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1 de II and III gliomas associated with 1p/19q co-deletion.
2 p53 dependent and markedly attenuated by p53 co-deletion.
3 ng serine/threonine-protein kinase 3 (Ripk3) co-deletion.
4 Pten deficiency on the backdrop of Smad4/Apc co-deletion.
6 diffuse glioma taxonomy (IDH mutation, 1p19q co-deletion and ATRX mutation), achieving a mean molecul
8 s of MGMT methylation, IDH mutations, 1p/19q co-deletion, ATRX mutation, and TERT mutations achieve a
9 ular (MGMT methylation, IDH mutation, 1p/19q co-deletion, ATRX mutation, and TERT mutations) predicti
11 oma subgroups (IDHmt, with or without 1p/19q co-deletion [IDHmt/codel], or IDH wild type [IDHwt]; p=0
15 n-free survival by molecular markers (1p/19q co-deletion, MGMT promoter methylation status, and IDH1/
16 lternations in IDH1/2, ATRX, TERT, TP53, and co-deletion of 1p/19q have the ability to reclassify gli
20 at occur early during tumorigenesis, such as co-deletion of chromosome arms 1p and 19q (1p/19q codele
21 as characterized by IDH mutation but without co-deletion of chromosome arms 1p/19q, and further conve
22 eficient RER (Rnaseh2b(DeltaIEC)), bearing a co-deletion of disrupted autophagy (Atg16l1/Rnaseh2b(Del
23 lasm of cornifying lingual keratinocytes and co-deletion of DNase1L2 and Trex2 causes massive accumul
26 ty of the fet3delta strain was suppressed by co-deletion of FRE1, suggesting that the cytotoxic speci
32 ovides a vulnerability for tumors carrying a co-deletion of MTAP and the adjacent CDKN2A tumor suppre
40 engineered murine liver models, we show that co-deletion of Rac1 with Nf2 blocks tumor initiation but
42 netically engineered mouse model of PSCC, by co-deletion of Smad4 and Apc in the androgen-responsive
45 th p16/p14ARF deletion were also studied for co-deletion of the contiguous methylthioadenosine phosph
46 organoid cultures, we show that conditional co-deletion of the LATS1 and LATS2 kinases, key effector
52 develop renal cysts and those with inherited co-deletions of the autosomal dominant polycystic kidney
54 ult mice, we show that either PTEN and SOCS3 co-deletion, or co-overexpression of osteopontin (OPN)/i
55 9q34.3/19p13.3 (NOTCH1/STK11/GNA11) showed a co-deletion pattern, which was associated with a signifi
58 ssification based on IDH mutation and 1p/19q co-deletion status were recapitulated through analysis o
59 confirmed that MTR(asym) could discriminate co-deletion status with an area under the curve of 0.85.
62 uires the presence of both IDH-mt and 1p/19q co-deletion, whereas anaplastic astrocytoma is divided i
63 permethylation and unintentional monoallelic co-deletion with phosphatase and tensin homolog (PTEN) i