ライフサイエンスコーパス: tumor suppression

1 al antibody nivolumab, has shown efficacy in tumor suppression.

2 ine kinase that functions in development and tumor suppression.

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

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

5 cycle is essential for genomic stability and tumor suppression.

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

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

8 explicates a mechanism utilized by BCCIP in tumor suppression.

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

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

11 rently affect development, tissue growth and tumor suppression.

12 n as a potential mechanism of loading-driven tumor suppression.

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

14 bolism is essential for tissue functions and tumor suppression.

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

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

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

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

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

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

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

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

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

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

25 infusion method, to safely achieve effective tumor suppression.

26 3 in response to DNA damage is essential for tumor suppression.

27 s in metabolic rewiring and context-specific tumor suppression.

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

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

30 19(Arf) and DNA damage-signaling pathways in tumor suppression.

31 tochondrial p53 is involved in apoptosis and tumor suppression.

32 in the regulation of cell deformability and tumor suppression.

33 (TIL) induces cellular senescence and limits tumor suppression.

34 evelopment and establish a novel paradigm of tumor suppression.

35 functional dysregulation and contributing to tumor suppression.

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

37 1 pathway downstream of TGFbeta signaling in tumor suppression.

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

39 olyamine metabolism and ferroptosis-mediated tumor suppression.

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

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

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

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

44 n mediator complex in genome maintenance and tumor suppression.

45 otein signaling, alveolar specification, and tumor suppression.

46 ealing that PKCbeta is haploinsufficient for tumor suppression.

47 ions that contribute to genome integrity and tumor suppression.

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

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

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

51 f TET dioxygenases during development and in tumor suppression.

52 including development, differentiation, and tumor suppression.

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

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

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

56 be explored for extending longevity and for tumor suppression.

57 in landscape in senescent cells and enforces tumor suppression.

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

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

60 esponse (DDR) and pinpointing their roles in tumor suppression.

61 -translational modification is essential for tumor suppression.

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

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

64 thylation and silencing of genes involved in tumor suppression.

65 ht contribute to stability of senescence and tumor suppression.

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

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

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

69 iomedical problems such as wound healing and tumor suppression.

70 y aimed at maintaining genomic stability and tumor suppression.

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

72 laborate in controlling autophagy to support tumor suppression.

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

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

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

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

77 integrity during organismal development and tumor suppression.

78 sal p53 protein levels in p53 activation and tumor suppression.

79 ilon) is required for genome duplication and tumor suppression.

80 loci on PWD chromosome 5 each contributed to tumor suppression.

81 ing genome stability, and may play a role in tumor suppression.

82 egulator and a key component of p53-mediated tumor suppression.

83 graft models, ATO reactivates mutant p53 for tumor suppression.

84 ns cement the importance of these domains in tumor suppression.

85 decorin (DCN) as a mechanism of MEIS1-driven tumor suppression.

86 ays a major role in cellular homeostasis and tumor suppression.

87 k between the transcriptional regulation and tumor suppression.

88 tion by p53 provides powerful, organism-wide tumor suppression.

89 omous stress response, integral to long-term tumor suppression.

90 t express abundant ANGPTL2 and contribute to tumor suppression.

91 response to stress signals are critical for tumor suppression.

92 ed in opposing functions in tumor growth and tumor suppression.

93 (+) T cells are required for CXCL14-mediated tumor suppression.

94 n that gap junctions have been implicated in tumor suppression.

95 pment of drugs that release WT p53 and allow tumor suppression.

96 ed ferroptosis and implicates ferroptosis in tumor suppression.

97 -STAT signaling genes critically involved in tumor suppression.

98 abolism, development, stress resistance, and tumor suppression.

99 , impairing cell viability as a tradeoff for tumor suppression.

100 n inhibition of hepatocyte proliferation and tumor suppression.

101 iocyte primary cilia acts as a mechanism for tumor suppression.

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

103 in mammary luminal cell differentiation and tumor suppression.

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

105 IRF2 protected LCLs against Blimp1-mediated tumor suppression.

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

107 of SIRT2 mutations in genome maintenance and tumor suppression.

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

109 and apoptosis are established mechanisms of tumor suppression, accumulating evidence reveals that fe

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

111 Our results suggest that besides tumor suppression activities, TMEM127 is a nutrient-sens

112 s study describes a new ceRNA with potential tumor suppression activity and helps us better understan

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

114 Shisa3 performs the tumor suppression activity through WNT signaling predict

115 OMES, MPEG1, PDK4, CCLI10, K60 and FST), and tumor suppression (ADAMTS2, LXN, ARRDC3, WNT7A, CLDN1 an

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

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

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

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

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

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

122 H3K27me3-targeted genes that are involved in tumor suppression and cell differentiation, leading to s

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

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

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

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

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

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

129 terochromatin is becoming more recognized in tumor suppression and may thus serve as a potential targ

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

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

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

133 d breast cells, suggesting distinct roles in tumor suppression and oncogenesis.

134 is a crucial component of p53-mediated liver tumor suppression and outline the mechanism by which thi

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

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

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

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

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

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

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

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

143 ns in the p53 pathway to bypass p53-mediated tumor suppression, and inactivate p53 itself only at lat

144 roved theranostic nanomedicine for efficient tumor suppression, and more importantly, inhibition of n

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

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

147 ium is required for endometrial homeostasis, tumor suppression, and postpartum endometrial regenerati

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

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

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

151 The molecular pathways underlying tumor suppression are incompletely understood.

152 , the mechanisms involved in ABHD5-dependent tumor suppression are not known.

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

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

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

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

157 mutation devoid of DNA binding results in no tumor suppression but surprising retention of an apoptot

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

159 3's apoptosis proficiency is dispensable for tumor suppression, but could prognosticate better surviv

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

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

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

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

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

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

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

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 new platform using dendronized polymers for tumor suppression by targeting cancer cell metabolism.

173 Loss of tumor suppression by the p53 protein involves altered or

174 at p53-mediated transcriptional function and tumor suppression can be achieved independently of its r

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

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

177 m, improved tumor selectivity, and increased tumor suppression compared to free IM, which accumulates

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

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

180 estored SOX17 expression, in addition to its tumor suppression effect, induces selective chemosensiti

181 estored SOX17 expression, in addition to its tumor suppression effect, induces selective chemosensiti

182 /PD-L1 blockade treatment showed synergistic tumor suppression efficacy.

183 n of these retroelements may help to explain tumor suppression encoded by p53, since erupting LINE1s

184 1 (liver kinase B1) plays important roles in tumor suppression, energy metabolism, and, recently, in

185 or talazoparib in murine xenografts provides tumor suppression equivalent to a month of daily dosing

186 I expression in HNC cells results in loss of tumor suppression even with CXCL14 expression.

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

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

189 ay be developed to balance between aging and tumor suppression, for example, by differentially regula

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

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

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

193 ion sites (p53-5KR) diminished its remaining tumor suppression function.

194 raised the possibility that RhoA may have a tumor suppression function.

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

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

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

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

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

200 nical evidence reveal dual roles for GJs, in tumor suppression, generally referred to as dormancy, an

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

202 t for such dramatic protein stabilization in tumor suppression has not been well addressed.

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

204 damage is critical for cellular homeostasis, tumor suppression, immunity, and gametogenesis.

205 The classic model of tumor suppression implies that malignant transformation

206 dage inside the body enables almost complete tumor suppression in an orthotopic liver cancer mouse mo

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

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

209 r mechanisms being proposed for p53-mediated tumor suppression in different contexts.

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

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

212 omimetic HK2-T473D rescued cisplatin-induced tumor suppression in Skp2 knockdown stable cells.

213 tablished roles in epigenetic regulation and tumor suppression in the endocrine pancreas; however, in

214 n therapy using both classes of Abs enhanced tumor suppression in the mouse immunogenic tumor model.

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

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

217 f the functional mechanisms of TP53-mediated tumor suppression in various cancers, using SEMA, and id

218 ther mutant p53 antagonizes p63/p73-mediated tumor suppression in vivo by using mutant p53-R270H knoc

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

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

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

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

223 r BRUCE in ATR activation in vitro and liver tumor suppression in vivo.

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

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

226 rtant role in both embryonic development and tumor suppression, independent of cell cycle arrest, sen

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

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

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

230 A significant tumor suppression is achieved by Fenton reaction-mediate

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

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

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

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

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

236 owever, the contribution of this function to tumor suppression is poorly understood.

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

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

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

240 ted in multiple diseases, and functions as a tumor suppression mechanism.

241 ation, has been recently identified as a new tumor suppression mechanism.

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

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

244 /6 effectively counter cancer cell-intrinsic tumor suppression mechanisms, senescence and apoptosis,

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

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

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

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

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

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

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

252 Here, we asked whether during tumor suppression p53 might instead regulate a wide rang

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

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

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

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

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

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

259 dependent transcriptional programs mediating tumor suppression remain incompletely understood.

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

261 STAG2 in gene regulation, hematopoiesis, and tumor suppression remains unresolved.

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

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

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

265 the underlying molecular mechanisms for its tumor suppression role remain largely unclear.

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

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

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

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

270 f the PI3K-AKT signaling pathway and greater tumor suppression than with BYL719 alone.

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

272 Tumor suppression that is mediated by oncogene-induced s

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

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

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

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

277 ment, the mechanism by which CXCL14 mediates tumor suppression through NK and/or T cells remained und

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

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

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

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

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

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

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

287 ver critical components downstream of p53 in tumor suppression, we perform unbiased RNAi and CRISPR-C

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

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

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

291 senescence throughout the lifespan promotes tumor suppression, whereas the persistence of senescent

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 downregulation of antigenicity and intrinsic tumor suppression, which provides the basis for developi

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

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

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

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

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

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