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1 athways and eventual sporadic development of malignant mesothelioma.
2 n highly differentiated breast carcinoma and malignant mesothelioma.
3 stos is a major factor in the development of malignant mesothelioma.
4 d mesothelial cells, the progenitor cells of malignant mesothelioma.
5 n malignancies of nonneuronal origin such as malignant mesothelioma.
6 iation therapy and subsequent development of malignant mesothelioma.
7 predispose to several cancers, in particular malignant mesothelioma.
8 shown promising results for the treatment of malignant mesothelioma.
9 ibitor, SM16, in the AB12 syngeneic model of malignant mesothelioma.
10 placebo in patients with previously treated malignant mesothelioma.
11 in patients with previously treated advanced malignant mesothelioma.
12 phase III clinical trials as a treatment for malignant mesothelioma.
13 as a result of Dishevelled overexpression in malignant mesothelioma.
14 cal trials for the treatment of unresectable malignant mesothelioma.
15 ng pathways may be a strategy for therapy of malignant mesothelioma.
16 beta gene (Ad.muIFN-beta) in mouse models of malignant mesothelioma.
17 trated frequent deletions from 15q11.1-15 in malignant mesothelioma.
18 (+/-) knockout mice with asbestos to induce malignant mesotheliomas.
19 ism in the etiology of the majority of human malignant mesotheliomas.
20 ven of 15 patients had histologically proven malignant mesotheliomas (10 epithelial, 1 sarcomatoid).
22 multicenter clinical registration trials for malignant mesothelioma: amatuximab in the first-line set
23 lly blocking HMGB1, may decrease the risk of malignant mesothelioma among asbestos-exposed cohorts.
24 ates many of the molecular features of human malignant mesothelioma and has significant implications
25 tand the significance of NF2 inactivation in malignant mesothelioma and identify tumor suppressor gen
27 or pathways critical for the pathogenesis of malignant mesothelioma and other NF2-related malignancie
28 y expressed in many human cancers, including malignant mesothelioma and pancreatic, ovarian, and lung
30 tion of asbestos-exposed individuals develop malignant mesothelioma, and because mesothelioma cluster
31 clinical characteristics of epithelial type malignant mesothelioma are distinct from those of biphas
35 The clinicopathologic characteristics of malignant mesotheliomas arising in these patients have n
36 rwent treatment for pathologically confirmed malignant mesothelioma at Brigham and Women's Hospital a
37 aluated telomerase activity in seven primary malignant mesothelioma biopsies and matched lung specime
38 with asbestos in the development of diffuse malignant mesothelioma, but its precise role in the path
42 luate if talc directly effects cell death of malignant mesothelioma cells (MMC) or normal pleural mes
43 Taken together, our findings indicate that malignant mesothelioma cells rely on HMGB1, and they off
46 at HMGB1 establishes an autocrine circuit in malignant mesothelioma cells that influences their proli
47 horage-independent growth of HMGB1-secreting malignant mesothelioma cells was inhibited in vitro by t
49 otheliomas from Nf2 (+/-) mice and in 50% of malignant mesotheliomas from asbestos-exposed WT mice.
50 n, was observed in all nine asbestos-induced malignant mesotheliomas from Nf2 (+/-) mice and in 50% o
54 treatment of non-small cell lung cancer and malignant mesothelioma, has adverse effects including ne
55 ibers may significantly increase the risk of malignant mesothelioma in genetically predisposed indivi
57 tumors unrelated to the NF2 syndrome such as malignant mesothelioma, indicating a broader role for th
66 benign and malignant tumor types, including malignant mesothelioma, melanoma, and kidney carcinoma.
67 the causal relationship established between malignant mesothelioma (MM) and asbestos exposure, the e
69 ays, to fine map genomic imbalances in human malignant mesothelioma (MM) cell lines derived from prim
70 identify chromosomal imbalances in 24 human malignant mesothelioma (MM) cell lines derived from untr
71 e expression changes in rat asbestos-induced malignant mesothelioma (MM) cells were investigated by d
72 nt study, we determined IL-8 levels in human malignant mesothelioma (MM) effusions and congestive hea
78 -like mineral, causes unprecedented rates of malignant mesothelioma (MM) mortality in some Turkish vi
80 the effect of the micronutrient selenium on malignant mesothelioma (MM) progression, we cultured fou
84 ng to the development and chemoresistance of malignant mesothelioma (MM), an aggressive asbestos-asso
86 tion of subjects exposed to asbestos develop malignant mesothelioma (MM), suggesting that additional
90 We compared the methylation profile of 66 malignant mesotheliomas (MMs) and 40 lung adenocarcinoma
94 ications for the further characterization of malignant mesothelioma pathogenesis and preclinical test
95 that cooperate with NF2 loss of function in malignant mesothelioma pathogenesis, we treated Nf2 (+/-
97 orted an association between pleural diffuse malignant mesothelioma (PDMM) and chest radiation for ly
99 d for other diseases, including lung cancer, malignant mesothelioma, pulmonary inflammation, surfacta
102 opriate treatment for selected patients with malignant mesothelioma selected using a revised staging
103 equent losses of chromosome 1p21-22 in human malignant mesothelioma, suggesting that the loss or inac
105 developed a multicellular spheroid model of malignant mesothelioma to investigate molecular mechanis
107 f2 (+/-) mice exhibited markedly accelerated malignant mesothelioma tumor formation compared with asb
108 ows potent activity against established AB12 malignant mesothelioma tumors using an immune-mediated m
111 ensity loss of heterozygosity analysis of 46 malignant mesotheliomas, using 26 polymorphic microsatel
114 imary tumor specimens and cell lines from 50 malignant mesotheliomas were examined for loss of hetero
115 and is present in the serum of patients with malignant mesothelioma, which could negatively affect th
116 ents with unresectable pleural or peritoneal malignant mesothelioma who had progressed after one or t
117 GB1 inhibition in vivo reduced the growth of malignant mesothelioma xenografts in severe-combined imm
118 strongly associated with the development of malignant mesothelioma, yet the mechanistic basis of thi
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