX9 expression in MDA-MB-231 breast cancer cells is necessary to maintain

145 Furthermore, LRIG1 expression in MDA-MB-231 breast cancer cells significantly slows their

146 Spry1 shRNAs to suppress Spry1 expression in MDA-MB-231, an established TNBC cell line.

147 0 fibrosarcoma cells and MT1-MMP function in MDA-MB231 breast cancer cells were not affected by DDR k

148 Finally, re-expression of c-JUN in MDA-MB-231 cells promoted radioresistance and abrogated

149 titatively assess ATP, ADP, and pH levels in MDA-MB-231 metastatic cancer cells as a function of the

150 itor MK2206 reduced phosphocholine levels in MDA-MB-468 cells.

151 d not alter the acetylation level of LSD1 in MDA-MB-231 cells.

152 t occurred in a TNFalpha-dependent manner in MDA-MB-468 cells.

153 ecreased the nuclear level of H3K4me1/me2 in MDA-MB-231 cells, whereas loss of HDAC5 by siRNA diminis

154 K1) mutant K46N increased lung metastases in MDA-MB-231 xenograft mouse models.

155 X-ray (carbon K-shell, 278 eV) microbeam in MDA-MB-231 breast cancer and AG01522 fibroblast cells wi

156 cell lines while the NP accumulated more in MDA-MB-231 than MCF-7 potentially due to binding of hyal

157 Moreover, in MDA-MB-231-bearing nude mice, H3L2 induced dysfunctional

158 ment compliance of at least 75% is needed in MDA to control human morbidity attributable to parasitic

159 tide, enhanced the cellular uptake of NPs in MDA-MB-468, an EFGR-overexpressing triple negative breas

160 ugh two mechanisms: apoptosis and oncosis in MDA-MB-468 cells.

161 eted phase-change contrast agents (PCCAs) in MDA-MB-231 and MCF-7 breast cancer cells in vitro.

162 dulated PARylation and cell proliferation in MDA-MB-436 cells (BRAC1 mutation).

163 Furthermore, suppressing Spry1 in MDA-MB-231 cells impaired the induction of Snail and Slu

164 h PET imaging and biodistribution studies in MDA-MB-231 and MDA-MB-157 xenografts and a patient-deriv

165 Further studies in MDA-MB-231 breast cancer cells reveal that TS subpopulat

166 nd target individuals who are not treated in MDA.

167 e of nodes at risk for refusing treatment in MDA to below 25%.

168 gnificantly decreased upon drug treatment in MDA-MB-231 and MDA-MB-157 cells (P < 0.01-0.001).

169 Loss of PRMT5 or WDR77 in MDA-MB-231 cells leads to defects in alternative splicin

170 Increased MDA and plasma creatinine levels also became evident aft

171 Increased MDA levels became evident at 2 hours of slow BD inductio

172 d heme-oxygenase 1 expression, and increased MDA and plasma creatinine levels.

173 hymic nude mice bearing estrogen-independent MDA-MB-231 human breast cancer xenografts.

174 guided fragment-based drug design, inhibited MDA-9/Syntenin binding to EGFRvIII, which increased foll

175 ll protectants, can again be fragmented into MDA.

176 Mesenchymal and invasive MDA-MB-231 tumors display higher vascularization and les

177 ort efficient matrix degradation in invasive MDA-MB-231 breast cancer cells.

178 xenografts originating from Spry1 knockdown MDA-MB-231 cells grew slower, had increased E-cadherin e

179 -1 deficiency abrogated malondialdehyde-LDL (MDA-LDL) uptake by hepatic macrophages and was associate

180 C2-like MDA-MB-231 cells dominated in untreated animals, but C3-

181 type was also observed in the TNBC cell line MDA-MB-157.

182 that in the basal-like metastatic cell line MDA-MB-231 and primary triple-negative breast cancer tum

183 riple-negative basal breast cancer cell line MDA-MB-231 and the luminal breast cancer cell line MCF7:

184 cell lines including breast cancer cell line MDA-MB-231, lung cancer cell line PC-9, and leukemia cel

185 invasiveness of the breast cancer cell line MDA-MB-231.

186 is model derived from human cancer cell line MDA-MB-231.

187 hly metastatic human breast cancer cell line MDA-MB-231HM.

188 vo studies, a human breast cancer cell line (MDA-231) was implanted in five mice per group.

189 d chimerism compared with products of liquid MDA reactions.

190 ged the absolute uptake of (18)F-FLT in live MDA-MB-231 cells grown under different serum conditions.

191 oteins showed higher ROS and T-AOC but lower MDA levels than non-meat proteins, which may be due to t

192 28) by the oxidative adduct malondialdehyde (MDA).

193 tes, glutathione (GSH), and malondialdehyde (MDA) concentrations in liver; and serum levels of alanin

194 rotein content, proline and malondialdehyde (MDA) content as well as O2*(-) production rate, the gene

195 The soluble proteins and malondialdehyde (MDA) contents were stimulated by all tested irradiation

196 amino acid, carotenoid, and malondialdehyde (MDA) in egg yolk.

197 xidative damage biomarkers, malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), aconitase-2 and 8-hydrox

198 entation products including malondialdehyde (MDA), an archetypal marker of PUFA oxidation.

199 cteristics, including lower malondialdehyde (MDA) content, lower water loss rates, lower relative Na(

200 ation of lipofuscine (LPS), malondialdehyde (MDA) and activity of total superoxide dismutase (SOD), a

201 The increased production of malondialdehyde (MDA) suggests that Ga stress could cause oxidative damag

202 xidative damage by reducing malondialdehyde (MDA) concentration and increasing antioxidant enzymes ac

203 xidation, measured as serum malondialdehyde (MDA) levels, correlates with delayed graft function in r

204 We further show that malondialdehyde (MDA) epitopes, products of lipid peroxidation and marker

205 Urinary malondialdehyde (MDA), a marker of lipid peroxidation, was measured in 24

206 ss and can be evaluated via malondialdehyde (MDA) levels.

207 480, HCT-15, RKO, and HCT 116) and melanoma (MDA-MB-435S and SK-MEL-28) cell lines using short hairpi

208 the myeloid lineage, in BCa bone metastases, MDA-MB-231 BCa cells were intra-tibially or intra-cardia

209 tly expressed in breast tumor and metastatic MDA-MB-231 cells and its level was significantly higher

210 troducing exogenous E-cadherin in metastatic MDA-MB-231 cells increases the micropattern dimension at

211 Depletion of CAP1 in the metastatic MDA-MB-231 and BT-549 cancer cells stimulated the metast

212 Methylenedianiline (MDA) is a common industrial chemical with health and pro

213 Characterization of methylenedianiline (MDA) 2-ring isomers (2,2'-, 2,4'-, and 4,4'-MDA) is repo

214 anged between approximately 0.15 and 0.30 mg MDA/kg appeared least at end of storage for 100% N2 trea

215 cells and in a preclinical xenograft model, MDA PCa 118b, also significantly suppressed tumor angiog

216 ake was evaluated in 3 breast cancer models: MDA-MB-231, MCF-7, and ZR-75-1.

217 Moreover, MDA-MB-231 human breast cancer cells could be separated

218 een studied during the course of a multiyear MDA program.

219 By using ER-negative MDA-MB-231 breast cancer cells, clonal lines were create

220 sma angiogenic secretomes in triple negative MDA-MB-231 breast cancer xenografts compared to ER-posit

221 of elevated LDL-C in human triple-negative (MDA-MB-231) and mouse Her2/Neu-overexpressing (MCNeuA) b

222 d PKCdelta completely ablated the ability of MDA-7/IL-24 to reduce the Bcl-x(L)/(s) mRNA ratio and ce

223 hat the increase in the migration ability of MDA-MB-231 cells co-cultured with HMEpiC cells was relat

224 rane disintegration allows quick ablation of MDA-MB-231 cells.

225 Accumulation of MDA epitopes plays a major role during diet-induced hepa

226 dhesion process of motile cells, adhesion of MDA-MB-231 cancer cells on glass substrate coated with f

227 f trachoma up to 10 years after cessation of MDA in 4 districts in children in Nepal.

228 d 10 years, respectively, after cessation of MDA.

229 e distribution, and morphological changes of MDA-MB-231 and MCF-7 cells.

230 Ectopic expression of MDA-5 has been shown to induce cancer cell death, but th

231 e, we demonstrate that ectopic expression of MDA-5 via replication-incompetent adenovirus (Ad.Mda-5)

232 estoration, through either the generation of MDA-MB-231-stable clones or peritumoral delivery in MDA-

233 rescue study showed that increased growth of MDA-MB-231 cells by HDAC5 overexpression was reversed by

234 invasion, and inhibited the tumor growth of MDA-MB-231 TNBC cell xenografts in the mammary fat pads

235 elded an additive reduction in the growth of MDA-MB-231 tumor xenografts.

236 we introduce lattice-light sheet imaging of MDA-MB-231 human breast cancer cells genetically enginee

237 gistically increased cisplatin inhibition of MDA-MB-231 triple-negative breast cancer cell proliferat

238 resulted in synergistic growth inhibition of MDA-MB453 cells, implicating Src as a mediator of resist

239 A specific inhibitor of MDA-9/Syntenin activity, PDZ1i (113B7), identified throu

240 ndependent growth, migration and invasion of MDA-MB-231 human breast cancer cells and Py8119 mouse ma

241 Knockdown of MDA-9/Syntenin sensitizes GBM cells to radiation, reduci

242 At lower levels of MDA, mammographic density and telomere length were inver

243 nversely associated; while at high levels of MDA, there was evidence of a J-shaped association betwee

244 -x(s) expression is an important mediator of MDA-7/IL-24-induced cytotoxicity requiring the SRC/PKCde

245 bition attenuates invasion and metastasis of MDA-MB-231 cells and prolongs life span of mice injected

246 also inhibited TGF-beta-induced migration of MDA-MB-231 cells by blocking nuclear export of NR4A1, wh

247 and assessment to accompany the roll-out of MDA programmes to ensure that the considerable health be

248 ycerol (18:3-16:3-MGDG) as an end-product of MDA incorporation.

249 Length of time since the last round of MDA and the prevalence of TF among children aged 1 to 9

250 reviously received between 1 and 9 rounds of MDA with praziquantel.

251 m II and is likely a major in vivo source of MDA in photosynthetic tissues.

252 increase in endoplasmic reticulum stress of MDA-MB-468 cells with time and with increasing oxygen te

253 investigations revealed that the survival of MDA-MB-231 TNBC cells relied heavily on the BCL-2/BCL-XL

254 ath in 3D spheroids and extended survival of MDA-MB-231-bearing mice.

255 -9) and pharmacological (PDZ1i) targeting of MDA-9/Syntenin reduced invasion gains in GBM cells follo

256 MC) in NOD/SCID mice harboring xenografts of MDA-MB-231, a triple-negative breast cancer line constit

257 from baseline were realized after 1 year of MDA: we did not identify factors that moderated this rel

258 was significantly higher in breast tumor or MDA-MB-231 cells than in distal non-tumor tissue and low

259 performed with mice bearing either U87MG or MDA-MB-435 tumor xenografts immediately before and after

260 ncer xenograft model, miR-221-overexpressing MDA-MB-231 clones were more aggressive and resistant to

261 brain metastasis of a breast cancer patient (MDA-MB-361).

262 Delivered as a volatile to intact plants, MDA was efficiently incorporated into lipids.

263 ymic mice bearing subcutaneous EGFR-positive MDA-MB-468 human breast cancer tumors.

264 ved (i) the mammalian antioxidant responses (MDA, GSH and SOD2 levels), (ii) tissue nutrient (glucose

265 In ESI, 2-ring MDA isomers formed single unique [M + H](+) (199 Da) par

266 more consecutive treatments, even at routine MDA doses (150 microg/kg) and frequencies (annual).

267 icant positive correlations between salivary MDA levels and periodontal clinical parameters as well a

268 s study is the first to investigate salivary MDA levels in patients with ACS and their correlations w

269 The results indicate that salivary MDA levels could be a biomarker for cardiovascular and/o

270 Moreover, elevated levels of secreted MDA-modified vimentin were detected in the plasma of age

271 Trastuzumab-sensitive MDA-MB-231/H2N and trastuzumab-resistant TrR1 tumors wer

272 e bearing subcutaneous trastuzumab-sensitive MDA-MB-231/H2N or trastuzumab-resistant TrR1 tumors were

273 ctivities and 5 signaling proteins in single MDA-MB-231 breast cancer cells.

274 type I IFN signaling was crucial for in situ MDA-5-induced protective antitumor immunity.

275 CF7, MCF7/VP16, BT474, T47D, ZR-75-1, SKBR3, MDA-MB-468) than normal breast cells (MCF-10A) or cell l

276 CF7, MCF7/VP16, BT474, T47D, ZR-75-1, SKBR3, MDA-MB-468, BT20, MDA-MB-231); normal breast cells (MCF-

277 topes by intravenous injection of a specific MDA antibody results in decreased hepatic inflammation i

278 t and cost-effectiveness of scaling up a STH MDA programme targeting Ascaris lumbricoides.

279 jection in athymic mice bearing subcutaneous MDA-MB-231/H2N tumors.

280 4 hours after slow BD induction, superoxide, MDA, and plasma creatinine levels increased further, whe

281 s in immunocompromised mice demonstrate that MDA-MB-231 TS cells form more and bigger xenograft tumor

282 haliana leaves, raising the possibility that MDA is metabolized.

283 The MDA strategies were less effective at reducing prevalenc

284 The MDA-MB-231 embedded spheroid tumor model exhibited the m

285 s of an aggressive metastatic variant of the MDA-MB-231 human TNBC cell line, LM2-4.

286 mes related gene expression, and reduced the MDA content and O2*(-) production rate compared to no GS

287 ing results reveal that the probe stains the MDA-MB-231 cell membrane in 30 min, which is followed by

288 Among these, MDA-MB231 and B16F10 had none to minimal expression in c

289 FRvIII signaling, which is abrogated through MDA-9/Syntenin down-regulation.

290 d HER2-targeted lapatinib, were delivered to MDA-MB-231 and SKBR3 (overexpressing HER2) breast cancer

291 quantel in schools with a higher exposure to MDA may pose a threat to the effectiveness of schistosom

292 from the mammary fat pad after transfecting MDA-MB-231 breast cancer cells, while BMD cells were iso

293 onounced endogenous overexpression of TRPV4, MDA-MB-468 and HCC1569.

294 Using the CARD-truncated MDA-5 mutant, silencing of IPS-1, and antibody blockade

295 , and was positively correlated with urinary MDA.

296 nce to the drug compared to 2D culture where MDA-MB-231 attained a drug-resistant tumor-initiating ph

297 death, but the mechanism of action by which MDA-5 exerts these cytotoxic effects is unclear.

298 treatment with HER-family inhibitors, while MDA-MB-453 was comparatively resistant.

299 rt-term impact of 2 rounds of community-wide MDA and household-level (focal) MDA with DHAp compared w

300 of nude mice, which had been inoculated with MDA-MB-231 cells, with inhibitor 38u via oral administra