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1 1p15.5 H19/ICR1 epigenetic hypermethylation (loss of imprinting).
2 id incompatibility has indeed been linked to loss of imprinting.
3  methyltransferase DNMT1 causes a widespread loss of imprinting.
4 In vitro culture of mouse embryos results in loss of imprinting.
5 is biallelic in G9a -/- ES cells, indicating loss of imprinting.
6           Removal of a gene's DMD leads to a loss of imprinting.
7 ence of methylation of SNRPN consistent with loss of imprinting.
8 of 27 tumors informative for IGF2 manifested loss of imprinting.
9 tion in both wild-type and mutant mice, with loss of imprinting.
10 3 promoter in primary human gliomas led to a loss of imprinting and decreased PEG3 mRNA expression th
11  Choriocarcinomas are embryonal tumours with loss of imprinting and hypermethylation at the insulin-l
12         The overexpression of Dnmt3b1 caused loss of imprinting and increased expression of Igf2 as w
13  normally silent maternal Dlk1 in offspring (loss of imprinting) and increased DNA methylation at the
14 elapse with loss of heterozygosity, 25% with loss of imprinting, and 3.3% relapse with retention of t
15 vents, such as promoter hypermethylation and loss of imprinting, are also involved in carcinogenesis.
16                                              Loss of imprinting at 11p15 was identified in one of 42
17 tations in WT1 and loss of heterozygosity or loss of imprinting at 11p15, which results in biallelic
18 the constitutional imprinting and six showed loss of imprinting at either H19 or IGF2.
19                                              Loss of imprinting at IGF2, generally through an H19-ind
20                  We propose a model in which loss of imprinting at the 14q32 domain leads to overexpr
21                      These data suggest that loss of imprinting at the IGF2 and H19 loci play a role
22                                   In humans, loss of imprinting at this locus is associated with tumo
23 hese data indicating environmentally induced loss of imprinting at VTRNA2-1 constitute a plausible ca
24  and the vulnerability of imprinted genes to loss of imprinting changes, there has been extensive spe
25 hat misregulation of non-imprinted genes and loss-of-imprinting characterize the ART-induced overgrow
26 this dynamic period and to determine whether loss of imprinting continues at later stages of developm
27                               As a result of loss of imprinting, DLX5 was upregulated in 69% of preec
28                         To determine whether loss of imprinting in cancer might be reversed by alteri
29  The maternally expressed gene DLX5 showed a loss of imprinting in lymphoblastoid cells from individu
30     The discrepancy between IGF2 and IGF2-AS loss of imprinting in some tumors demonstrates the contr
31 ted head and neck squamous carcinoma for the loss of imprinting in the IGF2 and H19 genes to determin
32 ncreased maternal allele expression of Igf2 (loss of imprinting) in adenoma which form, despite pater
33  occurs through a loss of heterozygosity- or loss of imprinting-independent process.
34  by in vitro reprogramming, and suggest that loss of imprinting is associated with the loss of activi
35 f 5-aza-2'-deoxycytidine on tumor cells with loss of imprinting is not random but specific to one all
36 arental inheritance of chromosome 11p15, and loss of imprinting is observed in several cancers includ
37                                              Loss of imprinting is the silencing of active imprinted
38 olved in maintenance of imprinting (MOI) and loss of imprinting (LOI) are unresolved.
39                                              Loss of imprinting (LOI) associated with hypomethylation
40                                     Although loss of imprinting (LOI) at fetal promoters contributes
41                                     Maternal loss of imprinting (LOI) at the H19/IGF2 locus results i
42                                              Loss of imprinting (LOI) at the IGF2/H19 locus on the ma
43                              We also found a loss of imprinting (LOI) for Igf2 in a limited number of
44                                              Loss of imprinting (LOI) has been observed in many types
45         Alterations of genomic imprinting or loss of imprinting (LOI) have been observed in a number
46 s, and some developmental disorders, exhibit loss of imprinting (LOI) in key genes such as insulin-li
47                                              Loss of imprinting (LOI) is a common epigenetic event in
48                                              Loss of imprinting (LOI) is an epigenetic alteration inv
49                                              Loss of imprinting (LOI) is an epigenetic alteration of
50                                              Loss of imprinting (LOI) is an epigenetic event that rel
51                                         IGF2 loss of imprinting (LOI) is fairly prevalent and implica
52                                              Loss of imprinting (LOI) is the most common molecular ab
53                                              Loss of imprinting (LOI) is the reactivation of the sile
54 tion patterns at imprinted loci resulting in loss of imprinting (LOI) may lead to serious imprinting
55                                              Loss of imprinting (LOI) of H19 is observed in human mal
56 ic acid supplementation during pregnancy and loss of imprinting (LOI) of IGF2 and H19 genes in placen
57                                 Constitutive loss of imprinting (LOI) of IGF2 has been associated wit
58  expression, and suggest a new mechanism for loss of imprinting (LOI) of Igf2, which may be important
59 nts (50%) showed biallelic expression, i.e., loss of imprinting (LOI) of LIT1.
60                                              Loss of imprinting (LOI) of the insulin-like growth fact
61                                              Loss of imprinting (LOI) of the insulin-like growth fact
62 a recent study showing that a mouse model of loss of imprinting (LOI) of the insulin-like growth fact
63 thylation and promoter hypermethylation, and loss of imprinting (LOI) of the insulin-like growth fact
64          We applied the assay to analysis of loss of imprinting (LOI) of the insulin-like growth fact
65                          We hypothesize that loss of imprinting (LOI) of the insulin-like growth fact
66       Recently, we and others have described loss of imprinting (LOI) of the insulin-like growth fact
67                   Loss of heterozygosity and loss of imprinting (LOI) of this region are frequently o
68                                              Loss of imprinting (LOI) results in severe developmental
69                                              Loss of imprinting (LOI), an epigenetic alteration affec
70 ics recapitulate those observed in the human loss-of-imprinting (LOI) overgrowth syndrome Beckwith-Wi
71  locus in LOI cancer cells suggests that the loss of imprinting may lead to a variety of changes in g
72              Thus, loss of heterozygosity or loss of imprinting might simultaneously affect several g
73 egulated in testicular germ cell tumors, and loss of imprinting occurs frequently in testicular semin
74 ly inherited chromosome causes bidirectional loss of imprinting of all genes in the cluster.
75     A deletion within this region results in loss of imprinting of both H19 and Igf2.
76 t synthesize gamma-aminobutyric acid (GABA), loss of imprinting of Dlx5 may alter GABAergic neuron ac
77 ncluding infrequent mutation of p57(KIP2) or loss of imprinting of either of two imprinted gene domai
78      Paternal inheritance of Ex1A-T leads to loss of imprinting of Gsalpha and loss of expression of
79  Paternal inheritance of Ex1A-T-CON leads to loss of imprinting of Gsalpha, resulting in preweaning g
80 t a similar mechanism may be responsible for loss of imprinting of IGF-II in normal brain and Wilms'
81 that show loss of heterozygosity of 11p15 or loss of imprinting of IGF2 also silence HOTS (7/7 and 10
82                                              Loss of imprinting of IGF2 is the most common molecular
83  informative for the ApaI IGF2 polymorphism, loss of imprinting of IGF2 was observed in both normal a
84                        Some patients display loss of imprinting of IGF2, a fetal-specific growth fact
85 e LOI of IGF2, only two of six tumors showed loss of imprinting of IGF2-AS, whereas four of six tumor
86 a disease that has also been associated with loss of imprinting of IGF2.
87                                              Loss of imprinting of insulin-like growth factor-II gene
88                                              Loss of imprinting of the IGF2 gene is frequently observ
89  with a luciferase reporter gene resulted in loss of imprinting of the transgene.
90         These findings strongly suggest that loss of imprinting or switching of allelic expression of
91                             Different from a loss of imprinting pattern, loss of IR and IGF1R causes
92 1c activation, whereas BET inhibitor-induced loss of imprinting was specific to mESCs.
93 overed a novel genetic alteration in cancer, loss of imprinting, which affects several of these genes