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1 h high-risk and low-risk patients with acute promyelocytic leukaemia.
2 c acid (RA)-induced differentiation of acute promyelocytic leukaemia and HL-60 cells, CD38 is one of
3 s and co-repressors contribute towards acute promyelocytic leukaemia and thyroid hormone resistance s
4 c leukaemia (PML) tumour suppressor of acute promyelocytic leukaemia (APL) accumulates in the PML nuc
5                                        Acute promyelocytic leukaemia (APL) arises following a recipro
6 t of all-trans-retinoic acid resistant acute promyelocytic leukaemia (APL) cases, encodes a DNA bindi
7                        The PML gene of acute promyelocytic leukaemia (APL) encodes a cell growth and
8                                        Acute promyelocytic leukaemia (APL), associated with chromosom
9                  Here we show that, in acute promyelocytic leukaemia (APL), ILC2s are increased and h
10  discovered in patients suffering from acute promyelocytic leukaemia (APL).
11 de a new model for the pathogenesis of acute promyelocytic leukaemia (APL).
12 cus, are oncogenic and result in human acute promyelocytic leukaemia (APL).
13 for acute myeloid leukaemia (excluding acute promyelocytic leukaemia) compared with chemotherapy alon
14 gible patients (aged >/=16 years) with acute promyelocytic leukaemia, confirmed by the presence of th
15  previously unknown role for the cytoplasmic promyelocytic leukaemia (cPML) tumour suppressor in TGF-
16          The outlook for patients with acute promyelocytic leukaemia has improved vastly with the use
17 (CBMNCyt) assay conducted with respectively, promyelocytic leukaemia (HL-60) and colon adenocarcinoma
18  myelomonocytic leukaemia (WEHI-3) and Human promyelocytic leukaemia (HL-60) cell lines.
19 d that PTEN is aberrantly localized in acute promyelocytic leukaemia, in which PML function is disrup
20                                        Acute promyelocytic leukaemia is a chemotherapy-sensitive subg
21 omal translocations with either the PML (for promyelocytic leukaemia) or the PLZF (for promyelocytic
22 r discrete nuclear structures known as ND10, promyelocytic leukaemia (PML) bodies or PODs.
23 Furthermore, the cytoplasmic localization of promyelocytic leukaemia (PML) is mediated by its nuclear
24                      SnoN interacts with the promyelocytic leukaemia (PML) protein and is recruited t
25 f SnoN results from its interaction with the promyelocytic leukaemia (PML) protein and the accumulati
26                                          The promyelocytic leukaemia (PML) protein controls multiple
27  Expression of TAp73beta efficiently induced promyelocytic leukaemia (PML) protein expression and PML
28     Here, we show that the tumour suppressor promyelocytic leukaemia (PML) protein is a circadian clo
29                                  Loss of the promyelocytic leukaemia (PML) tumour suppressor has been
30                                          The promyelocytic leukaemia (PML) tumour suppressor of acute
31 signatures, including the linear form of the promyelocytic leukaemia (PML)-defined structure in iPSCs
32                 Here we show that functional promyelocytic leukaemia protein (PML) nuclear bodies co-
33 Here we present data indicating that (i) the promyelocytic leukaemia protein (PML) physically interac
34      Here we define the critical role of the promyelocytic leukaemia protein (PML) tumour suppressor
35  nuclear matrix-associated domain containing promyelocytic leukaemia protein.
36                 We excluded those with acute promyelocytic leukaemia, those seen only for a one-time
37         Here the authors show that, in acute promyelocytic leukaemia, tumour-activated ILC2s secrete
38  target of differentiation therapy for acute promyelocytic leukaemia, wherein retinoic acid dissociat
39 n low-risk and high-risk patients with acute promyelocytic leukaemia, with a high cure rate and less
40                                          The promyelocytic leukaemia zinc finger (Plzf) protein (enco
41                          Here we report that promyelocytic leukaemia zinc finger (PLZF), the BTB-zinc
42 istinct lineage that originates from a novel promyelocytic leukaemia zinc finger (PLZF)-expressing IL
43 or promyelocytic leukaemia) or the PLZF (for promyelocytic leukaemia zinc finger) locus, are oncogeni
44 Gli3 (GLI-Kruppel family member 3) and Plzf (promyelocytic leukaemia zinc finger, also known as Zbtb1

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