ライフサイエンスコーパス: TERT

1 TERT co-localizes detectably with only 5-7 % of the telo

2 TERT expression improved the kinetics of double-strand c

3 TERT expression promotes oncogene-transformed cell growt

4 TERT has previously been found in rodent neurons, and we

5 TERT mRNA expression levels were significantly higher in

6 TERT overexpression was required for cellular interactio

7 TERT promoter can also be affected by copy number variat

8 TERT promoter methylation provided an additional deregul

9 TERT promoter mutations (TPMs) are the most common nonco

10 TERT promoter mutations alone did not predict adverse ou

11 TERT promoter mutations resulted in an increased prolife

12 TERT promoter mutations when combined with BRAF/NRAS mut

13 TERT protein colocalized with mitochondria in the hippoc

14 TERT rearrangements (23%), ATRX deletions (11%) and MYCN

15 TERT stabilized MYC levels on chromatin, contributing to

16 TERT-based adoptive immunotherapy selectively eliminated

17 TERT-deficient mice displayed marked delays in polyomavi

18 TERT-p mutations may identify the rare subset of spitzoi

19 TERT-specific cytotoxic T lymphocytes (CTL) have been de

20 red genes were TP53 (47.0%), CDKN2A (18.0%), TERT (17.0%), and KRAS (16.0%), and the majority of pati

21 In an extended case series (n = 217), TERT rearrangements defined a subgroup of high-risk tumo

22 ns at 9q34.2 (ABO), 13q22.1 (KLF5), 5p15.33 (TERT and CLPTM1), 13q12.2 (PDX1), 1q32.1 (NR5A2), 7q32.3

23 Four loci, 5p15.33 (TERT), 6p21.3 (BTNL2), 3q28 (TP63) and 17q24.2 (BPTF), p

24 riations (SNVs), with each case containing a TERT promoter (TERT-p) mutation, 13/15 containing an act

25 Dimerization was suppressed by removing a TERT domain linker with atypical sequence bias, which di

26 The most frequent mutations affect TERT promoter (60%), associated with an increased telome

27 genes, including BRAF, NRAS, NF1, EGFR, ALK, TERT, and APC.

28 er of the genetic duet>>>>BRAF V600E alone = TERT promoter mutation alone > wild-type for both genes,

29 er of the genetic duet>>>>BRAF V600E alone = TERT promoter mutation alone > wild-type for both genes,

30 arboring neither mutation, BRAF V600E alone, TERT mutation alone, or both mutations were 0.80 (95% CI

31 arboring neither mutation, BRAF V600E alone, TERT mutation alone, or both mutations were 0.80 (95% CI

32 TERC(-/-) mice at generation 2 and TERT(-/-) mice at generations 2, 3, and 4 developed less

33 upregulation of oncogenes such as ERBB2 and TERT.

34 Hence, combined targeting of RAS-ERK and TERT promoter remodeling is a promising avenue to limit

35 g of tumor-promoting genes, such as IGF2 and TERT, results from a defective TGF-beta pathway and is r

36 , IL6ST, CTNNB1, FRK, STAT3, GNAS, JAK1, and TERT) in 607 samples of 533 HCAs from 411 patients, coll

37 significant increases in telomere length and TERT were observed in the silica group at 4 and 32 wk.

38 ma risk, including in or near MC1R, MX2, and TERT/CLPTM1L (P < 1 x 10(-10)).

39 the chromosome-number changes persisted, and TERT-positive ALT cells surviving genotoxic events propa

40 C/EBPalpha, p53, FXR, SIRT1, PGC1alpha, and TERT by C/EBPbeta-HDAC1 complexes.

41 genesis, including CLK1, CASP3, PPFIBP1, and TERT, validate as alternatively spliced by EWS-FLI1.

42 Telomere length, RTEL1 and TERT expression may serve as potential biomarkers relate

43 omere length and the regulation of RTEL1 and TERT.

44 candidate genes, including IRS4, SMARCA1 and TERT.

45 Variants in TERC and TERT can impede telomere elongation causing stem cells t

46 hrough KLF8 upregulation, increased TERC and TERT expression, or altered splicing of DVL2 transcript,

47 lomere length differed between TERC(-/-) and TERT(-/-) mice, whereas PH severity was similar in the 2

48 ells with recombinant expression of TERT and TERT variants: TERT-positive ALT cells showed higher tol

49 two decades, structures of domains of TR and TERT as well as other telomerase- and telomere-interacti

50 BRAF V600E and TERT promoter mutation patterns and associated patient d

51 Main Outcomes and Measures: BRAF V600E and TERT promoter mutation patterns and associated patient d

52 al correlation study examined BRAF V600E and TERT promoter mutations (chr5:1,295,228C>T and chr5:1,29

53 al correlation study examined BRAF V600E and TERT promoter mutations (chr5:1,295,228C>T and chr5:1,29

54 Importance: BRAF V600E and TERT promoter mutations can coexist in papillary thyroid

55 BRAF V600E and TERT promoter mutations can coexist in papillary thyroid

56 growth and survival of NSCLC cells, such as TERT and CDK4.

57 ter; reverting a recurrent cancer-associated TERT promoter mutation in a urothelial cancer cell line

58 ons of genetic alternations in IDH1/2, ATRX, TERT, TP53, and co-deletion of 1p/19q have the ability t

59 Because TERT promoter (TERT-p) mutations are common in inherentl

60 h previous studies found no relation between TERT promoter mutations and UC patient outcome, we find

61 onstitutions yielded heterogeneous DNA-bound TERT monomer and dimer complexes in relative amounts tha

62 in unpaired, potentially providing access by TERT to this high affinity binding site during an early

63 86 case subjects with sporadic IPF confirmed TERT, RTEL1, and PARN as study-wide significant contribu

64 5HTT(+) mice while simultaneously decreasing TERT expression.

65 We identified telomere synthesis-defective TERT variants that bestowed similar genotoxic stress tol

66 hylation provided an additional deregulatory TERT expression mechanism.

67 to TERT, which allows us to reliably detect TERT in western blots, immunopurify it for biochemical a

68 n, a 12 kb PTEN deletion, and a dinucleotide TERT promoter substitution.

69 mmortality, but the molecular events driving TERT activation are largely unknown.

70 Here, we found that ectopic TERT expression increases cell proliferation, while acut

71 nd UC patient outcome, we find that elevated TERT mRNA expression strongly correlates with reduced di

72 ZNF148 in a manner consistent with elevated TERT in carriers of the C allele.

73 in several cancers, associated with elevated TERT mRNA levels.

74 port that delivery of modified mRNA encoding TERT to human fibroblasts and myoblasts increases telome

75 nic stem cell lines revealed that endogenous TERT, driven by mutant promoters or oncogenes, directly

76 duce precise modifications at the endogenous TERT locus in human cell lines.

77 f pathological tau did not appear to express TERT protein.

78 he remaining 22% of tumors neither expressed TERT nor harbored alterations in ATRX or DAXX.

79 Intriguingly, hippocampal neurons expressing TERT did not contain hyperphosphorylated tau.

80 and minimal recombinant enzyme monomeric for TERT had catalytic activity.

81 ered to carry any of the three most frequent TERT promoter mutations showed only a modest increase in

82 ion of EWS-FLI1 produces an isoform of gamma-TERT that has increased telomerase activity compared wit

83 f the telomerase reverse transcriptase gene (TERT).

84 Here, we demonstrated that first-generation TERT-null mice, unlike Terc-null mice, show delayed onse

85 Mutations in the essential telomerase genes TERT and TR cause familial pulmonary fibrosis; however,

86 pancreatic ductal epithelial (HPDE) cells, h-TERT transformed HPDE cells (HPNE), and four gain-of-fun

87 s, less than 1% were triple-positive, 2% had TERT and IDH mutations, 7% had only IDH mutations, 17% w

88 rations (i.e., were triple-positive), 5% had TERT and IDH mutations, 45% had only IDH mutations, 7% w

89 diate lesions and melanomas in situ harbored TERT promoter mutations, a finding that indicates that t

90 ere significantly higher in tumors harboring TERT promoter mutation and/or hypermethylation than thos

91 primary atypical meningiomas do not harbour TERT promoter mutations, which have been reported in aty

92 t H/ACA RNP assembly enhances endogenous hTR-TERT interaction.

93 l receptor (TCR) with high avidity for human TERT from vaccinated HLA-A*0201 transgenic mice.

94 lizing a high-avidity TCR specific for human TERT.

95 ording to tumor stage progression identified TERT promoter mutation as an early event, whereas FGF3,

96 We identified TERT, RTEL1, and PARN-three telomere-related genes previ

97 leterious, nonsynonymous variants implicated TERT and RTEL1, and a model specifically qualifying loss

98 B sites, we found no corresponding change in TERT levels at these sites, implying that SSB1-TERT inte

99 red tRNA levels and proliferation defects in TERT-depleted cells.

100 r mutations showed only a modest increase in TERT transcription with no impact on telomerase activity

101 COPD cases carried deleterious mutations in TERT (1%).

102 herited loss-of-function coding mutations in TERT or poly(A)-specific ribonuclease (PARN), another ge

103 ell proliferation, while acute reductions in TERT levels lead to a dramatic loss of proliferation wit

104 GF-beta-defective mice and BWS, resulting in TERT overexpression.

105 ffinity binding site during an early step in TERT-TER assembly.

106 )) case enrichment of qualifying variants in TERT, RTEL1, and PARN.

107 nt molecular mechanisms leading to increased TERT expression may guide development of prognostic assa

108 Corroborating this hypothesis were increased TERT expression, decreased telomere length, and activati

109 earrangements were associated with increased TERT expression and targeted regions immediately up- and

110 ferative phenotype associated with increased TERT expression, which was suppressed by imetelstat trea

111 plained by rs36115365, a variant influencing TERT expression via ZNF148 in a manner consistent with e

112 Our analysis integrates TERT abnormalities, telomerase activity and genomic alte

113 GABP thus directly links TERT promoter mutations to aberrant expression in multip

114 Here, we investigated lung TERT in human and experimental pulmonary hypertension (P

115 Marked TERT expression or activity was found in lungs from pati

116 higher levels of TERT messenger RNA (mRNA), TERT protein, telomerase enzymatic activity, and telomer

117 d recruitment of RNA polymerase II at mutant TERT promoters.

118 Genes of cells that express mutant TERT and NLRP3 proteins are presumed to be at increased

119 ed in multiple cancer cell lines that mutant TERT promoters exhibit the H3K4me2/3 mark of active chro

120 Our study provides evidence that the mutant TERT promoter is a key substrate downstream of the RAS-E

121 expression of STAT3, IL-10, ELL2, XBP1, MYC, TERT, and ADA.

122 chromosome 5p telomere loop to a region near TERT in human cells with long telomeres that is disengag

123 -identified CRC polymorphism, rs2736100 near TERT, was associated with EC risk (odds ratio (OR) = 1.0

124 ained an activating NRAS Q61 mutation and no TERT-p mutations.

125 g data analysis determined that ATRX but not TERT promoter mutations are associated with increased te

126 raak Stages I-VI) in situ and the ability of TERT to protect against oxidative damage in an in vitro

127 ur in vitro data suggest that the absence of TERT increases ROS generation and oxidative damage in ne

128 context of full-length TER in the absence of TERT, due to formation of a competing structure that seq

129 d kinase signaling in 40%, and an absence of TERT-p mutations, except for the one SM that succumbed t

130 t that genetic and epigenetic alterations of TERT are associated with TERT upregulation and may predi

131 Application of TERT-p mutational assays for risk stratification in the

132 melanoma, we investigated the association of TERT promoter mutations, as well as promoter methylation

133 ilable follow-up data for the association of TERT-p mutations, biallelic CDKN2A deletion, biallelic P

134 ed regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoi

135 omere length, suggesting that the effects of TERT could be telomere independent.

136 status correlates with altered expression of TERT and genes near to TERT, indicating a change in chro

137 of ALT cells with recombinant expression of TERT and TERT variants: TERT-positive ALT cells showed h

138 Here, we investigated the expression of TERT at different stages of Alzheimer's disease patholog

139 These data support the feasibility of TERT-based adoptive immunotherapy in clinical oncology,

140 The low expression level of TERT and the lack of adequate antibodies have made it di

141 In addition, CIRP regulates the level of TERT mRNAs.

142 Finally, we determined that levels of TERT and tRNA correlated in breast and liver cancer samp

143 er mutations correlate with higher levels of TERT messenger RNA (mRNA), TERT protein, telomerase enzy

144 rse outcomes (P = 0.50), but the presence of TERT promoter methylation, alone or concurrent with prom

145 Presence of TERT-p mutations was the most significant predictor of h

146 Prevalence of TERT reactivation over the ALT mechanism was linked to s

147 There were high rates of TERT promoter mutation in recurrent and metastatic HPV-n

148 However, while reactivation of TERT has been functionally linked to the acquisition of

149 these data, we conclude that reactivation of TERT, a direct transcriptional MYC target in tumors, pro

150 It is known that the reactivation of TERT, the catalytic subunit of telomerase, is limiting f

151 encing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five ca

152 rminal (TEN) domain is a conserved region of TERT proposed to mediate DNA substrate interactions.

153 facilitates TGF-beta-mediated repression of TERT transcription via interactions with beta2SP and SMA

154 se findings provide insight into the role of TERT in ALM tumorigenesis and reveal preliminary evidenc

155 Supporting a functional role of TERT, neuroblastoma cell lines bearing rearrangements or

156 ntext abrogates transcriptional silencing of TERT in high-risk neuroblastoma and places telomerase ac

157 es in tumor cells has elevated the status of TERT as a potential universal target for selective and b

158 uced massive transcriptional upregulation of TERT.

159 sa revealed a transcribed region upstream of TERT in the opposite orientation, suggesting the TERT pr

160 To determine the prognostic value of TERT alterations in AYA melanoma, we investigated the as

161 L-8, and CXCL5 from THP-1 monocytes and OKF6/TERT-2 cells than LPS alone.

162 CXCL5 expression by THP-1 monocytes and OKF6/TERT-2 cells.

163 In vitro stimulation of OKF6/TERT-2 cells and THP-1 monocytes was performed with comb

164 ing mutations that likely activate oncogenes TERT and PIK3CA, and alter chromatin-associated proteins

165 , 17% were triple-negative, and 74% had only TERT mutations.

166 s, 7% were triple-negative, and 10% had only TERT mutations; 5% had other combinations.

167 rs) among patients who had gliomas with only TERT mutations.

168 onstrate that PML depletion in U2OS cells or TERT-immortalized normal human diploid fibroblasts resul

169 Ectopic expression of either RPC32 or TERT restored tRNA levels and proliferation defects in T

170 atus of newly identified variants in TERC or TERT can be quite challenging.

171 , with each case containing a TERT promoter (TERT-p) mutation, 13/15 containing an activating BRAF V6

172 Because TERT promoter (TERT-p) mutations are common in inherently aggressive cu

173 direct interaction of the telomerase protein TERT with the telomeric protein TPP1.

174 The telomerase reverse transcriptase protein TERT has recently been demonstrated to have a variety of

175 a specialized reverse transcriptase protein (TERT) for activity in vitro.

176 Reactivating TERT and hence reconstituting telomerase is an important

177 lioblastomas (GBMs), harbor highly recurrent TERT promoter mutations of unknown function but specific

178 Knockdown of ZNF148 results in reduced TERT expression, telomerase activity and telomere length

179 Deletion of SSB1 reduces TERT interaction with telomeres and leads to G-overhang

180 n a known lung cancer susceptibility region (TERT-CLPTM1L) P = 6.6 x 10(-6)).

181 the dual roles that CIRP plays in regulating TERT and TERC, and reveal a new class of telomerase modu

182 y, the mouse genomic context did not repress TERT transcription until late during differentiation.

183 lencing of this regulatory element repressed TERT expression in an allele-specific manner.

184 Two additional SNPs, rs2736100 (TERT) and rs9376092 (HBS1L/MYB), achieve genome-wide sig

185 33, PON1 rs662, REV3L rs462779, SOD2 rs4880, TERT rs2736098, and TP53 rs1042522) showed significant a

186 er the ALT mechanism was linked to secondary TERT function unrelated to telomere length maintenance.

187 The identification of several TERT epitopes in tumor cells has elevated the status of

188 th TERT promoter mutations failed to silence TERT expression, resulting in increased telomerase activ

189 In cultured mouse PA-SMCs, TERT was expressed on growth stimulation by serum.

190 1 copy gains in 15% of patients, and somatic TERT translocations, copy gains, and missense and promot

191 We sorted TERT-positive cells with cytogenetic changes and followe

192 RT levels at these sites, implying that SSB1-TERT interaction relies upon a specific chromatin struct

193 To study TERT regulation, we generated mouse embryonic stem cell

194 tion in cytological abnormalities, surviving TERT-positive ALT cells were found to have gross chromos

195 In different cellular systems, TERT protein has been shown to be protective through its

196 (OR) = 2.38), followed by DEF6, IL12B, TCF7, TERT, CD226, PCNXL3, RASGRP1, SYNGR1 and SIGLEC6.

197 Telomerase (TERT) is overexpressed in 80% to 90% of primary tumors a

198 At the lower temperature, TERT mRNA is upregulated in a CIRP-dependent manner to c

199 , the telomerase holoenzyme consists of TER, TERT, and eight additional proteins, including the telom

200 elomerase holoenzyme catalytic core (p65-TER-TERT) was recently modeled in our 9 A resolution cryo-el

201 rders (GATA2, RUNX1), telomeropathies (TERC, TERT, RTEL1), ribosome disorders (SBDS, DNAJC21, RPL5),

202 a better marker of aggressive UC tumors than TERT promoter mutations alone.

203 We conclude that TERT-p mutations identify a clinically high-risk subset

204 We further determined that TERT is a regulator of MYC stability in cancer.

205 These data establish that TERT promoter mutations can promote immortalization and

206 genesis and reveal preliminary evidence that TERT inhibition represents a potential therapeutic strat

207 We observed that TERT determines the growth rate of cancer cells by direc

208 Our data reveal that TERT is expressed in vitro in mouse neurons and microgli

209 We have previously shown that TERT expression is upregulated in tumors with integratio

210 Together, our findings suggest that TERT protein persists in neurons of the adult human brai

211 The TERT inhibitor imetelstat and the TERT activator TA65 ab

212 The TERT mutations compromised telomerase catalytic activity

213 The TERT promoter mutations were found more frequently in ci

214 Mutations affecting the TERT promoter were the most frequent of all; however, ne

215 The TERT inhibitor imetelstat and the TERT activator TA65 abrogated and stimulated PA-SMC grow

216 he low CRISPR-Cas9 editing efficiency at the TERT locus, we develop a two-step "pop-in/pop-out" strat

217 e-molecule imaging, applied to determine the TERT content of complexes assembled in cells or cell ext

218 uman and mouse genomic DNAs encompassing the TERT genes and neighboring loci.

219 genome-wide significant associations in the TERT gene (rs7705526: OR = 1.8, P = 1.1 x 10(-32)), in S

220 regulatory sites include known sites in the TERT promoter and many new sites, including a subset in

221 he data suggest that ALV integrations in the TERT promoter region drive the overexpression of a novel

222 regulated in tumors with integrations in the TERT promoter region.

223 e use of three alterations: mutations in the TERT promoter, mutations in IDH, and codeletion of chrom

224 noncoding drivers, such as mutations in the TERT promoter.

225 erform single base-pair modifications in the TERT promoter; reverting a recurrent cancer-associated T

226 This study reveals the paths of TER in the TERT-TER-p65 catalytic core and single-stranded DNA exit

227 The 5p15.33 rearrangements juxtapose the TERT coding sequence to strong enhancer elements, result

228 of a variant on 5p15.33 (rs2736100 near the TERT gene) and present a stronger association result for

229 V integrations driving overexpression of the TERT antisense RNA suggest it may have a role in tumorig

230 exit; extensive subunit interactions of the TERT essential N-terminal domain, p50, and TEB; and othe

231 Analyses of the TERT locus have indicated that non-coding regulatory mut

232 6 and 3,552 nucleotides (nt) upstream of the TERT transcription start site, predominantly in the oppo

233 in the opposite orientation, suggesting the TERT promoter is bidirectional.

234 requently in cis with the WT allele than the TERT coding sequence mutation.

235 While the TERT protein is well-conserved across taxa, TR is highly

236 SSB1 interacts with the TERT catalytic subunit and regulates its interaction wit

237 nce to genotoxic insults compared with their TERT-negative counterparts.

238 ammary epithelial cells immortalized through TERT expression and human carcinoma HEp-2 cells were inf

239 Thus, TERT promoter mutations are sufficient to overcome the p

240 ion, an epigenetic alteration also linked to TERT upregulation, with TERT mRNA expression and outcome

241 altered expression of TERT and genes near to TERT, indicating a change in chromatin.

242 the opposite transcriptional orientation to TERT Transcriptome-sequencing (RNA-seq) analysis of norm

243 ique, we fuse an N-terminal FLAG-SNAP-tag to TERT, which allows us to reliably detect TERT in western

244 ing a higher frequency of mutations in TP53, TERT promoter, PI3K/AKT/mTOR pathway effectors, SWI/SNF

245 ovided a framework for understanding how TR, TERT, and other proteins from ciliate as well as vertebr

246 ds and consists of the reverse transcriptase TERT and the RNA subunit TERC.

247 ve site in telomerase reverse transcriptase (TERT) and an integral RNA subunit template.

248 catalytic telomerase reverse transcriptase (TERT) and telomerase RNA (TR) that provides the template

249 g a unique telomerase reverse transcriptase (TERT) and template in the telomerase RNA (TR), thereby h

250 d genes including the reverse transcriptase (TERT) and the RNA component (TERC) of the telomerase com

251 e gene for telomerase reverse transcriptase (TERT) are the most common noncoding mutations in cancer.

252 ivation of telomerase reverse transcriptase (TERT) expression enables cells to overcome replicative s

253 ivation of telomerase reverse transcriptase (TERT) expression is found in more than 85% of human canc

254 d that the telomerase reverse transcriptase (TERT) gene promoter is a common ALV integration target.

255 ons in the telomerase reverse transcriptase (TERT) gene promoter occur at high frequency in multiple

256 n 3 of the telomerase reverse transcriptase (TERT) gene that predisposes to CH (rs34002450; P = 7.4 x

257 ulation of telomerase reverse transcriptase (TERT) genes contribute to distinct aging and tumorigenic

258 tations in telomerase reverse transcriptase (TERT) in blood leukocytes of approximately 5% of individ

259 nts in the telomerase reverse transcriptase (TERT) promoter and isocitrate dehydrogenase 1 (IDH1).

260 the human telomerase reverse transcriptase (TERT) promoter are the most frequent non-coding mutation

261 units: the telomerase reverse transcriptase (TERT) protein and an associated telomerase RNA (TER).

262 ivation of telomerase reverse transcriptase (TERT) reconstitutes telomerase activity in the majority

263 confirmed in telomere reverse transcriptase (TERT) upstream regions in several cancers, associated wi

264 ic subunit telomerase reverse transcriptase (TERT) uses the RNA subunit (TER) as a template.

265 s IGF2 and telomerase reverse transcriptase (TERT) were overexpressed in fibroblasts from BWS patient

266 omoter for telomerase reverse transcriptase (TERT), along with BRAF alterations, has recently been no

267 elomerase, telomerase reverse transcriptase (TERT), alters sensitivity to HSV-dependent apoptosis.

268 RTEL1) and telomerase reverse transcriptase (TERT), genes involved in telomere regulation and functio

269 sites for telomerase reverse transcriptase (TERT), minimized hTR assembled biologically active enzym

270 n level of telomerase reverse transcriptase (TERT), the catalytic subunit of the ribonucleoprotein co

271 ay express telomerase reverse transcriptase (TERT), the dual function of which consists of maintainin

272 expressed telomerase reverse transcriptase (TERT), which was associated with TERT point mutations, r

273 (TER) and telomerase reverse transcriptase (TERT).

274 (TER) and telomerase reverse transcriptase (TERT).

275 ulates the telomerase reverse transcriptase (TERT)/Wnt/beta-catenin cascade, leading to improvement o

276 PARP1 also transformed TERT-immortalized melanocytes expressing BRAF(V600E).

277 In the remaining high-risk tumours, TERT expression was also elevated in MYCN-amplified tumo

278 tic activity requires cooperation across two TERT subunits remains under debate.

279 ESC lines with chimeric BACs, in which two TERT promoters were swapped, were also generated.

280 , highlighting a shared mechanism underlying TERT reactivation.

281 cent of cases, characterized by undetectable TERT expression and alterations in ATRX or DAXX, demonst

282 or amplified MYCN exhibited both upregulated TERT expression and enzymatic telomerase activity.

283 ated bone regeneration, and also upregulates TERT/FASL signaling, leading to improvement of SHED-medi

284 binant expression of TERT and TERT variants: TERT-positive ALT cells showed higher tolerance to genot

285 We further show that in vitro TERT inhibition has cytotoxic effects on primary ALM cel

286 e existence of a unifying mechanism by which TERT enhances translation in cells to regulate cancer ce

287 While TERT promoter mutations were rare and subclonal in PTCs,

288 Genome-wide TERT binding across 5 cancer cell lines and 2 embryonic

289 ) with BRAF V600E alone; 4 of 64 (6.3%) with TERT promoter mutation alone; and 15 of 66 (22.7%) with

290 ) with BRAF V600E alone; 4 of 64 (6.3%) with TERT promoter mutation alone; and 15 of 66 (22.7%) with

291 for BRAF V600E alone; 8.18 (2.04-32.75) with TERT mutation alone; and 37.77 (12.50-114.09) with both

292 TR assembles with TERT and species-specific proteins, and telomerase funct

293 nscriptase (TERT), which was associated with TERT point mutations, rearrangements, DNA amplifications

294 etic alterations of TERT are associated with TERT upregulation and may predict clinical outcomes in A

295 hich normally silence telomerase, cells with TERT promoter mutations failed to silence TERT expressio

296 cell lines (LCLs) derived from subjects with TERT promoter mutations showed increased telomerase expr

297 core domains that can assemble in trans with TERT and reconstitute active telomerase enzyme in vitro

298 ation also linked to TERT upregulation, with TERT mRNA expression and outcome using a well-characteri

299 omeres was present in neuroblastomas without TERT or MYCN alterations, suggesting that telomere lengt

300 merase activity compared with wild-type (WT) TERT.