Relevant bibliographies by topics / HTERC

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'HTERC'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "HTERC"

1

Xin, Zhong-Tao, Adam D. Beauchamp, Rodrigo T. Calado, Jennifer W. Bradford, Joshua A. Regal, Aarthi Shenoy, Yuying Liang, Peter M. Lansdorp, Neal S. Young, and Hinh Ly. "Functional characterization of natural telomerase mutations found in patients with hematologic disorders." Blood 109, no. 2 (September 21, 2006): 524–32. http://dx.doi.org/10.1182/blood-2006-07-035089.

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Abstract Human telomerase hTERC RNA serves as a template for the catalytic hTERT protein to synthesize telomere repeats at chromosome ends. We have recently shown that some patients with bone marrow failure syndromes are heterozygous carriers for hTERC or hTERT mutations. These sequence variations usually lead to a compromised telomerase function by haploinsufficiency. Here, we provide functional characterization of an additional 8 distinct hTERT sequence variants and 5 hTERC variants that have recently been identified in patients with dyskeratosis congenita (DC) or aplastic anemia (AA). Among the mutations, 2 are novel telomerase variants that were identified in our cohort of patients. Whereas most of the sequence variants modulate telomerase function by haploinsufficiency, 2 hTERC variants with sequence changes located within the template region appear to act in a dominant-negative fashion. Inherited telomerase gene mutations, therefore, operate by various mechanisms to shorten telomere lengths, leading to limited marrow stem cell reserve and renewal capacity in patients with hematologic disorders.
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2

Yang, Jing-Hua, Ming-Zhe Wu, Xu-Bo Wang, Shiyu Wang, Xue-Shan Qiu, En-Hua Wang, and Guang-Ping Wu. "HPV16 E6/E7 upregulate hTERC mRNA and gene amplification levels by relieving the effect of LKB1 on Sp1 phosphorylation in lung cancer cells." Therapeutic Advances in Medical Oncology 12 (January 2020): 175883592091756. http://dx.doi.org/10.1177/1758835920917562.

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Background: There is an immediate need for research on the mechanism underlying telomerase activation and overexpression. Materials & Methods: A total of 174 patients with lung cancer ( n = 106) and benign lung disease ( n = 68) were recruited for the current study. The mRNA expression levels of E6, E7, LKB1, Sp1, and hTERC in brushing cells were detected by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), and hTERC amplification was also detected by fluorescence in situ hybridization (FISH). To investigate the potential mechanism, bidirectional genetic manipulation was performed in well-established lung cancer cell lines. Results: Our results indicated that the mRNA expression levels of E6, E7, Sp1, and hTERC and the amplification level of hTERC were significantly increased in the malignant group compared with those of the benign group ( p < 0.01). Conversely, the mRNA expression level of LKB1 was significantly decreased in the malignant group ( p < 0.01). The correlation between E6, E7, Sp1, and hTERC expression was positive but was negative with LKB1 ( p < 0.01). Our results also showed that HPV16 E6/E7 downregulated the expression of LKB1 at both the protein and mRNA levels. The loss of LKB1 upregulated Sp1 expression, and also promoted Sp1 activity. Sp1 further upregulated hTERC at the mRNA and gene amplification levels. Thus, we proposed a HPV–LKB1–Sp1–hTERC axis of E6/E7 upregulation of hTERC expression. Conclusion: We demonstrated for the first time that E6 and E7 promoted hTERC mRNA expression and the amplification of hTERC by relieving the effect of LKB1 on the phosphorylation of Sp1. Sp1 further activated hTERC by directly binding to the promoter regions of hTERC.
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Garrels, W., W. Kues, U. Baulain, and H. Niemann. "161 MODULATION OF TELOMERASE ACTIVITY IN BOVINE EMBRYOS USING CYTOPLASMATIC PLASMID INJECTION." Reproduction, Fertility and Development 22, no. 1 (2010): 239. http://dx.doi.org/10.1071/rdv22n1ab161.

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Telomeres are repetitive, noncoding sequences at the ends of linear chromosomes that shorten with each cell division. They play an important role in aging and affect the regenerative capacity of cells. The holoenzyme telomerase rebuilds telomeres and is composed of 2 components, i.e. the catalytic protein component telomerase reverse transcriptase (TERT) and the telomerase RNA component (TERC). In mammals, telomerase is active during embryogenesis, in germ cells and a subset of stem and progenitor cells. In the present study, we set out to express the TERC component alone and then in combination with TERT, the human telomerase complex, in bovine embryos. The human telomerase components are highly homologous to bovine telomerase genes. Here, 3 different expression constructs encoding hTERC, hTERT, and a green fluorescent protein (GFP) reporter were co-injected into bovine zygotes cytoplasm, and three groups of 528, 1865, and 110 zygotes were constituted; hTERC/GFP (Group 1), hTERT/hTERC/GFP (Group 2), and GFP alone (Group 3), respectively. GFP fluorescence was used to identify successfully injected embryos. This method has recently been established in our laboratory. Injected and control embryos were cultured for 7 days to the blastocyst stage in vitro and the impact on early embryonic development and the physiological consequences of an ectopic overexpression of telomerase in early bovine embryos were assayed. We obtained 45 blastocysts with green fluorescence in the first, 192 in the second, and 28 in the third group. Embryos with GFP fluorescence were frozen for subsequent PCR analysis and telomerase activity measurement. Some blastocyts were analyzed using quantitative fluoresence in situ hybridization to monitor telomere length. Control groups were analyzed for the endogenous levels of TERC and TERT. Results indicate that endogenous TERC and TERT are up-regulated in morulae and blastocyts. In this study, we show that human TERC and TERT can be expressed in blastocysts by cytoplasmic plasmid injection in bovine zygotes. Statistical analyses were performed using the JMP 7.0.1 for Windows software (SAS Institute Inc., Cary, NC, USA). The Tukey-Kramer test was applied to compare the group means. The expression of hTERC alone resulted in a significant extension of telomere length of 280 telomere fluorescence units. Expression of both components also resulted in a significant extension of telomere length. In conclusion, TERC component alone is sufficient to elongate telomere length. The activity measurement showed that telomerase activity in the hTERT and hTERC injected group is 1.77 times higher than in the control group. Findings from this study will allow a comprehensive analysis of the functions of TERT and TERC in early embryogenesis. The ectopic expression of telomerase components in bovine embryos could pave new avenues for generating stem cells and for the development of novel regenerative therapies. Funded by DFG.
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Alnafakh, Rafah, Fiona Choi, Alice Bradfield, Meera Adishesh, Gabriele Saretzki, and Dharani K. Hapangama. "Endometriosis Is Associated with a Significant Increase in hTERC and Altered Telomere/Telomerase Associated Genes in the Eutopic Endometrium, an Ex-Vivo and In Silico Study." Biomedicines 8, no. 12 (December 9, 2020): 588. http://dx.doi.org/10.3390/biomedicines8120588.

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Telomeres protect chromosomal ends and they are maintained by the specialised enzyme, telomerase. Endometriosis is a common gynaecological disease and high telomerase activity and higher hTERT levels associated with longer endometrial telomere lengths are characteristics of eutopic secretory endometrial aberrations of women with endometriosis. Our ex-vivo study examined the levels of hTERC and DKC1 RNA and dyskerin protein levels in the endometrium from healthy women and those with endometriosis (n = 117). The in silico study examined endometriosis-specific telomere- and telomerase-associated gene (TTAG) transcriptional aberrations of secretory phase eutopic endometrium utilising publicly available microarray datasets. Eutopic secretory endometrial hTERC levels were significantly increased in women with endometriosis compared to healthy endometrium, yet dyskerin mRNA and protein levels were unperturbed. Our in silico study identified 10 TTAGs (CDKN2A, PML, ZNHIT2, UBE3A, MCCC2, HSPC159, FGFR2, PIK3C2A, RALGAPA1, and HNRNPA2B1) to be altered in mid-secretory endometrium of women with endometriosis. High levels of hTERC and the identified other TTAGs might be part of the established alteration in the eutopic endometrial telomerase biology in women with endometriosis in the secretory phase of the endometrium and our data informs future research to unravel the fundamental involvement of telomerase in the pathogenesis of endometriosis.
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Xu, Chenzhong, Nan Xie, Yuanyuan Su, Zhaomeng Sun, Yao Liang, Na Zhang, Doudou Liu, et al. "HnRNP F/H associate with hTERC and telomerase holoenzyme to modulate telomerase function and promote cell proliferation." Cell Death & Differentiation 27, no. 6 (December 20, 2019): 1998–2013. http://dx.doi.org/10.1038/s41418-019-0483-6.

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AbstractHuman telomerase RNA component hTERC comprises multiple motifs that contribute to hTERC biogenesis, holoenzyme activity, and enzyme recruitment to telomeres. hTERC contains several guanine tracts (G-tracts) at its 5′-end, but its associated proteins and potential roles in telomerase function are still poorly understood. The heterogeneous nuclear ribonucleoproteins F, H1, and H2 (hnRNP F/H) are splicing factors that preferentially bind to poly(G)-rich sequences RNA. Here, we demonstrate that hnRNP F/H associate with both hTERC and telomerase holoenzyme to regulate telomerase activity. We reveal hnRNP F/H bind to the 5′-end region of hTERC in vitro and in vivo, and identify the first three G-tracts of hTERC and qRRM1 domain of hnRNP F/H are required for their interaction. Furthermore, hnRNP F/H also directly interact with telomerase holoenzyme. Functionally, we show that hnRNP F/H plays important roles in modulating telomerase activity and telomere length. Moreover, hnRNP F/H deletion greatly impair cancer and stem cell proliferation, and induce stem cell senescence, while hnRNP F/H overexpression delay stem cell senescence. Collectively, our findings unveil a novel role of hnRNP F/H as the binding partners of hTERC and telomerase holoenzyme to regulate telomerase function.
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Eckburg, Adam, Joshua Dein, Joseph Berei, Zachary Schrank, and Neelu Puri. "Oligonucleotides and microRNAs Targeting Telomerase Subunits in Cancer Therapy." Cancers 12, no. 9 (August 19, 2020): 2337. http://dx.doi.org/10.3390/cancers12092337.

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Telomerase provides cancer cells with replicative immortality, and its overexpression serves as a near-universal marker of cancer. Anti-cancer therapeutics targeting telomerase have garnered interest as possible alternatives to chemotherapy and radiotherapy. Oligonucleotide-based therapies that inhibit telomerase through direct or indirect modulation of its subunits, human telomerase reverse transcriptase (hTERT) and human telomerase RNA gene (hTERC), are a unique and diverse subclass of telomerase inhibitors which hold clinical promise. MicroRNAs that play a role in the upregulation or downregulation of hTERT and respective progression or attenuation of cancer development have been effectively targeted to reduce telomerase activity in various cancer types. Tumor suppressor miRNAs, such as miRNA-512-5p, miRNA-138, and miRNA-128, and oncogenic miRNAs, such as miRNA-19b, miRNA-346, and miRNA-21, have displayed preclinical promise as potential hTERT-based therapeutic targets. Antisense oligonucleotides like GRN163L and T-oligos have also been shown to uniquely target the telomerase subunits and have become popular in the design of novel cancer therapies. Finally, studies suggest that G-quadruplex stabilizers, such as Telomestatin, preserve telomeric oligonucleotide architecture, thus inhibiting hTERC binding to the telomere. This review aims to provide an adept understanding of the conceptual foundation and current state of therapeutics utilizing oligonucleotides to target the telomerase subunits, including the advantages and drawbacks of each of these approaches.
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Ly, Hinh, Rodrigo T. Calado, Paulette Allard, Gabriela M. Baerlocher, Peter M. Lansdorp, Neal S. Young, and Tristram G. Parslow. "Functional characterization of telomerase RNA variants found in patients with hematologic disorders." Blood 105, no. 6 (March 15, 2005): 2332–39. http://dx.doi.org/10.1182/blood-2004-09-3659.

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AbstractHuman telomerase uses a specific cellular RNA, called hTERC, as the template to synthesize telomere repeats at chromosome ends. Approximately 10% to 15% of patients with aplastic anemia or other bone marrow failure syndromes are carriers of hTERC sequence variants whose functional significance, in most cases, is unknown. We screened 10 reported and 2 newly discovered hTERC variants from such patients and found that 10 of these negatively affected telomerase enzymatic function when they were used to reconstitute telomerase enzymatic function in human cells. Most functional deficits were due to perturbations of hTERC secondary structure and correlated well with the degrees of telomere shortening and reduced telomerase activity observed in peripheral blood lymphocytes of the representative patients. We also found no evidence of dominant-negative activity in any of the mutants. Therefore, loss of telomerase activity and of telomere maintenance resulting from inherited hTERC mutations may limit marrow stem cell renewal and predispose some patients to bone marrow failure.
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Carroll, Kathryn A., Rodrigo Calado, Neal S. Young, Shamika Danzy, and Hinh Ly. "Identification and Functional Characterization of Novel Telomerase Variant Alleles in Patients with Bone-Marrow Failure Syndromes." Blood 112, no. 11 (November 16, 2008): 4113. http://dx.doi.org/10.1182/blood.v112.11.4113.4113.

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Abstract As multiple studies have shown a link between mutations in telomerase components and the disease pathogenesis of bone-marrow failure syndromes (BMFS), we screened blood or marrow cells from patients with various forms of blood disorders for novel pathogenic mutations in the telomerase hTERC and hTERT genes. We identified several heterozygous mutations in these genes, which were observed only in patient samples and not in controls. As these mutations are predicted to affect proper telomerase function, we introduced these and other mutations identified previously in patients with other forms of blood disorders into telomerase-negative cells in order to reconstitute telomerase enzymatic activity and to assess the effect of the individual mutations on modulating a wild-type telomerase function. All disease-associated mutations disrupted telomerase function to various degrees and most modulated a wildtype telomerase enzymatic function by haploinsufficiency based on results obtained from the telomeric repeat amplification protocol (TRAP). We also tested several previously reported natural sequence changes in the promoter region of the hTERC gene for their effect on gene expression and telomerase function via luciferase-reporter assay, TRAP, and Northern blot. The results obtained from these studies appear to contradict those that have recently been reported for some of the naturally occurring hTERC-promoter associated mutations. This study, therefore, offers new insights into the mechanism of natural telomerase mutations in regulating telomere lengths and marrow stem cell renewal capacity in patients with hematological disorders.
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Zheng, Xiuhui, Peihe Liang, Yingru Zheng, Ping Yi, Qiang Liu, Jian Han, Yinhu Huang, Yuanguo Zhou, Jianxin Guo, and Li Li. "ATL." International Journal of Gynecologic Cancer 23, no. 5 (June 2013): 785–90. http://dx.doi.org/10.1097/igc.0b013e31828f39a0.

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ObjectiveTo investigate the clinical significance of abnormal human telomerase RNA gene component (hTERC) gene amplification tested by fluorescence in situ hybridization in cervical lesions.MethodsIn 373 patients with cytologic abnormalities, high-risk human papilomavirus (HR-HPV) was detected by the hybrid capture II method, and abnormal amplification of the hTERC gene in exfoliated cells was detected by fluorescence in situ hybridization.ResultsCell smear findings suggested atypical squamous cells in 148 patients, low-grade squamous intraepithelial lesion in 62 patients, and high-grade squamous intraepithelial lesion in 107 patients, squamous cell carcinoma in 56 patients, and cervical biopsy-revealed inflammation in 89 patients, cervical intraepithelial neoplasia (CIN) I in 36 patients, CIN II in 43 patients, CIN III in 129 patients, and infiltrating carcinoma in 76 patients. In the inflammation, CIN I, CIN II, CIN III, and infiltrating carcinoma groups, the infection rates of HR-HPV were 29.21%, 52.78%, 74.42%, 92.25%, and 93.42% (P < 0.01), respectively; the positive rates of hTERC gene amplification were 0.00%, 13.89%, 41.86%, 78.29%, and 89.47% (P < 0.01), respectively. With respect to advanced cervical lesions (≥CIN II), cytology (≥ low-grade squamous intraepithelial lesion), HR-HPV testing, and hTERC testing differed insignificantly in the negative predictive value (P > 0.05), but they differed significantly in the sensitivity, specificity, and positive predictive value (P < 0.01). Among the 3 methods, hTERC testing showed the highest specificity and positive predictive value, and HR-HPV testing showed the highest sensitivity. In 41 patients with untreated CIN I and CIN II, the sensitivity of detection of hTERC gene amplification to predict lesion progression was 88.89%, and the specificity was 93.75%.ConclusionDetection of abnormal amplification of the hTERC gene can assist in screening cervical lesions and identifying CIN I/II patients with a high progression risk.
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Zappacosta, Roberta, Manuel Maria Ianieri, Danilo Buca, Elena Repetti, Alessandra Ricciardulli, and Marco Liberati. "Clinical Role of the Detection of Human Telomerase RNA Component Gene Amplification by Fluorescence in situ Hybridization on Liquid-Based Cervical Samples: Comparison with Human Papillomavirus-DNA Testing and Histopathology." Acta Cytologica 59, no. 4 (2015): 345–54. http://dx.doi.org/10.1159/000438719.

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Objective: This study was designed to evaluate whether the adjunct of human telomerase RNA component (hTERC) fluorescence in situ hybridization (FISH) analysis to cytological diagnosis and human papillomavirus (HPV)-DNA testing may serve as a predictive marker for distinguishing cervical lesions destined to regress from those at high risk of progression towards invasive cancer. Study Design: hTERC FISH analysis was performed on 54 residual liquid-based cytology specimens obtained from women referred to colposcopy for the detection of atypical squamous cells of undetermined significance or worse (ASCUS+) lesions. Histological diagnosis was considered the gold standard and cervical intraepithelial neoplasia of grade 2 or worse (CIN2+) as the worst outcome. Results: Oncogenic HPV-DNA was found in 96.3% of the specimens. Among these, 38.5% revealed a CIN2+ diagnosis. hTERC gene amplification was detected in 37% of the cases; among these, 70% showed up as CIN2+. hTERC FISH analysis significantly improves the specificity and positive predictive value of HPV-DNA testing, thus differentiating patients with a CIN2+ diagnosis from those with a CIN2- diagnosis. Conclusions: Despite the limitation of a small study sample, our findings provide promising data, indicating the possible role of hTERC analysis in the assessment of the risk of developing cervical cancer. This approach would implement the specificity of DNA testing, avoiding overtreatment at the same time. Prospective follow-up studies are needed with the aim of introducing hTERC FISH into decision-making algorithms.
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More sources

Dissertations / Theses on the topic "HTERC"

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Gros, Julien. "Quadruplexes de Guanines en ADN et en ARN." Paris 6, 2009. http://www.theses.fr/2009PA066054.

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Les quadruplexes de guanines (G4) sont des structures non canoniques d’acide nucléique formées à partir de séquences ADN ou ARN riches en guanines (G) et basées sur la formation puis l’empilement de G-quartets. D’un point de vue technologique, la formation de ces structures peut être imaginée dans de nombreux domaines d’application allant de la chimie supra-moléculaire aux nanotechnologies. In vivo, ces structures pourraient être impliquées de façon transitoire dans de nombreux processus biologiques, en particulier au niveau des télomères. Les travaux de thèse présentés dans ce manuscrit relèvent de deux objectifs poursuivis. Dans le but de comprendre les mécanismes d'association et de dissociation de ces quadruplexes, nous avons étudié dans un premier temps l’association et la dissociation de G4 tétramoléculaires en ADN. L’utilisation de séquences modifiées nous a permis d’établir un certain nombre de règles régissant chacun de ces deux processus. En particulier, on peut difficilement accommoder d’autres nucléobases que des guanines au sein d’un G-quartet pour former un G4, même si certains analogues de G modifiés en positon 8 peuvent s'avérer favorables en 5' du G4. La stabilisation de G4 aux télomères à l’aide de molécules spécifiques pourrait limiter la prolifération de cellules tumorales. Dans ce cas, le(s) mécanisme(s) d’action de ces ligands demandent à être clarifié(s). Nous avons proposé une nouvelle cible G4 à l’extrémité 5’ d’hTERC, sous-unité ARN de la télomérase humaine. L’utilisation d’un système modèle nous a permis de valider la formation d’un G4 à l’extrémité 5’ d’hTERC in vitro. La formation de ce G4 est en compétition avec la formation de l’hélice P1 impliquée dans fonctionnement de la télomérase humaine. Il nous reste à valider cette hypothèse de travail sur une télomérase entière et active. Pour ce faire, nous avons modifié hTERC (mutations, délétions) et avons mis en place un test direct de l’activité télomérase reconstituée in vitro.
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Toutain, Jérôme. "Cytogénétique placentaire des retards de croissance intra-utérins : intérêts de la recherche des anomalies chromosomiques limitées au placenta et de l’estimation de la longueur télomérique placentaire." Thesis, Bordeaux 2, 2012. http://www.theses.fr/2012BOR21957/document.

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Ce travail de thèse se propose d’étudier le retard de croissance intra-utérin sous l’angle de la cytogénétique placentaire, avec deux approches distinctes et complémentaires. La première approche visera à réévaluer l’influence des anomalies chromosomiques limitées au placenta sur la croissance fœtale, car des études précédentes ont rapporté des résultats contradictoires à ce sujet. La première partie de ce travail permettra en outre d’étudier l’incidence et l’influence de la disomie uniparentale chez les fœtus issus des grossesses compliquées d’une anomalie chromosomique limitée au placenta. La deuxième approche de notre travail s’intéressera à la longueur de structures chromosomiques particulières, les télomères, au niveau placentaire. Il a récemment été décrit que la longueur des télomères des cellules placentaires était réduite au terme des grossesses compliquées d’un retard de croissance intra-utérin. La longueur télomérique placentaire n’a jamais été évaluée au cours de ces grossesses et pourrait potentiellement être utilisée comme biomarqueur placentaire du retard de croissance intra-utérin. La deuxième partie de ce travail nous permettra également d’évaluer le nombre de copies des régions chromosomiques portant les gènes codant pour les principales sous-unités du complexe enzymatique télomérase et de rechercher la présence d’agrégats télomériques au niveau placentaire en cas de retard de croissance intra-utérin
This thesis proposes to study intrauterine growth restriction in terms of cytogenetics of placenta, with two distinct and complementary approaches. The first approach will be to reassess the influence of confined placental mosaicism on fetal growth, as previous studies have reported conflicting results on this issue. The first part of this work will also study the influence of fetal uniparental disomy in case of confined placental mosaicism. The second approach of our work will focus on the length of terminal chromosomal structures, telomeres, at the placental level. It has recently been reported that telomere length was reduced in placental cells collected at term in pregnancies complicated by intrauterine growth restriction. Placental telomere length has never been evaluated in ongoing pregnancies and it could potentially be used as a placental biomarker of intrauterine growth restriction. The second part of this work will also focus on the copy number of chromosomal regions carrying genes encoding the main subunits of the telomerase enzyme complex and will look for the presence of placental telomeric aggregates in case of intrauterine growth restriction
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Silva, de Araujo Bruno Eduardo [Verfasser], Stefan [Akademischer Betreuer] Biesterfeld, and Monika [Gutachter] Hampl. "Multicolour fluorescence in situ hybridization in cervical smears: detection of amplification of hTERC, MYC, and EGFR for the diagnosis of intraepithelial neoplasia. / Bruno Eduardo Silva de Araujo ; Gutachter: Monika Hampl ; Betreuer: Stefan Biesterfeld." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2019. http://d-nb.info/1201882044/34.

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Ahmed, Shaheda Sameena. "hTERT protects mitochondria but not telomeres under oxidative stress." Thesis, University of Newcastle Upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435571.

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Bund, Dagmar. "hTERT, CD23 und CD229 als Tumorantigene bei der B-CLL." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-145282.

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Nimmo, Graeme A. M. "Mapping telomerase reverse transcriptase (hTERT) domains that contribute to tumorigenesis." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112547.

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Telomerase is a ribonucleoprotein that maintains telomere. It is activated in greater than 85% of human neoplasms. Traditionally, reactivation of telomerase during tumorigenesis was thought to be required solely to impart an indefinite lifespan. Recently, however, several studies have suggested that telomerase may contribute to tumorigenesis via an additional mechanism that is independent of its role in telomere lengthening. We sought to identify the region(s) of hTERT that contribute to this non-classical role of telomerase. We proposed to identify such regions by their ability to impart a tumorigenic phenotype in ALT cells transduced with activated Ras. Also, we attempted to develop methods to demonstrate that this role is not dependant of telomerase localizing to the telomere. The strategies employed and the progress gained toward each goal is presented in this thesis.
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Schaeper, Anja [Verfasser]. "Hoher prognostischer Wert der hTERT-Expression in Gastrointestinalen Stromatumoren / Anja Schaeper." Magdeburg : Universitätsbibliothek, 2012. http://d-nb.info/1052827829/34.

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Rodrigues, Katherine de Souza. "Polimorfismo rs2736100 do gene hTERT em pacientes com câncer de mama." reponame:Repositório Institucional da UnB, 2017. http://repositorio.unb.br/handle/10482/23505.

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Dissertação (mestrado)—Universidade de Brasília, Faculdade em Ciências da Saúde, Programa de Pós-Graduação em Ciências da Saúde, 2017.
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O câncer de mama é o mais comum em mulheres e é responsável por 23% dos novos casos de câncer. O seu diagnóstico precoce assume papel decisivo para um melhor prognóstico devido à sua etiopatogenia complexa e multifatorial, já que não pode ser prevenido. Desta forma, os esforços para melhoria dos indicadores do câncer de mama são direcionados na busca por medidas que antecipem seu diagnóstico. A telomerase, uma enzima importante no processo de carcinogênese, está presente na maioria dos tumores e apresenta indícios de ser um bom marcador molecular, por isso deve ser estudada para avaliar sua relação com o câncer de mama. Este estudo analisou o polimorfismo rs2736100 da telomerase em pacientes com câncer de mama e testou a correlação de tais dados com o prognóstico e variáveis clínicas diversas. Para isso, o DNA de pacientes com câncer de mama foi extraído, submetido a PCR com os primers da região do polimorfismo e sequenciado. Ao todo, 119 pacientes com câncer de mama aceitaram participar do estudo. Foi encontrada associação em diversas características gerais do paciente (altura, idade e IMC) e características do tumor (RE, RP e Ki67), reafirmando a importância deles na clínica para a definição do melhor e mais fidedigno prognóstico. Através do sequenciamento foi identificada a região do polimorfismo rs2736100 da telomerase em 63 amostras, divididos entre aqueles com detecção do genótipo GG e AG. Foi encontrada uma deleção em 11,11% da população estudada que ainda não foi relatada na literatura. Nosso estudo demonstrou que este polimorfismo tem algumas associações com variáveis clínicas e de prognóstico do câncer de mama. Entretanto, para o polimorfismo rs2736100 da telomerase ser utilizado como marcador prognóstico no câncer de mama estudos mais detalhados devem ser realizados para confirmar seu valor clínico.
Breast cancer is the most common in women and accounts for 23% of new cases of cancer. Its early diagnosis plays a decisive role for a better prognosis because of its complex and multifactorial etiopathogenesis, which can not be prevented. Thus, efforts to improve indicators of breast cancer are targeted seeking measures that anticipate their diagnosis. Telomerase, an important enzyme in the carcinogenesis process, is present in most tumors and shows signs of being a good molecular marker, so it should be studied to evaluate its relationship with breast cancer. This study analyzed the rs2736100 polymorphism of telomerase in breast cancer patients and tested the correlation of such data with the prognosis and various clinical variables. For this, the DNA of patients with breast cancer was extracted, subjected to PCR with primers and sequenced region of the polymorphism. In all, 119 breast cancer patients agreed to participate in the study. An association was found in several general patient characteristics (height, age and BMI) and tumor characteristics (ER, PR and Ki67), reaffirming their importance in clinical settings for the definition of the best and most reliable prognosis. Through sequencing the telomerase rs2736100 polymorphism region was identified in 63 samples, divided among those with GG and AG genotype detection. A deletion was found in 11.11% of the studied population that has not yet been reported in the literature. Our study demonstrated that this polymorphism has some associations with clinical and prognostic variables of breast cancer. However, for the rs2736100 polymorphism of telomerase to be used as a prognostic marker in breast cancer more detailed studies should be performed to confirm its clinical value.
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Chebly, Alain. "L'épigénétique comme modulateur de l'expression de hTERT dans les lymphomes T cutanés." Thesis, Bordeaux, 2020. http://www.theses.fr/2020BORD0321.

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Les lymphomes T-cutanés (CTCL) sont des tumeurs télomérase-positives exprimant hTERT, dans lesquelles ni l'amplification, ni les réarrangements, ni les mutations hotspots du promoteur peuvent expliquer la ré-expression du gène. Comme le promoteur de hTERT est riche en CpG, nous avons étudié la contribution des mécanismes épigénétiques dans sa ré-expression, puisqu’aucune étude à ce jour n’a été rapporté dans les CTCL. Nous avons analysé le statut de méthylation du promoteur de hTERT dans des lignées cellulaires, des cellules de patients ainsi que dans des cellules issues de donneurs sains. Nous avons également étudié la présence sur le promoteur de hTERT des histones H3K27ac et H3K27me3. Les analyses de méthylation spécifiques des cellules CTCL ont révélé un profil de méthylation caractéristique limité aux cellules tumorales, englobant une région distale hyperméthylée de -650 pb à -150 pb et une région proximale hypométhylée de -150 pb à + 150 pb, à partir du TSS. Ce double profil de méthylation observé sur le promoteur de hTERT est identique à celui observé dans d’autres types de tumeurs. La région distale hyperméthylée identifiée dans les cellules tumorales CTCL correspond à la région nommée récemment « région TERT oncogénique hyperméthylée » (THOR) et qui est rapportée associée à la réactivation de la télomérase dans les tumeurs, mais jusqu'à présent non rapportée dans les lymphomes. Nous avons évalué l'effet sur THOR de deux inhibiteurs d’histone désacétylases (HDACi), la romidepsine et le vorinostat, tous deux approuvés pour le traitement des CTCL ainsi que d'un inhibiteur de l'ADN méthyltransférase (DNMTi) 5-azacytidine, non approuvé pour les CTCL. Nos résultats obtenus à partir d’une cohorte limitée semblent suggérer, que la 5-azacytidine ne provoque pas la déméthylation de la région hyperméthylée du promoteur de hTERT alors que ce traitement s’accompagne d’une diminution de l’expression de hTERT et, fonctionnellement d’une baisse des capacités clonogènes des cellules. La romidepsine et le vorinostat modifient peu les marques d'histones H3K27ac et H3K27me3 présentes au niveau du promoteur hTERT. En conclusion, les résultats obtenus dans les cellules CTCL comparées à ceux de cellules saines confirment que la méthylation du promoteur de hTERT dans les cellules tumorales est particulière et spécifique à ces cellules, faisant de cette méthylation un biomarqueur de la cellule tumorale. De plus, ils révèlent que la méthylation du promoteur hTERT est relativement stable même sous la pression de thérapies épigénétiques, suggérant que la régulation de hTERT par ces thérapies s’opère en priorité de manière indirecte
Cutaneous T-lymphomas (CTCL) are telomerase-positive tumors expressing hTERT, in which neither amplification, nor rearrangement, nor promoter hotspot mutations can explain the re-expression of the gene. As the hTERT promoter is rich in CpG, we investigated the contribution of epigenetic mechanisms in its re-expression, since no studies to date have been reported in CTCL. We analyzed the methylation status of the hTERT promoter in cell lines, patients’ cells and in cells from healthy donors. We also studied the presence, on the hTERT promoter, of histones H3K27ac and H3K27me3. Methylation analyzes in CTCL cells revealed a characteristic methylation profile specific to tumor cells, encompassing a distal hypermethylated region from -650 bp to -150 bp and a proximal hypomethylated region from -150 bp to +150 bp, relatively to the TSS. This dual methylation profile on hTERT promoter is identical to the profile seen in other types of tumors. The hypermethylated distal region identified in CTCL tumor cells corresponds to the region recently named “TERT hypermethylated oncogenic region” (THOR) and which is reported to be associated with telomerase reactivation in several tumors, but so far not reported in lymphomas. We evaluated the effect on THOR of two histone deacetylases inhibitors (HDACi), romidepsin and vorinostat, both approved for the treatment of CTCL as well as a DNA methyltransferase inhibitor (DNMTi) 5- azacytidine, not approved for CTCL. Our results, obtained from a limited cohort, seem to suggest that 5-azacytidine does not cause a demethylation of the hypermethylated region on hTERT promoter, while this treatment is accompanied by a decrease in the expression of hTERT and, functionally with a decrease in the clonogenic capacities of tumor cells. Romidepsin and vorinostat can slightly modify the H3K27ac and H3K27me3 histone marks present on hTERT promoter. In conclusion, the results obtained in CTCL cells compared with those of healthy cells confirm that hTERT promoter methylation is specific to CTCL cells, making this methylation a biomarker of tumor cells. Furthermore, they reveal that the methylation of hTERT promoter is relatively stable even under the pressure of epigenetic therapies, suggesting that the regulation of hTERT by these therapies can happen indirectly
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Wen, Victoria Wei-Yu Women's &amp Children's Health Faculty of Medicine UNSW. "Molecular alterations during immortalisation of human endothelial cells." Awarded by:University of New South Wales. Women's & Children's Health, 2009. http://handle.unsw.edu.au/1959.4/44743.

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Replicative exhaustion of endothelial cells (ECs) contributes to the pathogenesis of age-related vascular disorders, including atherosclerosis and impaired wound healing. Conversely, abnormal proliferation of ECs underlies the development of EC-derived malignancies, such as haemangioblastoma and angiosarcoma. The central objective of this thesis was to delineate mechanisms that regulate the replicative lifespan of human ECs and molecular alterations that occur during immortalisation of ECs. The gradual shortening of telomeres (chromosome-end structures) is one mechanism that restricts the replicative lifespan of human ECs. Telomere shortening initiates an irreversible growth arrest or senescence through activation of a TP53-mediated DNA damage response. Expression of the cyclin-dependent kinase inhibitor, p16INK4a, is also increased and reinforces senescence via the retinoblastoma pathway. Overexpression of telomerase reverse transcriptase (hTERT) reconstitutes telomerase activity and extends the lifespan of human ECs, but is not sufficient for immortalisation. The current study demonstrated that p16INK4a repression by promoter methylation was a frequent event during immortalisation of hTERT-transduced bone marrow ECs (BMECs), occurring in 5 of 12 clones. Repression of p16INK4a concurred with the development of recurring chromosomal aberrations, which appeared to be a consequence of telomere dysfunction and chromosome fusions. Loss of p16INK4a and the development of a complex karyotype were associated with a more transformed phenotype in hTERT-immortalised BMECs. The investigations described in this thesis were the first to associate loss of p16INK4a expression with the accumulation of chromosome aberrations. Repression of p16INK4a in only a subset of immortal BMECs provided impetus for investigating whether there was a functionally analogous defect in the hTERT-immortalised BMECs that retained p16INK4a expression. In normal human cells, oncogenic Ras upregulates p16INK4a and induces senescence independently of telomere shortening. This thesis demonstrates that the immortal BMECs that retained p16INK4a expression had a defective response to oncogenic Ras, which may have contributed to the immortalisation of these cells. Whole genome and proteome analyses identified additional alterations in gene copy number and protein expression specific to p16INK4a-positive or -negative immortal BMECs. Overall, these investigations provide new insight to the potential consequences of p16INK4a repression during carcinogenesis and describe novel molecular alterations that occur during immortalisation of human ECs.
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Books on the topic "HTERC"

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Daug hters of Lancaster County: [the series. Uhrichsville, OH: Barbour Publishing, 2006.

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International Conference on High Temperature and Energy-related Materials (5th 1987 Rome, Italy). 5th HTERM: Fifth International Conference on High Temperature and Energy-related Materials, Rome, Italy, 25-29 May 1987. London, England: Pion, 1989.

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Book chapters on the topic "HTERC"

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Fujiki, Tsukasa, Yoshinori Katakura, Takumi Miura, and Sanetaka Shirahata. "Application of hTERT Promoter to Cancer Therapy." In Animal Cell Technology: From Target to Market, 562–64. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0369-8_133.

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Rosenberg, Robert, Ralf Gertler, Dominik Stricker, Silke Lassmann, Martin Werner, Hjalmar Nekarda, and Joerg Ruediger Siewert. "Telomere Length and hTERT Expression in Patients with Colorectal Carcinoma." In Molecular Staging of Cancer, 177–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59349-9_16.

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Lai, Serene R., Lucy G. Andrews, and Trygve O. Tollefsbol. "hTERT Knockdown in Human Embryonic Kidney Cells Using Double-Stranded RNA." In Telomerase Inhibition, 23–29. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-60327-070-0_3.

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Huang, Yi-Yuan, Jing-Wen Shih, and Jing-Jer Lin. "Establishing Cell-Based Reporter Systems for the Analysis of hTERT Expression." In Telomerase Inhibition, 87–96. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-60327-070-0_8.

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Gertler, Ralf, R. Rosenberg, D. Stricker, M. Werner, H. Nekarda, and J. R. Siewert. "Bedeutung von Telomerlänge und hTERT Expression für Entwicklung und Prognose kolorektaler Karzinome." In Deutsche Gesellschaft für Chirurgie, 135–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19024-7_38.

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Gertler, R., R. Rosenberg, D. Stricker, M. Werner, H. Nekarda, and J. R. Siewert. "Bedeutung von Telomerlänge und hTERT-Expression für Entwicklung und Prognose kolorektaler Karzinome." In Zurück in die Zukunft, 494–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55611-1_313.

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Frodermann, Bernd, and Christopher Poremba. "Expression Analysis of Telomerase-Genes hTERT and hTR by Quantitative PCR on LightCycler." In Rapid Cycle Real-Time PCR — Methods and Applications, 187–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-59397-0_20.

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Jacob, Dietmar, G. Schumacher, M. Bahra, J. M. Langrehr, J. Davis, F. C. Marini, P. Neuhaus, and B. Fang. "Tumorsuppression durch ein RGD modifiziertes, hTERT reguliertes, TRAIL exprimierendes Adenovirus in einem orthotopen Pankreas Tumormodell." In Deutsche Gesellschaft für Chirurgie, 123–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18547-2_39.

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Würl, Peter, M. Kappler, H. Taubert, A. Meye, F. Bartel, T. Köhler, and D. Henne-Bruns. "Coexpression von Survivin und hTERT — ein hoch signifikanter unabhängiger molekularer Prognosefaktor für Weichtelsarkome des Erwachsenen." In Deutsche Gesellschaft für Chirurgie, 143–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19024-7_40.

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Würl, P., M. Kappler, H. Taubert, A. Meye, F. Bartel, T. Köhler, and D. Henne-Bruns. "Coexpression von Survivin und hTERT — ein hoch signifikanter unabhängiger molekularer Prognoseparameter für Weichteilsarkome des Erwachsenen." In Zurück in die Zukunft, 483. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55611-1_302.

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Conference papers on the topic "HTERC"

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Moreno-Acosta, Pablo, Mónica Molano, Nicolas Morales, Alfredo Romero-Rojas, Oscar Gamboa, Jinneth Acosta, Raynner Alvarez, Nicolas Magné, and Nubia Muñoz. "Abstract 4328: hTERT protein expression, hTERT methylation and HPV infection in uterine cervical cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4328.

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Snover, Matthew, Nitin Madnani, Bonnie J. Dorr, and Richard Schwartz. "Fluency, adequacy, or HTER?" In the Fourth Workshop. Morristown, NJ, USA: Association for Computational Linguistics, 2009. http://dx.doi.org/10.3115/1626431.1626480.

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Moreno-Acosta, Pablo, Nicolas Morales, Marcela Burgos, Oscar Gamboa, Juan Carlos Mejia, Alfredo Romero-Rojas, Alba Lucia Combita, and Monica Molano. "Abstract C88: HPV infections, hTERT methylation and hTERT expression in patients with invasive cervical cancer." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-c88.

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Kim, Nam Deuk, Gi-Young Kim, and Yung Hyun Choi. "Abstract 3799: Cordyceptin induces apoptosis through repressing hTERT expression and inducing extranuclear export of hTERT." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3799.

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Bollam, Saumya Reddy, Hyun-Jin Kang, Sen Peng, Vijay Gokhale, Laurence Hurley, Michael Berens, and Harshil Dhruv. "Abstract 4798: Targeting hTERT for treatment of glioblastoma (GBM)." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4798.

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Judong Luo, Shuyu Zhang, Ling Chen, Xifa Zhou, Xujing Lu, Hua Tang, Yang Ling, and Jianping Cao. "ATM modulates hTERT expression after irradiated by 60Coγ-ray." In 2012 4th Electronic System-Integration Technology Conference (ESTC). IEEE, 2012. http://dx.doi.org/10.1109/estc.2012.6485645.

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Arish, N., SB Wallach-Dayan, and R. Breuer. "The Role of hTERT in Fas-Induced Epithelial Cell Apoptosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1987.

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Huang, Fei, Jian-Ming Xu, Abraham Ittycheriah, and Salim Roukos. "Adaptive HTER Estimation for Document-Specific MT Post-Editing." In Proceedings of the 52nd Annual Meeting of the Association for Computational Linguistics (Volume 1: Long Papers). Stroudsburg, PA, USA: Association for Computational Linguistics, 2014. http://dx.doi.org/10.3115/v1/p14-1081.

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Kroeker, AL, A. Yamasaki, T. Tran, R. Gosens, G. Dueck, KD McNeill, M. Mutawe, et al. "hTERT-Immortalized Human Airway Smooth Muscle Cells Retain a Multifunctional Phenotype." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3915.

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Denton, Michael L., Debbie M. Eikum, Gary D. Noojin, David J. Stolarski, Randolph D. Glickman, and Benjamin A. Rockwell. "Photo-oxidation from mode-locked laser exposure to hTERT-RPE1 cells." In Biomedical Optics 2004, edited by Steven L. Jacques and William P. Roach. SPIE, 2004. http://dx.doi.org/10.1117/12.529355.

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Reports on the topic "HTERC"

1

Stampfer, Martha R. Regulation of hTERT Expression and Function in Newly Immortalized p53(+) Human Mammary Epithelial Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada491221.

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Stampfer, Martha R. Regulation of hTERT Expression and Function in Newly Immortalized p53 (+) Human Mammary Epithelial Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada440296.

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Stampfer, Martha R. Regulation of hTERT Expression and Function in Newly Immortalized p53(+) Human Mammary Epithelial Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada457687.

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Stampfer, Martha R. Regulation of hTERT Expression and Function in Newly Immortalized p53(+) Human Mammary Epithelial Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, June 2007. http://dx.doi.org/10.21236/ada472883.

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