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1  The gene encoding MTAP, MTAP, is frequently codeleted along with the tumor suppressor gene p16 in ma
2                         Patients with 1p/19q codeleted anaplastic oligodendroglial tumors who partici
3 ting 60 of 127 patients, virtually all 1p19q codeleted and IDH mutated (59 of 60).
4       For the subset of patients with 1p/19q codeleted AO/AOA, PCV plus RT may be an especially effec
5 showed reduced survival, compared with their codeleted counterparts with weaker EGFR expression.
6 ma [AOA]), are chemosensitive, especially if codeleted for 1p/19q, but whether patients live longer a
7 n region in TgPWS mice, with 2 nonimprinted, codeleted genes reduced twofold.
8  and poorer outcome in patients with a 1p19q codeleted glioma.
9                          CIC mutant grade II codeleted gliomas spontaneously grew faster than WTs.
10                                 In the 1p19q codeleted gliomas, CIC mutations were associated with a
11 c carcinoma cell lines were p16(-), MTAP was codeleted in all five cases.
12                                Patients with codeleted mutated tumors (14.7 v 6.8 years; HR, 0.49; 95
13 HG concentration decreased rapidly in 1p/19q codeleted oligodendrogliomas and with a slower time cour
14 tomas, class II tumors are similar to 1p/19q codeleted oligodendrogliomas, and class III represents i
15 ic astrocytomas, a second grouped the 1p/19q codeleted oligodendrogliomas, and the mixture of remaini
16                      Genes in the frequently codeleted region 17p13 and 18q21/22 were associated with
17                                       1p/19q-codeleted tumors derive more benefit from adjuvant PCV c
18                                Patients with codeleted tumors lived longer than those with noncodelet
19                       Although patients with codeleted tumors lived longest, patients with noncodelet
20 .001), and the median survival of those with codeleted tumors treated with PCV plus RT was twice that
21 The INK4A-exon 1beta and the INK4B gene were codeleted with INK4A in all of the homozygously deleted
22 tromeric of tumor protein p53 (Tp53), and is codeleted with Tp53, we propose that loss of miR-3676 ca

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