Literatura académica sobre el tema "Telomeres"
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Artículos de revistas sobre el tema "Telomeres"
Lin, Chi-Ying, Hsih-Hsuan Chang, Kou-Juey Wu, Shun-Fu Tseng, Chuan-Chuan Lin, Chao-Po Lin y Shu-Chun Teng. "Extrachromosomal Telomeric Circles Contribute to Rad52-, Rad50-, and Polymerase δ-Mediated Telomere-Telomere Recombination in Saccharomyces cerevisiae". Eukaryotic Cell 4, n.º 2 (febrero de 2005): 327–36. http://dx.doi.org/10.1128/ec.4.2.327-336.2005.
Texto completoBrault, Marie Eve y Chantal Autexier. "Telomeric recombination induced by dysfunctional telomeres". Molecular Biology of the Cell 22, n.º 2 (15 de enero de 2011): 179–88. http://dx.doi.org/10.1091/mbc.e10-02-0173.
Texto completoBechard, Laura H., Bilge D. Butuner, George J. Peterson, Will McRae, Zeki Topcu y Michael J. McEachern. "Mutant Telomeric Repeats in Yeast Can Disrupt the Negative Regulation of Recombination-Mediated Telomere Maintenance and Create an Alternative Lengthening of Telomeres-Like Phenotype". Molecular and Cellular Biology 29, n.º 3 (24 de noviembre de 2008): 626–39. http://dx.doi.org/10.1128/mcb.00423-08.
Texto completoKondratieva, Yu A. y L. P. Mendeleeva. "Characteristics of telomere length in patients with hematological diseases (literature review)". Oncohematology 16, n.º 1 (14 de abril de 2021): 23–30. http://dx.doi.org/10.17650/1818-8346-2021-16-1-23-30.
Texto completoBasenko, Evelina, Zeki Topcu y Michael J. McEachern. "Recombination Can either Help Maintain Very Short Telomeres or Generate Longer Telomeres in Yeast Cells with Weak Telomerase Activity". Eukaryotic Cell 10, n.º 8 (10 de junio de 2011): 1131–42. http://dx.doi.org/10.1128/ec.05079-11.
Texto completoCook, Brandoch D., Jasmin N. Dynek, William Chang, Grigoriy Shostak y Susan Smith. "Role for the Related Poly(ADP-Ribose) Polymerases Tankyrase 1 and 2 at Human Telomeres". Molecular and Cellular Biology 22, n.º 1 (1 de enero de 2002): 332–42. http://dx.doi.org/10.1128/mcb.22.1.332-342.2002.
Texto completoPerera, Omesha N., Alexander P. Sobinoff, Erdahl T. Teber, Ashley Harman, Michelle F. Maritz, Sile F. Yang, Hilda A. Pickett et al. "Telomerase promotes formation of a telomere protective complex in cancer cells". Science Advances 5, n.º 10 (octubre de 2019): eaav4409. http://dx.doi.org/10.1126/sciadv.aav4409.
Texto completoChan, Simon R. W. L. y Elizabeth H. Blackburn. "Telomeres and telomerase". Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, n.º 1441 (29 de enero de 2004): 109–22. http://dx.doi.org/10.1098/rstb.2003.1370.
Texto completoMondello, Chiara y A. Ivana Scovassi. "Telomeres, telomerase, and apoptosis". Biochemistry and Cell Biology 82, n.º 4 (1 de agosto de 2004): 498–507. http://dx.doi.org/10.1139/o04-048.
Texto completoDreesen, Oliver y George A. M. Cross. "Telomerase-Independent Stabilization of Short Telomeres in Trypanosoma brucei". Molecular and Cellular Biology 26, n.º 13 (1 de julio de 2006): 4911–19. http://dx.doi.org/10.1128/mcb.00212-06.
Texto completoTesis sobre el tema "Telomeres"
Shakirov, Yevgeniy Vitalievich. "Telomeres and telomere binding proteins in Arabidopsis thaliana". Diss., Texas A&M University, 2004. http://hdl.handle.net/1969.1/422.
Texto completoMaddison, Rachelle Louise. "Telomeres in the absence of telomerase in Saccharomyces cerevisiae". Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/30365.
Texto completoMoye, Aaron Lavel. "Understanding the relationship between telomeres, telomerase, and DNA G-quadruplexes". Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17713.
Texto completoLee, Joyce Hiu Yan. "Detection of Alternative Lengthening of Telomeres in Telomerase-Positive Cancers". Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17252.
Texto completoLee, Michael. "Next Generation Sequencing Strategies to Investigate Telomeres in Cancer". Thesis, The University of Sydney, 2019. https://hdl.handle.net/2123/21844.
Texto completoSherwood, Rebecca. "The Effect of the Copy Number of the Telomerase RNA Gene on the Elongation of Telomeres in Saccharomyces cerevisiae". Thesis, Boston College, 2008. http://hdl.handle.net/2345/532.
Texto completoTelomeres are repeated sequences at the ends of chromosomes, which promote chromosome stability by preventing the loss of necessary nucleotides from the DNA with successive rounds of replication. Telomeres are elongated by the enzyme telomerase, which has both a protein component and an RNA component. In the yeast Saccharomyces cerevisiae, the TLC1 gene encodes the RNA component of the enzyme. Telomerase RNA interacts with several proteins to perform its function, including the Ku protein, which binds to the end of the DNA and helps to recruit telomerase to the chromosome thereby facilitating the lengthening of chromosome ends. Ku interacts with telomerase RNA at the site of a 48-nucleotide stem-loop on the RNA's structure. Previous experiments have shown that yeast strains engineered to carry two copies of the TLCI gene exhibit higher levels of telomerase RNA than those that have only one copy of the gene. Also, a yeast strain carrying a copy of the mutant tlc1Δ48 gene, which contains a deletion of the 48-nucleotide stem-loop, contains lower levels of telomerase RNA than a strain with the wild type TLC1 gene. This series of experiments is investigating whether the copy number of the telomerase RNA gene affects the elongation of telomeres in S. cerevisiae. In order to determine this effect, the de novo telomere addition of four strains was examined, as were the native telomere lengths of these strains. The assay indicated that the efficiency of telomere elongation was unchanged by increasing the copy number of the wild type gene but was increased upon increasing the copy number of the mutant gene. Analysis of the native telomere lengths showed that increasing the copy number of either the wild type or the mutant gene allowed the cells to maintain their telomeres at a longer length
Thesis (BS) — Boston College, 2008
Submitted to: Boston College. College of Arts and Sciences
Discipline: Biology
Discipline: College Honors Program
Schuller, Christine Children's Cancer Institute Australia for Medical Research Faculty of Medicine UNSW. "Telomeres and telomerase in haematopoietic progenitors and bone marrow endothelial cells". Publisher:University of New South Wales. Children's Cancer Institute Australia for Medical Research, 2008. http://handle.unsw.edu.au/1959.4/41098.
Texto completoHenson, Jeremy D. "The role of Alternative Lengthening of Telomeres in human cancer". Thesis, The University of Sydney, 2006. http://hdl.handle.net/2123/1533.
Texto completoHenson, Jeremy D. "The role of Alternative Lengthening of Telomeres in human cancer". University of Sydney, 2006. http://hdl.handle.net/2123/1533.
Texto completoActivation of a telomere maintenance mechanism is a vital step in the development of most cancers and provides a target for the selective killing of cancer cells. Cancers can use either telomerase or Alternative Lengthening of Telomeres (ALT) to maintain their telomeres and inhibition of either telomere maintenance mechanism can cause cancer cells to undergo senescence or apoptosis. Although telomerase inhibitors are undergoing clinical trials, on commencing this study very little was known about the role of ALT in cancer, what proteins were involved in its mechanism and regulation and how it could be targeted clinically. The primary aim of this thesis was to develop an assay for ALT suitable for examining archived tumour specimens and to begin using it to examine the prevalence and clinical significance of ALT in cancer. This assay and gene expression analysis was also used to identify genes that are involved in or associated with the activation of the ALT mechanism, to contribute towards the overall goal of an ALT cancer therapy. The ALT mechanism involves recombination mediated replication and ALT cells have a marked increase in a range of recombinational events specifically at their telomeres. Presumably, as a consequence of this the telomere lengths of ALT cells are very heterogeneous and on average long. This can be detected by terminal restriction fragment (TRF) Southern analysis, which has been used previously as the definitive test for ALT activity. However, TRF analysis requires intact genomic DNA and is unsuitable for tumour specimens which are commonly archived by paraffin embedding. Another hallmark of ALT is ALT-associated PML bodies (APBs) which are the subset of PML bodies that contain telomeric DNA. Work done in this study to consolidate APBs as a hallmark of ALT, combined with published data, showed 29/31 ALT[+], 3/31 telomerase[+] and 0/10 mortal cell lines/strains are APB[+]. The three APB[+]/telomerase[+] cell lines identified here had an order of magnitude lower frequency of APB[+] nuclei than the ALT[+] cell lines. APBs may be functionally linked to the ALT mechanism and contain the recombination proteins that are thought to be involved in the ALT mechanism. This study, in collaboration with Dr W-Q Jiang, strengthened this functional link by demonstrating that loss of ALT activity (as determined by TRF analysis) coincided with the disruption of APBs. The detection of APBs was developed into a robust assay for ALT in archived tumour specimens using a technique of combined immunofluorescence and telomere fluorescence in situ hybridisation. It was demonstrated that the APB assay concurred exactly with the standard assay for ALT (TRF analysis) in 60 tumours for which TRF analysis gave unequivocal results. The APB assay may be a more appropriate technique in the case of tumour specimen heterogeneity, which may explain why the APB assay was able to give definitive results when TRF analysis was equivocal. We demonstrated that intratumoral heterogeneity for ALT does exist and this could explain why about 3% of tumours in this study were APB[+] but with more than a ten-fold reduction in the frequency of APB[+] nuclei. This study also made the novel discovery of single stranded C-rich telomeric DNA inside APBs which potentially could be used to make the APB assay more suitable for routine pathology laboratory use. The APB assay was used to show that ALT is a significant concern for oncology. ALT was utilised in approximately one quarter of glioblastoma multiforme (GBM), one third of soft tissue sarcomas (STS) including three quarters of malignant fibrous histiocytomas (MFH), half of osteosarcomas and one tenth of non-small cell lung carcinomas (NSCLC). Furthermore, the patients with these ALT[+] tumours had poor survival; median survivals were 2 years for ALT[+] GBM, 4 years for ALT[+] STS including 3.5 years for ALT[+] MFH and 5 years for ALT[+] osteosarcoma. ALT[+] STS and osteosarcomas were also just as aggressive as their ALT[-] counterparts in terms of grade and patient outcome. ALT status was not found to be associated with response to chemotherapy in osteosarcomas or survival in STS. ALT was however, less prevalent in metastatic STS. The APB assay was a prognostic indicator for GBM and was correlated with three fold increased median survival in GBM (although this survival was still poor). ALT was more common in lower grade astrocytomas (88% ALT[+]) than GBM (24% ALT[+]) and ALT[+] GBM had an identical median age at diagnosis to that reported for secondary GBM. It is discussed that these data indicate that ALT was indirectly associated with secondary GBM and is possibly an early event in its progression from lower grade astrocytoma. This is relevant because secondary GBM have distinct genetic alterations that may facilitate activation of the ALT mechanism. Putative repressors of ALT could explain why this study found that ALT varied among the different STS subtypes. ALT was common in MFH (77%), leiomyosarcoma (62%) and liposarcoma (33%) but rare in rhabdomyosarcoma (6%) and synovial sarcoma (9%). ALT was not found in colorectal carcinoma (0/31) or thyroid papillary carcinoma (0/17) which have a high prevalence of telomerase activity and a reduced need for a telomere maintenance mechanism (low cell turnover), respectively. A yeast model of ALT predicts that one of the five human RecQ helicases may be required for ALT. Using the APB assay to test for the presence of ALT in tumours from patients with known mutations in either WRN or RECQL4 it was demonstrated that neither of these RecQ helicases is essential for ALT. Although p53 and mismatch repair (MMR) proteins have been suggested to be possible repressors of ALT, there was no apparent increase in the frequency of ALT in tumours from patients with a germline mutation in p53 codon 273 or in colorectal carcinomas that had microsatellite instability and thus MMR deficiency. Also contrary to being a repressor of ALT but consistent with its ability to interact with a protein involved in the ALT mechanism, the MMR protein MLH1, was demonstrated to be present in the APBs of an ALT[+] cell line. To further test for genes that may be involved in the ALT mechanism or associated with its activation, RNA microarray was used to compare the gene expression of 12 ALT[+] with 12 matched telomerase[+] cell lines; 240 genes were identified that were significantly differentially expressed (p<0.005) between the ALT[+] and telomerase[+] cell lines. Only DRG2 and SFNX4 were significantly differentially expressed after adjusting for the estimated false positive rate. Overall, DRG2, MGMT and SATB1 were identified as most likely to be relevant to the ALT[+] tumours and Western analysis indicated that DRG2 and MGMT levels were down-regulated after activation of ALT and up-regulated after activation of telomerase, whereas SATB1 protein levels appeared to be up-regulated after immortalisation but to a higher degree with activation of ALT compared to telomerase. Since lack of MGMT is known to be a determinant of temozolomide sensitivity in GBM, the possibility that ALT and the APB assay could be used to predict temozolomide sensitivity is discussed. The microarray data was consistent with MGMT expression being suppressed by EGF (p < 0.05), indicating that caution may be needed with combining EGFR inhibitors with temozolomide in ALT cancers. One ALT[+] cell line which did not express MGMT had TTAA sequence in its telomeres. This could possibly have resulted from mutations due to lack of MGMT expression and a possible role for MGMT in the ALT mechanism is discussed. Further analysis of the microarray data identified two groups of co-regulated genes (p < 5x10-5): CEBPA, TACC2, SFXN4, HNRPK and MGMT, and SIGIRR, LEF1, NSBP1 and SATB1. Two thirds of differentially expressed genes were down-regulated in ALT. Chromosomes 10 and 15 had a bias towards genes with lower expression in ALT while chromosomes 1, 4, 14 and X had a bias towards genes with higher expression levels in ALT. This work has developed a robust assay for ALT in tumour specimens which was then used to show the significance of ALT in sarcomas, astrocytomas and NSCLC. It has also identified genes that could possibly be molecular targets for the treatment of ALT[+] cancers.
Dagg, Rebecca Ann. "The extensive proliferation of human cancer cells with ever-shorter telomeres". Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17341.
Texto completoLibros sobre el tema "Telomeres"
Double, John A. y Michael J. Thompson. Telomeres and Telomerase. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592591892.
Texto completoSongyang, Zhou, ed. Telomeres and Telomerase. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6892-3.
Texto completoSongyang, Zhou, ed. Telomeres and Telomerase. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8.
Texto completoFoundation, Ciba, ed. Telomeres and telomerase. Chichester: John Wiley & Sons, 1997.
Buscar texto completoHiyama, Keiko, ed. Telomeres and Telomerase in Cancer. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-879-9.
Texto completoTelomeres and telomerase in cancer. New York: Springer, 2009.
Buscar texto completoTelomeres and telomerase: Methods and protocols. 2a ed. Totowa, N.J: Humana/Springer, 2011.
Buscar texto completoA, Double John y Thompson Michael J, eds. Telomeres and telomerase: Methods and protocols. Totowa, N.J: Humana Press, 2002.
Buscar texto completoTitia, De Lange, Lundblad Vicki y Blackburn Elizabeth H, eds. Telomeres. 2a ed. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2006.
Buscar texto completoH, Blackburn Elizabeth y Greider Carol W, eds. Telomeres. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1995.
Buscar texto completoCapítulos de libros sobre el tema "Telomeres"
Joseph, Nithila A., Chi-Fan Chen, Jiun-Hong Chen y Liuh-Yow Chen. "Monitoring Telomere Maintenance During Regeneration of Annelids". En Methods in Molecular Biology, 467–78. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2172-1_24.
Texto completoSongyang, Zhou. "Introduction to Telomeres and Telomerase". En Telomeres and Telomerase, 1–11. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_1.
Texto completoXin, Huawei. "Telomeric Repeat Amplification Protocol: Measuring the Activity of the Telomerase". En Telomeres and Telomerase, 107–11. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_10.
Texto completoWilliams, Eli S., Michael N. Cornforth, Edwin H. Goodwin y Susan M. Bailey. "CO-FISH, COD-FISH, ReD-FISH, SKY-FISH". En Telomeres and Telomerase, 113–24. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_11.
Texto completoAbreu, Eladio, Rebecca M. Terns y Michael P. Terns. "Visualization of Human Telomerase Localization by Fluorescence Microscopy Techniques". En Telomeres and Telomerase, 125–37. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_12.
Texto completoMultani, Asha S. y Sandy Chang. "Cytogenetic Analysis of Telomere Dysfunction". En Telomeres and Telomerase, 139–43. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_13.
Texto completoRai, Rekha y Sandy Chang. "Probing the Telomere Damage Response". En Telomeres and Telomerase, 145–50. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_14.
Texto completoMa, Wenbin. "Analysis of Telomere Proteins by Chromatin Immunoprecipitation (ChIP)". En Telomeres and Telomerase, 151–59. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_15.
Texto completoMa, Wenbin, Hyeung Kim y Zhou Songyang. "Studying of Telomeric Protein–Protein Interactions by Bi-Molecular Fluorescence Complementation (BiFC) and Peptide Array-Based Assays". En Telomeres and Telomerase, 161–71. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_16.
Texto completoWang, Feng y Ming Lei. "Human Telomere POT1-TPP1 Complex and Its Role in Telomerase Activity Regulation". En Telomeres and Telomerase, 173–87. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-092-8_17.
Texto completoActas de conferencias sobre el tema "Telomeres"
Soboleva, O. A., A. V. Torgunakova y V. I. Minina. "TELOMERE LENGTH IN PATIENTS WITH LUNG CANCER". En X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-373.
Texto completoSannikova, A. V., M. R. Sharipova, E. V. Shakirov y L. R. Valeeva. "THE ROLE OF TRFL PROTEINS IN THE REGULATION OF TELOMERE LENGTH MARCHANTIA POLYMORPHA". En X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-368.
Texto completoShay, Jerry. "Abstract ED04-01: Aging and cancer: are telomeres and telomerase the connection?" En Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-ed04-01.
Texto completoLin, Clement, Guanhui Wu, Kaibo Wang, Buket Onel, Saburo Sakai y Danzhou Yang. "Abstract 1856: Targeting human telomeres by binding of epiberberine to telomeric G-quadruplex". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1856.
Texto completoLin, Clement, Guanhui Wu, Kaibo Wang, Buket Onel, Saburo Sakai y Danzhou Yang. "Abstract 1856: Targeting human telomeres by binding of epiberberine to telomeric G-quadruplex". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1856.
Texto completoPoon, S. S. S., R. W. Ward y P. M. Lansdorp. "Segmenting telomeres and chromosomes in cells". En 1999 IEEE International Conference on Acoustics, Speech, and Signal Processing. Proceedings. ICASSP99 (Cat. No.99CH36258). IEEE, 1999. http://dx.doi.org/10.1109/icassp.1999.757575.
Texto completoHuang, Chenhui, Xueyu Dai y Weihang Chai. "Abstract 2039: Human Stn1 protects telomere integrity by promoting efficient lagging strand synthesis at telomeres". En Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2039.
Texto completoCao, En-Hua, Ai Chen, Xueguang Sun, Xiaoyan Zhang, Jingfen Qin, Dage Liu, Chen Wang y Chunli Bai. "Formation of sequence-specific telomeric DNA loops via direct effects of psoralen-photosensitization on telomeres". En Optics and Optoelectronic Inspection and Control: Techniques, Applications, and Instruments, editado por Hong Liu y Qingming Luo. SPIE, 2000. http://dx.doi.org/10.1117/12.403922.
Texto completoBechter, Oliver E. y Margit Dlaska. "Abstract 2993: Homologous recombination between telomeres is present in ALT and telomerase-positive immortal cells". En Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2993.
Texto completoHeaphy, Christopher M., Michael C. Haffner y Alan K. Meeker. "Abstract A06: A novel cell line model of the alternative lengthening of telomeres (ALT) telomere maintenance mechanism". En Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-a06.
Texto completoInformes sobre el tema "Telomeres"
Paul, Satashree. How Early Life Stress Effects Telomeres in Later Life. Spring Library, abril de 2021. http://dx.doi.org/10.47496/nl.blog.25.
Texto completoWahl, G. M. [An homologous recombination strategy to directly clone mammalian telomeres]. Progress report. Office of Scientific and Technical Information (OSTI), julio de 1994. http://dx.doi.org/10.2172/10163039.
Texto completoLundblad, Victoria. Telomere Maintenance in the Absence of Telomerase. Fort Belvoir, VA: Defense Technical Information Center, abril de 2000. http://dx.doi.org/10.21236/ada392106.
Texto completoZwang, Yaara. Systematic Characterization of the Molecular Mechanisms That Regulate and Mediate Alternative Lengthening of Telomeres in Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, abril de 2014. http://dx.doi.org/10.21236/ada607152.
Texto completoZwang, Yaara. Systematic Characterization of the Molecular Mechanisms That Regulate and Mediate Alternative Lengthening of Telomeres in Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, abril de 2013. http://dx.doi.org/10.21236/ada581164.
Texto completoWahl, G. M. An homologous recombination strategy to directly clone mammalian telomeres. Final progress report, March 15, 1991--March 14, 1994. Office of Scientific and Technical Information (OSTI), junio de 1994. http://dx.doi.org/10.2172/10196406.
Texto completoFordyca, Colleen y Jeffrey Griffith. Telomere DNA Content, Telomerase, and c-Myc Amplification in Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, julio de 2001. http://dx.doi.org/10.21236/ada396805.
Texto completoBroccoli, Dominique. Telomerase Independent Telomere Maintenance in Ovarian Cancer: A Molecular Genetic Analysis. Fort Belvoir, VA: Defense Technical Information Center, julio de 2002. http://dx.doi.org/10.21236/ada407268.
Texto completoBroccoli, Dominique. Telomerase Independent Telomere Maintenance in Ovarian Cancer: A Molecular Genetic Analysis. Fort Belvoir, VA: Defense Technical Information Center, julio de 2004. http://dx.doi.org/10.21236/ada428241.
Texto completoPennock, Erin y Vicki Lundblad. Identification of New Genes that Regulate Telomerase and Telomere Length in Budding Yeast. Fort Belvoir, VA: Defense Technical Information Center, junio de 2001. http://dx.doi.org/10.21236/ada395954.
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