ライフサイエンスコーパス: sulindac

1 ioprine/6-mercaptopurine, 5-fluorouracil and sulindac.

2 ion from Apc+/-, p21+/+, +/- or -/- mice fed sulindac.

3 p27 is not necessary for tumor inhibition by sulindac.

4 gastrointestinal ulcerations than high-dose sulindac.

5 ergoing primary chemoprevention therapy with sulindac.

6 tive of a shortened clonal evolution treated sulindac.

7 ercent methylation when comparing placebo vs sulindac.

8 the nonsteroidal anti-inflammatory compound, sulindac.

9 morigenesis was suppressed by treatment with sulindac.

10 ponsive elements were repressed by the NSAID sulindac.

11 phase IIb/III chemoprevention trial of DFMO/sulindac.

12 brogated the ischemic protection afforded by sulindac.

13 OX-2) inhibitor, exerted a similar effect as sulindac.

14 stablished tumors with NSAIDs (piroxicam and sulindac, 0.5 and 0.6 mg/mouse/day, respectively) for 6

15 FAP will be randomized to: CPP-1X 750 mg and sulindac 150 mg, CPP-1X placebo and sulindac 150 mg, or

16 0 mg and sulindac 150 mg, CPP-1X placebo and sulindac 150 mg, or CPP-1X 750 mg and sulindac placebo o

17 Participants with FAP were randomized to sulindac (150 mg) twice daily and erlotinib (75 mg) dail

18 Among the subset of patients taking sulindac, 3 of 5 prostaglandin levels were statistically

19 et (WD), WD + ASA (200 mg/kg food), and WD + sulindac (300 mg/kg food).

20 y of the nonsteroidal anti-inflammatory drug sulindac (400 ppm in drinking water) alone, the CCK2/gas

21 Sulindac, a non-steroidal anti-inflammatory prodrug, is

22 nse was also compared in detail with that of sulindac, a nonsteroidal anti-inflammatory drug with sig

23 Both the sulfide and sulfone metabolites of sulindac, a nonsteroidal anti-inflammatory drug, display

24 Sulindac, a nonsteroidal anti-inflammatory drug, inhibit

25 ent to abrogate duodenal tumor inhibition by sulindac, a nonsteroidal anti-inflammatory drug.

26 In the present study, sulindac, a nonsteroidal antiinflammatory drug (NSAID),

27 One of the drugs was sulindac, a prototypical non-steroidal anti-inflammatory

28 In conclusion, daily sulindac administration in FAP patients significantly al

29 In H. pylori-infected mice, sulindac alone or YM022 alone had no protective effect o

30 (P = 0.053) and 36 +/- 2.1 (NS) with 80 ppm sulindac alone; and to 116 +/- 8.1 (P = 0.004) and 28 +/

31 We have recently shown that sulindac, an anti-inflammatory drug, enhances the killin

32 The combination of sulindac and antimicrobial H. pylori eradication was ben

33 signed to examine the safety and efficacy of sulindac and DFMO (alone or in combination) for preventi

34 Among participants with FAP, the use of sulindac and erlotinib compared with placebo resulted in

35 ine, ibuprofen, acetaminophen (paracetamol), sulindac and indomethacin, was also achieved in supramol

36 n was tested with the anti-inflammatory drug sulindac and its metabolite, sulindac sulfone, which wer

37 ly ameliorated by the anti-inflammatory drug sulindac and largely prevented by statin treatment.

38 ptotic response to the chemopreventive agent sulindac and other nonsteroidal anti-inflammatory drugs

39 Unlike sulindac and other nonsteroidal anti-inflammatory drugs,

40 s polyposis have consistently indicated that sulindac and other nonsteroidal antiinflammatory drugs o

41 Sulindac and selective cyclooxygenase (COX)-2 inhibitors

42 Combined treatment with sulindac and ursodeoxycholate was more effective than ei

43 nd growth rate were similar for the control, sulindac, and analogue groups.

44 Other traditional NSAIDs, particularly sulindac, and selective COX-2 inhibitors are now given t

45 for the nonsteroidal anti-inflammatory drug, sulindac, and the chemotherapeutic drug, 5-fluorouracil.

46 e hydrophobic small drug molecules curcumin, sulindac, and triamterene is demonstrated.

47 nsteroidal anti-inflammatory drugs including sulindac are promising chemopreventive agents for colore

48 0.66 (95% CI, 0.36 to 1.24) for eflornithine-sulindac as compared with eflornithine.

49 nterval [CI], 0.39 to 1.32) for eflornithine-sulindac as compared with sulindac (P = 0.29) and 0.66 (

50 (3) P-S is much safer than sulindac as evidenced by its in vitro toxicologic evalua

51 Both the sulfide and sulfone metabolites of sulindac as well as more potent cyclic GMP-dependent pho

52 afety of the combination of eflornithine and sulindac, as compared with either drug alone, in adults

53 of combination therapy with eflornithine and sulindac, as compared with either drug alone, in delayin

54 ine kinase inhibitor erlotinib and GPCR with sulindac at low doses of 6 and 310 micromol/L, respectiv

55 utations are likely to develop resistance to sulindac but not to SC-'236-like NSAIDs.

56 As shown here, sulindac can also protect RPE cells from chemical oxidat

57 The results suggest that low levels of sulindac can induce a preconditioning response, triggere

58 cells to validate the basic observation that sulindac can protect retinal cells against oxidative str

59 Sulindac causes regression of precancerous adenomatous p

60 However, sulindac combined with H. pylori antimicrobial eradicati

61 the compound sulindac sulfide (SS), because sulindac compounds are well-established colon cancer che

62 tes that addition of a benzylamide moiety to sulindac compounds results in markedly altered pharmacol

63 idative stress in RPE cells and suggest that sulindac could be used therapeutically for slowing the p

64 Low levels of sulindac could protect cardiac myocytes against cell dea

65 e transcription inhibitors (CT-ARM, ICAT, or sulindac) could disrupt the LEF-1-beta-cat complex after

66 The non-steroidal anti-inflammatory drug sulindac decreases size and number of adenomas after 4-6

67 zed phospho-sulindac (P-S; OXT-328), a novel sulindac derivative.

68 Standard doses of sulindac did not prevent the development of adenomas in

69 Sulindac did not slow the development of adenomas, accor

70 dal anti-inflammatory drugs (NSAIDs) such as sulindac effectively prevent colon cancer in humans and

71 We conclude that sulindac enhances H. pylori gastritis and may promote in

72 and 2 adverse events were more common in the sulindac-erlotinib group, with an acne-like rash observe

73 Importantly, sulindac exacerbated the severity of H. pylori-associate

74 that the sulfide and sulfone derivatives of sulindac exert COX-dependent effects by distinct mechani

75 The nonsteroidal anti-inflammatory drug sulindac exerts a significant antineoplastic effect on s

76 biomarker levels modified the effect of DFMO/sulindac for CRA prevention.

77 oped in 9 of 21 subjects (43 percent) in the sulindac group and 11 of 20 subjects in the placebo grou

78 in tag diversity over time was found in the sulindac group compared to the placebo group (*p = 0.018

79 ere statistically significantly lower in the sulindac group than in the placebo group.

80 18 of 56 patients (32%) in the eflornithine-sulindac group, 22 of 58 (38%) in the sulindac group, an

81 ithine-sulindac group, 22 of 58 (38%) in the sulindac group, and 23 of 57 (40%) in the eflornithine g

82 ate of compliance exceeded 76 percent in the sulindac group, and mucosal prostaglandin levels were lo

83 .001) and polyp area (70%; P < 0.001) in the sulindac group.

84 ddition to its anti-inflammatory properties, sulindac has been demonstrated to have a role in the pre

85 s its established antiinflammatory activity, sulindac has previously been shown to protect cardiac ti

86 Aspirin and sulindac have been shown to be effective in selecting fo

87 l anti-inflammatory drugs (NSAIDs) including sulindac have shown potent chemopreventive and tumor reg

88 Five organic acids (sulindac, ibuprofen, ketoprofen, diclofenac, and norflox

89 trasts with the abrogation of the effects of sulindac in Apc(+/-),p21(+/-) or Apc(+/-),p21(-/-) mice,

90 , attenuated the tumor-suppressive effect of sulindac in APC(Min/+) mice by blocking apoptosis and re

91 Y-294002 (PI3kinase inhibitor), retinol, and sulindac in colon cancer cell lines expressing the poor

92 significantly reversed by the application of sulindac in the drinking water of the L2D1(+)/p53(+/-) m

93 However, p21 was not induced by sulindac in the duodenal flat mucosa and tumors of Apc+/

94 dicate that the primary protective effect of sulindac in these experiments does not involve its role

95 colorectal cancer cells with the prooxidant sulindac increased the half-life of gamma-GCSh mRNA.

96 st, the nonsteroidal anti-inflammatory drug, sulindac, increased c-myc expression, an effect attribut

97 ell cycle progression, although butyrate and sulindac induce a similar G0-G1 arrest, elevation of bet

98 We found that dietary sulindac induced apoptosis to remove the intestinal stem

99 Sulindac induced complex alterations in gene expression,

100 nhibition of the PGE2 synthesis pathway with sulindac induced HNSCC cytotoxicity at high doses (EC(50

101 Sulindac induced iNOS and Hsp70, late-phase IPC markers

102 on) did not induce colitis whereas the NSAID sulindac induced severe colitis.

103 ibition of MEK/ERK activity is necessary for sulindac-induced apoptosis of human colon cancer cells,

104 Lovastatin, 10-30 micromol/L, augmented sulindac-induced apoptosis up to 5-fold in 3 colon cance

105 Sulindac induces apoptotic cell death in cancer cells in

106 Nonsteroidal anti-inflammatory drugs such as sulindac inhibit Wnt signaling, which is critical to mai

107 olateral and canalicular membrane fractions, sulindac inhibited cholyltaurine transport competitively

108 As expected, sulindac inhibited colonic ACF formation (P < 0.001) and

109 To dissect the role of p21 in sulindac inhibition of intestinal tumor development in A

110 However, the mechanisms by which sulindac inhibits tumor cell growth are not completely u

111 lammatory drugs (NSAIDs) such as aspirin and sulindac is associated with a decreased mortality from c

112 Sulindac is metabolized in vivo to sulfide and sulfone d

113 Sulindac is the most extensively investigated clinically

114 d with clinically used NSAIDs (indomethacin, sulindac, ketoprofen, ibuprofen, diclofenac, ketorolac,

115 account for the growth inhibitory effect of sulindac, less is known about its biochemical mechanism(

116 on of TRAIL/Apo2L with either irradiation or sulindac may be highly effective against both p53-profic

117 hibitory and anti-inflammatory properties of sulindac may be regulated in part by inhibition of kinas

118 These results suggest that sulindac may have therapeutic potential as a preconditio

119 events when given with rofecoxib, celecoxib, sulindac, meloxicam, and indometacin but not when given

120 Sulindac metabolites and other nonsteroidal anti-inflamm

121 We studied the effects of these sulindac metabolites in human colon cancer-derived Caco-

122 We previously reported that sulindac metabolites inhibit the mitogen-activated prote

123 ibition of ERK1/2 phosphorylation induced by sulindac metabolites.

124 necessary for the induction of apoptosis by sulindac metabolites.

125 of the induction of programmed cell death by sulindac metabolites.

126 drugs (NSAIDs), we evaluated the effects of sulindac on 14-3-3epsilon protein expression in colorect

127 nation of difluoromethylornithine (DFMO) and sulindac on biomarkers and investigated factors that mod

128 To further study the protective effect of sulindac on cells exposed to oxidative stress, we have i

129 as used to detect COX-independent effects of sulindac on gene expression in human colorectal cells.

130 e stress, we have investigated the effect of sulindac on rat cardiac myocytes subjected to hypoxia/re

131 Therefore, the effect of sulindac on stem cell dynamics was studied.

132 s, aspirin (acetyl-salicylic acid; ASA), and sulindac, on neointimal formation in a mouse femoral art

133 d 14-3-3epsilon proteins from elimination by sulindac or indomethacin.

134 Patients received either sulindac or placebo for 48 months, and development of ne

135 Sulindac or YM022 combined with antimicrobial eradicatio

136 or antagonist YM022 (45 mg/kg/wk) alone, and sulindac or YM022 combined with H. pylori eradication th

137 In infected mice, sulindac or YM022 treatment did not alter gastric expres

138 to receive 750 mg of eflornithine, 150 mg of sulindac, or both once daily for up to 48 months.

139 The subjects received either 75 or 150 mg of sulindac orally twice a day or identical-appearing place

140 ) for eflornithine-sulindac as compared with sulindac (P = 0.29) and 0.66 (95% CI, 0.36 to 1.24) for

141 en these limitations, we synthesized phospho-sulindac (P-S; OXT-328), a novel sulindac derivative.

142 (1) Compared with sulindac, P-S is much more potent in inhibiting the grow

143 0.024, and 0.010 mM for aspirin, ibuprofen, sulindac, phenylbutazone, naproxen, indomethacin, diclof

144 0.013, and 0.008 mM for aspirin, ibuprofen, sulindac, phenylbutazone, naproxen, indomethacin, diclof

145 bo and sulindac 150 mg, or CPP-1X 750 mg and sulindac placebo once daily for 24 months.

146 20 ppm of the nonsteroidal anti-inflammatory sulindac (positive control); or 30 ppm of SC-51 with 500

147 nti-inflammatory drug (NSAID) treatment with sulindac prevented NASH and subsequent HCC development.

148 A unique feature of the sulindac protective response is that it involves activat

149 In the Langendorff model sulindac provided significant protection against cell de

150 activity of phospho-aspirin (PA) and phospho-sulindac (PS) in inhibiting tumor growth in established

151 These results demonstrate sulindac reduces neointimal formation in both normolipid

152 Treatment with piroxicam and sulindac resulted in 95% and 52% fewer tumors, respectiv

153 owed that short-term treatment of cells with sulindac resulted in a large reduction of phosphorylated

154 mbined with maximal PA export using low-dose sulindac, results in greatly reduced levels of normal mu

155 In addition, indomethacin and sulindac significantly enhanced the apoptosis-inducing e

156 A combination of DFMO and sulindac significantly suppressed production of rectal m

157 In the group that received DFMO/sulindac, spermidine-to-spermine ratio (Spd:Spm) in rect

158 Sulindac sulfide (10 microm) altered the expression of 6

159 Neither sulindac sulfide (a cyclooxygenase inhibitor) nor sulind

160 and evaluated a series of (E)-2'-des-methyl-sulindac sulfide (E-DMSS) analogues for inhibition of CO

161 Here, we show that the NSAID, sulindac sulfide (SS) can potently inhibit the invasion

162 For comparison, we included the compound sulindac sulfide (SS), because sulindac compounds are we

163 In this study, we show that sulindac sulfide acts both as a PPARgamma agonist and a

164 In this report, we demonstrate that sulindac sulfide also engaged the membrane death recepto

165 Thus, our results demonstrate that sulindac sulfide also engages the membrane DR pathway in

166 stern analysis supported the conclusion that sulindac sulfide altered the expression of these protein

167 Sulindac sulfide and 5'-DMI inhibited intracellular cycl

168 Both sulindac sulfide and ciglitazone, a defined peroxisome p

169 ical inhibitors specific for Ras activation, sulindac sulfide and farnesytranferase inhibitor I, mark

170 D/GSM activity, we determined the effects of sulindac sulfide and flurbiprofen on gamma-cleavage of a

171 not impaired by the Abeta42-lowering NSAIDs, sulindac sulfide and ibuprofen.

172 a critical role in the induction of NAG-1 by sulindac sulfide and other NSAIDs.

173 tosolic phospholipase A(2), COX-1, or COX-2, sulindac sulfide and PPARgamma agonists also inhibited t

174 Here we report that two different NSAIDs, sulindac sulfide and SC-'236 engage the death receptor 5

175 We show that sulindac sulfide and SC-'236-induced apoptosis is couple

176 We further show that sulindac sulfide and SC-'236-induced DR5 upregulation oc

177 rentially modulates the apoptotic effects of sulindac sulfide and SC-'236.

178 also found that the anti-inflammatory drugs sulindac sulfide and sulindac sulfone, which attenuate b

179 sis, and potentiated the apoptotic effect of sulindac sulfide and sulindac sulfone.

180 l anti-inflammatory drugs (NSAIDs) including sulindac sulfide are known to exert cancer chemopreventa

181 Similarly, pretreatment with sulindac sulfide blocks the ability of EGF to induce ERK

182 hysiological pattern (high Abeta40); and (4) sulindac sulfide directly and preferentially decreases A

183 We find that sulindac sulfide does not induce drastic architectural c

184 Recent evidence suggests that sulindac sulfide engages the mitochondrial pathway invol

185 he novel-type 5-LO inhibitors licofelone and sulindac sulfide exhibited higher potencies in human blo

186 Sulindac sulfide had little effect on COX-2 in this mode

187 The NSAIDs indomethacin and sulindac sulfide have been shown to induce apoptosis of

188 report, we demonstrate that indomethacin and sulindac sulfide induce apoptosis of human leukemic Jurk

189 ion of PPARgamma, as well as ciglitazone and sulindac sulfide induced expression of E-cadherin, which

190 Sulindac sulfide inhibited 14-3-3epsilon proteins in HT-

191 Sulindac sulfide inhibited PPARdelta protein expression

192 Sulindac sulfide inhibits cyclooxygenase (COX) enzyme ac

193 state NMR study demonstrating that the NSAID sulindac sulfide interacts specifically with Alzheimer d

194 Sulindac sulfide is one of the major metabolites of suli

195 Further, in Bax-deficient cells, neither sulindac sulfide nor SC-'236 in combination with Apo2L/T

196 Importantly, the concentration of sulindac sulfide required to inhibit NSCLC cell growth g

197 Sulindac sulfide specifically up-regulated the DR5 level

198 At micromolar concentrations, sulindac sulfide stimulated apoptosis and inhibited the

199 nation for this finding is the metabolism of sulindac sulfide to inactive metabolites by the peroxida

200 and p21WAF1/CIP1 upregulation in response to sulindac sulfide treatment in PNT1A cells.

201 Sulindac sulfide treatment restored DR-5 expression and,

202 Sulindac sulfide up-regulated DR5 and activated the prox

203 For example, sulindac sulfide upregulates DR5 in both Bax-deficient a

204 nonsteroidal anti-inflammatory drug (NSAID) sulindac sulfide were synthesized as potential agonists

205 Selective COX-2 (NS398) and nonselective (sulindac sulfide) COX inhibitors, as well as 5-fluoroura

206 Sulindac sulfide, a COX inhibitor, inhibited the growth

207 e evaluated the growth-inhibitory effects of sulindac sulfide, a COX-1 and COX-2 inhibitor; exisulind

208 anti-inflammatory drug), R-flurbiprofen and sulindac sulfide, affect only Abeta and not Notch beta f

209 and the nonsteroidal anti-inflammatory drug sulindac sulfide, analogous to those reported previously

210 Indomethacin, sulindac sulfide, and zomepirac displaced [3H]PGD2 bindi

211 mma-Secretase cleavage of APP was altered by sulindac sulfide, but CD44 and Notch-1 were either insen

212 Sulindac sulfide, but not sulindac sulfone, inhibits cyc

213 studies showed synergistic interactions for sulindac sulfide, exisulind, and NDGA with paclitaxel, c

214 anti-inflammatory drugs (R)-flurbiprofen and sulindac sulfide, have been suggested to modulate the Al

215 conclusion, this is the first report showing sulindac sulfide, independent of cyclooxygenase, altered

216 st potent agent (IC50 = 0.003-0.150 microM); sulindac sulfide, NDGA, and 13-cis-retinoic acid had int

217 Treatment of the cells with Exisulind, sulindac sulfide, OSI-461, the guanylyl cyclase activato

218 ollectively, our results suggest that unlike sulindac sulfide, SC-'236 in combination with Apo2L/TRAI

219 To test this hypothesis sulindac sulfide, which is used to treat familial adenom

220 lls, but Apo2L/TRAIL efficiently potentiates sulindac sulfide-induced apoptosis as well as activation

221 ligand, the ligand for DR5, also potentiated sulindac sulfide-induced apoptosis in all of the cell li

222 als originating from the endogenous DR5, and sulindac sulfide-induced apoptosis was investigated.

223 To further delineate the role of DR5 in sulindac sulfide-induced apoptosis, we used JCA-1 prosta

224 s-associated death domain did indeed inhibit sulindac sulfide-induced apoptosis.

225 further supporting the involvement of DR5 in sulindac sulfide-induced apoptosis.

226 oduct of cyclooxygenase, only suppressed the sulindac sulfide-induced expression of two genes, with l

227 icient HCT-116 cells were more responsive to sulindac sulfide-induced gene expression than SW-480 cel

228 h inhibition and also dramatically inhibited sulindac sulfide-mediated p21WAF1/CIP1 upregulation.

229 or the nonsteroidal anti-inflammatory drug, sulindac sulfide.

230 rs such as NS-398, nimesulide, SC-58125, and sulindac sulfide.

231 of Min/+ mice with the chemopreventive drug sulindac sulfide.

232 bridge is not affected upon interacting with sulindac sulfide.

233 e first generation GSMs (R)-flurbiprofen and sulindac sulfide.

234 e substrates have different sensitivities to sulindac sulfide.

235 We used the NSAIDs sulindac sulfone (COX-2-independent) and NS-398 (a COX-2

236 ic leukemia (CLL), we studied the effects of sulindac sulfone (exisulind), a non- cyclooxygenase-inhi

237 Sulindac sulfone (exisulind), although a nonsteroidal an

238 investigate the chemopreventive efficacy of sulindac sulfone (exisulind), the sulfone metabolite of

239 uction of apoptosis in cancer cells, because sulindac sulfone (exisulind, Aptosyn) and certain deriva

240 tment of SW480 human colon cancer cells with sulindac sulfone (Exisulind, Aptosyn) or the related der

241 ves, or the cGMP phosphodiesterase inhibitor sulindac sulfone (exisulind, aptosyn, hereafter called e

242 Treatment of IL-10(-/-) mice with sulindac sulfone (which does not inhibit PG production)

243 Here, we demonstrate that sulindac, sulindac sulfone and indomethacin activate the NF-kappaB

244 te, is required for the induction of SSAT by sulindac sulfone and is specifically bound by PPAR gamma

245 Sulindac sulfone at 600 mumol/L inhibited 14-3-3epsilon

246 is not required for the induction of SSAT by sulindac sulfone but can be bound by both PPAR delta and

247 c enzyme, was induced by clinically relevant sulindac sulfone concentrations.

248 dac sulfide (a cyclooxygenase inhibitor) nor sulindac sulfone induced G(2)-M arrest, Bcl2 phosphoryla

249 Sulindac sulfone inhibited COX-2 protein expression, whi

250 These data suggest that apoptosis induced by sulindac sulfone is mediated, in part, by the COX-indepe

251 Sulindac sulfone reduced cellular polyamine contents in

252 However, the mechanisms by which sulindac sulfone suppresses cancer growth are not as def

253 of human colon cancer cells with exisulind (sulindac sulfone) and related compounds induces apoptosi

254 ide, a COX-1 and COX-2 inhibitor; exisulind (sulindac sulfone), a novel proapoptotic agent that does

255 e focused on a novel benzylamide analogue of sulindac sulfone, CP461, which is in clinical trials as

256 Sulindac sulfide, but not sulindac sulfone, inhibits cyclooxygenase (COX) enzyme a

257 anti-inflammatory drugs sulindac sulfide and sulindac sulfone, which attenuate beta-catenin transcrip

258 flammatory drug sulindac and its metabolite, sulindac sulfone, which were readily distinguished.

259 and mutational studies were done to map the sulindac sulfone-dependent response sequences in the SSA

260 the apoptotic effect of sulindac sulfide and sulindac sulfone.

261 Here, we demonstrate that sulindac, sulindac sulfone and indomethacin activate the

262 that the NSAIDs ibuprofen, indomethacin and sulindac sulphide preferentially decrease the highly amy

263 In Apc+/-, p21 wild-type mice fed the sulindac supplemental diet, both p21 mRNA and protein we

264 Sulindac suppressed 14-3-3epsilon promoter activity.

265 nonsteroidal anti-inflammatory drug (NSAID) sulindac, suppresses the growth of tRXRalpha-mediated co

266 in the skin was lower in wild-type mice fed sulindac than in similarly treated PPARbeta-null mice.

267 wer with the combination of eflornithine and sulindac than with either drug alone.

268 rry structurally and functionally related to sulindac that also has chemopreventive activity.

269 enase-inhibitory end metabolite of the NSAID sulindac that has been reported to inhibit cGMP phosphod

270 c sulfide is one of the major metabolites of sulindac that is believed to mediate its antitumorigenic

271 hat showed similar responses to butyrate and sulindac, the data were characterized by the extensive d

272 h I kappa B kinase activity was inhibited by sulindac to a similar level as in melanocytes, the phosp

273 The ability of sulindac to block ERK1/2 signaling by the EGF receptor m

274 of p21 completely eliminated the ability of sulindac to both inhibit mitotic activity in the duodena

275 eptor gamma did not attenuate the ability of sulindac to down-regulate Stat3.

276 hypermethylation, and that the inability of sulindac to inhibit tumor formation in Apc+/-, p21+/- mi

277 ts were laser microdissected in placebo- and sulindac- treated FAP patient tissue after which the met

278 A sulindac-treated group (n = 10) was used as a positive c

279 er ratio of apoptosis:mitosis in tumors from sulindac-treated mice as compared with controls.

280 uding head and neck SCCa, we studied whether sulindac treatment affects the Stat3 signaling pathway i

281 In contrast, 3 days of sulindac treatment eliminated both phosphorylated and un

282 Also, sulindac treatment exerted a significant time-dependent

283 Compared with ASA or WD alone, sulindac treatment resulted in approximately 70% (P = 0.

284 ps, but remarkably, none was detectable with sulindac treatment, despite hyperlipidemia, suggesting e

285 t down-modulation of Stat3 can be induced by sulindac treatment, thus possibly contributing to the an

286 Secondly, after feeding of sulindac, two end-effectors of preconditioning, inducibl

287 d clopidogrel or the anti-inflammatory agent sulindac vs mice on a chow (control) diet.

288 Furthermore, sulindac was able to disrupt the ability of PPARdelta to

289 with the nonsteroidal anti-inflammatory drug sulindac was evaluated.

290 Combined treatment with low-dose sulindac was less toxic, with normal weight gain and few

291 Furthermore, tumor inhibition by sulindac was linked to the induction of p21 expression b

292 In biliary fistula rats, sulindac was recovered in bile in unconjugated form and

293 Sulindac was secreted normally in Tr(-) rats, indicating

294 p1), the nonsteroidal anti-inflammatory drug sulindac was still effective in inhibiting intestinal tu

295 Sulindac was tested in combination with ursodeoxycholic

296 (P = 0.02) when 50 ppm lovastatin and 80 ppm sulindac were combined.

297 lfone (exisulind), the sulfone metabolite of sulindac, when administered during the promotion/progres

298 ammatory drugs (NSAIDs), such as aspirin and sulindac, which inhibit COX activity, reduce colorectal

299 The sulfone metabolite of sulindac, which lacks cyclooxygenase-inhibitory activity

300 ines between treatment groups or in those on sulindac who were polyp free compared with those who dev