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1 rt by inducing expression of the FOXO1 tumor suppressor gene.
2 uman tumors, pointing to its role as a tumor suppressor gene.
3 ssible explanation why Parkin may be a tumor suppressor gene.
4  phosphatase and tensin homolog (Pten) tumor-suppressor gene.
5  might contribute to its function as a tumor suppressor gene.
6 velopment is driven by loss of the Apc tumor suppressor gene.
7 egulates muscle contraction, and is a tumour-suppressor gene.
8 irming that the cystatin E/M gene is a tumor suppressor gene.
9 pporting a putative role for CHD2 as a tumor suppressor gene.
10 ted by somatic inactivation of the VHL tumor suppressor gene.
11 tic evidence that MCPH1 is a bona fide tumor suppressor gene.
12 he E3 ligase HACE1 as HER2 cooperative tumor suppressor gene.
13  tumorigenesis, making GR an authentic tumor suppressor gene.
14 those predicted to target oncogenes or tumor suppressor gene.
15 cers, as widely documented for the p53 tumor suppressor gene.
16  originates from the first intron of a tumor suppressor gene.
17 ntified in Peutz-Jeghers syndrome as a tumor suppressor gene.
18 her in these patients, particularly in tumor suppressor genes.
19 ressing critical oncogenes and lacking tumor suppressor genes.
20  of which are associated with putative tumor suppressor genes.
21 used by mutations in the TSC1 and TSC2 tumor suppressor genes.
22 global oncogene expression and disrupt tumor suppressor genes.
23 ed out to be one of the most important tumor suppressor genes.
24 cribed as a prototype for the class of tumor suppressor genes.
25 ranscription inactivation of candidate tumor-suppressor genes.
26 loss and the reduced dosage of linked tumour suppressor genes.
27 ts had protein-truncating mutations in tumor-suppressor genes.
28 rward genetic screen to identify three novel suppressor genes.
29 ignaling and loss of heterozygosity of tumor-suppressor genes.
30 epression of Dnmt3b and possibly other tumor suppressor genes.
31 mulation of mutations in oncogenes and tumor suppressor genes.
32 ncer related mutations in oncogenes or tumor suppressor genes.
33 sting that they constitute a family of tumor suppressor genes.
34  indicate that most of mutant PTPs are tumor suppressor genes.
35 ous CRISPR/Cas9-mediated knockout of 3 tumor-suppressor genes.
36  acetylation and promote expression of tumor suppressor genes.
37 demonstrated to repress tumor and metastasis suppressor genes.
38 with cancer-associated genes including tumor suppressor genes.
39 activate proto-oncogenes or inactivate tumor-suppressor genes.
40  are rare in cancers and often target tumour suppressor genes.
41 reakpoints and recurrently inactivated tumor-suppressor genes.
42 part, by repressing the expression of tumour suppressor genes.
43 specific overexpression of variants in tumor-suppressor genes.
44 these DMRs overlapped with 1,145 known tumor suppressor genes.
45 e magnitude and mode of action of many tumor-suppressor genes.
46 tivating mutations in the TSC1 or TSC2 tumor suppressor genes.
47 mb repressor complex 2 (PRC2)-silenced tumor suppressor genes.
48                             The Wilms' tumor suppressor gene 1 (WT1) encodes a zinc finger transcript
49 phosphorylated state mediated by large tumor suppressor gene 1 and 2 (LATS1/2).
50     These data link oncogene, loss of tumour suppressor gene and drug-induced replication stress with
51         Germline mutations in the PTEN tumor-suppressor gene and germline variations in succinate deh
52 we show that cylindromatosis (CYLD), a tumor suppressor gene and negative regulator of NF-kappaB sign
53 etic evidence that Bap1 is a bona fide tumor suppressor gene and offer key insights into the contribu
54 stablishes TRIM29 as a hypoxia-induced tumor suppressor gene and provides a novel molecular mechanism
55 nduces the expression of p16(INK4a), a tumor suppressor gene and senescence/aging biomarker.
56                          Both the LKB1 tumor suppressor gene and the oncogene DeltaN-LKB1 are express
57 essing tumors revealed upregulation of tumor-suppressor genes and downregulation of molecules involve
58 on changes leading to upregulation of tumour suppressor genes and downregulation of oncogenes.
59 is often associated with silencing of tumour suppressor genes and hypomethylation with activation of
60 e and phosphatome harbor oncogenes and tumor suppressor genes and important regulators of angiogenesi
61  mutations, which can be found in both tumor suppressor genes and oncogenes, produce proteins with en
62 he emerging wealth of novel candidate tumour suppressor genes and the generation of faithful animal m
63                                        Tumor suppressor genes and the immune system are critical play
64 variety of tumor types and can silence tumor suppressor genes and, therefore, is important for carcin
65 tion as a traditional loss-of-function tumor suppressor gene, and they provide a fully penetrant anim
66 er by silencing certain genes, such as tumor suppressor genes, and by reactivating other regions, suc
67 of cellular oncogenes, inactivation of tumor-suppressor genes, and dysregulation of multiple signal-t
68 rmed that miR-210 directly targets the tumor suppressor gene APC (adenomatous polyposis coli), thereb
69                        Deletion of the tumor suppressor gene Apc using the Car1(CreER) KI caused tumo
70                   Mutations in the p53 tumor suppressor gene are the most frequent genetic alteration
71 n the tuberous sclerosis complex (TSC) tumor suppressor genes are associated closely with the pathoge
72 terogeneous carcinoma in which various tumor-suppressor genes are lost by mutation, deletion, or sile
73 located in the promoter region of some tumor suppressor genes are very common in human diseases such
74 established that many genes, including tumor suppressor genes, are hypermethylated and transcriptiona
75                            MAP3K7 is a tumor suppressor gene associated with poor disease-free surviv
76 lar necrosis by negatively regulating tumour suppressor genes associated with the death-receptor-medi
77  domain family protein 1a (RASSF1A), a tumor suppressor gene at 3p21.3, plays a very important role i
78                    Known oncogenes and tumor suppressor genes, beyond those engineered, are mutated,
79 of both the RAD52 gene, and the HR and tumor suppressor gene, BRCA2, in human cells synergistically r
80 reasing histone methylation to silence tumor suppressor genes, but how EZH2 levels become elevated in
81  the replacement of single, functional tumor suppressor genes by the mutant alleles.
82 wever, little is known about whether a tumor suppressor gene can function through both immune-depende
83                     Thus, mutations in tumor suppressor genes can create a state of increased cellula
84 ity that, in the absence of functional tumor suppressor genes, can contribute to tumorigenesis.
85  three genes: NNAT (suggested to be a tumour suppressor gene), CDC14B (involved in cell cycle control
86 e identify recurrent mutations in the tumour suppressor gene CDC27 (11.9%).
87 se of its chromosomal proximity to the tumor suppressor gene CDKN2A.
88 ed with reduced expression of the cell cycle suppressor genes CDKN2A (p16 and p14) and CDKN2B (p15) a
89 adenosine phosphorylase (MTAP) and the tumor suppressor genes CDKN2A-CDKN2B are frequently deleted in
90  its proximity to the commonly deleted tumor suppressor gene, CDKN2A.
91  caused by an inactivating mutation in tumor suppressor genes coding the TSC1/TSC2 complex, resulting
92                     Comutated, myeloid tumor-suppressor genes contribute to phenotypic variability, p
93                               SIRT2, a tumor suppressor gene, contributes to the control of this chec
94 t mutations in the novel penile cancer tumor suppressor genes CSN1(GPS1) and FAT1 Expression of CSN1
95 s caused by germline mutations in the tumour suppressor gene, CYLD.
96     Since its development in 2012, the Tumor Suppressor Gene database (TSGene), has become a popular
97 ence for PPP2R4 as a haploinsufficient tumor suppressor gene, defining a high-penetrance genetic mech
98 rp53(-/-)) or double (Trp53(-/-);Brca2(-/-)) suppressor gene deletions.
99 g therapeutic targets in cancers with tumour-suppressor gene deletions.
100 which can act as either an oncogene or tumor suppressor gene depending on signaling context.
101 to create genetic mosaic zebrafish for tumor suppressor gene discovery.
102  melanocytes, whereas the proapoptotic tumor suppressor gene DPPIV/CD26 was down-regulated, followed
103 tor TBX5, leading to repression of the tumor suppressor genes DYRK1A and PTEN In clinical specimens o
104                               The LKB1 tumor suppressor gene encodes a master kinase that coordinates
105   The adenomatous polyposis coli (APC) tumor suppressor gene encodes a multifunctional protein that i
106                    Inactivation of the tumor suppressor gene encoding the transcriptional regulator I
107 ethylation with the down-regulation of tumor suppressor gene epithelial cadherin CDH1.
108 iallelic inactivation events affecting tumor suppressor genes, especially TP53, the end result being
109      Notch may act as an oncogene or a tumor-suppressor gene even within the same tumor type.
110 retinoblastoma), altered oncogenes and tumor suppressor gene expression, and disrupted the normal res
111 down to 0.00003% abundance, or to scan tumor-suppressor genes for rare mutations.
112 a rapid and scalable strategy to study tumor suppressor gene function in cancer.
113 tively regulate D3 was mediated by the tumor suppressor gene GRHL3, a hitherto unrecognized D3 transc
114  (WWOX), originally marked as a likely tumor suppressor gene, has over the years become recognized fo
115 essor genes Tbx5 and Pten and the metastasis suppressor gene Hoxd10 are significantly upregulated by
116 ic-ultrasound (TUS) to deliver a human tumor suppressor gene, hSef-b, to prostate tumors in vivo.
117  two broad categories: inactivation of tumor suppressor genes (hypomorph, antimorph or amorph) or act
118 nregulates DNA methylation of the CDH1 tumor suppressor gene in association with induction of E-cadhe
119  functionally validate CEP350 as a new tumor-suppressor gene in human melanoma.
120 oncogene and PRUNE2 as an unrecognized tumor suppressor gene in human prostate cancer, and their regu
121   The mutational pattern for the TP53 tumour suppressor gene in lung tumours differs to other cancer
122 n is lacking on the status of this key tumor suppressor gene in pleural lesions preceding mesotheliom
123 ur findings established that Ets2 is a tumor suppressor gene in prostate cancer, and its loss along w
124    Our results indicate that Cftr is a tumor suppressor gene in the intestinal tract as Cftr mutant m
125           Expression of the TUSC2/FUS1 tumor suppressor gene in TUSC2 deficient EGFR wildtype lung ca
126 ors, suggesting that REST may act as a tumor-suppressor gene in Wilms tumor pathogenesis.
127     However, the discovery of new metastasis suppressor genes in breast cancer using genomic efforts
128      Investigating the in vivo role of tumor suppressor genes in cancer is technically challenging du
129 as9-based editing of the Apc and Trp53 tumor suppressor genes in colon epithelial cells and by orthot
130            Recent studies of conserved tumor-suppressor genes in Drosophila showed how protumor cells
131 rgizes with DNA methylation to silence tumor-suppressor genes in human fibroblasts.
132 reens in multiple cancer types, as new tumor suppressor genes in prostate cancer.
133 polygenic up-regulation of dozens of biofilm suppressor genes in strains isolated from human patients
134 ostate cancers, which retain potential tumor-suppressor genes in the interstitial regions between TMP
135 d, placing PARD3 among the most common tumor suppressor genes in this malignancy.
136          Our validation of several new tumor suppressor genes in TNBC demonstrate the utility of two-
137 tionally express oncogenes or silence tumour suppressor genes in vivo.
138 ents of menin, the product of the MEN1 tumor suppressor gene, in coordinating the transcription and s
139 tor 3 (RUNX3) is widely regarded as a tumour-suppressor gene inactivated by DNA hypermethylation of i
140 discovery uncovers novel mechanisms of tumor-suppressor gene inactivation and highlights a new approa
141 ion (H3K27me3), and (ii) activation of tumor suppressor genes, including BRCA1.
142 identified upregulation of 17 putative tumor suppressor genes, including DNA methyltransferase Dnmt3b
143 on and increased expression of several tumor suppressor genes, including Src homology region 2 domain
144 t evidence that DAXX represses several tumor suppressor genes, including the DAPK1 and DAPK3 protein
145 lidation studies identified eight TNBC tumor suppressor genes, including the GATA-like transcriptiona
146 itation experiments identified several tumor suppressor genes, including the protein tyrosine phospha
147 nd clonal driver mutations occurred in tumor-suppressor genes, including TP53, KMT2D and ZNF750, amon
148 used by a germline mutation in the NF1 tumor suppressor gene, individuals with NF1 are prone to optic
149 eptibility loci: 11q23.3 CADM1, a metastasis suppressor gene involved in modifying tumour interaction
150                               The LKB1 tumor suppressor gene is frequently mutated and inactivated in
151            The von Hippel-Lindau (VHL) tumor suppressor gene is inactivated in the majority of clear
152               The product of the Brca1 tumor-suppressor gene is involved in multiple aspects of the c
153            The von Hippel-Lindau (VHL) tumor suppressor gene is mutated as an early event in almost a
154            The tumor protein 53 (TP53) tumor suppressor gene is the most frequently somatically alter
155   We observed that hypermethylation of tumor suppressor genes is a frequent event in ocular tumors, b
156           The loss of function of metastasis suppressor genes is a major rate-limiting step in breast
157        The epigenetic dysregulation of tumor suppressor genes is an important driver of human carcino
158 nt DNA hypermethylation of promoter of tumor suppressor genes is commonly observed in cancer, and its
159 pel Lindau (Vhl) protein, encoded by a tumor suppressor gene, is an E3 ubiquitin ligase that targets
160 cohorts of pancreatic NET-bearing Men1 tumor-suppressor gene KO mice, a transgenic model of functioni
161 n of oncogenes and/or deactivation of tumour suppressor genes lead to uncontrolled cell cycle progres
162 zygous missense mutations in SAMD9L, a tumor suppressor gene located on chromosome arm 7q.
163 DAC) frequently contains deletions of tumour suppressor gene loci, most notably SMAD4, which is homoz
164  therapeutic targets for counteracting tumor suppressor gene loss is needed.
165 iple endocrine neoplasia type 1 (Men1) tumor suppressor gene, mediates the cell proliferation and dif
166  Foxp2 negatively interacts with the synapse suppressor gene Mef2c.
167 stance caused by downregulation of the tumor suppressor gene miR-34a.
168 nes sp7, runx2, bmp2a, spp1, opg, and muscle suppressor gene mstn.
169 channel catfish, Ictalurus punctatus, muscle suppressor gene MSTN.
170 ntified RASA2, encoding a RasGAP, as a tumor-suppressor gene mutated in 5% of melanomas.
171 order due to germline mutations in the tumor suppressor gene NF1.
172  symptoms caused by alterations of the tumor suppressor genes NF1 (encoding the protein neurofibromin
173 rough analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila wing imaginal dis
174 esis of cancer either by silencing key tumor suppressor genes or by activating oncogenes.
175 instability and aberrant expression of tumor suppressor genes or oncogenes.
176 f-target sites and no modifications in tumor suppressor genes or other genes associated with patholog
177 ere, we have identified a role for the tumor suppressor gene p53 in regulating venous thrombus resolu
178                                        Tumor suppressor gene p53 plays an important role in the maint
179                   NO de-represses the tumour suppressor gene p53 via nitrosylation of Mdm2.
180 C) DNA mutations, including within the tumor-suppressor gene p53, and chronic exposure is associated
181 ythroid 2-related factor 2 (Nrf2), and tumor suppressor gene (p53) when children or adults were expos
182                            Analysis of tumor suppressor gene patterns revealed disease specificity fo
183                       A panel of three tumor suppressor genes (PCDHGB6, HOXA9 and RASSF1A) was assess
184 ough transcriptional repression of the tumor suppressor gene PDZ-LIM domain-containing protein 2 (PDL
185 cated in human melanoma, including the tumor-suppressor genes phosphatase and tensin homolog (PTEN),
186           Structural compromise of the tumor suppressor gene, phosphatase and tensin homolog (PTEN),
187   We therefore propose that the cystatin E/M suppressor gene plays an important role in the regulatio
188        Heritable mutations in the BAP1 tumor suppressor gene predispose individuals to mesothelioma a
189                          In patients, tumour suppressor gene promoters are markedly more methylated i
190 as been shown that hypermethylation of tumor suppressor genes promoters is a common feature of cancer
191            BRCA1-a breast and ovarian cancer suppressor gene-promotes genome integrity.
192 lity of MBD2 to repress the methylated tumor suppressor gene PRSS8 in MDA-MB-435 breast cancer cells.
193 recurrent somatic inactivations of the tumor suppressor gene Ptch1 and a recapitulation of the sonic
194  where deletions and mutations in the tumour suppressor gene PTEN (phosphatase and tensin homolog) ar
195 nslation initiation factor EIF4A1, the tumor suppressor gene PTEN and the long non-coding RNA NEAT1.
196 own that miRNA-based regulation of the tumor suppressor gene PTEN can be modulated by the expression
197  Mice with T-cell-specific loss of the tumor suppressor gene PTEN early in T-cell ontogeny develop th
198                            Loss of the tumor suppressor gene PTEN exerts diverse outcomes on cancer i
199                            Loss of the tumor suppressor gene PTEN is implicated in breast cancer prog
200  miR-181a/b targets the ATRA-regulated tumor suppressor gene RASSF1A by direct binding to its 3'-untr
201                    Inactivation of the tumor suppressor gene RASSF1A by promoter hypermethylation rep
202                                    The tumor suppressor gene RASSF1A is epigenetically silenced in mo
203        Mutations in the retinoblastoma tumor suppressor gene Rb are involved in many forms of human c
204            Although the retinoblastoma tumor-suppressor gene (RB1) is frequently lost together with T
205        Mutations of the retinoblastoma tumor-suppressor gene (RB1) or components regulating the CDK-R
206                                        Tumor suppressor genes regulate cell growth and prevent sponta
207          Mutations disabling the TP53 tumour suppressor gene represent the most frequent events in hu
208  Hypermethylation of the promoters of tumour suppressor genes represses transcription of these genes,
209 ne mutations in the Folliculin (FLCN) tumour suppressor gene result in fibrofolliculomas, lung cysts
210 s are associated with mutations in NF1 tumor suppressor gene, resulting in activation of Ras and its
211 an retinoblastoma are mutations in the tumor-suppressor gene retinoblastoma (RB) and amplification of
212 ks (DSB) in cancer cells that lack the tumor suppressor gene RUNX3 Loss of RUNX3 resulted in transcri
213 for the identification of a novel metastasis suppressor gene, serum deprivation response (SDPR), loca
214 mutations, testing of CTNNA1 and other tumor suppressor genes should be considered.
215 y neurons (MBn) of a newly discovered memory suppressor gene, Solute Carrier DmSLC22A, a member of th
216                      The chromosome 8p tumor suppressor genes SORBS3 and SH2D4A are physically and fu
217         In addition, the chromosome 8p tumor suppressor genes Src homology 2 domain containing 4A (SH
218 tion, differential gene expression and tumor suppressor gene status.
219 deletion of the liver kinase B1 (LKB1) tumor suppressor gene, Stk11 (serine threonine kinase 11), in
220 program several hypoxia associated and tumor suppressor genes such as MAT2A and PDK-1, in addition to
221 ed tumorigenesis through repression of tumor suppressor genes such as Ras suppressor 1 and stromal an
222 arget genes include frequently mutated tumor suppressor genes such as TNFAIP3, SOCS3 and TNFRSF14.
223  ranging from 4% to 35%, even at known tumor suppressor genes such as TWIST2.
224 mutation and loss of heterozygosity of tumor suppressor genes, such as APC and TP53; (3) CpG island m
225 is unclear whether the inactivation of tumor suppressor genes, such as STK11/LKB1, exerts similar eff
226 f proliferation and differentiation by tumor suppressor genes suggests that evolution of divergent tu
227 complex (TSC) is an autosomal dominant tumor-suppressor gene syndrome caused by inactivating mutation
228          Tuberous sclerosis (TSC) is a tumor suppressor gene syndrome that is associated with the wid
229 Among the target genes of miR-10b, the tumor suppressor genes Tbx5 and Pten and the metastasis suppre
230 Cdkn1c promoters and expression of the tumor-suppressor genes Tff2 and Cdkn1c was increased.
231      Mutations at CpG sites on the p53 tumor suppressor gene that can result from these adductions ar
232                    TP53, a well-known tumour suppressor gene that encodes p53, is frequently inactiva
233 s TP53 is the most frequently mutated tumour-suppressor gene that functions in a context-dependent ma
234  our data suggest that SPEN is a novel tumor-suppressor gene that may be clinically useful as a predi
235 sociated protein 1 (BAP1) is a potent tumour suppressor gene that modulates environmental carcinogene
236  novel somatic L1 insertion in the APC tumor suppressor gene that provided us with a unique opportuni
237                Therefore, MIR-491 is a tumor suppressor gene that, by utilizing both mature forms, co
238 growth by perturbing the expression of tumor suppressor genes that control B cell-activating pathways
239 ooperative repressors of a network of tumour suppressor genes that included PDCD4, BTG2, and NEDD4L.
240 vation of oncogenes or inactivation of tumor suppressor genes, these processes become deregulated in
241                                   For tumour suppressor genes this has proven more challenging due to
242 and TGFB1) and increased expression of tumor suppressor genes (TNFRSF14 and HSD17B14).
243 usceptibility gene (RB1) was the first tumor suppressor gene to be molecularly defined.
244 c silencing mechanisms to downregulate tumor suppressor genes to maintain its own expression.
245 ation of this information identified a tumor suppressor gene TOB1 as a critical determinant of estrog
246 ephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53 copy
247                                    The tumor suppressor gene TP53 is mutated exclusively with the HYD
248  along with increases in the levels of tumor suppressor gene TP53, cell cycle inhibitors CDKN1A and C
249 giogenesis, including mutations in the tumor suppressor gene TP53, which occur frequently in many hum
250 ignaling and the negative regulator of tumor suppressor gene TP53-mediated cell cycle arrest and cell
251 le phase II study in patients with p53 tumor suppressor gene ( TP53)-mutated ovarian cancer refractor
252 able to simultaneously inactivate five tumor suppressor genes (TP53, PTEN, APC, BRCA1, and BRCA2) and
253 isruption of the cell cycle checkpoint tumor-suppressor genes Trp53 and Rb1 using Prx1-Cre, Collagen-
254  have found that KANK1 was a candidate tumor suppressor gene (TSG) for human MPNSTs.
255 able to inhibit the CpG methylation of tumor suppressor gene (TSG) promoters and reactivate their exp
256  defined for initiating and supporting tumor suppressor gene (TSG) silencing in human colorectal canc
257 ation-mediated oncogene activation, or tumor suppressor gene (TSG) silencing mechanisms, widely contr
258  interactions among orthologs of human tumor suppressor genes (TSG) and genes encoding drug targets a
259                    Genomic deletion of tumor suppressor genes (TSG) is a rite of passage for virtuall
260 ly mutated, and the identity of key 8p tumor-suppressor genes (TSG) is unknown.
261 ases sensitivity to hotspot regions in tumor suppressor genes (TSG).
262      We elucidated a broad spectrum of tumor suppressor genes (TSGs) and oncogenes (OGs) that can gen
263                                        Tumor suppressor genes (TSGs) are a major type of gatekeeper g
264               NMD-elicit mutations in tumour suppressor genes (TSGs) are associated with significant
265 tic SNVs associated with oncogenes and tumor suppressor genes (TSGs) induce very different changes in
266 rally believed to encode oncogenes and tumor suppressor genes (TSGs) that drive cancer growth.
267  that presumably contain oncogenes and tumor-suppressor genes (TSGs).
268  as kidney cells with mutations in the tumor suppressor genes tuberous sclerosis complex (TSC)1 or TS
269 ficient in the von Hippel-Lindau (VHL) tumor suppressor gene use glutamine to generate citrate and li
270                     Lesions affecting tumour suppressor genes usually occur as single events, whereas
271 s of function of the von Hippel-Lindau tumor suppressor gene (VHL) predisposes renal epithelial cells
272 inactivation of the von Hippel-Lindau tumour suppressor gene (VHL).
273 ons and epigenetic inactivation of the tumor suppressor gene von Hippel-Lindau (VHL) are major causes
274                       Mutations of the tumor suppressor gene von Hippel-Lindau (VHL) can lead to beni
275 erefore, haploinsufficiency of one TSC tumor suppressor gene was required for tumor initiation, but f
276                            The RASSF1A tumor suppressor gene was shown to be often inactivated by hyp
277  changes and biallelic inactivation of tumor suppressor genes was increased in GEP70 high risk, consi
278 LN first identified as a p53-dependent tumor suppressor gene, was believed to bind randomly to DNA an
279 multi-methylated sites, a well-studied tumor suppressor gene, was used as the target DNA sequence mod
280 G1-S phase arrest and act as potential tumor suppressor genes, we aimed to study potential methylatio
281         In the High-M set, a number of tumor-suppressor genes were methylated and repressed.
282 r diploid but carry deletions spanning tumor suppressor genes, whereas P53 inactivation allowed Caph2
283 the expression of methylation-silenced tumor suppressor genes, whereas PKC412 inhibits hyperactive ki
284 ults suggest that VGLL4 is a candidate tumor suppressor gene which acts by selectively antagonizing Y
285                               The MEN1 tumor suppressor gene, which encodes the protein menin, is kno
286 4 could be a potential novel prostate cancer suppressor gene, which may prevent cancer progression an
287 ema 3A in coordination with a chain of tumor-suppressor genes, which in turn inhibits breast cancer c
288 nction mutations of the PBRM1 and BAP1 tumor suppressor genes, which occur in a mutually exclusive ma
289  findings suggest that KMT2D acts as a tumor suppressor gene whose early loss facilitates lymphomagen
290  canonical androgen-regulated putative tumor suppressor gene whose expression is inhibited by androge
291 Cellular stress response 1 (CSR1) is a tumor suppressor gene whose expression was frequently down-reg
292 erefore identify KLF12 as a novel metastasis-suppressor gene whose loss of function is associated wit
293  represent an antilymphangiogenic metastasis suppressor gene widely lost during cancer progression, h
294           CTCF is a haploinsufficient tumour suppressor gene with diverse normal functions in genome
295 A (Methyltransferase Like 7A), a novel tumor suppressor gene with multiple editing sites at its 3'UTR
296 ified miR-192 as an epigenetically regulated suppressor gene with predictive value in this disease.
297 road quantification of the function of tumor-suppressor genes with unprecedented resolution, parallel
298 n of the ST/PE lineage-specific Wilms' tumor suppressor gene (Wt1) in the ST/PE of G2-Gata4(Cre) mice
299  progenitor cells expressing the Wilms tumor suppressor gene, WT1, are induced to differentiate in re
300  tumor progression and a new human CRC tumor-suppressor gene, ZNF292, that might also function in oth

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