ライフサイエンスコーパス: addicted

1 y a small percentage of alcohol users become addicted.

2 ic driver mutations to which tumor cells are addicted.

3 genetic lesion to which the cancer cells are addicted.

4 confirming that these tumors remain oncogene addicted.

5 stress than those of individuals who are not addicted.

6 d by mutant p53 to which cancer cells become addicted.

7 cription to which cancer cells become highly addicted.

8 , illustrating that cancers can be 'oncogene addicted' [1-10].

9 mers (24 +/- 2.8 yrs; 88.64% Male), 30% were addicted, 30% were problematic, 8% were engaged and 32%

10 Therefore, drug-addicted adolescents may have a higher risk of relapse t

11 ostasis and withdrawal relate, both in a non-addicted and addicted state.

12 ne expression changes common to both cocaine-addicted and alcoholic individuals that may reflect neur

13 pplying the monetary incentive delay task in addicted and at-risk adult populations are reviewed, wit

14 Generalized reward processing in addicted and at-risk populations is often characterized

15 strate that the CML stem cell is not BCR-ABL addicted and have important implications for developing

16 ions and socioeconomic disadvantage are more addicted and less likely to quit and experience greater

17 d state to which the tumor cells have become addicted and make them vulnerable to therapies and targe

18 addicted obese people is compared to alcohol-addicted and non-addicted lean controls.

19 Brain activity in food-addicted and non-food-addicted obese people is compared

20 ib with other c-MET inhibitors in both c-MET-addicted and nonaddicted cancer cells.

21 viability with similar potency in both c-MET-addicted and nonaddicted cells.

22 Drugs of abuse are rewarding to addicted and nonaddicted subjects, but they trigger crav

23 st that primitive CML cells are not oncogene addicted and that therapies that biochemically target BC

24 er suggest that cancer cells are "telomerase-addicted" and uncover functions of telomerase in tumor g

25 strategy in which cells with LOI are "IGF-II addicted" and undergo reduced tumorigenesis in the colon

26 ., non-problematic, engaged, problematic and addicted) and (3) the predictive power of socioeconomic

27 cocaine exposure are responsible for cocaine-addicted behaviors, the underlying molecular mechanism a

28 Long-lasting changes in the addicted brain are mediated by a complex circuit of brai

29 is a key adaptation occurring in the cocaine-addicted brain, but the effect of cocaine on the fundame

30 bute to persistent functional changes in the addicted brain.

31 We found that the cystine-addicted breast cancer cells and tumors have strong acti

32 Not everyone who takes drugs becomes addicted, but the likelihood of developing drug addictio

33 ically suppressed the growth of multiple Wnt-addicted cancer cell lines in soft agar.

34 es that showed enhanced ability to kill PI3K-addicted cancer cells and to inhibit Akt phosphorylation

35 ng incomplete tumor cell killing in oncogene-addicted cancer cells, we investigated the role of EGFR

36 t of cellular drug resistance in an oncogene-addicted cancer.

37 We found that many drug-treated "oncogene-addicted" cancer cells engage a positive feedback loop l

38 A subset of Wnt-addicted cancers are sensitive to targeted therapies tha

39 that targeting nutrient metabolism in energy-addicted cancers with high mTORC1 signaling may be an ef

40 mors, suggesting that treatment of glutamine-addicted cancers with mTOR inhibitors might have benefic

41 nd [hepatocyte growth factor receptor (MET)] addicted cancers, and reactivation of ErbB3 is a promine

42 d PHA-665752, suppressed the growth of c-MET-addicted cancers, but not the growth of cancers that are

43 s show efficacy in preclinical models of Wnt-addicted cancers, including RNF43-mutant pancreatic canc

44 e have previously shown that, unlike glucose-addicted cancers, Kaposi's sarcoma-associated herpesviru

45 hance clinical benefit for patients with MET-addicted cancers.

46 new approach for treating transcriptionally addicted cancers.

47 xcessive degradation of MET and triggers MET-addicted carcinoma cell death in vitro and in vivo.

48 " pathway induced by targeted therapy in Met-addicted carcinoma cells.

49 murafenib resistance in BRAF-mutated and MET-addicted carcinomas.

50 rols, we hypothesized and found that cocaine-addicted carriers of a 9R-allele exhibited higher respon

51 ighly effective to inhibit the growth of RTK-addicted cell lines and hepatocellular (HCC) cells in vi

52 ion as a mechanism of cell death in oncogene-addicted cells and establish Par-4 as a negative regulat

53 w that despite increased glucose uptake, GLN addicted cells do not metabolize glucose via the TCA cyc

54 GLN addicted cells exhibit reduced PDH activity, increased P

55 inhibition of GDH converted these glutamine-addicted cells to glucose-addicted cells.

56 Consequently, ABT-263 failed to kill BCL-XL-addicted cells with low activator BH3s and BCL-XL overab

57 nges following drug treatment of mutant EGFR-addicted cells, we identified the stem cell transcriptio

58 ed these glutamine-addicted cells to glucose-addicted cells.

59 d response to targeted therapies of oncogene-addicted cells.

60 tion with pro-oxidants selectively kills GLN addicted cells.

61 Here we studied how "glutamine-addicted" cells react to interruptions of glutamine meta

62 ce self-administration paradigm to identify 'addicted' cocaine-preferring (CP) individuals and resist

63 However food-addicted differ from non-food-addicted obese people by o

64 therapeutic strategies that target oncogene addicted diseases.

65 also promotes counterselection of NF-kappaB-addicted DLBCL lines by a dual mechanism involving kinas

66 previously drug-naive individuals who become addicted following legitimate prescriptions for medical

67 B oncogene pathway, to which KM12C cells are addicted for growth.

68 previous studies, reporting problematic and addicted gamers show poorer health outcomes compared wit

69 t overexpresses miR-155 and develops miR-155-addicted hematological malignancy, we describe here a mu

70 ued regarding the neurobiology of the opiate-addicted human brain.

71 Sensitivity of six MET-addicted human tumor cells to three MET kinase inhibitor

72 Here, using a panel of kinase-'addicted' human cancer cell lines, we found that most ce

73 ethod reveals that the response of 'oncogene-addicted' human cancer cells to tyrosine kinase inhibito

74 increased relapse-like behavior, and, as in addicted humans, major increases in opioid economic dema

75 ncreasingly uncontrolled cocaine use seen in addicted humans.

76 lf-administration, and in the NAc of cocaine-addicted humans.

77 that continue to take the drug compulsively (addicted) in the presence of footshocks.

78 oral dependent variables in 73 human cocaine-addicted individuals and 47 healthy controls, we hypothe

79 The brains of addicted individuals are altered and respond very differ

80 ug abstinence is frequently compromised when addicted individuals are re-exposed to environmental sti

81 uring cognitive processing characterize drug addicted individuals as compared with healthy controls.

82 ioral trait frequently seen not only in drug-addicted individuals but also in individuals who patholo

83 ing behavior that resemble the ways in which addicted individuals consume drugs.

84 explanation for the puzzling question of why addicted individuals continue drug consumption despite n

85 Addicted individuals continue substance use despite the

86 ned cues (stimuli associated with the drug), addicted individuals experience an intense desire for th

87 trate fMRI response to drug words in cocaine-addicted individuals in mesencephalic regions as possibl

88 ntions to change the maladaptive behavior of addicted individuals mainly rely on psychosocial approac

89 This functional overlap results in addicted individuals making poor choices despite awarene

90 een 1 month and 6 months of abstinence, when addicted individuals may be most vulnerable to, and perh

91 in prescription opiates may reduce harm, but addicted individuals may switch to other opiates such as

92 Addicted individuals pursue substances of abuse even in

93 umption opportunities, are inappropriate for addicted individuals seeking treatment or abstaining.

94 ng positive for cocaine in urine, 26 cocaine addicted individuals testing negative for cocaine in uri

95 Sixteen cocaine addicted individuals testing positive for cocaine in uri

96 ically diagnosed drug addiction, siblings of addicted individuals, and control volunteers.

97 ism is more common among men and that, among addicted individuals, men are more responsive to mu-opio

98 dered neurobiology in a minority of severely addicted individuals, which undermines the implementatio

99 ay perpetuate drug use or trigger relapse in addicted individuals.

100 on, and increased drug taking and relapse in addicted individuals.

101 a variety of abnormalities in the brains of addicted individuals.

102 red to treatment-seeking and abstaining drug-addicted individuals.

103 ople is compared to alcohol-addicted and non-addicted lean controls.

104 al targeting of aPKC impairs human oncogenic addicted leukemias.

105 T1L-target genes, and proliferation of DOT1L-addicted leukemic cells.

106 tant colonies that arose from a single, EGFR-addicted lung cancer cell.

107 ependent IL-6 secretion unleashed previously addicted lung tumor cells from their EGFR dependency.

108 ng SCARB1 with HDL NPs in cholesterol uptake-addicted lymphoma cells abolishes GPX4, resulting in can

109 ation and survival of lymphocytes and CARMA1-addicted lymphoma types.

110 e target for abrogating tumorigenesis in MYC-addicted lymphoma.

111 in a subpopulation of SIV-infected morphine addicted macaques, the presence of drugs of abuse may ca

112 rus (SIV) infections in control and morphine-addicted macaques, we found that two of the most signifi

113 mmunodeficiency virus infections in morphine-addicted macaques.

114 ion-related measures identified a subset of "addicted" mice ( approximately 19%) that exhibited inten

115 tostatic HER TKIs, re-affirming the oncogene-addicted nature of HER2-driven tumours and the therapeut

116 As a result, adoptive transfer of such IL-15-addicted NK cells is associated with cellular stress bec

117 ving a food-addicted obese group, a non-food addicted obese group and a lean control group.

118 ere performed in 66 people, involving a food-addicted obese group, a non-food addicted obese group an

119 However food-addicted differ from non-food-addicted obese people by opposite activity in the anteri

120 Brain activity in food-addicted and non-food-addicted obese people is compared to alcohol-addicted an

121 ated upon inhibition of Wnt signaling in Wnt-addicted pancreatic and colorectal cancer models.

122 H-Ras signal output and the growth of K-Ras-addicted pancreatic and non-small cell lung cancer cells

123 herapies, especially in BRAF-mutated and MET-addicted papillary thyroid carcinomas.

124 -glutamine levels in the striatum of cocaine-addicted participants (n = 15) compared with healthy con

125 f principle that targeting multiple oncogene addicted pathways can prevent therapeutic resistance.

126 Positron emission tomography studies in drug-addicted patients have shown that exposure to drug-relat

127 Here we report on impairments in cocaine-addicted patients to act purposefully toward a given goa

128 In addicted patients, decision making may also strongly dep

129 Here I argue that addicted people become unable to make drug-use choices o

130 Safety data were obtained on 461 opiate-addicted persons who participated in an open-label study

131 tes and the craving for opiates among opiate-addicted persons who receive these medications in an off

132 lacebo-controlled trial involving 326 opiate-addicted persons who were assigned to office-based treat

133 critically involved in the development of an addicted phenotype in females.

134 e examined its role in the development of an addicted phenotype in intact male and female rats, and i

135 food rewards following the development of an addicted phenotype in male and female rats.

136 nistration, confirming the development of an addicted phenotype in the extended-access group.

137 nd females, indicating the development of an addicted phenotype in these groups.

138 are sex differences in the magnitude of the addicted phenotype under optimized conditions that induc

139 e less cocaine exposure before developing an addicted phenotype with evidence implicating estradiol a

140 additional measure for the development of an addicted phenotype, separate groups of rats were screene

141 e an enhanced vulnerability to developing an addicted phenotype, they may be similar to males once ad

142 tration, both males and females developed an addicted phenotype, with 9 of 11 males and 8 of 10 femal

143 known to produce either a nonaddicted or an addicted phenotype.

144 s to alter drug responses and aspects of the addicted phenotype.

145 stream pathways that relieve the cell of its addicted phenotype.

146 across abstinent, recreationally using, and addicted populations demonstrate complexities in interpr

147 In addicted populations, both hyporesponsiveness and hyperr

148 In addicted populations, however, the causal relationship b

149 s, drug metabolites, and treatment status in addicted populations.

150 sing in abstinent, recreationally using, and addicted populations.

151 unctioning have been observed in healthy and addicted populations; however, there is limited evidence

152 ibits miR-155 and slows the growth of these "addicted" pre-B-cell tumors in vivo, suggesting a promis

153 Maintaining addicted pregnant women on long-acting opioid receptor a

154 We found that METH-addicted rats did indeed show differential DNA hydroxyme

155 ferential DNA hydroxymethylation observed in addicted rats occurred mostly at intergenic sites locate

156 s when compared with mRNA expression in METH-addicted rats.

157 edicting which nutrients cancer cells become addicted remains difficult.

158 222 nuclear families with multiple nicotine-addicted siblings.

159 Computational models of addiction depict the addicted state as a feature of a valuation disease, wher

160 of the BCR-ABL kinase transforms cells to an addicted state that requires glucose metabolism for surv

161 ccount for the near-permanent quality of the addicted state.

162 whose function is suppressed in the oncogene-addicted state.

163 airments of prefrontal cortex in the alcohol-addicted state.

164 icated in the expression of a multiphenotype addicted state.

165 ithdrawal relate, both in a non-addicted and addicted state.

166 expression have been studied as mediators of addicted states.

167 ptor tyrosine kinase inhibitors for oncogene-addicted subgroups of non-small-cell lung cancer (for ex

168 ponses (marker of brain function) of cocaine-addicted subjects (n = 21) and controls (n = 15) to iden

169 usly shown to be involved in drug craving in addicted subjects (orbitofrontal cortex, hippocampus, ce

170 s of the amygdala and hippocampus in cocaine-addicted subjects and matched healthy controls and deter

171 here methylphenidate increased metabolism in addicted subjects but decreased metabolism in controls.

172 brain regions that are uniquely activated in addicted subjects by intravenous methylphenidate (a drug

173 The cocaine-addicted subjects demonstrated bilateral activation of t

174 They are activated in addicted subjects during intoxication, craving, and bing

175 A consistent finding in drug-addicted subjects is a lower level of dopamine D2 recept

176 ened activation with procaine in the cocaine-addicted subjects is similar to the pattern of intericta

177 The findings for the cocaine-addicted subjects may thus represent evidence of localiz

178 ience attribution and motivation) in cocaine-addicted subjects may underlie the strong emotional resp

179 avenous methylphenidate (a drug that cocaine-addicted subjects report to be similar to cocaine).

180 ested during early or protracted withdrawal, addicted subjects show lower levels of D2 receptors in s

181 In contrast, addicted subjects show significant DA increases in stria

182 After receiving placebo, the cocaine-addicted subjects showed markedly lower rCBF in the bila

183 We tested eighteen cocaine-addicted subjects using positron emission tomography and

184 ased "desire for methylphenidate" and in the addicted subjects with "cocaine craving." In addicted su

185 effects but have unexpectedly shown that in addicted subjects, drug-induced DA increases (as well as

186 addicted subjects with "cocaine craving." In addicted subjects, increases in BA 25 were also associat

187 ve for food and drugs seen in obese and drug-addicted subjects, respectively.

188 d PET to characterize the brain DA system in addicted subjects.

189 ens and that this regulation is disrupted in addicted subjects.

190 rlie the decreased sensitivity to rewards in addicted subjects.

191 rigger craving and compulsive intake only in addicted subjects.

192 may contribute to compulsive drug intake in addicted subjects.

193 f control and compulsive drug intake in drug-addicted subjects.

194 er recovery and ensure relapse prevention in addicted subjects.

195 In this manner, the cells are drug-addicted, suggesting that melanoma cells evolve a 'just

196 targeting non-oncogenes to which cancers are addicted supports the future development and potential a

197 bey and colleagues describe a unique antigen-addicted T cell population bearing characteristics of bo

198 Through targeting "HR-addicted" temozolomide-resistant glioblastoma cells via

199 g pre-existing oncogenic pathways in cystine-addicted TNBC with prominent mesenchymal features.

200 ed kinase inhibitors shows that they are not addicted to a single survival pathway.

201 proneural" and "classical" subtypes that are addicted to aberrant signaling from integrin alphavbeta3

202 based on the assumption that PDAC cells are addicted to activated KRAS, but this assumption remains

203 question the degree to which PDAC cells are addicted to activated KRAS, by illustrating adaptive non

204 Indeed, individuals addicted to alcohol also crave alcoholic beverages and s

205 -resolution structural images of 42 patients addicted to alcohol and 32 healthy control participants.

206 the major behavioral characteristic of those addicted to alcohol but it is not the only one.

207 icity effects in bilateral CA2+3 in patients addicted to alcohol.

208 bstinence and prevent relapse in individuals addicted to alcohol.

209 tered in most myelomas, they are nonetheless addicted to an aberrant IRF4 regulatory network that fus

210 Many tumors become addicted to autophagy for survival, suggesting inhibitio

211 trast, using an Myc-dependent leukemic model addicted to autophagy, we show that knockdown of Grasp55

212 mely common, suggesting that melanoma is not addicted to B-raf.

213 Tumor cells become addicted to both activated oncogenes and to proliferativ

214 , but not the growth of cancers that are not addicted to c-MET.

215 vide further evidence that myeloma cells are addicted to c-MYC activity and that c-MYC is a promising

216 bitors, approved for a breast cancer subtype addicted to CDK4/6 activation, could be repurposed to tr

217 cur to conditioned stimuli in human subjects addicted to cocaine and whether this is associated with

218 Individuals addicted to cocaine spend much of their time foraging fo

219 g, and Participants: Seventy-six individuals addicted to cocaine with varying durations of abstinence

220 Results: Among the 76 individuals addicted to cocaine, 19 (25%) were abstinent for 2 days,

221 Although both males and females become addicted to cocaine, females transition to addiction fas

222 lified MYCC, indicating that these cells are addicted to continued MYCC overexpression.

223 Cancer cells are dysregulated and addicted to continuous supply and metabolism of nutritio

224 nduce growth suppression in the cancer cells addicted to cyclin D1 expression.

225 t cells transformed by oncogenic RasV12 were addicted to DDX5, because reduction of DDX5 was sufficie

226 this difficulty, a cancer cell often becomes addicted to DNA repair pathways other than the one that

227 dual differences in the propensity to become addicted to drugs, leading to the description of addicti

228 n obese rats, as has been reported in humans addicted to drugs.

229 ram tumor metabolism and render cancer cells addicted to extracellular nutrients.

230 e large B cell lymphomas (DLBCLs) are mostly addicted to EZH2 but not the more differentiated activat

231 o understand which cancers are oncogenically addicted to FGF19 amplification as well as the role it s

232 tant plus c-Myc appeared to be become highly addicted to FGFR-dependent prosurvival activities, as sm

233 suggesting that some FLT3/ITD AML may not be addicted to FLT3 signaling.

234 d metabolism, rendering the transformed cell addicted to glucose for the maintenance of survival.

235 hondrial dysfunction, TOP1MT-KO cells become addicted to glycolysis, which limits synthetic building

236 tumour cells are more proliferative but not addicted to HER2, consistent with activation of multiple

237 kinases and the reason why some kinases are addicted to Hsp90 while closely related family members a

238 Here we show that ALCLs of both subtypes are addicted to IRF4 signaling, as knockdown of IRF4 by RNA

239 ata demonstrate that miR-125a-induced MPN is addicted to its sustained overexpression, and highlight

240 n the degree to which pancreatic cancers are addicted to KRAS by illustrating adaptive nongenetic and

241 Indeed, these cells are addicted to maintenance of low cAMP concentrations in a

242 Here we show that a subset of MCLs is addicted to MALT1, as its inhibition by either RNA or ph

243 Cells with BRAF(V600E) amplification are addicted to MEKi to maintain a precise level of ERK1/2 s

244 we demonstrated that MYC-induced tumors are addicted to mutant beta-catenin, and the combined inacti

245 tion for treating pancreatic tumors that are addicted to mutant KRAS, thus offering opportunities for

246 erapeutic strategy to manage tumors that are addicted to mutant p53 for survival.

247 tumor, suggesting that tumors continue to be addicted to MYC.

248 ma (DLBCL) is an aggressive lymphoma that is addicted to NF-kappaB signaling through the CARD11-BCL10

249 who think them safe or by those sufficiently addicted to nicotine to not be able to quit e-cigarette

250 g effects that increase the risk of becoming addicted to nicotine.

251 id in HCC1599 breast cancer cells, which are addicted to NOTCH1 for growth/viability.

252 results demonstrate that tumours can become addicted to oncomiRs and support efforts to treat human

253 ous diseases in people who misuse and/or are addicted to opioids and to concurrently address the unde

254 phase 3, randomised trial with men and women addicted to opioids who were starting antiretroviral the

255 annabis users progress to using and becoming addicted to other drugs, but the reasons for this progre

256 ain that increase the likelihood of becoming addicted to other drugs.

257 ts suggest that tumors induced by MYC remain addicted to overexpression of this oncogene.

258 melanomas with BRAF inhibitors renders them addicted to oxidative phosphorylation.

259 tion sensitizers or as monotherapy in tumors addicted to particular DNA-repair pathways.

260 PI3K/AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that phar

261 including Bortezomib-resistant MM cells are addicted to RelB-p52 for survival.

262 Our society is addicted to steel.

263 cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling pathways.

264 utant allelic ratios and, in vitro, are more addicted to the aberrant signaling from the FLT3/ITD onc

265 PDA is addicted to the activity of the mutated KRAS oncogene wh

266 RBB2-amplified breast tumour lines are truly addicted to the ERBB2 oncogene at the mRNA level and dis

267 and CRC cells with BRAF(V600E) mutations are addicted to the ERK1/2 pathway for repression of BIM and

268 Tumour cells become addicted to the expression of initiating oncogenes like

269 large B-cell lymphoma (DLBCL) cell lines are addicted to the expression of OCT2 and its coactivator O

270 Thus, CLL is a disease "addicted to the host" and is dependent on pathways that

271 d that tumor cells carrying a mutant p53 are addicted to the mutant for cell survival and resistance

272 carcinoma cells that carry a mutant p53, are addicted to the mutant for their survival and resistance

273 (MM) cell lines and primary tumor cells are addicted to the MYC oncoprotein for survival.

274 he hypothesis that tumors become irrevocably addicted to the oncogenes that initiated tumorigenesis.

275 gy enables melanomas that would otherwise be addicted to the Ras-Raf pathway to instead tolerate path

276 cause patients to commit suicide and become addicted to their medication may have disconcerted the p

277 tablished that glioblastomas are selectively addicted to this pathway as a strategy to evade oncogene

278 the world where women are just now becoming addicted to tobacco.

279 ut tumor cells are also affected by, or even addicted to, signals from the microenvironment.

280 cci with high transformation capability are "addicted" to a "hypertransformable" state for optimal fi

281 Such cancers are "addicted" to EGFR, and treatment with a TKI invariably l

282 gly, MYCN-amplified neuroblastoma cells are "addicted" to LDHA enzymatic activity, as its depletion c

283 ors displaying c-MET gene amplification are "addicted" to MET signaling and therefore are very sensit

284 lls, which explains why cancer cells become "addicted" to this heat shock protein.

285 In these contexts, transformed cells 'addicted' to AP-1 activity are rendered susceptible to S

286 on-small cell lung cancer (NSCLC) cells are 'addicted' to basal autophagy that reprograms cellular me

287 tumour cells expressing activated AKT1 are 'addicted' to FoxM1, as they require continuous presence

288 recent findings suggest that tumors can be 'addicted' to miRNA overexpression, yielding a possible t

289 hese genetic aberrations cause tumors to be 'addicted' to NF-kappaB, which can be exploited therapeut

290 Notably, KIAA1199 silencing in oncogene-addicted tumor cells improved therapeutic responses and

291 Notably, increased NRP2 expression in EGFR-addicted tumor cells led to downregulation of EGFR prote

292 The withdrawal of TKI from addicted tumors in vitro and in vivo leads to overwhelmi

293 er, STK38 knockdown suppresses growth of MYC-addicted tumors in vivo, thus providing a novel viable t

294 er, STK38 knockdown suppresses growth of MYC-addicted tumors in vivo, thus providing a novel viable t

295 represents a promising approach to treat RAS-addicted tumors.

296 is as a druggable target to antagonize STAT3-addicted tumors.

297 show great promise for the treatment of PI3K-addicted tumors.

298 Following the scans, the cocaine-addicted volunteers performed cocaine self-administratio

299 and strategies for the treatment of cancers addicted with glutamine metabolism.

300 The usual treatment for opioid-addicted youth is detoxification and counseling.