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1 s that lack telomerase in pathways known as 'alternative lengthening of telomeres'.
2 t telomere maintenance mechanism termed ALT (alternative lengthening of telomeres).
3 sing a recombinational mechanism termed ALT (alternative lengthening of telomeres).
4 hanism of telomere lengthening known as ALT (alternative lengthening of telomeres).
5 telomerase (+) and ALT (+) cell lines (ALT = alternative lengthening of telomeres).
6  of pNETs, in association with activation of alternative lengthening of telomeres.
7 ls of genomic instability, and activation of alternative lengthening of telomeres.
8 e foci in both telomerase-active (TA(+)) and alternative lengthening of telomere (ALT) cells and decr
9 telomere stability in cells that rely on the alternative lengthening of telomere (ALT) mechanism.
10 nce of detectable telomerase activity by the alternative lengthening of telomere (ALT) mechanism.
11 is maintain telomeres both by telomerase and alternative lengthening of telomere (ALT) mechanisms in
12                    There was no evidence for alternative lengthening of telomere (ALT) pathway activa
13 s associated with transient activation of an alternative lengthening of telomere (ALT) pathway, but f
14 esultant tumors maintained telomeres via the alternative lengthening of telomere (ALT) pathway.
15 RF1 and TRF2 in immortalized cells using the alternative lengthening of telomere (ALT) pathways.
16                                              Alternative lengthening of telomere (ALT) tumors maintai
17 veal a higher level of genome instability in alternative lengthening of telomere (ALT)-positive tumor
18 owth subsequently resumed as tumors acquired alternative lengthening of telomeres (ALT) and aberrant
19  that maintain their chromosome ends through alternative lengthening of telomeres (ALT) display persi
20 ce of telomerase suggested activation of the alternative lengthening of telomeres (ALT) in the UV-exp
21                                              Alternative lengthening of telomeres (ALT) is a telomera
22                                              Alternative lengthening of telomeres (ALT) is a telomera
23 comas lack telomerase expression and use the alternative lengthening of telomeres (ALT) mechanism to
24 n cancers maintain their telomeres using the alternative lengthening of telomeres (ALT) mechanism; a
25                                              Alternative lengthening of telomeres (ALT) necessitates
26 arily at the telomeres of cells that use the alternative lengthening of telomeres (ALT) pathway as th
27 in cells that use the recombination-mediated alternative lengthening of telomeres (ALT) pathway elici
28 pes are often found in tumor cells using the alternative lengthening of telomeres (ALT) pathway for t
29 more prevalent in tumor cells engaged in the alternative lengthening of telomeres (ALT) pathway of te
30       Cancer cells rely on telomerase or the alternative lengthening of telomeres (ALT) pathway to ov
31 roteins found at telomeres maintained by the alternative lengthening of telomeres (ALT) pathway to pr
32 ecombination-driven, telomerase-independent, alternative lengthening of telomeres (ALT) pathway, like
33 raction utilizes the recombination dependent alternative lengthening of telomeres (ALT) pathway.
34 the homologous recombination (HR)-associated alternative lengthening of telomeres (ALT) pathway.
35 rase activity and are classified as using an alternative lengthening of telomeres (ALT) pathway.
36 f homologous recombination implicated in the alternative lengthening of telomeres (ALT) pathway.
37 ecombination in human cells that utilize the Alternative Lengthening of Telomeres (ALT) pathway.
38 ugh the upregulation of telomerase or by the alternative lengthening of telomeres (ALT) pathway.
39 elomeres in a telomerase-independent manner [alternative lengthening of telomeres (ALT) pathway].
40 re maintained through telomerase-independent alternative lengthening of telomeres (ALT) pathways.
41 endent telomere maintenance pathway known as alternative lengthening of telomeres (ALT) that is chara
42 ion of sarcomas, use the recombination-based alternative lengthening of telomeres (ALT) to maintain t
43                 Notably, in contrast to TRD, alternative lengthening of telomeres (ALT) was suppresse
44  Some human cancers maintain telomeres using alternative lengthening of telomeres (ALT), a process th
45            The remaining cancers rely on the alternative lengthening of telomeres (ALT), a recombinat
46  use telomerase, but 5% to 20% of tumors use alternative lengthening of telomeres (ALT), a telomerase
47 l lines use a recombination-based mechanism, alternative lengthening of telomeres (ALT), to maintain
48  HPV-16 E7 induces an increased formation of alternative lengthening of telomeres (ALT)-associated pr
49  structures, suppresses the proliferation of alternative lengthening of telomeres (ALT)-positive cell
50 maintain chromosome ends in cells relying on alternative lengthening of telomeres (ALT).
51 s in a telomerase-independent manner, termed alternative lengthening of telomeres (ALT).
52 d by a telomerase-independent pathway termed alternative lengthening of telomeres (ALT).
53 endent telomere maintenance mechanism termed alternative lengthening of telomeres (ALT).
54  mechanisms, the activation of telomerase or alternative lengthening of telomeres (ALT).
55            These cells maintain telomeres by alternative lengthening of telomeres (ALT).
56  the expression of telomerase or through the alternative lengthening of telomeres (ALT).
57 s or a telomerase-independent pathway termed alternative lengthening of telomeres (ALT).
58 on (TA) and, more rarely, the process termed alternative lengthening of telomeres (ALT).
59 led clear evidence of telomerase-independent alternative lengthening of telomeres (ALT).
60 merase-independent mechanism, referred to as alternative lengthening of telomeres (ALT).
61       19 patients (25%) had tumours with the alternative-lengthening-of-telomere (ALT) phenotype.
62 ess maintain telomeres via a process termed "alternative lengthening of telomeres" (ALT).
63 h somatic ATRX mutations are associated with alternative lengthening of telomeres and clinically aggr
64 ntenance mechanism not involving telomerase (alternative lengthening of telomeres), and point mutatio
65 whether loss of DAXX or ATRX, and consequent alternative lengthening of telomeres, are related to CIN
66 ductions in the fraction of cells containing alternative lengthening of telomere-associated promyeloc
67  hTERT-negative astrocytes, fibroblasts, and alternative lengthening of telomeres cells.
68 ch maintain their telomere length through an alternative lengthening of telomeres DNA recombination p
69 requently lost in cancer cells that use ALT (alternative lengthening of telomeres) for telomere maint
70 results suggest that NBS1 may be involved in alternative lengthening of telomeres in telomerase-negat
71                            We concluded that alternative lengthening of telomeres is important in epi
72 telomerase-independent mechanism called ALT (alternative lengthening of telomeres) is activated as fr
73 Ink4a/Arf-/- tumors showed activation of the alternative lengthening of telomere mechanism, underscor
74 intenance in cancerous human cells using the alternative lengthening of telomeres mechanism and in bu
75 ain long heterogeneous telomeres by the ALT (alternative lengthening of telomeres) mechanism; such tu
76 ough a recombination-based mechanism, termed alternative lengthening of telomeres or ALT.
77 ed cells maintaining telomeres by either the alternative lengthening of telomeres pathway (U2OS) or t
78 e cellular activities, including DNA repair, alternative lengthening of telomeres, transcriptional co
79  elevated in MYCN-amplified tumours, whereas alternative lengthening of telomeres was present in neur
80             Loss of DAXX or ATRX protein and alternative lengthening of telomeres were associated wit
81 DAXX, or ATRX, expression, and activation of alternative lengthening of telomeres with data from comp

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