ライフサイエンスコーパス: addicted

1 cription to which cancer cells become highly addicted.

2 y a small percentage of alcohol users become addicted.

3 ic driver mutations to which tumor cells are addicted.

4 genetic lesion to which the cancer cells are addicted.

5 confirming that these tumors remain oncogene addicted.

6 stress than those of individuals who are not addicted.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 bute to persistent functional changes in the addicted brain.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 GLN addicted cells exhibit reduced PDH activity, increased P

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

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

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

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

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

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

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

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

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

53 therapeutic strategies that target oncogene addicted diseases.

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

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

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

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

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

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

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

61 neurochemical processes occurring in cocaine-addicted humans [1].

62 ncreasingly uncontrolled cocaine use seen in addicted humans.

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

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

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

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

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

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

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

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

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

72 Addicted individuals continue substance use despite the

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

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

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

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

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

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

79 Addicted individuals pursue substances of abuse even in

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

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

82 Sixteen cocaine addicted individuals testing positive for cocaine in uri

83 Therefore, those addicted individuals who are incarcerated for the sale o

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

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

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

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

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

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

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

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

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

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

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

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

96 mmunodeficiency virus infections in morphine-addicted macaques.

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

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

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

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

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

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

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

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

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

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

107 In addicted patients, decision making may also strongly dep

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

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

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

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

112 underlying compulsive drug administration in addicted persons.

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

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

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

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

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

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

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

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

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

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

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

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

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

126 In addicted populations, both hyporesponsiveness and hyperr

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

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

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

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

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

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

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

134 edicting which nutrients cancer cells become addicted remains difficult.

135 222 nuclear families with multiple nicotine-addicted siblings.

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

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

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

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

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

141 produce the complex behaviors that define an addicted state.

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

143 hdrawal symptoms through maintenance of the 'addicted' state with methadone.

144 expression have been studied as mediators of addicted states.

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

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

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

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

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

150 The cocaine-addicted subjects demonstrated bilateral activation of t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 rlie the decreased sensitivity to rewards in addicted subjects.

168 rigger craving and compulsive intake only in addicted subjects.

169 may contribute to compulsive drug intake in addicted subjects.

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

171 ay contribute to drug craving and relapse in addicted subjects.

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

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

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

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

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

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

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

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

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

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

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

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

184 bstinence and prevent relapse in individuals addicted to alcohol.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 and fortunately a peculiar set of humans are addicted to solving the problems.

230 Our society is addicted to steel.

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

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

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

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

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

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

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

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

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

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

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

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

243 Society, which likes to live well, is addicted to the products of science, and fortunately a p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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