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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
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
13 s associated with transient activation of an alternative lengthening of telomere (ALT) pathway, but f
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
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
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
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
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
44 Some human cancers maintain telomeres using alternative lengthening of telomeres (ALT), a process th
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
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
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
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
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
81 DAXX, or ATRX, expression, and activation of alternative lengthening of telomeres with data from comp
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