ライフサイエンスコーパス: tumor suppression

1 in mammary luminal cell differentiation and tumor suppression.

2 solHVEM((P37-V202))) binds BTLA and restores tumor suppression.

3 repair, which is thought to be critical for tumor suppression.

4 ling but can also trigger DNA damage-induced tumor suppression.

5 and in HR, a DNA repair pathway critical for tumor suppression.

6 n mediator complex in genome maintenance and tumor suppression.

7 ealing that PKCbeta is haploinsufficient for tumor suppression.

8 ions that contribute to genome integrity and tumor suppression.

9 ation of p73 in order to efficiently restore tumor suppression.

10 ever, studies have also reported its role in tumor suppression.

11 IRF2 protected LCLs against Blimp1-mediated tumor suppression.

12 the function of MCPH1 has been implicated in tumor suppression.

13 f TET dioxygenases during development and in tumor suppression.

14 s in the maintenance of genome stability and tumor suppression.

15 tity, cell function, tissue homeostasis, and tumor suppression.

16 ht to control the cell cycle, senescence and tumor suppression.

17 nd genome integrity, normal development, and tumor suppression.

18 be explored for extending longevity and for tumor suppression.

19 in landscape in senescent cells and enforces tumor suppression.

20 of SIRT2 mutations in genome maintenance and tumor suppression.

21 Bcl-xL partially reverses the RBM4-mediated tumor suppression.

22 on, genome stability, normal development and tumor suppression.

23 ine kinase that functions in development and tumor suppression.

24 Tumor suppressor p53 plays a central role in tumor suppression.

25 -translational modification is essential for tumor suppression.

26 validates in humans the "continuum" model of tumor suppression.

27 ng potential in contributing to p53-mediated tumor suppression.

28 ht contribute to stability of senescence and tumor suppression.

29 essential for HDR-mediated DSB repair or for tumor suppression.

30 yogenesis, wound healing, host immunity, and tumor suppression.

31 lorectal cancers, supporting a WDR48 role in tumor suppression.

32 mbers of chromosomes leads to cell death and tumor suppression.

33 y aimed at maintaining genomic stability and tumor suppression.

34 s, which resulted in apoptosis induction and tumor suppression.

35 laborate in controlling autophagy to support tumor suppression.

36 cell cycle control, genomic maintenance, and tumor suppression.

37 cycle is essential for genomic stability and tumor suppression.

38 ion factor p53 plays a central role in human tumor suppression.

39 tes Kras-induced DNA damage and p53-mediated tumor suppression.

40 glutamine metabolism, cell cycle arrest, and tumor suppression.

41 integrity during organismal development and tumor suppression.

42 ction of Notch3 in senescence regulation and tumor suppression.

43 s, and finger 4 was selectively required for tumor suppression.

44 a potent antiangiogenic factor implicated in tumor suppression.

45 ial effects in the CNS, without compromising tumor suppression.

46 mplicated in cellular processes that promote tumor suppression.

47 ment of an estrogen-Nrf2 connection in BRCA1 tumor suppression.

48 omplexes may constitute a major mechanism of tumor suppression.

49 J are crucial for the genome maintenance and tumor suppression.

50 contribute to cellular protection as well as tumor suppression.

51 than transcription and how MIC-1 exerts its tumor suppression.

52 rtial loss of Spartan impairs DPC repair and tumor suppression.

53 ng and has cell-specific functions including tumor suppression.

54 anoikis sensitivity, a pivotal mechanism in tumor suppression.

55 sting a novel mechanism for RASSF1A-mediated tumor suppression.

56 mplicating this as one possible mechanism of tumor suppression.

57 apoptosis, which is an important process for tumor suppression.

58 p53 has been widely studied for its role in tumor suppression.

59 tin remodeling enzyme which is implicated in tumor suppression.

60 unique function for 53BP1 in end-joining and tumor suppression.

61 ell pluripotency, embryonic development, and tumor suppression.

62 regulation, normal development, and possibly tumor suppression.

63 explicates a mechanism utilized by BCCIP in tumor suppression.

64 whether they are the rate-limiting steps in tumor suppression.

65 immunogenic cell death, suggesting a role in tumor suppression.

66 n of an Arf-independent function for Dmp1 in tumor suppression.

67 ated hypertension and enhance antiangiogenic tumor suppression.

68 n caused chromosomal instability and in vivo tumor suppression.

69 distinct aneuploidy-causing Bub1 defects in tumor suppression.

70 s with distinct functions in development and tumor suppression.

71 le arrested state, assumed to be involved in tumor suppression.

72 l control, response to genotoxic insult, and tumor suppression.

73 s an important constituent of role of p53 in tumor suppression.

74 Yap pathway that is integral to p53-mediated tumor suppression.

75 s coordinate development, tissue growth, and tumor suppression.

76 rently affect development, tissue growth and tumor suppression.

77 logue (PTEN) protein levels are critical for tumor suppression.

78 bolism is essential for tissue functions and tumor suppression.

79 ng fundamental new insight into p53-mediated tumor suppression.

80 ontributing to long-term senescence-mediated tumor suppression.

81 ut Tpl2-depenednt role of NF-kappaB1 in lung tumor suppression.

82 gulators of the cell cycle and contribute to tumor suppression.

83 ng, higher rates of CIN cause cell death and tumor suppression.

84 in the cell cycle and is implicated in lung tumor suppression.

85 F10 melanoma to explore the role of NLRC4 in tumor suppression.

86 e the function of H4K20me3 in senescence and tumor suppression.

87 s recombination (HR), which is important for tumor suppression.

88 f p53 compromised p53-mediated apoptosis and tumor suppression.

89 infusion method, to safely achieve effective tumor suppression.

90 3 in response to DNA damage is essential for tumor suppression.

91 (DDR), are also essential for p53-dependent tumor suppression.

92 and DDR, both of which play crucial roles in tumor suppression.

93 19(Arf) and DNA damage-signaling pathways in tumor suppression.

94 tochondrial p53 is involved in apoptosis and tumor suppression.

95 in the regulation of cell deformability and tumor suppression.

96 evelopment and establish a novel paradigm of tumor suppression.

97 functional dysregulation and contributing to tumor suppression.

98 a that are involved in epithelial repair and tumor suppression.

99 1 pathway downstream of TGFbeta signaling in tumor suppression.

100 s a novel and critical mechanism for CUL3 in tumor suppression.

101 olyamine metabolism and ferroptosis-mediated tumor suppression.

102 l cancer and p73 activation elicits p53-like tumor suppression.

103 gical and pathological conditions, including tumor suppression [2], embryonic development [3, 4], tis

104 f rb1, revealing a conserved role for rb1 in tumor suppression across vertebrates.

105 P53 cancer mutants not only lose tumor suppression activity but, more problematically, al

106 miR-122* is an important contributor to the tumor suppression activity previously attributed solely

107 Shisa3 performs the tumor suppression activity through WNT signaling predict

108 h active site mutant E411A presented similar tumor suppression activity.

109 uggesting that it plays an important role in tumor suppression, although the underlying mechanisms ar

110 end-joining (NHEJ) factor, also functions in tumor suppression, although this molecular mechanism rem

111 ro results were further confirmed by in vivo tumor suppression and a matrigel plug angiogenesis assay

112 known activities Ate1 gene is essential for tumor suppression and also likely participates in suppre

113 phosphorylation of Mdm2 in regulation of p53 tumor suppression and bone marrow failure.

114 double-strand break repair is important for tumor suppression and cancer therapy resistance.

115 gene repression and have been implicated in tumor suppression and carcinogenesis, but the roles of m

116 e identified STAT1/ASPP2 pathway may connect tumor suppression and cell polarity to neuroinflammation

117 ms of the DDR is important for understanding tumor suppression and cellular resistance to clastogenic

118 in human nevi undermines senescence-mediated tumor suppression and enhances the probability of malign

119 cancers in which p53 has lost its ability in tumor suppression and gained function in promoting tumor

120 reveal an important mechanism for Parkin in tumor suppression and HIF-1alpha regulation.

121 p53 to regulate transcription is crucial for tumor suppression and implies that inherited polymorphis

122 deacetylation is integral to SIRT6-mediated tumor suppression and inhibition of metastasis.

123 critical downstream target of MEN1-dependent tumor suppression and is required for tumorigenic prolif

124 transcription factor, a central regulator of tumor suppression and metabolism, plays a unique role in

125 ergy stress regulators are also important in tumor suppression and metabolism.

126 Due to the role of p73 in tumor suppression and neural development, its expression

127 of the p53 family, plays a critical role in tumor suppression and neural development.

128 tumor suppressors, plays a critical rule in tumor suppression and neuronal development.

129 tes that caspase-2 has putative functions in tumor suppression and protection against cellular stress

130 nd apoptosis-independent function of SMAC in tumor suppression and provide new insights into the biol

131 e, both the liposomes demonstrated excellent tumor suppression and reduction for 3months.

132 G2D ligand-expressing cells was important in tumor suppression and that NKG2D ligand expression is a

133 ltered secretory pathway, thought to promote tumor suppression and tissue aging.

134 erative response with essential functions in tumor suppression and tissue homeostasis.

135 nduced apoptosis contributes to p53-mediated tumor suppression and treatment response.

136 th a substantial fraction also implicated in tumor suppression and/or mental disorders.

137 aN isoforms, both of which are implicated in tumor suppression and/or promotion.

138 tor SIRT6 plays pivotal roles in metabolism, tumor suppression, and aging biology.

139 ytokine receptors, kinase and Ras signaling, tumor suppression, and chromatin modification.

140 , including in differentiation, mitogenesis, tumor suppression, and neuronal plasticity.

141 with critical roles in ribosome biogenesis, tumor suppression, and nucleolar stress response.

142 events in development, cellular homeostasis, tumor suppression, and prevention of neurodegeneration a

143 g proliferation, signaling, differentiation, tumor suppression, and survival.

144 ular and the molecular mechanisms of CUL9 in tumor suppression are currently unknown.

145 cets of the DNA damage response required for tumor suppression are dictated by the proliferative stat

146 The molecular pathways underlying tumor suppression are incompletely understood.

147 g/kg, orally) exerted synergistic effects on tumor suppression, as compared with sorafenib and anti-C

148 ronal guidance molecule SLIT plays a role in tumor suppression, as SLIT-encoding genes are inactivate

149 These findings provide insight into tumor suppression at the cross-roads of apoptosis, cell

150 apoptotic function appears insufficient for tumor suppression, because these mutations are also foun

151 function in maintaining genome stability and tumor suppression but may also point to a previously unr

152 Thus, p53 transactivation is essential for tumor suppression but, intriguingly, in association with

153 ays important roles in normal physiology and tumor suppression, but accumulation of senescent cells w

154 3's apoptosis proficiency is dispensable for tumor suppression, but could prognosticate better surviv

155 53-RNPC1 loop is critical for modulating p53 tumor suppression, but it is not clear how the loop is r

156 nce is widely believed to play a key role in tumor suppression, but the molecular pathways that regul

157 at NRF2 is a major target of p53-independent tumor suppression by ARF and also suggest that the ARF-N

158 Here, I argue that tumor suppression by BRCA1 and BRCA2 originates from the

159 study, we present an additional mechanism of tumor suppression by Bre1 through maintenance of genomic

160 cells, expression of wild-type Riz1 restored tumor suppression by decreasing proliferation and increa

161 ecretory phenotype (SASP) that contribute to tumor suppression by enforcing arrest and recruiting imm

162 The mechanism of p53 tumor suppression by loss of SK1 is mediated by elevatio

163 e signaling in the uterus, where it mediates tumor suppression by modulating endometrial stromal-epit

164 Oncogenic stress provokes tumor suppression by p53 but the extent to which this re

165 We show that tumor suppression by p53 can occur via an alternate rout

166 Tumor suppression by p53 occurs via both transcription-d

167 Mutations inactivate tumor suppression by p53, and some endow the protein wit

168 l relevance of metabolism and ferroptosis to tumor suppression by p53.

169 n vivo, which correlates with restoration of tumor suppression by PML.

170 ese proteins may synergistically function in tumor suppression by regulating these processes.

171 onstrated a novel mechanism of regulation of tumor suppression by Sema 3A in coordination with a chai

172 onsidering downstream biological effects, as tumor suppression cannot be inferred from potent PKC bin

173 Tumor suppression caused by loss of Mnt was linked to in

174 Consistent with tumor suppression, CCN1 expression is downregulated in h

175 hoid development, cell-cycle regulation, and tumor suppression; cytokine receptor, kinase, and Ras si

176 Cellular senescence and associated tumor suppression depend on control of chromatin.

177 Activation of p53 target genes for tumor suppression depends on the stress-specific regulat

178 cell differentiation, cell cycle regulation, tumor suppression, drug responsiveness, and apoptosis ha

179 L(+), and decitabine and vorinostat-mediated tumor-suppression efficacy was significantly decreased i

180 1 (liver kinase B1) plays important roles in tumor suppression, energy metabolism, and, recently, in

181 reveal a novel role for HP1 as a cofactor in tumor suppression, expand our mechanistic understanding

182 in transferrin-bearing vesicles resulted in tumor suppression for 30% of A431 and 60% of B16-F10 tum

183 with transdermal vaccine and around 9 times tumor suppression for the combination route of delivery

184 While the tumor suppression function of EAG2 knockdown is independ

185 ide clinical candidates for reactivating the tumor suppression function of p53 in cancer by dual targ

186 Thus, our findings clearly demonstrate the tumor suppression function of PER2 and elucidate a pathw

187 udy further reveal the mechanisms underlying tumor suppression function of VentX and suggest a role o

188 Thus, Smurf2 has a tumor suppression function that normally maintains genom

189 ing 14-3-3sigma, thus turning off TGF-beta's tumor suppression function.

190 pts predicted to encode a BRCA1 protein with tumor suppression function.We confirm that BRCA1c.[594-2

191 stabilize the differentiated state and have tumor suppression functions are expected to exist.

192 The mechanisms underlying Palb2 mammary tumor suppression functions can now be explored genetica

193 Mutant (Mt) p53 abrogates tumor suppression functions of wild-type (WT) p53 throug

194 Our work demonstrates that TGF-beta tumor suppression functions through an EMT-mediated disr

195 Despite its tumor suppression functions, BRCA1 is most highly expres

196 sms underlying PALB2-mediated DNA repair and tumor suppression functions, we targeted Palb2 in the mo

197 mote mitochondrial apoptosis (Nix, PUMA) and tumor suppression (GDF-15, IGFBP-6), particularly in cel

198 While the critical role of wild-type p53 in tumor suppression has been firmly established, mounting

199 igenesis, and data consistent with a role in tumor suppression have been reported as well.

200 Nuclear localization of PTEN is vital for tumor suppression; however, outside of cancer, the molec

201 The classic model of tumor suppression implies that malignant transformation

202 ovel therapeutic approach for restoration of tumor suppression in B-cell lymphoma.

203 e that together provide a novel mechanism of tumor suppression in basal keratinocytes of zebrafish em

204 Vaccine alone resulted in around 1.5 times tumor suppression in case of transdermal and combination

205 of conservative DSB repair may contribute to tumor suppression in human cells.

206 function and that caspase-2 may also impact tumor suppression in humans.

207 gene-induced senescence in growth arrest and tumor suppression in melanocytic nevi and melanoma.

208 lved in apoptosis, NF-kappaB regulation, and tumor suppression in mice.

209 Here we show they function in prostate tumor suppression in the mouse.

210 oncogenic function, thereby contributing to tumor suppression in TP53-mutated cancer.

211 pid tumor regression, overcoming established tumor suppression in tumor-bearing mice.

212 fied that resulted in complete and sustained tumor suppression in vivo.

213 nd triggering massive apoptosis in vitro and tumor suppression in vivo.

214 A cells, resulting in CCA cell apoptosis and tumor suppression in vivo.

215 r FasL in decitabine and vorinostat-mediated tumor suppression in vivo.

216 the p53-mediated DNA damage response or p53 tumor suppression in vivo.

217 that Rad18 confers DNA damage tolerance and tumor-suppression in a physiological setting.

218 e cellular processes that might be linked to tumor suppression, including promoting proper spindle or

219 NA end resection, chromosomal stability, and tumor suppression, indicating that the enzymatic functio

220 Inactivation of RB-mediated tumor suppression induced surface epithelial proliferati

221 y of genes involved in apoptosis regulation, tumor suppression, innate immune response, and cell adhe

222 The loss of tumor suppression involves the NF-kappaB and p63 pathway

223 describe a novel mechanism of NOTCH-induced tumor suppression involving modulation of the deacetylas

224 This is in contrast to suggestions that tumor suppression is a trade-off for regenerative capaci

225 Restoration of tumor suppression is an attractive onco-therapeutic appr

226 ent and specificity of caspase-2 function in tumor suppression is currently unclear.

227 , but precisely how p53 functions to mediate tumor suppression is not well understood.

228 However, the molecular mechanism of tumor suppression is not yet understood.

229 rlying the tissue-specific nature of BRCA1's tumor suppression is obscure.

230 ole for Abeta in differentiation and perhaps tumor suppression may lie partly in its ability to negat

231 These findings define an important tumor suppression mechanism and uncover adaptive mechani

232 ession network in cancer and reveals a novel tumor suppression mechanism involving regulation of spec

233 tophagic degradation of HIF2alpha is a novel tumor suppression mechanism.

234 Cellular senescence is an important tumor suppression mechanism.

235 Cell senescence, a putative tumor-suppression mechanism, depends on high-intensity E

236 MDM2 to p53 has been described as a crucial tumor-suppression mechanism.

237 /6 effectively counter cancer cell-intrinsic tumor suppression mechanisms, senescence and apoptosis,

238 Although cellular tumor-suppression mechanisms are widely studied, little

239 h in mice lacking myeloid A2A receptors, but tumor suppression mediated by CD8(+) T cells is more per

240 pathway expands our understanding of the p53 tumor suppression network in cancer and reveals a novel

241 nism of RPs in association with the MDM2-p53 tumor-suppression network, and the potential implication

242 te how, during developmental progression and tumor suppression, non-coding transcription orchestrates

243 pivotal factor required for neurogenesis and tumor suppression of medulloblastoma (MB).

244 Systemic therapeutic trial revealed potent tumor suppression of the proposed formulation via synerg

245 However, whether NKG2D ligands contribute to tumor suppression or progression clinically remains cont

246 d developmental pathways that promote either tumor suppression or progression.

247 ntial splicing of the SENP7 regulates either tumor suppression or progression.

248 ity control, prevention of genotoxic stress, tumor suppression, pathogen elimination, regulation of i

249 of multiple cellular growth, signaling, and tumor suppression pathways in the pathogenesis of B-ALL.

250 MLL-fusions induce latent, context-dependent tumor suppression programs.

251 an be improvised through harnessing inherent tumor suppression properties of individual oncogenic fus

252 KLF11-mediated HP1-HMT recruitment abolishes tumor suppression, providing direct evidence that HP1-HM

253 ependent cell cycle arrest and apoptosis for tumor suppression, recent studies have suggested that ot

254 those p53-inducible genes most critical for tumor suppression remain elusive.

255 the mechanisms of caspase-2 responsible for tumor suppression remain unclear.

256 However, the mechanism of GPx3-mediated tumor suppression remains unclear.

257 s to the maintenance of genome stability and tumor suppression remains unknown.

258 thus targeting UHRF1 to restore PML-mediated tumor suppression represents a promising, novel, antican

259 thus targeting UHRF1 to restore PML-mediated tumor suppression represents a promising, novel, antican

260 nonical roles of Arf in ExEn development and tumor suppression, respectively, may be conceptually lin

261 genes including several that are relevant to tumor suppression, revealing potential new targets for c

262 mice by forced expression of GPx3 suggests a tumor suppression role of GPx3 in prostate cancer.

263 tumor development, FA genes perform critical tumor-suppression roles.

264 This new function may be important in BRCA1 tumor suppression, since the expression of several inter

265 nlike in some tumors, where Spry may mediate tumor suppression, Spry1 plays a selective role in at le

266 iASPP expression and leads to p53-dependent tumor suppression, suggesting a therapeutic strategy to

267 ostic role of several critical mechanisms of tumor suppression that are regulated by TP63.

268 Tumor suppression that is mediated by oncogene-induced s

269 activated oncogenes is a failsafe program of tumor suppression that must be bypassed for tumorigenesi

270 been linked to cancer and implicate CHD5 in tumor suppression, the ATP-dependent activity of CHD5 is

271 ted secretory phenotype collaborate to enact tumor suppression, the former by blocking cell prolifera

272 In addition to it role in tumor suppression, the PTEN-PI3K pathway controls many c

273 us, in addition to well-established roles in tumor suppression, these findings identify a role for AT

274 protein expression and triggers ARF-mediated tumor suppression through a novel translational mechanis

275 egulator (TIGAR) has been thought to promote tumor suppression through metabolic fine-tuning, yet, TI

276 red that MOB1/Warts binding is essential for tumor suppression, tissue growth control, and developmen

277 of beta2SP switches TGF-beta signaling from tumor suppression to tumor promotion by engaging Notch s

278 The transition from tumor suppression to tumor promotion is mediated by a tu

279 ed, which in essence turn ERK functions from tumor suppression to tumor promotion.

280 nzymes regulates myriad processes, including tumor suppression, transcription, protein trafficking, a

281 Thus, MIC-1 displays two opposing effects: tumor suppression versus promotion.

282 1 START domain and CAV-1 contributes to DLC1 tumor suppression via a RhoGAP-independent mechanism, an

283 en presentation phenotype, likely to promote tumor suppression via activation of the adaptive immune

284 d and that the FDXR-p53 loop is critical for tumor suppression via iron homeostasis.

285 Tumor suppression was associated with squamous different

286 This mechanism of tumor suppression was validated in Ewing sarcoma cells,

287 -interacting motif in cell-cycle control and tumor suppression, we generated mouse embryonic fibrobla

288 Epidermal cell differentiation and skin tumor suppression were caused by a p53-dependent transcr

289 phagy-mediated miR-224 degradation and liver tumor suppression were further confirmed by the autophag

290 nclusion of interleukins resulted in 3 times tumor suppression when administered with transdermal vac

291 endritic cells were contributed to efficient tumor suppression, whereas perforin, NK cells, and CD4 T

292 microenvironment in RNASET2-mediated ovarian tumor suppression, which could eventually contribute to

293 To unravel mechanisms of p53-mediated tumor suppression, which have remained elusive, we analy

294 significance of p53 metabolic regulation in tumor suppression, while also alluding to the potential

295 Knockdown Gfi1b represses PRDM16-mediated tumor suppression, while Gfi1b overexpression mimics PRD

296 d reveal a novel mechanism for LKB1-mediated tumor suppression with direct therapeutic implications f

297 n the adult, with important repercussions in tumor suppression, wound healing, and aging.

298 ught to play important roles in aging and in tumor suppression, yet the dynamics by which senescent c

299 ally important for cell cycle regulation and tumor suppression, yet the underlying mechanisms are inc

300 Impaired retinoblastoma protein RB tumor suppression yields grade II histopathology.