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1 dgkin lymphoma (HL) is the binucleated giant Reed-Sternberg cell.
2 h is central to the biologic activity of the Reed-Sternberg cell.
3 s avidly with LP cells than with Hodgkin and Reed-Sternberg cells.
4 e IIB-IV disease; 8% had CD20(+) Hodgkin and Reed-Sternberg cells.
5 cal Hodgkin lymphoma contained CT45-positive Reed-Sternberg cells.
6 terations in B-cell identity seen in Hodgkin Reed-Sternberg cells.
7 consistently expressed on malignant Hodgkin Reed-Sternberg cells.
8 gnaling cascades that is impaired in Hodgkin-Reed-Sternberg cells.
9 genic activation of NF-kappaB in Hodgkin and Reed-Sternberg cells.
10 by most polyclonal T cells rosetting around Reed-Sternberg cells.
11 athway is also important in the formation of Reed-Sternberg cells.
12 HD patients (28%) had EBER1 expressed in the Reed-Sternberg cells.
13 tulated the major pathologic features of the Reed-Sternberg cell and concluded that KLHDC8B is essent
14 press CD25, it is expressed by a minority of Reed-Sternberg cells and by most polyclonal T cells rose
15 laser-capture microdissected primary Hodgkin Reed-Sternberg cells and primary MLBCLs and find that pr
16 peculiar activated phenotype of Hodgkin and Reed-Sternberg cells and their pattern of cytokine secre
17 e chain reaction and applied it to 51 single Reed-Sternberg cells and their variants from six cases o
19 ssues, is an extremely consistent marker for Reed-Sternberg cells and variants of Hodgkin's disease (
20 nd unclassified types (5), all or nearly all Reed-Sternberg cells and variants were immunoreactive fo
21 tor Xa receptor, EPR-1, as a novel marker of Reed-Sternberg cells, and suggest its potential role in
22 ce receptor, CD40, consistently expressed by Reed-Sternberg cells, and the first link in the pathway
23 oplastic cells in classical Hodgkin disease (Reed-Sternberg cells) are of B-lymphoid origin, but they
24 its nonproductive immunoglobulin genes, the Reed-Sternberg cell avoids the usual apoptotic fate of d
27 n this issue of Blood, Fhu et al report that Reed-Sternberg cell-derived lymphotoxin-alpha activates
29 sponses were observed both in patients whose Reed-Sternberg cells expressed CD25 and in those whose n
32 e sequence was determined from living single Reed-Sternberg cells, Hodgkin's tissue, and cell lines.
33 survival mechanisms of the malignant Hodgkin-Reed-Sternberg cell (HRS) in a disease whose pathophysio
34 ilencing several B-cell genes in Hodgkin and Reed-Sternberg cells (HRS) of Hodgkin lymphoma (HL), and
35 ivity of monoclonal antibodies to EPR-1 with Reed-Sternberg cells in 30 of 35 cases of nodular-sclero
37 and histiocytic (L&H) cells, the variants of Reed-Sternberg cells in nodular lymphocyte-predominant H
39 geting molecular mechanisms specific for the Reed-Sternberg cell may allow for less toxic and more ef
40 ivation state and resistance to apoptosis of Reed-Sternberg cells might be attributable to dysregulat
43 naplastic large cell lymphoma (ALCL) and the Reed-Sternberg cell of Hodgkin's disease (HD) remains la
46 expression pattern distinct from Hodgkin and Reed-Sternberg cells of classical Hodgkin lymphoma (CHL)
49 d in 1832, but the nature of the pathognomic Reed-Sternberg cell, on which diagnosis of the disease i
51 toward nonmalignant T cells rosetting around Reed-Sternberg cells provided meaningful therapy for sel
57 C (PLC)-gamma2 were consistently absent from Reed-Sternberg cells, whereas 2 other Src kinases (Lyn a
58 as (cHLs) include small numbers of malignant Reed-Sternberg cells within an extensive but ineffective
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