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1 tions, consistent with suppression of their 'immortality'.
2 telomerase (EC 2.7.7.49) to promote cellular immortality.
3 rk of cancer cells which enables replicative immortality.
4 exhibit comparable patterns of mortality and immortality.
5 tinue in this eternal cycle, termed germline immortality.
6 length maintenance is crucial to cancer cell immortality.
7 the hotspot mutations that confer tumor cell immortality.
8 CN through generations, supporting germline immortality.
9 ing how much telomerase is required for cell immortality.
10 ase pathway for telomere maintenance to gain immortality.
11 al role in chromosome stability and cellular immortality.
12 mere length, is sufficient to result in cell immortality.
13 e been overcome in a cancer cell's quest for immortality.
14 tion of the potential to achieve replicative immortality.
15 ibutes to the acquisition and maintenance of immortality.
16 ic BCL-2 family proteins to enforce cellular immortality.
17 east cells to overcome senescence and attain immortality.
18 m in addition to hTERT expression to achieve immortality.
19 ast known proliferative blockade to cellular immortality.
20 and essential feature of germ cells is their immortality.
21 el and may facilitate cell transformation to immortality.
22 maintenance mechanism to achieve replicative immortality.
23 allowing cancer cells to achieve replicative immortality.
24 to the role of telomere regulation in cancer immortality.
25 ere-based proliferative barriers and achieve immortality.
26 critical for the development of replicative immortality.
27 sent the genetic underpinnings of tumor cell immortality.
28 lomere length and are essential for germline immortality.
30 key pathways required to support replicative immortality and anchorage independent growth, a predicto
31 The roles of telomerase in both cellular immortality and cancer are vibrant areas of current rese
34 e tumor cells is sufficient to reverse their immortality and cause a phenotype that is, by all genera
35 its medusae reproduce, hinting at biological immortality and challenging our understanding of aging.
37 significant role in establishing cancer cell immortality and is under suspicion for its potential con
38 genetic changes, which follow acquisition of immortality and loss of senescence, are of consistent so
41 to investigate the contribution of cellular immortality and oncogenic transformation of primary huma
42 n of telomerase is crucial for cells to gain immortality and proliferation ability, we examined the r
43 elomere and genome stability to ensure their immortality and shed light on the regeneration medicine
44 rk is critical to understanding how cellular immortality and totipotency are retained, gained, and lo
45 suggest the existence of a suppressor of SCC immortality and tumour development at chromosome 6q14.3-
48 s, however, are able to sustain long-lasting immortality, as prominently exemplified by stem cells.
50 opose that RSD-2 and RSD-6 promote germ cell immortality at stressful temperatures by maintaining tra
51 Our previous work showed that acquisition of immortality at the dysplasia stage of oral cancer progre
52 te telomerase, contributing to proliferative immortality, but the molecular events driving TERT activ
53 Most glioblastomas (GBMs) achieve cellular immortality by acquiring a mutation in the telomerase re
55 both aging and rejuvenating lineages retain immortality by reaching their respective states of physi
58 e activity is closely linked to the cellular immortality characteristic of late stage carcinogenesis,
62 s review examines the mechanisms of germline immortality-how germline cells reset the aging of cells-
63 on the dominance of cellular senescence over immortality, immortal human cell lines have been assigne
66 lls experience multiple barriers to cellular immortality in culture (mortality mechanisms 0, 1, and 2
68 terized by serum independence in culture and immortality in vivo, when compared with wild type contro
69 bute to a molecular understanding of Hydra's immortality, indicate an evolutionarily conserved role o
70 sors, resist cell death, promote replicative immortality, induce angiogenesis, support invasion and m
71 phase transition between finite lifetime and immortality (infinite proliferation) of the cell populat
82 nce telomerase plays a critical role in cell immortality, it is an attractive target for a selective
84 n programs in vitro and in vivo, replicative immortality, malignancy, rapid tumor growth, pigmentatio
87 e is thought to be essential for replicative immortality, MYC, in conjunction with cofactors, confers
90 ans infection on the continuing survival and immortality of human peripheral blood mononuclear cells
91 The key to this methodology is the intrinsic immortality of normal intestinal stem cells (ISCs) and c
96 elomeres (ALT), is essential for replicative immortality of tumor cells, although its regulatory mech
100 ther, these observations imply that cellular immortality promotes epigenetic adaptation to highly pro
102 r output from stem cells as well as inducing immortality, self-renewal, and tumorigenesis in myeloid
103 The majority of human tumor cells acquire immortality through expression of the catalytic subunit
104 pected role for NRSS in maintaining germline immortality through maintenance of a vulnerable genomic
105 e between cellular life and death, achieving immortality through pathologic enforcement of survival p
107 lls are distinct from somatic cells in their immortality, totipotency, and ability to undergo meiosis
108 ence of cells with stem-cell properties (ie, immortality, transplantability, and resistance to therap
109 ify the genes that are required for germline immortality, we isolated Caenorhabditis elegans mutants
110 A hallmark of tumor cells is replicative immortality, which can be achieved, in part, by the acti
111 telomeres (ALT) to sustain their replicative immortality, yet there are currently no targeted therapi