ライフサイエンスコーパス: tumor suppressor gene

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

2 3sigma might contribute to its function as a tumor suppressor gene.

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

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

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

6 g genetic evidence that MCPH1 is a bona fide tumor suppressor gene.

7 fied the E3 ligase HACE1 as HER2 cooperative tumor suppressor gene.

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

9 ked to tumorigenesis, making GR an authentic tumor suppressor gene.

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

11 sociated with germ-line mutation in the TP53 tumor suppressor gene.

12 luding an insertion into an exon of the PTEN tumor suppressor gene.

13 ecurrent silencing mutations in ID3, a novel tumor suppressor gene.

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

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

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

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

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

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

20 on requires full "two-hit" inactivation of a tumor-suppressor gene.

21 nsin homolog mutated on chromosome 10 (PTEN) tumor-suppressor gene.

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

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

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

25 gment global oncogene expression and disrupt tumor suppressor genes.

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

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

28 dent repression of Dnmt3b and possibly other tumor suppressor genes.

29 l accumulation of mutations in oncogenes and tumor suppressor genes.

30 as cancer related mutations in oncogenes or tumor suppressor genes.

31 suggesting that they constitute a family of tumor suppressor genes.

32 tudies indicate that most of mutant PTPs are tumor suppressor genes.

33 crease acetylation and promote expression of tumor suppressor genes.

34 kely results in transcriptional silencing of tumor suppressor genes.

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

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

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

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

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

40 and transcription inactivation of candidate tumor-suppressor genes.

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

42 enic signaling and loss of heterozygosity of tumor-suppressor genes.

43 ultaneous CRISPR/Cas9-mediated knockout of 3 tumor-suppressor genes.

44 eneration sequencing (tNGS) of oncogenes and tumor-suppressor genes.

45 cer progression is through inhibition of key 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 The Wilms' tumor suppressor gene 1 (WT1) encodes a zinc finger tran

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

52 t, by differences in the location of two-hit tumor suppressor genes across the genome.

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

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

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

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

57 Both the LKB1 tumor suppressor gene and the oncogene DeltaN-LKB1 are e

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

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

60 Tumor suppressor genes and the immune system are critica

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

62 Germline mutations in the PTEN tumor-suppressor gene and germline variations in succina

63 erexpressing tumors revealed upregulation of tumor-suppressor genes and downregulation of molecules i

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

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

66 pliced genes included a number of oncogenes, tumor suppressor genes, and genes involved in regulation

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

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

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

70 Mutations in the PTEN tumor suppressor gene are found in a high proportion of

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

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

73 lands located in the promoter region of some tumor suppressor genes are very common in human diseases

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

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

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

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

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

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

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

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

82 Silencing of tumor-suppressor genes by DNA methyltransferase 1 (Dnmt1

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

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

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

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

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

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

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

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

91 SIRT2, a tumor suppressor gene, contributes to the control of thi

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

93 study, we identify a mechanism in which the tumor-suppressor gene, cylindromatosis (CYLD), confers p

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

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

96 -29b, which can act as either an oncogene or tumor suppressor gene depending on signaling context.

97 eases to create genetic mosaic zebrafish for tumor suppressor gene discovery.

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

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

100 The p53 tumor suppressor gene encodes a homotetrameric transcrip

101 The LKB1 tumor suppressor gene encodes a master kinase that coord

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

103 Inactivation of the tumor suppressor gene encoding the transcriptional regul

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

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

106 Notch may act as an oncogene or a tumor-suppressor gene even within the same tumor type.

107 ic and epigenetic alterations, e.g., loss of tumor suppressor gene expression (TP53, PTEN, RB) as wel

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

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

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

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

112 We recently reported that the p53 tumor suppressor gene has a bidirectional gene partner,

113 uctase (WWOX), originally marked as a likely tumor suppressor gene, has over the years become recogni

114 Several additional tumor suppressor genes have been identified near the VHL

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

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

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

118 ative oncogene and PRUNE2 as an unrecognized tumor suppressor gene in human prostate cancer, and thei

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

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

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

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

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

124 ion has been linked to aberrant silencing of tumor suppressor genes in cancer, and an imbalance in DN

125 (PTEN) is one of the most frequently mutated tumor suppressor genes in cancers.

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

127 n mouse models of pancreatic cancer, loss of tumor suppressor genes in conjunction with Kras mutation

128 tive assemblage could underlie repression of tumor suppressor genes in leukemia cells.

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

130 xamined, placing PARD3 among the most common tumor suppressor genes in this malignancy.

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

132 e also functionally validate CEP350 as a new tumor-suppressor gene in human melanoma.

133 pression of DLC1 (deleted in liver cancer 1) tumor-suppressor gene in metastatic prostate carcinoma (

134 Csk) is a genetic modifier of warts (wts), a tumor-suppressor gene in the Hippo pathway, and interact

135 wo tumors, suggesting that REST may act as a tumor-suppressor gene in Wilms tumor pathogenesis.

136 gements identifies ATF7IP and MGA as two new tumor-suppressor genes in ALL.

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

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

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

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

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

142 Chromosome 3p harbors several additional tumor suppressor genes, including BRCA1-associated prote

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

144 lysis identified upregulation of 17 putative tumor suppressor genes, including DNA methyltransferase

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

146 recent evidence that DAXX represses several tumor suppressor genes, including the DAPK1 and DAPK3 pr

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

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

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

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

151 The LKB1 tumor suppressor gene is frequently mutated and inactiva

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

153 The von Hippel-Lindau (VHL) tumor suppressor gene is mutated as an early event in al

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

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

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

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

158 The product of the Brca1 tumor-suppressor gene is involved in multiple aspects of

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

160 fferential isoform usage including CDKN2A, a tumor suppressor gene known to be inactivated in a major

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

162 sein kinase 1A1 gene (CSNK1A1) is a putative tumor suppressor gene located in the common deleted regi

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

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

165 e multiple endocrine neoplasia type 1 (Men1) tumor suppressor gene, mediates the cell proliferation a

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

167 es identified RASA2, encoding a RasGAP, as a tumor-suppressor gene mutated in 5% of melanomas.

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

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

170 age sequences identified the products of the tumor suppressor genes NF1 and NF2 as potent microtubule

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

172 more than biallelic inactivation of the NF1 tumor suppressor gene or expression of the KIAA1549:BRAF

173 pathways, synthetic lethality for a specific tumor suppressor gene or oncogene is likely cell context

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

175 enome instability and aberrant expression of tumor suppressor genes or oncogenes.

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

177 The tumor suppressor gene p53 and its family members p63/p73

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

179 Tumor suppressor gene p53 plays an important role in the

180 rmed both in the presence and absence of the tumor suppressor gene p53, enabling us to assess what ef

181 yte (KC) DNA mutations, including within the tumor-suppressor gene p53, and chronic exposure is assoc

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

183 Analysis of tumor suppressor gene patterns revealed disease specific

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

185 is through transcriptional repression of the tumor suppressor gene PDZ-LIM domain-containing protein

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

187 Tumor-suppressor genes phosphatase and tensin homolog de

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

189 induced silencing of promoter CpG islands in tumor suppressor genes plays an important role in human

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

191 , it has been shown that hypermethylation of tumor suppressor genes promoters is a common feature of

192 tivation of oncogenes and/or inactivation of tumor suppressor genes provide continuous proliferative

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

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

195 a p53 target gene that is homologous to the tumor suppressor gene PTCH1 and can function as a repres

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

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

198 Mice with T-cell-specific loss of the tumor suppressor gene PTEN early in T-cell ontogeny deve

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

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

201 r new potential cell polarity and colorectal tumor suppressor genes (RASA3, NUPL1, DENND5A and AVL9).

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

203 Inactivation of the tumor suppressor gene RASSF1A by promoter hypermethylati

204 The tumor suppressor gene RASSF1A is epigenetically silenced

205 significant promoter hypermethylation of the tumor-suppressor gene RASSF1A in 6 FTH samples (60%) com

206 Mutations in the retinoblastoma tumor suppressor gene Rb are involved in many forms of h

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

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

209 Tumor suppressor genes regulate cell growth and prevent

210 particular, whether the physical location of tumor suppressor genes relative to one another influence

211 LKB1/STK11 is a tumor suppressor gene responsible for Peutz-Jeghers synd

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

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

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

215 modification of the endogenous locus of the tumor-suppressor gene SFRP1, a pivotal regulator of the

216 CDH1 mutations, testing of CTNNA1 and other tumor suppressor genes should be considered.

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

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

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

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

221 characterized a specific subset of potential tumor suppressor genes subject to repression via the OGT

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

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

224 MT2D target genes include frequently mutated tumor suppressor genes such as TNFAIP3, SOCS3 and TNFRSF

225 levels ranging from 4% to 35%, even at known tumor suppressor genes such as TWIST2.

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

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

228 c lesions and accumulation of LOH at various tumor suppressor genes, suggesting a possible causal ass

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

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

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

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

233 2 and Cdkn1c promoters and expression of the tumor-suppressor genes Tff2 and Cdkn1c was increased.

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

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

236 Therefore, MIR-491 is a tumor suppressor gene that, by utilizing both mature for

237 encoding the G protein Galphas, as a potent tumor suppressor gene that, when expressed at low levels

238 SMARCA4 (BRG1) and SMARCB1 (INI1) are tumor suppressor genes that are crucially involved in th

239 nt outgrowth by perturbing the expression of tumor suppressor genes that control B cell-activating pa

240 ed as cooperative repressors of a network of tumor suppressor genes that included PDCD4, BTG2, and NE

241 a model in which dysregulated expression of tumor suppressor genes that induce DDR activation can be

242 ether, our data suggest that SPEN is a novel tumor-suppressor gene that may be clinically useful as a

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

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

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

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

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

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

249 The tumor suppressor gene TP53 is mutated exclusively with t

250 DK4/6, along with increases in the levels of tumor suppressor gene TP53, cell cycle inhibitors CDKN1A

251 nce angiogenesis, including mutations in the tumor suppressor gene TP53, which occur frequently in ma

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 p-lox-G12D/+) and K-Ras(lox-Stop-lox-G12D/+);tumor suppressor gene Trp53(F/F) mice infected with Aden

256 onal disruption of the cell cycle checkpoint tumor-suppressor genes Trp53 and Rb1 using Prx1-Cre, Col

257 is caused by germline mutation in one of two tumor suppressor genes, TSC1 and TSC2.

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 methylation-mediated oncogene activation, or tumor suppressor gene (TSG) silencing mechanisms, widely

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

263 Genomic deletion of tumor suppressor genes (TSG) is a rite of passage for vi

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

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

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

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

268 to identify novel biallelically inactivated tumor suppressor genes (TSGs) in sporadic invasive and p

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 ations that presumably contain oncogenes and tumor-suppressor genes (TSGs).

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

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

274 Loss of function of the von Hippel-Lindau tumor suppressor gene (VHL) predisposes renal epithelial

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

276 Mutations of the tumor suppressor gene von Hippel-Lindau (VHL) can lead t

277 Mutations in the tumor-suppressor gene von Hippel-Lindau (VHL) are associ

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

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

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

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

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

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

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

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

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

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

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

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

290 pe 1 (NF1) results from mutations in the NF1 tumor-suppressor gene, which encodes neurofibromin, a ne

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

292 These findings suggest that KMT2D acts as a tumor suppressor gene whose early loss facilitates lymph

293 F is a canonical androgen-regulated putative tumor suppressor gene whose expression is inhibited by a

294 Cellular stress response 1 (CSR1) is a tumor suppressor gene whose expression was frequently do

295 g 2 (DAB2) gene was recently identified as a tumor suppressor gene with its expression downregulated

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

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

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

299 nesis, progenitor cells expressing the Wilms tumor suppressor gene, WT1, are induced to differentiate

300 ignant tumor progression and a new human CRC tumor-suppressor gene, ZNF292, that might also function