ライフサイエンスコーパス: TERT

1 TERT aberrations and ATRX mutations are associated with

2 TERT expression improved the kinetics of double-strand c

3 TERT gene alterations (TERT-alt) have been linked to inc

4 TERT mRNA expression levels were significantly higher in

5 TERT promoter methylation provided an additional deregul

6 TERT promoter mutations (13.1% of R/M cases) were mutual

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

8 TERT promoter mutations alone did not predict adverse ou

9 TERT promoter mutations resulted in an increased prolife

10 TERT promoter mutations were the most prevalent mutation

11 TERT promoter mutations when combined with BRAF/NRAS mut

12 TERT-alt affected prognosis independent of WHO grades.

13 TERT-alt is an important biomarker for significantly hig

14 TERT-alt occurred in 4.7%, 7.9% and 15.4% of WHO-I/WHO-I

15 TERT-alt should be managed and surveilled aggressively.

16 TERT-associated breakpoints involve ~3% of cases, most f

17 TERT-deficient mice displayed marked delays in polyomavi

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

19 h encompasses BCL9, MCL1 and ARNT), 5p15.33 (TERT), 11q13.3 (CCND1), 19q12 (CCNE1) and 8q24.1 (MYC) w

20 iations at three of the 29 UL loci: 5p15.33 (TERT), 5q35.2 (FGFR4) and 11q22.3 (ATM).

21 ng to determine their potential in editing a TERT gene promoter-activating mutation, which occurs in

22 In comparison, little is known about TERT expression at the single-cell and single-molecule l

23 c approach for cancer and validate activated TERT-promoter mutations as a cancer-specific therapeutic

24 lterations occur at median 2.3 years of age, TERT at 3.8 years, and ATRX at 5.6 years.

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

26 currence-free survival was 14 months for all TERT-alt patients versus 101 months for all TERTp-wt pat

27 For all TERT-alt patients versus all TERTp-wt patients, the medi

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 alternative lengthening of telomeres (ALT)], TERT mRNA expression by RNA-sequencing, whole-genome/exo

33 TERT gene alterations (TERT-alt) have been linked to increased risk of recurren

34 Although TERT promoter mutations (TPMs) are a major cancer-associ

35 Although TERT promoter mutations have been associated with a wors

36 Event-free survival was similar among TERT-high, ALT(+), or TERT-low/non-ALT patients.

37 To address this, we analyzed TERT expression across 10 human cancer lines using singl

38 into three subgroups (TERT-high, ALT(+), and TERT-low/non-ALT) based on presence of C-circles and TER

39 most aberrations, including MYCN, ATRX, and TERT alterations, differ in frequency by age.

40 ferentiation of squamous carcinoma cells and TERT-immortalized keratinocytes.

41 /non-ALT) based on presence of C-circles and TERT mRNA expression (above or below median TERT express

42 upregulation of oncogenes such as ERBB2 and TERT.

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

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

45 ions, 1p/19q co-deletion, ATRX mutation, and TERT mutations achieve a test performance AUC of 0.83 +/

46 tion, 1p/19q co-deletion, ATRX mutation, and TERT mutations) prediction methods of low-grade gliomas

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

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

49 omere length and the regulation of RTEL1 and TERT.

50 candidate genes, including IRS4, SMARCA1 and TERT.

51 d a single tumor with both TERT(-124C>T) and TERT(-146C>T) mutations present at different allele freq

52 of BRAF(V600), NRAS(Q61), TERT(-124C>T), and TERT(-146C>T) mutations.

53 ytic core illustrates how domains of TER and TERT, including the TEN-TRAP complex, can interact in a

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

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

56 alterations of ATM in cMCL, whereas TP53 and TERT alterations were slightly enriched in nnMCL.

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

58 ERT promoter, reduced TERT transcription and TERT protein expression, and induced cancer-cell senesce

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

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

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

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

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

64 in which dosage effects predominate (such as TERT), whereas they lead to selection of function in oth

65 tion system whereby the associations between TERT mutations and their downstream molecular manifestat

66 No associations were found between TERT levels in plasma and telomere length in PBMC and th

67 of lines as having monoallelic or biallelic TERT expression was found to be inadequate for capturing

68 telomerase RNA because it is needed to bind TERT to form the core RNP enzyme.

69 seven of these had a single tumor with both TERT(-124C>T) and TERT(-146C>T) mutations present at dif

70 ion and poor prognosis in neuroblastoma, but TERT-associated oncogenic signaling remains unclear.

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

72 as targeting TERT gene expression driven by TERT promoter mutations.

73 Mutations in the catalytic TERT and TR subunits of telomerase compromise activity,

74 telomerase reverse transcriptase component (TERT) down-regulation, immediately after endoderm differ

75 Conclusion: TERT elevation by AR through integrated HBV and point mu

76 86 case subjects with sporadic IPF confirmed TERT, RTEL1, and PARN as study-wide significant contribu

77 However, what defines TERT and separates it from other reverse transcriptases

78 hylation provided an additional deregulatory TERT expression mechanism.

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

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

81 m of TERT upregulation, many cancers exhibit TERT upregulation without TPMs.

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

83 with hTERT and promote the production of FL TERT.

84 TERT transcripts to produce full-length (FL) TERT.

85 genes (range, approximately 90% and 60% for TERT and EGFR mutations, respectively), and such changes

86 The HR for TERT-alt was 2.77 compared with TERTp-wt.

87 The HR for TERT-alt was 3.74 in reference to TERTp-wt.

88 ime, we evaluated 60 melanoma cell lines for TERT promoter mutational status, copy number, gene expre

89 However, overall survival (OS) for TERT-low/non-ALT patients was significantly higher relat

90 essential binding site in telomerase RNA for TERT that is crucial to form the catalytic core of this

91 ncer-frequently activate the telomerase gene TERT.

92 n the telomerase reverse transcriptase gene (TERT) promoter, activate gene expression to drive carcin

93 Gene expression of 2 telomere-related genes (TERT and WRAP53) was significantly upregulated (164% and

94 SE: three telomerase activity-related genes (TERT, WRAP53 and MYC) and an independent telomerase acti

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

96 ad BRAF, NRAS, or NF1 mutations, and 62% had TERT promoter mutations.

97 Thirteen patients had TERT(mutant) discordant tumors; seven of these had a sin

98 e human CLB-GA neuroblastoma cells harboring TERT rearrangement uncovered genome-wide chromatin co-oc

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

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

101 E inhibited the growth of gliomas harbouring TERT-promoter mutations.

102 h as BCL9, MCL1, ARNT (also known as HIF1B), TERT and MYC) within separate subclones, were present in

103 High TERT levels in cancer tissues were independently associa

104 cuss the transcriptional regulation of human TERT, hTR processing, assembly of the telomerase complex

105 es of the TEN and IFD regions, we identified TERT residues that are critical for contacting TPP1 but

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

107 tistical coupling analysis on all identified TERTs and find that TEN and TRAP have coevolved as telom

108 The patterns of gene sets, including IDH1/TERT and IDH1/TP53 exhibited significant difference betw

109 rence rate was 4.8 times higher in WHO-I/-II TERT-alt patients compared with WHO-III TERTp-wt patient

110 was 2.7 times higher in the WHO-I and WHO-II TERT-alt patients compared with WHO-III TERTp-wt patient

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

112 Interestingly, changes in TERT expression were negatively correlated to changes in

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

114 H3K27Ac and robust enrichment of H3K36me3 in TERT and multiple TERT-associated genes.

115 rigenesis in affected tumors, such as HBV in TERT and KMT2B (also known as MLL4) gene loci in liver c

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

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

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

119 eneity, complexity, and unconventionality in TERT expression across human cancer cells.

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

121 ed genes impacted by this phenomenon include TERT, MDM2, CDK4, ERBB2, CD274, PDCD1LG2, and IGF2.

122 Besides, AR also increased TERT expression by targeting TERT promoter mutations in

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

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

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

126 res and decreasing viability occurred in low TERT-expressing, non-ALT patient-derived high-risk neuro

127 e activation, numerous studies have measured TERT mRNA levels in populations of cells or in tissues.

128 TERT mRNA expression (above or below median TERT expression).

129 MGMT, TERT, and EGFRvIII status was individually determined.

130 ocations activated oncogenes (BMI1, MIR17HG, TERT, MYC, and MYCN), generating gene amplifications and

131 atalytic protein subunit TERT into the mouse TERT backbone is sufficient to bias the species specific

132 ppressed the expression of TERT and multiple TERT-associated genes in neuroblastoma with TERT overexp

133 nd chromatin activation of TERT and multiple TERT-associated genes.

134 enrichment of H3K36me3 in TERT and multiple TERT-associated genes.

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

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

137 K) and two important cell lines, HaCaT and N/TERT-1.

138 d the immortalized keratinocyte cell line, N/TERT-1.

139 g HeLa, HEK 293T, K562, and keratinocytes (N/TERTs).

140 recurrent non-coding mutations, most notably TERT promoter mutations, have been reported.

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

142 n the expression and chromatin activation of TERT and multiple TERT-associated genes.

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

144 tly and are associated with amplification of TERT, CDK4, MDM2, CCND1, PAK1 and GAB2, indicating poten

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

146 tive inhibitors suppressed the expression of TERT and multiple TERT-associated genes in neuroblastoma

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

148 of sex hormone pathways on the expression of TERT with both genetic changes were investigated using a

149 of evidence indicates that the expression of TERT, the catalytic subunit of telomerase, is a biologic

150 Furthermore, the failure of TERT promoter mutations to consistently correlate with T

151 Given the importance of TERT in stem cells, we hypothesized that TERT plays an i

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

153 6 were associated with the highest levels of TERT gene expression but had no appreciable impact on ab

154 High levels of TERT transcripts in cancer cells represent a reliable pr

155 major cancer-associated genetic mechanism of TERT upregulation, many cancers exhibit TERT upregulatio

156 a cancer-associated epigenetic mechanism of TERT upregulation.

157 ary fibrosis spontaneously up to 9 months of TERT deficiency.

158 ce and transformation, and overexpression of TERT in mTert (-/-) cells rescued these phenotypes.

159 ncing of 25 genes and Digital Droplet PCR of TERT promoter, including sequential samples throughout t

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

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

162 Moreover, removal or down-regulation of TERT expression in mTert (+/+) and human primary fibrobl

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

164 To evaluate the role of TERT in epithelial cells, we generated type II alveolar

165 igated the predictive and prognostic role of TERT levels and telomere length in tissues and periphera

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

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

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

169 and allocated patients to TERT-alt (n=59) or TERT promoter wild-type (TERTp-wt; n=618).

170 ival was similar among TERT-high, ALT(+), or TERT-low/non-ALT patients.

171 e detected in BRAF (39%), NRAS (21%), and/or TERT (78%).

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

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

174 rmine the presence of BRAF(V600), NRAS(Q61), TERT(-124C>T), and TERT(-146C>T) mutations.

175 Reactivating TERT and hence reconstituting telomerase is an important

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

177 factor family to the TERT promoter, reduced TERT transcription and TERT protein expression, and indu

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

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

180 Unmethylated THOR repressed TERT promoter activity regardless of TPM status, and hyp

181 Deleting DDX11 in RPE1-TERT cells inhibits proliferation and survival in a TP53

182 33, PON1 rs662, REV3L rs462779, SOD2 rs4880, TERT rs2736098, and TP53 rs1042522) showed significant a

183 Moreover, selective TERT deficiency in AECII diminished their proliferation

184 1 copy gains in 15% of patients, and somatic TERT translocations, copy gains, and missense and promot

185 II alveolar epithelial cell (AECII)-specific TERT conditional knockout (SPC-Tert cKO) mice by crossin

186 These findings suggest that AECII-specific TERT deficiency enhances pulmonary fibrosis by heighteni

187 Finally, spliced TERT mRNA had primarily nuclear localization in cancer c

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

189 astoma were classified into three subgroups (TERT-high, ALT(+), and TERT-low/non-ALT) based on presen

190 e human telomerase catalytic protein subunit TERT into the mouse TERT backbone is sufficient to bias

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

192 Correction of the -124C>T TERT promoter mutation to -124C was achieved using a sin

193 ell as emerging approaches such as targeting TERT gene expression driven by TERT promoter mutations.

194 also increased TERT expression by targeting TERT promoter mutations in a GA binding protein transcri

195 ecurrent structural rearrangements targeting TERT, CDK4 and MDM2.

196 d that enhanced expression of both TelGenes (TERT, WRAP53, MYC and ZSCAN4) and Yamanaka factors might

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

203 We found that TERT inserts a mismatch or ribonucleotide ~1 in 10,000 a

204 of TERT in stem cells, we hypothesized that TERT plays an important role in epithelial repair and th

205 d previously in fibroblasts, indicating that TERT's role in pulmonary fibrosis is cell type-specific.

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

207 We propose that TERT-alt analysis should be implemented as a routine dia

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

209 Our results suggest that TERT has a protective role in AECII, unlike its pro-fibr

210 hese data together, this study suggests that TERT has a previously underappreciated, protective role

211 The TERT promoter mutations were found more frequently in ci

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

213 opment (BRAF other than V600E, NRAS, and the TERT promoter) can also be identified.

214 and noncoding drivers, such as TP53 and the TERT promoter.

215 ugh integrated HBV and point mutation at the TERT promoter region was identified as a mechanism for t

216 Integrations at the TERT promoter were associated with high telomerase expre

217 was found to be inadequate for capturing the TERT gene expression patterns.

218 In this study, we describe the TERT hypermethylated oncological region (THOR), a 433-bp

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

220 ration sites and the common mutations in the TERT promoter and tumor protein P53 (TP53) coding region

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

222 The discovery of prevalent mutations in the TERT promoter region in many cancers and recent advances

223 HBV integration and -124G>A mutation in the TERT promoter region, occurring in a mutually exclusive

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

225 HBV integration in the TERT promoter rendered the TERT transcription responsive

226 olving KLF TFs to different mutations in the TERT promoter, and gain of a MYB interaction with an 18-

227 urvival-promoting mutations, commonly in the TERT promoter, to form a detectable tumor.

228 a with TERT overexpression by inhibiting the TERT-associated gene expression networks.

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

230 pG sites located immediately upstream of the TERT core promoter, as a cancer-associated epigenetic me

231 Promoter rearrangement of the TERT gene juxtaposes the coding sequence to strong enhan

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

233 h to provide a comprehensive analysis of the TERT/telomere pathway and establish a classification sys

234 ntegration in the TERT promoter rendered the TERT transcription responsive to sex hormones, with enha

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

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

237 rified melanoma cell lines, suggest that the TERT promoter harbors a more complex mutational landscap

238 f the E26 transcription factor family to the TERT promoter, reduced TERT transcription and TERT prote

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

240 They achieve this through TERT activation or alternative telomere lengthening asso

241 TERT, we find that the 4-bp CEH RNA binds to TERT but the shorter-CEH constructs do not, consistent w

242 ence to strong enhancer elements, leading to TERT overexpression and poor prognosis in neuroblastoma,

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

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

245 from eight studies and allocated patients to TERT-alt (n=59) or TERT promoter wild-type (TERTp-wt; n=

246 atients was significantly higher relative to TERT-high or ALT patients (log-rank test; P < 0.01) inde

247 to assess binding of our CEH mutant RNAs to TERT, we find that the 4-bp CEH RNA binds to TERT but th

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

249 genes were telomerase reverse transcriptase (TERT) (58.1%), catenin beta 1 (CTNNB1) (30.7%), tumor pr

250 ic core of telomerase reverse transcriptase (TERT) and telomerase RNA (TER).

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

252 s encoding telomerase reverse transcriptase (TERT) and telomerase's RNA components as well as shorten

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

254 cludes the telomerase reverse transcriptase (TERT) and the non-coding human telomerase RNA (hTR), whi

255 tomas with telomerase reverse transcriptase (TERT) gene overexpression and coordinated activation of

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

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

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

259 tions into telomerase reverse transcriptase (TERT) immortalized oral keratinocytes (NOKs) that are ca

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

261 Because telomerase reverse transcriptase (TERT) is usually the limiting component for telomerase a

262 castaneum telomerase reverse transcriptase (TERT) throughout its catalytic cycle and mapped the acti

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

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

265 uch as the telomerase reverse transcriptase (TERT), but through differential effects on telomere leng

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

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

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

269 ulation of telomerase reverse transcriptase (TERT).

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

271 ulation of telomerase reverse-transcriptase (TERT) expression was detected in mTert (+/+) cells at th

272 scriptase (telomerase reverse transcriptase [TERT]).

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

274 nd TRAP are absent in the putative Tribolium TERT that has been used as a model for telomerase for ov

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

276 he structure of a previously uncharacterized TERT domain (TRAP) with unanticipated interactions with

277 ially different OS: a previously undescribed TERT-low/non-ALT cohort with superior OS (even after rel

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

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

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

281 uent mutations in ctDNA of advanced HCC were TERT promoter (51%), TP53 (32%), CTNNB1 (17%), PTEN (8%)

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

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

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

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

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

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

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

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

290 ter mutations to consistently correlate with TERT expression and telomere length suggests an alternat

291 s suggest that this binding interaction with TERT is dictated more by secondary than by primary struc

292 assess telomere maintenance mechanisms with TERT mRNA and the ALT DNA biomarker C-circles to stratif

293 ibe a unique mechanism in neuroblastoma with TERT overexpression and an epigenetically targeted novel

294 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated ge

295 TERT-associated genes in neuroblastoma with TERT overexpression or MYCN amplification.

296 with the observed higher OS in patients with TERT-low/non-ALT tumors, continuous shortening of telome

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

298 findings demonstrate that assaying TMM with TERT mRNA expression and C-circles provides precise stra

299 (ATRX/DAXX(trunc)) is increased, tumors with TERT modifications show a moderate decrease of telomere

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