ライフサイエンスコーパス: suppressor gene

1 cause they result in functional loss (tumour suppressor genes).

2 in the neurofibromatosis type 1 (NF1) tumor suppressor gene.

3 letion of MTAP and the adjacent CDKN2A tumor suppressor gene.

4 ociated mutants that arose in the DLC1 tumor suppressor gene.

5 ng a role for LTF as a prostate cancer tumor suppressor gene.

6 holipase C delta 1 (PLCD1), a proposed tumor suppressor gene.

7 cers, as widely documented for the p53 tumor suppressor gene.

8 ssible explanation why Parkin may be a tumor suppressor gene.

9 ted by somatic inactivation of the VHL tumor suppressor gene.

10 those predicted to target oncogenes or tumor suppressor gene.

11 loss of the Neurofibromatosis 2 (NF2) tumor suppressor gene.

12 originates from the first intron of a tumor suppressor gene.

13 e 5-hmC in the promoter region of MGMT tumor suppressor gene.

14 ntified in Peutz-Jeghers syndrome as a tumor suppressor gene.

15 m two hits to the same allele of PLCD1 tumor suppressor gene.

16 rt by inducing expression of the FOXO1 tumor suppressor gene.

17 uman tumors, pointing to its role as a tumor suppressor gene.

18 phosphatase and tensin homolog (Pten) tumor-suppressor gene.

19 , confirming the role of ADAMTS12 as a tumor suppressor gene.

20 yndrome caused by mutations in the NF1 tumor suppressor gene.

21 tic kinases and blockade of a putative tumor suppressor gene.

22 le in the development of melanoma as a tumor suppressor gene.

23 ed recurrence frequency, especially in tumor suppressor genes.

24 allelic mutations of the PTEN and TP53 tumor suppressor genes.

25 lating the expression of oncogenes and tumor-suppressor genes.

26 ments AML1-ETO-dependent repression of tumor suppressor genes.

27 of which are associated with putative tumor suppressor genes.

28 with cancer-associated genes including tumor suppressor genes.

29 activate proto-oncogenes or inactivate tumor-suppressor genes.

30 ut their combined role as oncogenes or tumor suppressor genes.

31 are rare in cancers and often target tumour suppressor genes.

32 reakpoints and recurrently inactivated tumor-suppressor genes.

33 part, by repressing the expression of tumour suppressor genes.

34 specific overexpression of variants in tumor-suppressor genes.

35 these DMRs overlapped with 1,145 known tumor suppressor genes.

36 e magnitude and mode of action of many tumor-suppressor genes.

37 tivating mutations in the TSC1 or TSC2 tumor suppressor genes.

38 mb repressor complex 2 (PRC2)-silenced tumor suppressor genes.

39 her in these patients, particularly in tumor suppressor genes.

40 onine phosphatases are important human tumor suppressor genes.

41 ressing critical oncogenes and lacking tumor suppressor genes.

42 used by mutations in the TSC1 and TSC2 tumor suppressor genes.

43 nd epigenetic changes in oncogenes and tumor suppressor genes.

44 global oncogene expression and disrupt tumor suppressor genes.

45 ed out to be one of the most important tumor suppressor genes.

46 cribed as a prototype for the class of tumor suppressor genes.

47 ranscription inactivation of candidate tumor-suppressor genes.

48 ncogenes and inactivating mutations in tumor-suppressor genes.

49 riptional repression, mainly targeting tumor-suppressor genes.

50 evealed 49 variants in 27 oncogenes or tumor suppressor genes.

51 t of indels residing in oncogenes and tumour suppressor genes.

52 e evaluated for inherited mutations in tumor suppressor genes.

53 tations on transcriptional splicing of tumor suppressor genes.

54 phosphorylated state mediated by large tumor suppressor gene 1 and 2 (LATS1/2).

55 Such genes act as both oncogenes and tumor suppressor genes, a scenario that is unlikely but theore

56 usual example, where inactivation of a tumor-suppressor gene and activation of an oncogene are incomp

57 These data link oncogene, loss of tumour suppressor gene and drug-induced replication stress with

58 etic evidence that Bap1 is a bona fide tumor suppressor gene and offer key insights into the contribu

59 g located on chromosome 10 (PTEN) is a tumor suppressor gene and one of the most frequently mutated/d

60 usion, FRMD6 was identified as a novel tumor suppressor gene and prognostic biomarker candidate in PC

61 ings herein identify TMIGD1 as a novel tumor suppressor gene and provide new insights into the pathog

62 stablishes TRIM29 as a hypoxia-induced tumor suppressor gene and provides a novel molecular mechanism

63 NF1, a tumor suppressor gene and RAS-GTPase, is one of the highly mut

64 nduces the expression of p16(INK4a), a tumor suppressor gene and senescence/aging biomarker.

65 is research implicates FBXL7 as a metastasis-suppressor gene and suggests therapeutic strategies to c

66 initiation through inactivation of two tumor suppressor genes and activation of one oncogene, account

67 on changes leading to upregulation of tumour suppressor genes and downregulation of oncogenes.

68 mutations, which can be found in both tumor suppressor genes and oncogenes, produce proteins with en

69 tion mutations in DNA repair and other tumor suppressor genes and overall survival following platinum

70 n WT mice via in utero deletion of key tumor suppressor genes and serially monitored cortical epilept

71 Tumor suppressor genes and the immune system are critical play

72 ons can be exploited to identify novel tumor suppressor genes and to obtain a deeper characterization

73 variety of tumor types and can silence tumor suppressor genes and, therefore, is important for carcin

74 tion as a traditional loss-of-function tumor suppressor gene, and they provide a fully penetrant anim

75 hich sometimes leads to the removal of tumor-suppressor genes, and can induce complex translocations

76 idizing the cDNA to the BROCA panel of tumor suppressor genes, and then multiplex sequencing to very

77 rmed that miR-210 directly targets the tumor suppressor gene APC (adenomatous polyposis coli), thereb

78 Deletion of the tumor suppressor gene Apc using the Car1(CreER) KI caused tumo

79 ited mutations in DNA repair and other tumor suppressor genes appear to particularly benefit from pla

80 n the tuberous sclerosis complex (TSC) tumor suppressor genes are associated closely with the pathoge

81 The order in which oncogenes or tumour suppressor genes are functionally selected for in a stem

82 terogeneous carcinoma in which various tumor-suppressor genes are lost by mutation, deletion, or sile

83 Repression effects on tumor suppressor genes are negligible as they are generally ex

84 ic pathways, and at the same time some tumor suppressor genes are under strong selection in deer.

85 established that many genes, including tumor suppressor genes, are hypermethylated and transcriptiona

86 uisition of mutations in oncogenes and tumor suppressor genes, as well as changes in the pancreatic e

87 on, leading to decreased expression of tumor suppressor genes, as well as with genome instability, le

88 MAP3K7 is a tumor suppressor gene associated with poor disease-free surviv

89 domain family protein 1a (RASSF1A), a tumor suppressor gene at 3p21.3, plays a very important role i

90 Known oncogenes and tumor suppressor genes, beyond those engineered, are mutated,

91 of both the RAD52 gene, and the HR and tumor suppressor gene, BRCA2, in human cells synergistically r

92 n, was recently identified as a novel memory suppressor gene, but its mechanism remained unknown.

93 T1 inhibitor, induces re-expression of tumor suppressor genes by removing/erasing methylation marks f

94 the replacement of single, functional tumor suppressor genes by the mutant alleles.

95 wever, little is known about whether a tumor suppressor gene can function through both immune-depende

96 Thus, mutations in tumor suppressor genes can create a state of increased cellula

97 ity that, in the absence of functional tumor suppressor genes, can contribute to tumorigenesis.

98 three genes: NNAT (suggested to be a tumour suppressor gene), CDC14B (involved in cell cycle control

99 nactivating germline mutations in the tumour suppressor gene CDH1, although pathogenic variants in CT

100 Targeting G-tract RNA to the tumor suppressor gene CDKN2A in malignant rhabdoid tumor cells

101 se of its chromosomal proximity to the tumor suppressor gene CDKN2A.

102 levels and increased expression of the tumor suppressor gene Cdkn2a/p16 in mammary tumors of HF offsp

103 its proximity to the commonly deleted tumor suppressor gene, CDKN2A.

104 o discriminate methylation levels of a tumor suppressor gene, CDO1, on a molecule-by-molecule basis.

105 caused by an inactivating mutation in tumor suppressor genes coding the TSC1/TSC2 complex, resulting

106 Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging

107 Comutated, myeloid tumor-suppressor genes contribute to phenotypic variability, p

108 oncogene and inactivation of the ATRX tumor-suppressor gene correlate with high-risk disease and poo

109 ene partners that are known oncogenes, tumor suppressor genes, COSMIC genes, and/or transcription fac

110 t mutations in the novel penile cancer tumor suppressor genes CSN1(GPS1) and FAT1 Expression of CSN1

111 Since its development in 2012, the Tumor Suppressor Gene database (TSGene), has become a popular

112 estigated the phenotype of the TMEM127 tumor suppressor gene deficiency in vivo.

113 ence for PPP2R4 as a haploinsufficient tumor suppressor gene, defining a high-penetrance genetic mech

114 Deleted in Liver Cancer 1 (DLC1) is a tumor suppressor gene deleted in many cancers, including angio

115 g therapeutic targets in cancers with tumour-suppressor gene deletions.

116 rp53(-/-)) or double (Trp53(-/-);Brca2(-/-)) suppressor gene deletions.

117 melanocytes, whereas the proapoptotic tumor suppressor gene DPPIV/CD26 was down-regulated, followed

118 tor TBX5, leading to repression of the tumor suppressor genes DYRK1A and PTEN In clinical specimens o

119 The adenomatous polyposis coli (APC) tumor suppressor gene encodes a multifunctional protein that i

120 Inactivation of the tumor suppressor gene encoding the transcriptional regulator I

121 onstrated that ANKDD1A is a functional tumor suppressor gene, especially in the hypoxia microenvironm

122 iallelic inactivation events affecting tumor suppressor genes, especially TP53, the end result being

123 retinoblastoma), altered oncogenes and tumor suppressor gene expression, and disrupted the normal res

124 deletions and duplications within the tumor suppressor gene FHIT Taking aneuploidy into account, we

125 screens as well as identification of natural suppressor genes for neurodegenerative diseases.

126 ation domain family 1 isoform A) is a tumour suppressor gene frequently silenced by promoter hypermet

127 The expression of the metabolic tumor suppressor gene fructose-1,6-bisphosphatase (FBP1), epig

128 Lung tumor suppressor gene Gprc5a-knockout (ko) mice are susceptibl

129 most frequently mutated oncogenes and tumour-suppressor genes have been studied for several decades,

130 These classical tumour-suppressor genes have tumorigenic effects associated wit

131 essor genes Tbx5 and Pten and the metastasis suppressor gene Hoxd10 are significantly upregulated by

132 ic-ultrasound (TUS) to deliver a human tumor suppressor gene, hSef-b, to prostate tumors in vivo.

133 two broad categories: inactivation of tumor suppressor genes (hypomorph, antimorph or amorph) or act

134 e experimentally validated METTL3 as a tumor suppressor gene in bladder cancer, providing support to

135 PBRM1, the second most highly mutated tumor suppressor gene in kidney cancer, encodes PBRM1.

136 TP53 is the most frequently mutated tumor suppressor gene in many cancers, yet biochemical charact

137 he Myc oncogene and deleting the Trp53 tumor suppressor gene in murine neural stem cells or progenito

138 n is lacking on the status of this key tumor suppressor gene in pleural lesions preceding mesotheliom

139 ur findings established that Ets2 is a tumor suppressor gene in prostate cancer, and its loss along w

140 Our results indicate that Cftr is a tumor suppressor gene in the intestinal tract as Cftr mutant m

141 We conclude that ERbeta is a tumor suppressor gene in the VP and MG where its loss increase

142 Expression of the TUSC2/FUS1 tumor suppressor gene in TUSC2 deficient EGFR wildtype lung ca

143 n the X chromosome (WTX) is a putative tumor suppressor gene in Wilms tumor, but its expression and f

144 as9-based editing of the Apc and Trp53 tumor suppressor genes in colon epithelial cells and by orthot

145 Recent studies of conserved tumor-suppressor genes in Drosophila showed how protumor cells

146 rgizes with DNA methylation to silence tumor-suppressor genes in human fibroblasts.

147 reens in multiple cancer types, as new tumor suppressor genes in prostate cancer.

148 Cas9 system to model loss of candidate tumor suppressor genes in SCLC, and we anticipate that this ap

149 polygenic up-regulation of dozens of biofilm suppressor genes in strains isolated from human patients

150 ostate cancers, which retain potential tumor-suppressor genes in the interstitial regions between TMP

151 Our validation of several new tumor suppressor genes in TNBC demonstrate the utility of two-

152 on of oncogenes and/or inactivation of tumor suppressor genes in tumor cells promotes tumorigenesis.

153 tionally express oncogenes or silence tumour suppressor genes in vivo.

154 ents of menin, the product of the MEN1 tumor suppressor gene, in coordinating the transcription and s

155 discovery uncovers novel mechanisms of tumor-suppressor gene inactivation and highlights a new approa

156 ion (H3K27me3), and (ii) activation of tumor suppressor genes, including BRCA1.

157 on and increased expression of several tumor suppressor genes, including Src homology region 2 domain

158 lidation studies identified eight TNBC tumor suppressor genes, including the GATA-like transcriptiona

159 nd clonal driver mutations occurred in tumor-suppressor genes, including TP53, KMT2D and ZNF750, amon

160 f consequences of abnormal splicing in tumor suppressor genes, including whole or partial exon skippi

161 used by a germline mutation in the NF1 tumor suppressor gene, individuals with NF1 are prone to optic

162 eptibility loci: 11q23.3 CADM1, a metastasis suppressor gene involved in modifying tumour interaction

163 The von Hippel-Lindau (VHL) tumor suppressor gene is inactivated in the majority of clear

164 The RB1 tumor suppressor gene is mutated in highly aggressive tumors i

165 tions as a medulloblastoma oncogene or tumor suppressor gene is not known.

166 Inactivation of the VHL tumor suppressor gene is the signature initiating event in cle

167 We observed that hypermethylation of tumor suppressor genes is a frequent event in ocular tumors, b

168 The loss of function of metastasis suppressor genes is a major rate-limiting step in breast

169 CpG islands in the promoter region of tumor suppressor genes is a promising biomarker for early canc

170 nt DNA hypermethylation of promoter of tumor suppressor genes is commonly observed in cancer, and its

171 ITH mapping to gene promoter areas or tumor suppressor genes is low.

172 OPCML, a tumor suppressor gene, is frequently silenced epigenetically i

173 ermethylation, within the promoters of tumor suppressor genes, is an important risk factor in cervica

174 ression; (iii) enhanced expression of tumour suppressor genes; (iv) downregulation of migration and m

175 growth factor receptor 2 protein, p53 tumor suppressor gene, Ki-67 proliferation marker, and tumor-i

176 cohorts of pancreatic NET-bearing Men1 tumor-suppressor gene KO mice, a transgenic model of functioni

177 mic dysfunction triggers expression of tumor-suppressor genes, limiting the development of aggressive

178 (BRCA2) (PALB2) has emerged as a major tumor suppressor gene linked to breast cancer (BC), pancreatic

179 zygous missense mutations in SAMD9L, a tumor suppressor gene located on chromosome arm 7q.

180 DAC) frequently contains deletions of tumour suppressor gene loci, most notably SMAD4, which is homoz

181 therapeutic targets for counteracting tumor suppressor gene loss is needed.

182 opose a framework where a heterozygous tumor suppressor gene microenvironment has antagonistic roles

183 stance caused by downregulation of the tumor suppressor gene miR-34a.

184 channel catfish, Ictalurus punctatus, muscle suppressor gene MSTN.

185 nes sp7, runx2, bmp2a, spp1, opg, and muscle suppressor gene mstn.

186 erations in epigenetic regulators, and tumor suppressor gene mutation.

187 ne downregulated the expression of the tumor suppressor gene N-myc downstream-regulated gene 1 (NDRG1

188 order due to germline mutations in the tumor suppressor gene NF1.

189 that is caused by inactivation of the tumor suppressor gene NF2 The NF2 gene product, Merlin, has no

190 rough analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila wing imaginal dis

191 berrations that result in silencing of tumor-suppressor genes, oncogene addictions, and enhancement o

192 esis of cancer either by silencing key tumor suppressor genes or by activating oncogenes.

193 f-target sites and no modifications in tumor suppressor genes or other genes associated with patholog

194 ere, we have identified a role for the tumor suppressor gene p53 in regulating venous thrombus resolu

195 ythroid 2-related factor 2 (Nrf2), and tumor suppressor gene (p53) when children or adults were expos

196 Analysis of tumor suppressor gene patterns revealed disease specificity fo

197 cated in human melanoma, including the tumor-suppressor genes phosphatase and tensin homolog (PTEN),

198 Structural compromise of the tumor suppressor gene, phosphatase and tensin homolog (PTEN),

199 logical role of BACE2 as a dose-sensitive AD-suppressor gene, potentially explaining the dementia del

200 In patients, tumour suppressor gene promoters are markedly more methylated i

201 s, and that dual inactivation of these tumor suppressor genes promotes myocyte cell-cycle reentry.

202 recurrent somatic inactivations of the tumor suppressor gene Ptch1 and a recapitulation of the sonic

203 diated by mutant U1 snRNA inactivates tumour-suppressor genes (PTCH1) and activates oncogenes (GLI2 a

204 where deletions and mutations in the tumour suppressor gene PTEN (phosphatase and tensin homolog) ar

205 Primary PCa with deletion of the tumor suppressor gene PTEN (PTEN-del) can be modeled through P

206 nslation initiation factor EIF4A1, the tumor suppressor gene PTEN and the long non-coding RNA NEAT1.

207 own that miRNA-based regulation of the tumor suppressor gene PTEN can be modulated by the expression

208 Loss of the tumor suppressor gene PTEN exerts diverse outcomes on cancer i

209 CDCP1 cooperates with the loss of the tumor suppressor gene PTEN to promote the emergence of metasta

210 a Sox2-induced miRNA that targets the tumor suppressor genes PTEN and FoxO1 and regulates the GBM st

211 Inactivation of the tumor suppressor gene RASSF1A by promoter hypermethylation rep

212 rbor loss-of-function mutations in the tumor suppressor gene RB1 The canonical function of the RB1 ge

213 The tumor suppressor genes RB1 (retinoblastoma) and CDKN2a (cyclin

214 nd UPS frequently lose function of the tumor suppressor genes RB1 and TP53 In this issue of Cancer Re

215 number alterations or mutations in the tumor suppressor genes RB1 and TP53.

216 Although the retinoblastoma tumor-suppressor gene (RB1) is frequently lost together with T

217 Mutations of the retinoblastoma tumor-suppressor gene (RB1) or components regulating the CDK-R

218 Tumor suppressor genes remain to be systemically identified fo

219 the overexpression of DNA repair and tumour suppressor genes, rendering these genes susceptible to m

220 ne mutations in the Folliculin (FLCN) tumour suppressor gene result in fibrofolliculomas, lung cysts

221 s are associated with mutations in NF1 tumor suppressor gene, resulting in activation of Ras and its

222 an retinoblastoma are mutations in the tumor-suppressor gene retinoblastoma (RB) and amplification of

223 We speculate that its tumor suppressor gene role may be real, while its high express

224 ks (DSB) in cancer cells that lack the tumor suppressor gene RUNX3 Loss of RUNX3 resulted in transcri

225 for the identification of a novel metastasis suppressor gene, serum deprivation response (SDPR), loca

226 xemplified by the frequent loss of the tumor suppressor gene SMAD4 in this malignancy.

227 The chromosome 8p tumor suppressor genes SORBS3 and SH2D4A are physically and fu

228 tion, differential gene expression and tumor suppressor gene status.

229 KB1) has been studied extensively as a tumor suppressor gene (Stk11) in the context of cancer.

230 deletion of the liver kinase B1 (LKB1) tumor suppressor gene, Stk11 (serine threonine kinase 11), in

231 program several hypoxia associated and tumor suppressor genes such as MAT2A and PDK-1, in addition to

232 genomic alterations, particularly in tumour suppressor genes such as TP53 and LKB1 (also known as ST

233 complex (TSC) is an autosomal dominant tumor-suppressor gene syndrome caused by inactivating mutation

234 Tuberous sclerosis (TSC) is a tumor suppressor gene syndrome that is associated with the wid

235 Among the target genes of miR-10b, the tumor suppressor genes Tbx5 and Pten and the metastasis suppre

236 Mutations at CpG sites on the p53 tumor suppressor gene that can result from these adductions ar

237 are typically caused by mutations of a tumor suppressor gene that lead to the early development of mu

238 sociated protein 1 (BAP1) is a potent tumour suppressor gene that modulates environmental carcinogene

239 novel somatic L1 insertion in the APC tumor suppressor gene that provided us with a unique opportuni

240 ing, cell fate determination, and as a tumor suppressor gene that restricts cell lineage progression

241 precipitation and sequencing to identify key suppressor genes that are silenced by histone methylatio

242 Unlike some pan-cancer oncogenes and tumour suppressor genes that drive transformation in virtually

243 to miR-486-5p-dependent modulation of tumor suppressor genes that feeds back to regulate glioma stem

244 romosome 17p loss, containing the TP53 tumor suppressor gene, that was significantly associated with

245 ith a DNA sequence related to the p53 tumour suppressor gene, the most commonly affected gene in huma

246 vation of oncogenes or inactivation of tumor suppressor genes, these processes become deregulated in

247 n the adenomatous polyposis coli (APC) tumor suppressor gene through inhibition of cholesterol biosyn

248 and TGFB1) and increased expression of tumor suppressor genes (TNFRSF14 and HSD17B14).

249 c silencing mechanisms to downregulate tumor suppressor genes to maintain its own expression.

250 ation of this information identified a tumor suppressor gene TOB1 as a critical determinant of estrog

251 F chromatin-remodeling complex and the tumor suppressor gene TP53 and provide preclinical evidence to

252 ephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53 copy

253 le phase II study in patients with p53 tumor suppressor gene ( TP53)-mutated ovarian cancer refractor

254 able to simultaneously inactivate five tumor suppressor genes (TP53, PTEN, APC, BRCA1, and BRCA2) and

255 RPINE1 and inactivation of TP53-family tumor suppressor gene TP73.

256 generated through the deletion of the tumor-suppressor gene Trp53 in conjunction with oncogenic acti

257 Here we report that inactivation of tumor suppressor genes Trp53 and Rb1 in the gastric squamous-c

258 have found that KANK1 was a candidate tumor suppressor gene (TSG) for human MPNSTs.

259 able to inhibit the CpG methylation of tumor suppressor gene (TSG) promoters and reactivate their exp

260 defined for initiating and supporting tumor suppressor gene (TSG) silencing in human colorectal canc

261 ly mutated, and the identity of key 8p tumor-suppressor genes (TSG) is unknown.

262 nscriptional repression of a number of tumor suppressor genes (TSG) via molecular mechanisms that rem

263 ation and gene silencing of hemizygous tumor suppressor genes (TSG), we thus hypothesized that this e

264 T3 can mediate epigenetic silencing of tumor suppressor genes (TSG).

265 ases sensitivity to hotspot regions in tumor suppressor genes (TSG).

266 We elucidated a broad spectrum of tumor suppressor genes (TSGs) and oncogenes (OGs) that can gen

267 Tumor suppressor genes (TSGs) are a major type of gatekeeper g

268 NMD-elicit mutations in tumour suppressor genes (TSGs) are associated with significant

269 g passenger genes, oncogenes (OGs) and tumor-suppressor genes (TSGs) for each cancer type is critical

270 tic SNVs associated with oncogenes and tumor suppressor genes (TSGs) induce very different changes in

271 rally believed to encode oncogenes and tumor suppressor genes (TSGs) that drive cancer growth.

272 hanges in the RT rate or set of driver tumor-suppressor genes (TSGs) were observed to alter the dynam

273 n, reactivates epigenetically silenced tumor suppressor genes (TSGs), and reduces CRC oncogenic prope

274 as kidney cells with mutations in the tumor suppressor genes tuberous sclerosis complex (TSC)1 or TS

275 ficient in the von Hippel-Lindau (VHL) tumor suppressor gene use glutamine to generate citrate and li

276 inactivation of the von Hippel-Lindau tumour suppressor gene (VHL).

277 h 3'-UTR shortening, and to inactivate tumor suppressor genes via the re-routing of microRNA competit

278 her curated VIS-involved oncogenes and tumor suppressor genes, virus-host interactions involved in no

279 ons and epigenetic inactivation of the tumor suppressor gene von Hippel-Lindau (VHL) are major causes

280 The RASSF1A tumor suppressor gene was shown to be often inactivated by hyp

281 Notably, the HIC1 tumor suppressor gene was stimulated by JMJD1A and MDFIC, but

282 changes and biallelic inactivation of tumor suppressor genes was increased in GEP70 high risk, consi

283 LN first identified as a p53-dependent tumor suppressor gene, was believed to bind randomly to DNA an

284 cally be selected for when targeting a tumor suppressor gene, we could effectively recapitulate oncog

285 G1-S phase arrest and act as potential tumor suppressor genes, we aimed to study potential methylatio

286 r diploid but carry deletions spanning tumor suppressor genes, whereas P53 inactivation allowed Caph2

287 ults suggest that VGLL4 is a candidate tumor suppressor gene which acts by selectively antagonizing Y

288 l death 4 (PDCD4) is a proinflammatory tumor-suppressor gene which helps to prevent the transition fr

289 The MEN1 tumor suppressor gene, which encodes the protein menin, is kno

290 4 could be a potential novel prostate cancer suppressor gene, which may prevent cancer progression an

291 nction mutations of the PBRM1 and BAP1 tumor suppressor genes, which occur in a mutually exclusive ma

292 overrepresented in anti-longevity and tumor-suppressor genes, while genes inhibiting cellular senesc

293 erefore identify KLF12 as a novel metastasis-suppressor gene whose loss of function is associated wit

294 d on searching for novel oncogenes and tumor suppressor genes whose abundance is positively or negati

295 CTCF is a haploinsufficient tumour suppressor gene with diverse normal functions in genome

296 A (Methyltransferase Like 7A), a novel tumor suppressor gene with multiple editing sites at its 3'UTR

297 ified miR-192 as an epigenetically regulated suppressor gene with predictive value in this disease.

298 road quantification of the function of tumor-suppressor genes with unprecedented resolution, parallel

299 n of the ST/PE lineage-specific Wilms' tumor suppressor gene (Wt1) in the ST/PE of G2-Gata4(Cre) mice

300 most frequently mutated, well-studied tumor-suppressor gene, yet the molecular basis of the switch f