ライフサイエンスコーパス: tumor suppressor gene

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

2 er-associated mutants that arose in the DLC1 tumor suppressor gene.

3 ic cancers, as widely documented for the p53 tumor suppressor gene.

4 one possible explanation why Parkin may be a tumor suppressor gene.

5 phospholipase C delta 1 (PLCD1), a proposed tumor suppressor gene.

6 initiated by somatic inactivation of the VHL tumor suppressor gene.

7 luded those predicted to target oncogenes or tumor suppressor gene.

8 STAiR2 originates from the first intron of a tumor suppressor gene.

9 st identified in Peutz-Jeghers syndrome as a tumor suppressor gene.

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

11 in part by inducing expression of the FOXO1 tumor suppressor gene.

12 unique 5-hmC in the promoter region of MGMT tumor suppressor gene.

13 mary human tumors, pointing to its role as a tumor suppressor gene.

14 ng from two hits to the same allele of PLCD1 tumor suppressor gene.

15 3sigma might contribute to its function as a tumor suppressor gene.

16 cer development is driven by loss of the Apc tumor suppressor gene.

17 , confirming that the cystatin E/M gene is a tumor suppressor gene.

18 hus supporting a putative role for CHD2 as a tumor suppressor gene.

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

20 tion syndrome caused by mutations in the NF1 tumor suppressor gene.

21 f mitotic kinases and blockade of a putative tumor suppressor gene.

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

23 co-deletion of MTAP and the adjacent CDKN2A tumor suppressor gene.

24 pporting a role for LTF as a prostate cancer tumor suppressor gene.

25 or the phosphatase and tensin homolog (Pten) tumor-suppressor gene.

26 ch augments AML1-ETO-dependent repression of tumor suppressor genes.

27 , some of which are associated with putative tumor suppressor genes.

28 ation with cancer-associated genes including tumor suppressor genes.

29 on about their combined role as oncogenes or tumor suppressor genes.

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

31 h inactivating mutations in the TSC1 or TSC2 tumor suppressor genes.

32 polycomb repressor complex 2 (PRC2)-silenced tumor suppressor genes.

33 so higher in these patients, particularly in tumor suppressor genes.

34 s, expressing critical oncogenes and lacking tumor suppressor genes.

35 is caused by mutations in the TSC1 and TSC2 tumor suppressor genes.

36 gment global oncogene expression and disrupt tumor suppressor genes.

37 s turned out to be one of the most important tumor suppressor genes.

38 en described as a prototype for the class of tumor suppressor genes.

39 e/threonine phosphatases are important human tumor suppressor genes.

40 etic and epigenetic changes in oncogenes and tumor suppressor genes.

41 sues revealed 49 variants in 27 oncogenes or tumor suppressor genes.

42 ma were evaluated for inherited mutations in tumor suppressor genes.

43 mic mutations on transcriptional splicing of tumor suppressor genes.

44 observed recurrence frequency, especially in tumor suppressor genes.

45 d, bi-allelic mutations of the PTEN and TP53 tumor suppressor genes.

46 that activate proto-oncogenes or inactivate tumor-suppressor genes.

47 heir breakpoints and recurrently inactivated tumor-suppressor genes.

48 llele-specific overexpression of variants in tumor-suppressor genes.

49 vel the magnitude and mode of action of many tumor-suppressor genes.

50 and transcription inactivation of candidate tumor-suppressor genes.

51 patients had protein-truncating mutations in tumor-suppressor genes.

52 ling oncogenes and inactivating mutations in tumor-suppressor genes.

53 transcriptional repression, mainly targeting tumor-suppressor genes.

54 y regulating the expression of oncogenes and tumor-suppressor genes.

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

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

57 Here we show that cylindromatosis (CYLD), a tumor suppressor gene and negative regulator of NF-kappa

58 de genetic evidence that Bap1 is a bona fide tumor suppressor gene and offer key insights into the co

59 homolog located on chromosome 10 (PTEN) is a tumor suppressor gene and one of the most frequently mut

60 conclusion, FRMD6 was identified as a novel tumor suppressor gene and prognostic biomarker candidate

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

62 tudy establishes TRIM29 as a hypoxia-induced tumor suppressor gene and provides a novel molecular mec

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

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

65 ancer initiation through inactivation of two tumor suppressor genes and activation of one oncogene, a

66 kinome and phosphatome harbor oncogenes and tumor suppressor genes and important regulators of angio

67 orphic mutations, which can be found in both tumor suppressor genes and oncogenes, produce proteins w

68 f-function mutations in DNA repair and other tumor suppressor genes and overall survival following pl

69 omas in WT mice via in utero deletion of key tumor suppressor genes and serially monitored cortical e

70 Tumor suppressor genes and the immune system are critica

71 mutations can be exploited to identify novel tumor suppressor genes and to obtain a deeper characteri

72 in a variety of tumor types and can silence tumor suppressor genes and, therefore, is important for

73 an unusual example, where inactivation of a tumor-suppressor gene and activation of an oncogene are

74 n function as a traditional loss-of-function tumor suppressor gene, and they provide a fully penetran

75 n cancer by silencing certain genes, such as tumor suppressor genes, and by reactivating other region

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

77 ome, which sometimes leads to the removal of tumor-suppressor genes, and can induce complex transloca

78 ation of cellular oncogenes, inactivation of tumor-suppressor genes, and dysregulation of multiple si

79 confirmed that miR-210 directly targets the tumor suppressor gene APC (adenomatous polyposis coli),

80 Deletion of the tumor suppressor gene Apc using the Car1(CreER) KI cause

81 inherited mutations in DNA repair and other tumor suppressor genes appear to particularly benefit fr

82 Mutations in the p53 tumor suppressor gene are the most frequent genetic alte

83 ions in the tuberous sclerosis complex (TSC) tumor suppressor genes are associated closely with the p

84 Repression effects on tumor suppressor genes are negligible as they are genera

85 ogenetic pathways, and at the same time some tumor suppressor genes are under strong selection in dee

86 and heterogeneous carcinoma in which various tumor-suppressor genes are lost by mutation, deletion, o

87 well established that many genes, including tumor suppressor genes, are hypermethylated and transcri

88 al acquisition of mutations in oncogenes and tumor suppressor genes, as well as changes in the pancre

89 hylation, leading to decreased expression of tumor suppressor genes, as well as with genome instabili

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

91 iation domain family protein 1a (RASSF1A), a tumor suppressor gene at 3p21.3, plays a very important

92 Known oncogenes and tumor suppressor genes, beyond those engineered, are mut

93 ssion of both the RAD52 gene, and the HR and tumor suppressor gene, BRCA2, in human cells synergistic

94 by increasing histone methylation to silence tumor suppressor genes, but how EZH2 levels become eleva

95 a DNMT1 inhibitor, induces re-expression of tumor suppressor genes by removing/erasing methylation m

96 ead to the replacement of single, functional tumor suppressor genes by the mutant alleles.

97 However, little is known about whether a tumor suppressor gene can function through both immune-d

98 Thus, mutations in tumor suppressor genes can create a state of increased c

99 stability that, in the absence of functional tumor suppressor genes, can contribute to tumorigenesis.

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

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

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

103 ylthioadenosine phosphorylase (MTAP) and the tumor suppressor genes CDKN2A-CDKN2B are frequently dele

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

105 lets to discriminate methylation levels of a tumor suppressor gene, CDO1, on a molecule-by-molecule b

106 It is caused by an inactivating mutation in tumor suppressor genes coding the TSC1/TSC2 complex, res

107 Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-dam

108 Comutated, myeloid tumor-suppressor genes contribute to phenotypic variabil

109 e MYCN oncogene and inactivation of the ATRX tumor-suppressor gene correlate with high-risk disease a

110 ning gene partners that are known oncogenes, tumor suppressor genes, COSMIC genes, and/or transcripti

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

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

113 We investigated the phenotype of the TMEM127 tumor suppressor gene deficiency in vivo.

114 e evidence for PPP2R4 as a haploinsufficient tumor suppressor gene, defining a high-penetrance geneti

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

116 -29b, which can act as either an oncogene or tumor suppressor gene depending on signaling context.

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

118 on factor TBX5, leading to repression of the tumor suppressor genes DYRK1A and PTEN In clinical speci

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

120 Inactivation of the tumor suppressor gene encoding the transcriptional regul

121 DNA methylation with the down-regulation of tumor suppressor gene epithelial cadherin CDH1.

122 st demonstrated that ANKDD1A is a functional tumor suppressor gene, especially in the hypoxia microen

123 e of biallelic inactivation events affecting tumor suppressor genes, especially TP53, the end result

124 WNT, retinoblastoma), altered oncogenes and tumor suppressor gene expression, and disrupted the norm

125 ecific deletions and duplications within the tumor suppressor gene FHIT Taking aneuploidy into accoun

126 tions down to 0.00003% abundance, or to scan tumor-suppressor genes for rare mutations.

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

128 sents a rapid and scalable strategy to study tumor suppressor gene function in cancer.

129 Lung tumor suppressor gene Gprc5a-knockout (ko) mice are susc

130 o positively regulate D3 was mediated by the tumor suppressor gene GRHL3, a hitherto unrecognized D3

131 rapeutic-ultrasound (TUS) to deliver a human tumor suppressor gene, hSef-b, to prostate tumors in viv

132 l into two broad categories: inactivation of tumor suppressor genes (hypomorph, antimorph or amorph)

133 -C downregulates DNA methylation of the CDH1 tumor suppressor gene in association with induction of E

134 We experimentally validated METTL3 as a tumor suppressor gene in bladder cancer, providing suppo

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 c

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

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

139 ely, our findings established that Ets2 is a tumor suppressor gene in prostate cancer, and its loss a

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

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

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

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

144 Investigating the in vivo role of tumor suppressor genes in cancer is technically challeng

145 ISPR-Cas9-based editing of the Apc and Trp53 tumor suppressor genes in colon epithelial cells and by

146 our screens in multiple cancer types, as new tumor suppressor genes in prostate cancer.

147 RISPR-Cas9 system to model loss of candidate tumor suppressor genes in SCLC, and we anticipate that t

148 Our validation of several new tumor suppressor genes in TNBC demonstrate the utility o

149 tivation of oncogenes and/or inactivation of tumor suppressor genes in tumor cells promotes tumorigen

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

151 t synergizes with DNA methylation to silence tumor-suppressor genes in human fibroblasts.

152 ive prostate cancers, which retain potential tumor-suppressor genes in the interstitial regions betwe

153 fragments of menin, the product of the MEN1 tumor suppressor gene, in coordinating the transcription

154 This discovery uncovers novel mechanisms of tumor-suppressor gene inactivation and highlights a new

155 thylation (H3K27me3), and (ii) activation of tumor suppressor genes, including BRCA1.

156 pression and increased expression of several tumor suppressor genes, including Src homology region 2

157 Validation studies identified eight TNBC tumor suppressor genes, including the GATA-like transcri

158 precipitation experiments identified several tumor suppressor genes, including the protein tyrosine p

159 iety of consequences of abnormal splicing in tumor suppressor genes, including whole or partial exon

160 ncal and clonal driver mutations occurred in tumor-suppressor genes, including TP53, KMT2D and ZNF750

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

162 The LKB1 tumor suppressor gene is frequently mutated and inactiva

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

164 The RB1 tumor suppressor gene is mutated in highly aggressive tu

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

166 The tumor protein 53 (TP53) tumor suppressor gene is the most frequently somatically

167 Inactivation of the VHL tumor suppressor gene is the signature initiating event

168 We observed that hypermethylation of tumor suppressor genes is a frequent event in ocular tum

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

170 The epigenetic dysregulation of tumor suppressor genes is an important driver of human c

171 Aberrant DNA hypermethylation of promoter of tumor suppressor genes is commonly observed in cancer, a

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

173 on Hippel Lindau (Vhl) protein, encoded by a tumor suppressor gene, is an E3 ubiquitin ligase that ta

174 OPCML, a tumor suppressor gene, is frequently silenced epigenetic

175 ed hypermethylation, within the promoters of tumor suppressor genes, is an important risk factor in c

176 dermal growth factor receptor 2 protein, p53 tumor suppressor gene, Ki-67 proliferation marker, and t

177 using cohorts of pancreatic NET-bearing Men1 tumor-suppressor gene KO mice, a transgenic model of fun

178 pigenomic dysfunction triggers expression of tumor-suppressor genes, limiting the development of aggr

179 cer 2 (BRCA2) (PALB2) has emerged as a major tumor suppressor gene linked to breast cancer (BC), panc

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

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

182 we propose a framework where a heterozygous tumor suppressor gene microenvironment has antagonistic

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

184 s, alterations in epigenetic regulators, and tumor suppressor gene mutation.

185 rly gene downregulated the expression of the tumor suppressor gene N-myc downstream-regulated gene 1

186 on disorder due to germline mutations in the tumor suppressor gene NF1.

187 apping symptoms caused by alterations of the tumor suppressor genes NF1 (encoding the protein neurofi

188 as and that is caused by inactivation of the tumor suppressor gene NF2 The NF2 gene product, Merlin,

189 how through analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila wing imagin

190 etic aberrations that result in silencing of tumor-suppressor genes, oncogene addictions, and enhance

191 thogenesis of cancer either by silencing key tumor suppressor genes or by activating oncogenes.

192 ial off-target sites and no modifications in tumor suppressor genes or other genes associated with pa

193 Here, we have identified a role for the tumor suppressor gene p53 in regulating venous thrombus

194 tor erythroid 2-related factor 2 (Nrf2), and tumor suppressor gene (p53) when children or adults were

195 Analysis of tumor suppressor gene patterns revealed disease specific

196 A panel of three tumor suppressor genes (PCDHGB6, HOXA9 and RASSF1A) was

197 implicated in human melanoma, including the tumor-suppressor genes phosphatase and tensin homolog (P

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

199 Heritable mutations in the BAP1 tumor suppressor gene predispose individuals to mesothel

200 yocytes, and that dual inactivation of these tumor suppressor genes promotes myocyte cell-cycle reent

201 he ability of MBD2 to repress the methylated tumor suppressor gene PRSS8 in MDA-MB-435 breast cancer

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

203 Primary PCa with deletion of the tumor suppressor gene PTEN (PTEN-del) can be modeled thr

204 ic translation initiation factor EIF4A1, the tumor suppressor gene PTEN and the long non-coding RNA N

205 has shown that miRNA-based regulation of the tumor suppressor gene PTEN can be modulated by the expre

206 Loss of the tumor suppressor gene PTEN exerts diverse outcomes on ca

207 Loss of the tumor suppressor gene PTEN is implicated in breast cance

208 tably, CDCP1 cooperates with the loss of the tumor suppressor gene PTEN to promote the emergence of m

209 -5p as a Sox2-induced miRNA that targets the tumor suppressor genes PTEN and FoxO1 and regulates the

210 d that miR-181a/b targets the ATRA-regulated tumor suppressor gene RASSF1A by direct binding to its 3

211 Inactivation of the tumor suppressor gene RASSF1A by promoter hypermethylati

212 The tumor suppressor gene RASSF1A is epigenetically silenced

213 Cs) harbor loss-of-function mutations in the tumor suppressor gene RB1 The canonical function of the

214 The tumor suppressor genes RB1 (retinoblastoma) and CDKN2a (

215 MFS and UPS frequently lose function of the tumor suppressor genes RB1 and TP53 In this issue of Can

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

217 Although the retinoblastoma tumor-suppressor gene (RB1) is frequently lost together

218 Mutations of the retinoblastoma tumor-suppressor gene (RB1) or components regulating the

219 Tumor suppressor genes remain to be systemically identif

220 MPSNTs are associated with mutations in NF1 tumor suppressor gene, resulting in activation of Ras an

221 in human retinoblastoma are mutations in the tumor-suppressor gene retinoblastoma (RB) and amplificat

222 We speculate that its tumor suppressor gene role may be real, while its high e

223 d breaks (DSB) in cancer cells that lack the tumor suppressor gene RUNX3 Loss of RUNX3 resulted in tr

224 , as exemplified by the frequent loss of the tumor suppressor gene SMAD4 in this malignancy.

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

226 In addition, the chromosome 8p tumor suppressor genes Src homology 2 domain containing

227 stribution, differential gene expression and tumor suppressor gene status.

228 B1 (LKB1) has been studied extensively as a tumor suppressor gene (Stk11) in the context of cancer.

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

230 lso reprogram several hypoxia associated and tumor suppressor genes such as MAT2A and PDK-1, in addit

231 promoted tumorigenesis through repression of tumor suppressor genes such as Ras suppressor 1 and stro

232 A and mutation and loss of heterozygosity of tumor suppressor genes, such as APC and TP53; (3) CpG is

233 ut it is unclear whether the inactivation of tumor suppressor genes, such as STK11/LKB1, exerts simil

234 trol of proliferation and differentiation by tumor suppressor genes suggests that evolution of diverg

235 Tuberous sclerosis (TSC) is a tumor suppressor gene syndrome that is associated with t

236 rosis complex (TSC) is an autosomal dominant tumor-suppressor gene syndrome caused by inactivating mu

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

238 Mutations at CpG sites on the p53 tumor suppressor gene that can result from these adducti

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

240 tify a novel somatic L1 insertion in the APC tumor suppressor gene that provided us with a unique opp

241 atterning, cell fate determination, and as a tumor suppressor gene that restricts cell lineage progre

242 emness to miR-486-5p-dependent modulation of tumor suppressor genes that feeds back to regulate gliom

243 d a chromosome 17p loss, containing the TP53 tumor suppressor gene, that was significantly associated

244 o activation of oncogenes or inactivation of tumor suppressor genes, these processes become deregulat

245 ions in the adenomatous polyposis coli (APC) tumor suppressor gene through inhibition of cholesterol

246 DGFB, and TGFB1) and increased expression of tumor suppressor genes (TNFRSF14 and HSD17B14).

247 toma susceptibility gene (RB1) was the first tumor suppressor gene to be molecularly defined.

248 genetic silencing mechanisms to downregulate tumor suppressor genes to maintain its own expression.

249 Integration of this information identified a tumor suppressor gene TOB1 as a critical determinant of

250 SWI/SNF chromatin-remodeling complex and the tumor suppressor gene TP53 and provide preclinical evide

251 the elephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53

252 ppaB signaling and the negative regulator of tumor suppressor gene TP53-mediated cell cycle arrest an

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

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

255 tor SERPINE1 and inactivation of TP53-family tumor suppressor gene TP73.

256 Here we report that inactivation of tumor suppressor genes Trp53 and Rb1 in the gastric squa

257 er was generated through the deletion of the tumor-suppressor gene Trp53 in conjunction with oncogeni

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

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

260 nt, is defined for initiating and supporting tumor suppressor gene (TSG) silencing in human colorecta

261 ential interactions among orthologs of human tumor suppressor genes (TSG) and genes encoding drug tar

262 he transcriptional repression of a number of tumor suppressor genes (TSG) via molecular mechanisms th

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

264 increases sensitivity to hotspot regions in tumor suppressor genes (TSG).

265 STAT3 can mediate epigenetic silencing of tumor suppressor genes (TSG).

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

267 We elucidated a broad spectrum of tumor suppressor genes (TSGs) and oncogenes (OGs) that c

268 Tumor suppressor genes (TSGs) are a major type of gateke

269 t somatic SNVs associated with oncogenes and tumor suppressor genes (TSGs) induce very different chan

270 e generally believed to encode oncogenes and tumor suppressor genes (TSGs) that drive cancer growth.

271 ylation, reactivates epigenetically silenced tumor suppressor genes (TSGs), and reduces CRC oncogenic

272 uishing passenger genes, oncogenes (OGs) and tumor-suppressor genes (TSGs) for each cancer type is cr

273 mall changes in the RT rate or set of driver tumor-suppressor genes (TSGs) were observed to alter the

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

275 lls deficient in the von Hippel-Lindau (VHL) tumor suppressor gene use glutamine to generate citrate

276 through 3'-UTR shortening, and to inactivate tumor suppressor genes via the re-routing of microRNA co

277 e further curated VIS-involved oncogenes and tumor suppressor genes, virus-host interactions involved

278 Mutations and epigenetic inactivation of the tumor suppressor gene von Hippel-Lindau (VHL) are major

279 Therefore, haploinsufficiency of one TSC tumor suppressor gene was required for tumor initiation,

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

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

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

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

284 cific multi-methylated sites, a well-studied tumor suppressor gene, was used as the target DNA sequen

285 chastically be selected for when targeting a tumor suppressor gene, we could effectively recapitulate

286 ed in G1-S phase arrest and act as potential tumor suppressor genes, we aimed to study potential meth

287 In the High-M set, a number of tumor-suppressor genes were methylated and repressed.

288 re near diploid but carry deletions spanning tumor suppressor genes, whereas P53 inactivation allowed

289 tores the expression of methylation-silenced tumor suppressor genes, whereas PKC412 inhibits hyperact

290 he results suggest that VGLL4 is a candidate tumor suppressor gene which acts by selectively antagoni

291 ed cell death 4 (PDCD4) is a proinflammatory tumor-suppressor gene which helps to prevent the transit

292 The MEN1 tumor suppressor gene, which encodes the protein menin,

293 -of-function mutations of the PBRM1 and BAP1 tumor suppressor genes, which occur in a mutually exclus

294 n by Sema 3A in coordination with a chain of tumor-suppressor genes, which in turn inhibits breast ca

295 cantly overrepresented in anti-longevity and tumor-suppressor genes, while genes inhibiting cellular

296 focused on searching for novel oncogenes and tumor suppressor genes whose abundance is positively or

297 METTL7A (Methyltransferase Like 7A), a novel tumor suppressor gene with multiple editing sites at its

298 the broad quantification of the function of tumor-suppressor genes with unprecedented resolution, pa

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

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