-
1
-
-
0000049842
-
The remaking of chromosomes
-
Muller HJ: The remaking of chromosomes. Collecting Net 1938, 8.
-
(1938)
Collecting Net
, pp. 8
-
-
Muller, H.J.1
-
2
-
-
0001294157
-
The stability of broken ends of chromosomes in Zea mays
-
McClintock B: The stability of broken ends of chromosomes in Zea mays. Genetics 1941, 26:234-282.
-
(1941)
Genetics
, vol.26
, pp. 234-282
-
-
McClintock, B.1
-
3
-
-
0013462065
-
A highly conserved repetitive DNA sequence, (TTAGGG)n, present at the telomeres of human chromosomes
-
Moyzis RK, Buckingham JM, Cram LS, et al.: A highly conserved repetitive DNA sequence, (TTAGGG)n, present at the telomeres of human chromosomes. Proc Natl Acad Sci U S A 1988, 85:6622-6626.
-
(1988)
Proc Natl Acad Sci U S A
, vol.85
, pp. 6622-6626
-
-
Moyzis, R.K.1
Buckingham, J.M.2
Cram, L.S.3
-
4
-
-
0022402513
-
Identification of a specific telomere terminal transferase activity in tetrahymena extracts
-
Greider CW, Blackburn EH: Identification of a specific telomere terminal transferase activity in tetrahymena extracts. Cell 1985, 43:405-413.
-
(1985)
Cell
, vol.43
, pp. 405-413
-
-
Greider, C.W.1
Blackburn, E.H.2
-
5
-
-
0037316266
-
Assessment of telomere length and factors that contribute to its stability
-
Saldanha SN, Andrews LG, Tollefsbol TO: Assessment of telomere length and factors that contribute to its stability. Eur J Biochem 2003, 270:389-403.
-
(2003)
Eur J Biochem
, vol.270
, pp. 389-403
-
-
Saldanha, S.N.1
Andrews, L.G.2
Tollefsbol, T.O.3
-
6
-
-
0038025489
-
Telomere repeat binding factors: Keeping the ends in check
-
Karlseder J: Telomere repeat binding factors: keeping the ends in check. Cancer Lett 2003, 194:189-197.
-
(2003)
Cancer Lett
, vol.194
, pp. 189-197
-
-
Karlseder, J.1
-
7
-
-
0036629255
-
Oxidative stress shortens telomeres
-
von Zglinicki T: Oxidative stress shortens telomeres. Trends Biochem Sci 2002, 27:339-344.
-
(2002)
Trends Biochem Sci
, vol.27
, pp. 339-344
-
-
Von Zglinicki, T.1
-
9
-
-
0037687623
-
Alternative lengthening of telomeres, telomerase, and cancer
-
Reddel RR: Alternative lengthening of telomeres, telomerase, and cancer. Cancer Lett 2003, 194:155-162.
-
(2003)
Cancer Lett
, vol.194
, pp. 155-162
-
-
Reddel, R.R.1
-
10
-
-
0042386051
-
Telomere dysfunction and the initiation of genome instability
-
Feldser DM, Hackett JA, Greider CW: Telomere dysfunction and the initiation of genome instability. Nat Rev Cancer 2003, 3:623-627.
-
(2003)
Nat Rev Cancer
, vol.3
, pp. 623-627
-
-
Feldser, D.M.1
Hackett, J.A.2
Greider, C.W.3
-
11
-
-
0034003333
-
A critical role for telomeres in suppressing and facilitating carcinogenesis
-
Artandi SE, DePinho RA: A critical role for telomeres in suppressing and facilitating carcinogenesis. Curr Opin Genet Dev 2000, 10:39-46.
-
(2000)
Curr Opin Genet Dev
, vol.10
, pp. 39-46
-
-
Artandi, S.E.1
DePinho, R.A.2
-
12
-
-
0034632717
-
Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice
-
Artandi SE, Chang S, Lee SL, et al.: Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice. Nature 2000, 406:641-645.
-
(2000)
Nature
, vol.406
, pp. 641-645
-
-
Artandi, S.E.1
Chang, S.2
Lee, S.L.3
-
13
-
-
0000839280
-
Telomere dysfunction provokes regional amplification and deletion in cancer genomes
-
O'Hagan RC, Chang S, Maser RS, et al.: Telomere dysfunction provokes regional amplification and deletion in cancer genomes. Cancer Cell 2002, 2:149-155. Use of array comparative genomic hybridization to compare tumors arising in p53-deficient mice with either normal or shortened telomeres. Shorter telomeres correlate with a higher degree of chromosomal instability plus recurrent amplifications and deletions of regions corresponding to hotspots in human tumors.
-
(2002)
Cancer Cell
, vol.2
, pp. 149-155
-
-
O'Hagan, R.C.1
Chang, S.2
Maser, R.S.3
-
14
-
-
0037421896
-
Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing
-
Wong KK, Maser RS, Bachoo RM, et al.: Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing. Nature 2003, 421:643-648. Telomerase knock-out virtually eliminates thymic lymphomas normally found in mice null for Atm. Doubly deficient mice show aggravated telomere shortening, chromosomal fusions, and aneuploidy in late generations. The apoptotic phenotype of the late generation telomerase knock-out is not rescued by loss of Atm.
-
(2003)
Nature
, vol.421
, pp. 643-648
-
-
Wong, K.K.1
Maser, R.S.2
Bachoo, R.M.3
-
15
-
-
0033605145
-
p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2
-
Karlseder J, Broccoli D, Dai Y, et al.: p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2. Science 1999, 283:1321-1325.
-
(1999)
Science
, vol.283
, pp. 1321-1325
-
-
Karlseder, J.1
Broccoli, D.2
Dai, Y.3
-
16
-
-
0042440603
-
Differential impact of telomere dysfunction on initiation and progression of hepatocellular carcinoma
-
Farazi PA, Glickman J, Jiang S, et al.: Differential impact of telomere dysfunction on initiation and progression of hepatocellular carcinoma. Cancer Res 2003, 63:5021-5027. This study examines the role of telomerase deficiency and shortened telomeres in three mouse models of hepatocellular carcinoma. Progressive telomere loss reduces hepatocellular carcinoma incidence in all three models due to decreased proliferation and increased apoptosis. However, careful histologic analysis reveals an increase in initiated lesions, thus pointing to differing effects of telomere shortening on cancer initiation versus progression.
-
(2003)
Cancer Res
, vol.63
, pp. 5021-5027
-
-
Farazi, P.A.1
Glickman, J.2
Jiang, S.3
-
17
-
-
0037402984
-
Role of short telomeres in inducing preferential chromosomal aberrations in human ovarian surface epithelial cells: A combined telomere quantitative fluorescence in situ hybridization and whole-chromosome painting study
-
Deng W, Tsao SW, Guan XY, et al.: Role of short telomeres in inducing preferential chromosomal aberrations in human ovarian surface epithelial cells: a combined telomere quantitative fluorescence in situ hybridization and whole-chromosome painting study. Genes Chromosomes Cancer 2003, 37:92-97. Telomerase-negative ovarian epithelial cells with extended lifespan (via HPV 16 E6/E7 expression) show that chromosomal abnormalities preferentially involve those chromosomes possessing very short telomeres.
-
(2003)
Genes Chromosomes Cancer
, vol.37
, pp. 92-97
-
-
Deng, W.1
Tsao, S.W.2
Guan, X.Y.3
-
18
-
-
0036858415
-
DNA amplification by breakage/fusion/bridge cycles initiated by spontaneous telomere loss in a human cancer cell line
-
Lo AW, Sabatier L, Fouladi B, et al.: DNA amplification by breakage/fusion/bridge cycles initiated by spontaneous telomere loss in a human cancer cell line. Neoplasia 2002, 4:531-538. The authors provide evidence that chromosome fusion and subsequent breakage-fusion-bridge cycles provide a mechanism for gene amplification in cancer cells.
-
(2002)
Neoplasia
, vol.4
, pp. 531-538
-
-
Lo, A.W.1
Sabatier, L.2
Fouladi, B.3
-
19
-
-
0642336728
-
Analysis of anaphase figures in routine histologic sections distinguishes chromosomally unstable from chromosomally stable malignancies
-
Montgomery E, Wilentz RE, Argani P, et al.: Analysis of anaphase figures in routine histologic sections distinguishes chromosomally unstable from chromosomally stable malignancies. Cancer Biol Ther 2003, 2:248-252. The presence of anaphase bridges in H&E-stained histologic tumor sections correlates with complex karyotypes (CIN phenotype) in sarcomas, pancreatic and colon carcinomas, whereas cases with MIN phenotype lack anaphase bridges. This article implies that telomere dysfunction may drive genetic instability in CIN tumors but is not necessary for MIN tumors, which have an alternate source of instability.
-
(2003)
Cancer Biol Ther
, vol.2
, pp. 248-252
-
-
Montgomery, E.1
Wilentz, R.E.2
Argani, P.3
-
20
-
-
0035252089
-
Normal human mammary epithelial cells spontaneously escape senescence and acquire genomic changes
-
Romanov SR, Kozakiewicz BK, Holst CR, et al.: Normal human mammary epithelial cells spontaneously escape senescence and acquire genomic changes. Nature 2001, 409:633-637.
-
(2001)
Nature
, vol.409
, pp. 633-637
-
-
Romanov, S.R.1
Kozakiewicz, B.K.2
Holst, C.R.3
-
21
-
-
0037380886
-
Methylation of p16(INK4a) promoters occurs in vivo in histologically normal human mammary epithelia
-
Holst CR, Nuovo GJ, Esteller M, et al.: Methylation of p16(INK4a) promoters occurs in vivo in histologically normal human mammary epithelia. Cancer Res 2003, 63:1596-1601. Fluctuation analysis indicates HMECs with the ability to bypass senescence preexist in culture, implying they may also exist in vivo. Examination of normal-appearing mammary epithelium in tissue sections reveals numerous foci of p16 promoter hypermethylation and corresponding loss of p16 protein, whereas p16 methylation was not observed in myoepithelial or stromal cells.
-
(2003)
Cancer Res
, vol.63
, pp. 1596-1601
-
-
Holst, C.R.1
Nuovo, G.J.2
Esteller, M.3
-
22
-
-
0037100745
-
Centrosomal abnormalities, multipolar mitoses, and chromosomal instability in head and neck tumours with dysfunctional telomeres
-
Gisselsson D, Jonson T, Yu C, et al.: Centrosomal abnormalities, multipolar mitoses, and chromosomal instability in head and neck tumours with dysfunctional telomeres. Br J Cancer 2002, 87:202-207. This study points to a potential link between telomere dysfunction and centrosomal abnormalities in human tumors. Anaphase bridges and multipolar mitoses were strongly correlated in cells from head and neck tumors. Chromosomes with very short telomeres were also preferentially involved in chromosomal aberrations.
-
(2002)
Br J Cancer
, vol.87
, pp. 202-207
-
-
Gisselsson, D.1
Jonson, T.2
Yu, C.3
-
23
-
-
0036184605
-
Treatment and prevention of intraepithelial neoplasia: An important target for accelerated new agent development
-
O'Shaughnessy JA, Kelloff GJ, Gordon GB, et al.: Treatment and prevention of intraepithelial neoplasia: an important target for accelerated new agent development. Clin Cancer Res 2002, 8:314-346.
-
(2002)
Clin Cancer Res
, vol.8
, pp. 314-346
-
-
O'Shaughnessy, J.A.1
Kelloff, G.J.2
Gordon, G.B.3
-
24
-
-
0036102606
-
Telomere length assessment in human archival tissues: Combined telomere fluorescence in situ hybridization and immunostaining
-
Meeker AK, Gage WR, Hicks JL, et al.: Telomere length assessment in human archival tissues: combined telomere fluorescence in situ hybridization and immunostaining. Am J Pathol 2002, 160:1259-1268. A method for assessing telomere lengths in standard clinical specimens is outlined and validated. Importantly, this method is quantitative, maintains intact tissue architecture, allows the identification of cell types/phenotype by simultaneous incorporation of immunofluorescence, and is applicable to very small tissue samples, such as clinical biopsy specimens.
-
(2002)
Am J Pathol
, vol.160
, pp. 1259-1268
-
-
Meeker, A.K.1
Gage, W.R.2
Hicks, J.L.3
-
25
-
-
0037112522
-
Telomere shortening is an early somatic DNA alteration in human prostate tumorigenesis
-
Meeker AK, Hicks JL, Platz EA, et al.: Telomere shortening is an early somatic DNA alteration in human prostate tumorigenesis. Cancer Res 2002, 62:6405-6409. Using in situ telomere length assessment (see [24]), the authors show marked telomere shortening in 93% of high-grade prostatic intraepithelial neoplasia (HGPIN) when compared with normal prostatic epithelium. The magnitude of telomere shortening was similar to that found in invasive carcinomas in the same tissues and was restricted to prostatic intraepithelial neoplasia luminal cells only.
-
(2002)
Cancer Res
, vol.62
, pp. 6405-6409
-
-
Meeker, A.K.1
Hicks, J.L.2
Platz, E.A.3
-
26
-
-
0037417131
-
Evidence of multifocalrty of telomere erosion in high-grade prostatic intraepithelial neoplasia (HPIN) and concurrent carcinoma
-
Vukovic B, Park PC, Al-Maghrahi J, et al.: Evidence of multifocalrty of telomere erosion in high-grade prostatic intraepithelial neoplasia (HPIN) and concurrent carcinoma. Oncogene 2003, 22:1978-1987. Use of in situ telomere assessment reveals telomere shortening in HGPIN. Centromere staining showed that aneusomy was also present in these same lesions.
-
(2003)
Oncogene
, vol.22
, pp. 1978-1987
-
-
Vukovic, B.1
Park, P.C.2
Al-Maghrahi, J.3
-
27
-
-
0036841802
-
Telomere shortening is nearly universal in pancreatic intraepithelial neoplasia
-
van Heek NT, Meeker AK, Kern SE, et al.: Telomere shortening is nearly universal in pancreatic intraepithelial neoplasia. Am J Pathol 2002, 161:1541-1547. Using in situ telomere length assessment, these authors found telomere shortening in nearly all premalignant pancreatic cancer precursor lesions (PanlNs), regardless of histologic grade or proliferation status.
-
(2002)
Am J Pathol
, vol.161
, pp. 1541-1547
-
-
Heek, N.T.1
Meeker, A.K.2
Kern, S.E.3
-
28
-
-
18644370262
-
Chromosomal instability in ulcerative colitis is related to telomere shortening
-
O'Sullivan JN, Bronner MP, Brentnall TA, et al.: Chromosomal instability in ulcerative colitis is related to telomere shortening. Nat Genet 2002, 32:280-284. This study strongly implicates telomere shortening/telomere dysfunction in the development of colon cancer in ulcerative colitis patients. The authors used FISH methodology to assess telomere lengths in nondysplastic tissue specimens from ulcerative colitis patients. Markedly reduced telomere signals, in association with losses of chromosomal material and an increased anaphase bridge index, were found in patients who developed cancer versus ulcerative colitis nonprogressors.
-
(2002)
Nat Genet
, vol.32
, pp. 280-284
-
-
O'Sullivan, J.N.1
Bronner, M.P.2
Brentnall, T.A.3
-
29
-
-
0042140590
-
Telomere dysfunction: A potential cancer predisposition factor
-
Wu X, Amos CI, Zhu Y, et al.: Telomere dysfunction: a potential cancer predisposition factor. J Natl Cancer Inst 2003, 95:1211-1218. This case-control study found an inverse correlation between PBL telomere lengths and four smoking-related cancers (bladder, head and neck, lung, and renal). These intriguing findings merit further study to determine whether such short PBL telomeres represent a proxy for telomere shortening in epithelial tissues or if such a relationship holds for other tumor types.
-
(2003)
J Natl Cancer Inst
, vol.95
, pp. 1211-1218
-
-
Wu, X.1
Amos, C.I.2
Zhu, Y.3
-
30
-
-
0037461928
-
Bypass of telomere-dependent replicative senescence (M1) upon overexpression of Cdk4 in normal human epithelial cells
-
Ramirez RD, Herbert BS, Vaughan MB, et al.: Bypass of telomere-dependent replicative senescence (M1) upon overexpression of Cdk4 in normal human epithelial cells. Oncogene 2003, 22:433-444. The authors find that Cdk4 overexpression allows human keratinocytes and HMECs to bypass both stress-induced premature senescence and telomere-dependent replicative senescence, despite expression of p16, p53, and p21.
-
(2003)
Oncogene
, vol.22
, pp. 433-444
-
-
Ramirez, R.D.1
Herbert, B.S.2
Vaughan, M.B.3
-
31
-
-
0141857636
-
Telomerase protects cancer-prone human cells from chromosomal instability and spontaneous immortalization
-
Elmore LW, Turner KC, Gollahon LS, et al.: Telomerase protects cancer-prone human cells from chromosomal instability and spontaneous immortalization. Cancer Biol Ther 2002, 1:391-397. This study demonstrates that ectopic expression of hTERT in HMECs derived from Li-Fraumeni syndrome (p53-deficient) provides both chromosomal and telomeric stability and, interestingly, prevents spontaneous immortalization.
-
(2002)
Cancer Biol Ther
, vol.1
, pp. 391-397
-
-
Elmore, L.W.1
Turner, K.C.2
Gollahon, L.S.3
-
32
-
-
0037038681
-
p16(INK4a) inactivation is not required to immortalize human mammary epithelial cells
-
Herbert BS, Wright WE, Shay JW: p16(INK4a) inactivation is not required to immortalize human mammary epithelial cells. Oncogene 2002, 21:7897-7900. The authors report that growth of HMEC on feeder layers prevents p16 up-regulation and p16-induced premature senescence. Such cells are immortalized by introduction of hTERT alone.
-
(2002)
Oncogene
, vol.21
, pp. 7897-7900
-
-
Herbert, B.S.1
Wright, W.E.2
Shay, J.W.3
-
33
-
-
0037308362
-
Telomerase reconstitution immortalizes human fetal hepatocytes without disrupting their differentiation potential
-
Wege H, Le HT, Chui MS, et al.: Telomerase reconstitution immortalizes human fetal hepatocytes without disrupting their differentiation potential. Gastroenterology 2003, 124:432-444.
-
(2003)
Gastroenterology
, vol.124
, pp. 432-444
-
-
Wege, H.1
Le, H.T.2
Chui, M.S.3
-
34
-
-
0037407652
-
Myofibroblast differentiation of normal human keratocytes and hTERT, extended-life human corneal fibroblasts
-
Jester JV, Huang J, Fisher S, et al.: Myofibroblast differentiation of normal human keratocytes and hTERT, extended-life human corneal fibroblasts. Invest Ophthalmol Vis Sci 2003, 44:1850-1858.
-
(2003)
Invest Ophthalmol Vis Sci
, vol.44
, pp. 1850-1858
-
-
Jester, J.V.1
Huang, J.2
Fisher, S.3
-
35
-
-
0035992840
-
Telomerase immortalization of human myometrial cells
-
Condon J, Yin S, Mayhew B, et al.: Telomerase immortalization of human myometrial cells. Biol Reprod 2002, 67:506-514.
-
(2002)
Biol Reprod
, vol.67
, pp. 506-514
-
-
Condon, J.1
Yin, S.2
Mayhew, B.3
-
36
-
-
0037369703
-
Characterisation of telomerase immortalised normal human oesophageal squamous cells
-
Morales CP, Gandia KG, Ramirez RD, et al.: Characterisation of telomerase immortalised normal human oesophageal squamous cells. Gut 2003, 52:327-333.
-
(2003)
Gut
, vol.52
, pp. 327-333
-
-
Morales, C.P.1
Gandia, K.G.2
Ramirez, R.D.3
-
37
-
-
0042169024
-
Extended lifespan of Barrett's esophagus epithelium transduced with the human telomerase catalytic subunit: A useful in vitro model
-
Palanca-Wessels MC, Klingelhutz A, Reid BJ, et al.: Extended lifespan of Barrett's esophagus epithelium transduced with the human telomerase catalytic subunit: a useful in vitro model. Carcinogenesis 2003, 24:1183-1190. hTERT introduced into premalignant, telomerase-negative, esophageal epithelial cells derived from Barrett's dysplasia produces long-lived cells in culture that retain features of chromosomal instability, providing a potentially valuable research tool.
-
(2003)
Carcinogenesis
, vol.24
, pp. 1183-1190
-
-
Palanca-Wessels, M.C.1
Klingelhutz, A.2
Reid, B.J.3
-
38
-
-
0344406970
-
Deletion of the telomerase reverse transcriptase gene and haploinsufficiency of telomere maintenance in Cri du chat syndrome
-
Zhang A, Zheng C, Hou M, et al.: Deletion of the telomerase reverse transcriptase gene and haploinsufficiency of telomere maintenance in Cri du chat syndrome. Am J Hum Genet 2003, 72:940-948. Demonstration of hTERT haploinsufficiency in humans: loss of the hTERT gene in Cri-du-chat syndrome (distal 5p deletion) results in decreased hTERT mRNA expression and short telomere phenotype in cultured cells. This phenotype is reversed upon introduction of ectopic hTERT.
-
(2003)
Am J Hum Genet
, vol.72
, pp. 940-948
-
-
Zhang, A.1
Zheng, C.2
Hou, M.3
-
39
-
-
0037064127
-
Stabilization of telomere length and karyotypic stability are directly correlated with the level of hTERT gene expression in primary fibroblasts
-
Cui W, Aslam S, Fletcher J, et al.: Stabilization of telomere length and karyotypic stability are directly correlated with the level of hTERT gene expression in primary fibroblasts. J Biol Chem 2002, 277:38531-38539.
-
(2002)
J Biol Chem
, vol.277
, pp. 38531-38539
-
-
Cui, W.1
Aslam, S.2
Fletcher, J.3
-
40
-
-
0037133668
-
Preferential maintenance of critically short telomeres in mammalian cells heterozygous for mTert
-
Liu Y, Kha H, Ungrin M, et al.: Preferential maintenance of critically short telomeres in mammalian cells heterozygous for mTert. Proc Natl Acad Sci U S A 2002, 99:3597-3602.
-
(2002)
Proc Natl Acad Sci U S A
, vol.99
, pp. 3597-3602
-
-
Liu, Y.1
Kha, H.2
Ungrin, M.3
-
41
-
-
0037133563
-
Haploinsufficiency of mTR results in defects in telomere elongation
-
Hathcock KS, Hemann MT, Opperman KK, et al.: Haploinsufficiency of mTR results in defects in telomere elongation. Proc Natl Acad Sci U S A 2002, 99:3591-3596.
-
(2002)
Proc Natl Acad Sci U S A
, vol.99
, pp. 3591-3596
-
-
Hathcock, K.S.1
Hemann, M.T.2
Opperman, K.K.3
-
42
-
-
0042169025
-
Transcriptional regulation of the telomerase hTERT gene as a target for cellular and viral oncogenic mechanisms
-
Horikawa I, Barrett JC: Transcriptional regulation of the telomerase hTERT gene as a target for cellular and viral oncogenic mechanisms. Carcinogenesis 2003, 24:1167-1176. Extensive review of transcriptional regulation of the hTERT gene, including viral cis-activation mechanisms.
-
(2003)
Carcinogenesis
, vol.24
, pp. 1167-1176
-
-
Horikawa, I.1
Barrett, J.C.2
-
43
-
-
0037404425
-
Putative telomere-recruiting domain in the catalytic subunit of human telomerase
-
Armbruster BN, Etheridge KT, Broccoli D, Counter CM: Putative telomere-recruiting domain in the catalytic subunit of human telomerase. Mol Cell Biol 2003, 23:3237-3246.
-
(2003)
Mol Cell Biol
, vol.23
, pp. 3237-3246
-
-
Armbruster, B.N.1
Etheridge, K.T.2
Broccoli, D.3
Counter, C.M.4
-
44
-
-
0242286004
-
The C terminus of the human telomerase reverse transcriptase is a determinant of enzyme processivity
-
Huard S, Moriarty TJ, Autexier C: The C terminus of the human telomerase reverse transcriptase is a determinant of enzyme processivity. Nucleic Acids Res 2003, 31:4059-4070.
-
(2003)
Nucleic Acids Res
, vol.31
, pp. 4059-4070
-
-
Huard, S.1
Moriarty, T.J.2
Autexier, C.3
-
45
-
-
0037871858
-
Integrations of the hepatitis B virus (HBV) and human papillomavirus (HPV) into the human telomerase reverse transcriptase (hTERT) gene in liver and cervical cancers
-
Ferber MJ, Montoya DP, Yu C, et al.: Integrations of the hepatitis B virus (HBV) and human papillomavirus (HPV) into the human telomerase reverse transcriptase (hTERT) gene in liver and cervical cancers. Oncogene 2003, 22:3813-3820. The authors document examples of HPV and HBV viral insertions at the hTERT gene, a potentially important mechanism for hTERT gene activation in cancers with viral etiology.
-
(2003)
Oncogene
, vol.22
, pp. 3813-3820
-
-
Ferber, M.J.1
Montoya, D.P.2
Yu, C.3
-
46
-
-
0038239507
-
Expression profile of a gamma-deletion variant of the human telomerase reverse transcriptase gene
-
Hisatomi H, Ohyashiki K, Ohyashiki JH, et al.: Expression profile of a gamma-deletion variant of the human telomerase reverse transcriptase gene. Neoplasia 2003, 5:193-197.
-
(2003)
Neoplasia
, vol.5
, pp. 193-197
-
-
Hisatomi, H.1
Ohyashiki, K.2
Ohyashiki, J.H.3
-
47
-
-
0037229067
-
Human chromosome 5 carries a putative telomerase repressor gene
-
Kugoh H, Shigenami K, Funaki K, et al.: Human chromosome 5 carries a putative telomerase repressor gene. Genes Chromosomes Cancer 2003, 36:37-47.
-
(2003)
Genes Chromosomes Cancer
, vol.36
, pp. 37-47
-
-
Kugoh, H.1
Shigenami, K.2
Funaki, K.3
-
48
-
-
0036782079
-
Hypermethylation of the human telomerase catalytic subunit (hTERT) gene correlates with telomerase activity
-
Guilleret I, Yan P, Grange F, et al.: Hypermethylation of the human telomerase catalytic subunit (hTERT) gene correlates with telomerase activity. Int J Cancer 2002, 101:335-341. These authors report the paradoxical finding that hTERT mRNA expression is tightly correlated with hTERT promoter hypermethylation in a number of cancer cell lines and tissues. These results agree with prior reports showing hTERT repression following 5-aza-cytidine treatment, but differ from other studies showing no clear-cut relationship between hTERT expression and promoter methylation status.
-
(2002)
Int J Cancer
, vol.101
, pp. 335-341
-
-
Guilleret, I.1
Yan, P.2
Grange, F.3
-
49
-
-
0036949605
-
The human telomerase RNA gene (hTERC) is regulated during carcinogenesis but is not dependent on DNA methylation
-
Guilleret I, Yan P, Guillou L, et al.: The human telomerase RNA gene (hTERC) is regulated during carcinogenesis but is not dependent on DNA methylation. Carcinogenesis 2002, 23:2025-2030.
-
(2002)
Carcinogenesis
, vol.23
, pp. 2025-2030
-
-
Guilleret, I.1
Yan, P.2
Guillou, L.3
-
50
-
-
0037821661
-
Multiple tumor suppressor pathways negatively regulate telomerase
-
Lin SY, Elledge SJ: Multiple tumor suppressor pathways negatively regulate telomerase. Cell 2003, 113:881-889. The authors use enhanced retroviral mutagenesis coupled with a GFP reporter under hTERT promoter control to randomly activate genes that negatively affect hTERT transcription. Several different pathways are identified that appear to function in telomerase suppression. For several candidates, use of RNAi to knock down their expression in telomerase negative cells leads to hTERT induction and, in the case of the tumor suppressor menin, apparent immortalization. Further work should identify additional candidates as the screen was not saturated.
-
(2003)
Cell
, vol.113
, pp. 881-889
-
-
Lin, S.Y.1
Elledge, S.J.2
-
51
-
-
0036711651
-
Subnuclear shuttling of human telomerase induced by transformation and DNA damage
-
Wong JM, Kusdra L, Collins K: Subnuclear shuttling of human telomerase induced by transformation and DNA damage. Nat Cell Biol 2002, 4:731-736. The localization of limiting amounts of functional GFP-hTERT expressed in normal, transformed, or tumor cells was followed by confocal microscopy. In normal cells, hTERT was primarily sequestered in the nucleolus, with transient release during S-phase. In contrast, transformed and cancer cells exhibited cell cycle-independent nucleoplasmic localization. Interestingly, all cell types showed enhanced nucleolar association in response to ionizing radiation. These findings point to a novel sequestration mechanism for telomerase regulation.
-
(2002)
Nat Cell Biol
, vol.4
, pp. 731-736
-
-
Wong, J.M.1
Kusdra, L.2
Collins, K.3
-
52
-
-
0036311278
-
Nucleolar localization of hTERT protein is associated with telomerase function
-
Yang Y, Chen Y, Zhang C, et al.: Nucleolar localization of hTERT protein is associated with telomerase function. Exp Cell Res 2002, 277:201-209. In agreement with Wong et al. [51], these authors find a predominant nucleoplasmic distribution of hTERT in transformed and cancer cells. Deletion mapping points to two regions, amino acids 1-14 and 471-686 of hTERT, important for nucleolar targeting.
-
(2002)
Exp Cell Res
, vol.277
, pp. 201-209
-
-
Yang, Y.1
Chen, Y.2
Zhang, C.3
-
53
-
-
0037025334
-
The nucleolar localization domain of the catalytic subunit of human telomerase
-
Etheridge KT, Banik SS, Armbruster BN, et al.: The nucleolar localization domain of the catalytic subunit of human telomerase. J Biol Chem 2002, 277:24764-24770. Deletion mapping indicates that the region encompassed by amino acids 326-620 of hTERT functions in nucleolar targeting. hTERT nucleolar localization was found to be independent of either the ability to bind hTR or the presence of hTR.
-
(2002)
J Biol Chem
, vol.277
, pp. 24764-24770
-
-
Etheridge, K.T.1
Banik, S.S.2
Armbruster, B.N.3
-
54
-
-
0043199578
-
Telomerase maintains telomere structure in normal human cells
-
Masutomi K, Yu EY, Khurts S, et al.: Telomerase maintains telomere structure in normal human cells. Cell 2003, 114:241-253. This provocative report demonstrates expression of hTERT mRNA and protein in normal human fibroblasts in culture, previously thought to be completely telomerase negative. Expression is cell cycle regulated and limited to S-phase, and the resultant telomerase activity is insufficient to prevent telomere shortening due to cell replication. The authors propose that telomerase is acting on the single stranded 3′ overhang in these cells to delay the onset of senescence.
-
(2003)
Cell
, vol.114
, pp. 241-253
-
-
Masutomi, K.1
Yu, E.Y.2
Khurts, S.3
-
55
-
-
0037382414
-
Erosion of the telomeric single-strand overhang at replicative senescence
-
Stewart SA, Ben-Porath I, Carey VJ, et al.: Erosion of the telomeric single-strand overhang at replicative senescence. Nat Genet 2003, 33:492-496. This study applies an assay that measures the aggregate length of the 3′ single-stranded telomeric overhang to cultured normal fibroblasts. The authors report that marked overhang loss occurs as cells near senescence and propose that overhang loss is used by the cell as a signal for entry into senescence.
-
(2003)
Nat Genet
, vol.33
, pp. 492-496
-
-
Stewart, S.A.1
Ben-Porath, I.2
Carey, V.J.3
-
56
-
-
0037457987
-
Evidence that exposure of the telomere 3′ overhang sequence induces senescence
-
Li GZ, Eller MS, Firoozabadi R, Gilchrest BA: Evidence that exposure of the telomere 3′ overhang sequence induces senescence. Proc Natl Acad Sci U S A 2003, 100:527-531.
-
(2003)
Proc Natl Acad Sci U S A
, vol.100
, pp. 527-531
-
-
Li, G.Z.1
Eller, M.S.2
Firoozabadi, R.3
Gilchrest, B.A.4
-
57
-
-
18644373013
-
Telomerase contributes to tumorigenesis by a telomere length-independent mechanism
-
Stewart SA, Hahn WC, O'Connor BF, et al.: Telomerase contributes to tumorigenesis by a telomere length-independent mechanism. Proc Natl Acad Sci U S A 2002, 99:12606-12611. These authors find that the expression of oncogenic ras in the telomerase negative ALT cell line GM847 is unable to convert them to the tumorigenic state. Additional introduction of hTERT allows tumorigenic conversion. Surprisingly, the same is also true of an hTERT mutant defective in telomere length maintenance, implying that hTERT may be supplying additional functions beyond telomeric DNA synthesis.
-
(2002)
Proc Natl Acad Sci U S A
, vol.99
, pp. 12606-12611
-
-
Stewart, S.A.1
Hahn, W.C.2
O'Connor, B.F.3
-
58
-
-
0037062454
-
Constitutive telomerase expression promotes mammary carcinomas in aging mice
-
-/- background. However, TERT transgenic mice exhibited an overall increase in cancer incidence, with a high proportion of breast carcinoma in aged female mice (compared to none in wt controls). The finding of increased tumorigenesis in a background of ample telomere reserve supports the concept of additional functions for TERT apart from telomere maintenance.
-
(2002)
Proc Natl Acad Sci U S A
, vol.99
, pp. 8191-8196
-
-
Artandi, S.E.1
Alson, S.2
Tietze, M.K.3
-
59
-
-
0038056347
-
Telomerase modulates expression of growth-controlling genes and enhances cell proliferation
-
Smith LL, Coller HA, Roberts JM: Telomerase modulates expression of growth-controlling genes and enhances cell proliferation. Nat Cell Biol 2003, 5:474-479. hTERT introduced into HMECs led to changes in expression of genes involved in cell proliferation. These cells also exhibited a growth advantage upon mitogen-withdrawal. Surprisingly, both responses were dependent on catalytically active hTERT.
-
(2003)
Nat Cell Biol
, vol.5
, pp. 474-479
-
-
Smith, L.L.1
Coller, H.A.2
Roberts, J.M.3
-
60
-
-
0037390962
-
TERT suppresses apoptotis at a premitochondrial step by a mechanism requiring reverse transcriptase activity and 14-3-3 protein-binding ability
-
Zhang P, Chan SL, Fu W, et al.: TERT suppresses apoptotis at a premitochondrial step by a mechanism requiring reverse transcriptase activity and 14-3-3 protein-binding ability. FASEB J 2003, 17:767-769.
-
(2003)
FASEB J
, vol.17
, pp. 767-769
-
-
Zhang, P.1
Chan, S.L.2
Fu, W.3
-
61
-
-
85047697807
-
TERT regulates cell survival independent of telomerase enzymatic activity
-
Cao Y, Li H, Deb S, Liu JP: TERT regulates cell survival independent of telomerase enzymatic activity. Oncogene 2002, 21:3130-3138.
-
(2002)
Oncogene
, vol.21
, pp. 3130-3138
-
-
Cao, Y.1
Li, H.2
Deb, S.3
Liu, J.P.4
-
62
-
-
0037115935
-
Nijmegen breakage syndrome gene, NBS1, and molecular links to factors for genome stability
-
Tauchi H, Matsuura S, Kobayashi J, et al.: Nijmegen breakage syndrome gene, NBS1, and molecular links to factors for genome stability. Oncogene 2002, 21:8967-8980.
-
(2002)
Oncogene
, vol.21
, pp. 8967-8980
-
-
Tauchi, H.1
Matsuura, S.2
Kobayashi, J.3
-
63
-
-
0036921562
-
Recruitment of NBS1 into PML oncogenic domains via interaction with SP100 protein
-
Naka K, lkeda K, Motoyama N: Recruitment of NBS1 into PML oncogenic domains via interaction with SP100 protein. Biochem Biophys Res Commun 2002, 299:863-871.
-
(2002)
Biochem Biophys Res Commun
, vol.299
, pp. 863-871
-
-
Naka, K.1
Lkeda, K.2
Motoyama, N.3
-
64
-
-
0036899106
-
The Bloom syndrome helicase BLM interacts with TRF2 in ALT cells and promotes telomeric DNA synthesis
-
Stavropoulos DJ, Bradshaw PS, Li X, et al.: The Bloom syndrome helicase BLM interacts with TRF2 in ALT cells and promotes telomeric DNA synthesis. Hum Mol Genet 2002, 11:3135-3144.
-
(2002)
Hum Mol Genet
, vol.11
, pp. 3135-3144
-
-
Stavropoulos, D.J.1
Bradshaw, P.S.2
Li, X.3
-
65
-
-
0038241878
-
Candidate chromosomal regions for genes involved in activation of alternative lengthening of telomeres in human immortal cell lines
-
Shigeeda N, Uchida M, Barrett JC, Tsutsui T: Candidate chromosomal regions for genes involved in activation of alternative lengthening of telomeres in human immortal cell lines. Exp Gerontol 2003, 38:641-651. Loss of heterozygosity analysis implicates a gene or genes on chromosome 8 as being involved in regulation of the ALT telomere maintenance pathway.
-
(2003)
Exp Gerontol
, vol.38
, pp. 641-651
-
-
Shigeeda, N.1
Uchida, M.2
Barrett, J.C.3
Tsutsui, T.4
-
66
-
-
0037426088
-
Alternative lengthening of telomeres and survival in patients with glioblastoma multiforme
-
Hakin-Smith V, Jellinek DA, Levy D, et al.: Alternative lengthening of telomeres and survival in patients with glioblastoma multiforme. Lancet 2003, 361:836-838. GBM patients with ALT-positive/telomerase-negative tumor phenotype (20% of the study group) show an approximately twofold greater median survival; thus, ALT may be a potential prognostic indicator in GBM.
-
(2003)
Lancet
, vol.361
, pp. 836-838
-
-
Hakin-Smith, V.1
Jellinek, D.A.2
Levy, D.3
-
67
-
-
0344837710
-
Absence of a telomere maintenance mechanism as a favorable prognostic factor in patients with osteosarcoma
-
Ulaner GA, Huang HY, Otero J, et al.: Absence of a telomere maintenance mechanism as a favorable prognostic factor in patients with osteosarcoma. Cancer Res 2003, 63:1759-1763. Unlike the results for GBM (see [66]), these authors found no difference in outcome for telomerase-positive versus ALT-positive osteosarcomas. However, lack of both telomere maintenance mechanisms (18% of study group) was associated with improved survival in this osteosarcoma series.
-
(2003)
Cancer Res
, vol.63
, pp. 1759-1763
-
-
Ulaner, G.A.1
Huang, H.Y.2
Otero, J.3
-
68
-
-
0042674370
-
A novel telomerase template antagonist (GRN 163) as a potential anticancer agent
-
Asai A, Oshima Y, Yamamoto Y, et al.: A novel telomerase template antagonist (GRN 163) as a potential anticancer agent. Cancer Res 2003, 63:3931-3939.
-
(2003)
Cancer Res
, vol.63
, pp. 3931-3939
-
-
Asai, A.1
Oshima, Y.2
Yamamoto, Y.3
-
69
-
-
0037442701
-
Blocking telomerase by dietary polyphenols is a major mechanism for limiting the growth of human cancer cells in vitro and in vivo
-
Naasani I, Oh-Hashi F, Oh-Hara T, et al.: Blocking telomerase by dietary polyphenols is a major mechanism for limiting the growth of human cancer cells in vitro and in vivo. Cancer Res 2003, 63:824-830.
-
(2003)
Cancer Res
, vol.63
, pp. 824-830
-
-
Naasani, I.1
Oh-Hashi, F.2
Oh-Hara, T.3
-
70
-
-
0347335811
-
Reotropic effects of genistein on MCF-7 breast cancer cells
-
Chinni SR, Alhasan SA, Multani AS, et al.: Reotropic effects of genistein on MCF-7 breast cancer cells. Int J Mol Med 2003, 12:29-34.
-
(2003)
Int J Mol Med
, vol.12
, pp. 29-34
-
-
Chinni, S.R.1
Alhasan, S.A.2
Multani, A.S.3
-
71
-
-
0041817848
-
Telomerase-inhibitory effects of sugar-modified nucleotide analogs
-
Jinmei H, Takahashi H, Amano R, et al.: Telomerase-inhibitory effects of sugar-modified nucleotide analogs. Nucleic Acids Res Suppl 2002:221-222.
-
(2002)
Nucleic Acids Res Suppl
, pp. 221-222
-
-
Jinmei, H.1
Takahashi, H.2
Amano, R.3
-
72
-
-
0037442425
-
Adenoviral-mediated retinoblastoma 94 produces rapid telomere erosion, chromosomal crisis, and caspase-dependent apoptosis in bladder cancer and immortalized human urothelial cells but not in normal urothelial cells
-
Zhang X, Multani AS, Zhou JH, et al.: Adenoviral-mediated retinoblastoma 94 produces rapid telomere erosion, chromosomal crisis, and caspase-dependent apoptosis in bladder cancer and immortalized human urothelial cells but not in normal urothelial cells. Cancer Res 2003, 63:760-765.
-
(2003)
Cancer Res
, vol.63
, pp. 760-765
-
-
Zhang, X.1
Multani, A.S.2
Zhou, J.H.3
-
73
-
-
0042674013
-
Telomerase-dependent oncolytic adenovirus for cancer treatment
-
Huang TG, Savontaus MJ, Shinozaki K, et al.: Telomerase-dependent oncolytic adenovirus for cancer treatment. Gene Ther 2003, 10:1241-1247.
-
(2003)
Gene Ther
, vol.10
, pp. 1241-1247
-
-
Huang, T.G.1
Savontaus, M.J.2
Shinozaki, K.3
-
74
-
-
0038745637
-
A telomerase-dependent conditionally replicating adenovirus for selective treatment of cancer
-
Wirth T, Zender L, Schulte B, et al.: A telomerase-dependent conditionally replicating adenovirus for selective treatment of cancer. Cancer Res 2003, 63:3181-3188.
-
(2003)
Cancer Res
, vol.63
, pp. 3181-3188
-
-
Wirth, T.1
Zender, L.2
Schulte, B.3
-
75
-
-
0036782884
-
Telomerase: A target for cancer therapeutics
-
Shay JW, Wright WE: Telomerase: a target for cancer therapeutics. Cancer Cell 2002, 2:257-265.
-
(2002)
Cancer Cell
, vol.2
, pp. 257-265
-
-
Shay, J.W.1
Wright, W.E.2
-
76
-
-
0038369786
-
Delivering antisense telomerase RNA by a hybrid adenovirus/ adeno-associated virus significantly suppresses the malignant phenotype and enhances cell apoptosis of human breast cancer cells
-
Zhang X, Chen Z, Chen Y, Tong T: Delivering antisense telomerase RNA by a hybrid adenovirus/ adeno-associated virus significantly suppresses the malignant phenotype and enhances cell apoptosis of human breast cancer cells. Oncogene 2003, 22:2405-2416.
-
(2003)
Oncogene
, vol.22
, pp. 2405-2416
-
-
Zhang, X.1
Chen, Z.2
Chen, Y.3
Tong, T.4
-
77
-
-
0036834259
-
Inhibition of human telomerase enhances the effect of chemotherapeutic agents in lung cancer cells
-
Misawa M, Tauchi T, Sashida G, et al.: Inhibition of human telomerase enhances the effect of chemotherapeutic agents in lung cancer cells. Int J Oncol 2002, 21:1087-1092.
-
(2002)
Int J Oncol
, vol.21
, pp. 1087-1092
-
-
Misawa, M.1
Tauchi, T.2
Sashida, G.3
-
78
-
-
0036845833
-
Inhibition of human telomerase enhances the effect of the tyrosine kinase inhibitor, imatinib, in BCR-ABL-positive leukemia cells
-
Tauchi T, Nakajima A, Sashida G, et al.: Inhibition of human telomerase enhances the effect of the tyrosine kinase inhibitor, imatinib, in BCR-ABL-positive leukemia cells. Clin Cancer Res 2002, 8:3341-3347.
-
(2002)
Clin Cancer Res
, vol.8
, pp. 3341-3347
-
-
Tauchi, T.1
Nakajima, A.2
Sashida, G.3
-
79
-
-
0037350830
-
Telomerase inhibition enhances apoptosis in human acute leukemia cells: Possibility of antitelomerase therapy
-
Nakajima A, Tauchi T, Sashida G, et al.: Telomerase inhibition enhances apoptosis in human acute leukemia cells: possibility of antitelomerase therapy. Leukemia 2003, 17:560-567.
-
(2003)
Leukemia
, vol.17
, pp. 560-567
-
-
Nakajima, A.1
Tauchi, T.2
Sashida, G.3
-
80
-
-
0038701811
-
Telomerase inhibition as cancer therapy
-
Saretzki G: Telomerase inhibition as cancer therapy. Cancer Lett 2003, 194:209-219.
-
(2003)
Cancer Lett
, vol.194
, pp. 209-219
-
-
Saretzki, G.1
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