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1 phase III clinical trials as a treatment for malignant mesothelioma.
2 as a result of Dishevelled overexpression in malignant mesothelioma.
3 cal trials for the treatment of unresectable malignant mesothelioma.
4 ng pathways may be a strategy for therapy of malignant mesothelioma.
5 e the most frequent genetic lesions in human malignant mesothelioma.
6 beta gene (Ad.muIFN-beta) in mouse models of malignant mesothelioma.
7 trated frequent deletions from 15q11.1-15 in malignant mesothelioma.
8 n highly differentiated breast carcinoma and malignant mesothelioma.
9 stos is a major factor in the development of malignant mesothelioma.
10 d mesothelial cells, the progenitor cells of malignant mesothelioma.
11 n malignancies of nonneuronal origin such as malignant mesothelioma.
12 iation therapy and subsequent development of malignant mesothelioma.
13 ferroptosis in an orthotopic mouse model of malignant mesothelioma.
14 athways and eventual sporadic development of malignant mesothelioma.
15 placebo in patients with previously treated malignant mesothelioma.
16 in patients with previously treated advanced malignant mesothelioma.
17 predispose to several cancers, in particular malignant mesothelioma.
18 shown promising results for the treatment of malignant mesothelioma.
19 ibitor, SM16, in the AB12 syngeneic model of malignant mesothelioma.
20 a rare and clinically distinct entity among malignant mesotheliomas.
21 (+/-) knockout mice with asbestos to induce malignant mesotheliomas.
22 ism in the etiology of the majority of human malignant mesotheliomas.
23 ven of 15 patients had histologically proven malignant mesotheliomas (10 epithelial, 1 sarcomatoid).
24 3 eligible patients with suspected or proven malignant mesothelioma, 41 could be included in the data
25 on Criteria in Solid Tumours version 1.1 for malignant mesothelioma, a predicted life expectancy of a
27 multicenter clinical registration trials for malignant mesothelioma: amatuximab in the first-line set
28 lly blocking HMGB1, may decrease the risk of malignant mesothelioma among asbestos-exposed cohorts.
29 ates many of the molecular features of human malignant mesothelioma and has significant implications
30 tand the significance of NF2 inactivation in malignant mesothelioma and identify tumor suppressor gen
33 or pathways critical for the pathogenesis of malignant mesothelioma and other NF2-related malignancie
34 y expressed in many human cancers, including malignant mesothelioma and pancreatic, ovarian, and lung
36 tion of asbestos-exposed individuals develop malignant mesothelioma, and because mesothelioma cluster
37 Nf2, and Cdkn2a results in rapid, aggressive malignant mesotheliomas, and that deletion of Bap1 contr
38 clinical characteristics of epithelial type malignant mesothelioma are distinct from those of biphas
42 The clinicopathologic characteristics of malignant mesotheliomas arising in these patients have n
43 ogenic tyrosine kinase receptor expressed in malignant mesothelioma as well as in a variety of cancer
44 rwent treatment for pathologically confirmed malignant mesothelioma at Brigham and Women's Hospital a
45 nical use for patients with glioblastoma and malignant mesothelioma, based on the principle of using
46 aluated telomerase activity in seven primary malignant mesothelioma biopsies and matched lung specime
47 with asbestos in the development of diffuse malignant mesothelioma, but its precise role in the path
49 ranscriptome in human normal mesothelial and malignant mesothelioma cell lines exposed or not exposed
52 luate if talc directly effects cell death of malignant mesothelioma cells (MMC) or normal pleural mes
53 m for the maintenance of EphB4-expression in malignant mesothelioma cells and other IGF-II-secreting
54 demonstrate that EphB4 protein expression in malignant mesothelioma cells depend upon a degradation r
56 Taken together, our findings indicate that malignant mesothelioma cells rely on HMGB1, and they off
59 at HMGB1 establishes an autocrine circuit in malignant mesothelioma cells that influences their proli
60 horage-independent growth of HMGB1-secreting malignant mesothelioma cells was inhibited in vitro by t
61 approved therapy for glioblastoma (GBM) and malignant mesothelioma, employ noninvasive application o
63 otheliomas from Nf2 (+/-) mice and in 50% of malignant mesotheliomas from asbestos-exposed WT mice.
64 n, was observed in all nine asbestos-induced malignant mesotheliomas from Nf2 (+/-) mice and in 50% o
66 with a median survival of only 12 weeks, and malignant mesotheliomas from these mice were consistentl
70 treatment of non-small cell lung cancer and malignant mesothelioma, has adverse effects including ne
71 either Nf2 or Cdkn2a to drive development of malignant mesothelioma in approximately 20% of double-CK
72 ibers may significantly increase the risk of malignant mesothelioma in genetically predisposed indivi
74 Cdkn2a, or Nf2 alone gave rise to few or no malignant mesotheliomas, inactivation of Bap1 cooperated
75 tumors unrelated to the NF2 syndrome such as malignant mesothelioma, indicating a broader role for th
88 benign and malignant tumor types, including malignant mesothelioma, melanoma, and kidney carcinoma.
90 the causal relationship established between malignant mesothelioma (MM) and asbestos exposure, the e
93 ays, to fine map genomic imbalances in human malignant mesothelioma (MM) cell lines derived from prim
94 identify chromosomal imbalances in 24 human malignant mesothelioma (MM) cell lines derived from untr
95 e expression changes in rat asbestos-induced malignant mesothelioma (MM) cells were investigated by d
96 nt study, we determined IL-8 levels in human malignant mesothelioma (MM) effusions and congestive hea
104 -like mineral, causes unprecedented rates of malignant mesothelioma (MM) mortality in some Turkish vi
106 the effect of the micronutrient selenium on malignant mesothelioma (MM) progression, we cultured fou
110 Gemcitabine plus cisplatin is active in malignant mesothelioma (MM), although single-arm phase I
111 ng to the development and chemoresistance of malignant mesothelioma (MM), an aggressive asbestos-asso
114 tion of subjects exposed to asbestos develop malignant mesothelioma (MM), suggesting that additional
119 We compared the methylation profile of 66 malignant mesotheliomas (MMs) and 40 lung adenocarcinoma
124 onse in patients with chemotherapy-resistant malignant mesothelioma of the pleura or peritoneum.
127 ications for the further characterization of malignant mesothelioma pathogenesis and preclinical test
128 that cooperate with NF2 loss of function in malignant mesothelioma pathogenesis, we treated Nf2 (+/-
130 orted an association between pleural diffuse malignant mesothelioma (PDMM) and chest radiation for ly
132 d for other diseases, including lung cancer, malignant mesothelioma, pulmonary inflammation, surfacta
133 s with advanced, recurrent ovarian cancer or malignant mesothelioma received anetumab ravtansine at t
134 response predicts survival in patients with malignant mesothelioma receiving high-dose pembrolizumab
135 response predicts survival in patients with malignant mesothelioma receiving high-dose pembrolizumab
138 opriate treatment for selected patients with malignant mesothelioma selected using a revised staging
139 equent losses of chromosome 1p21-22 in human malignant mesothelioma, suggesting that the loss or inac
140 is project was to evaluate, in patients with malignant mesothelioma, the relationship between inherit
142 developed a multicellular spheroid model of malignant mesothelioma to investigate molecular mechanis
144 f2 (+/-) mice exhibited markedly accelerated malignant mesothelioma tumor formation compared with asb
145 ows potent activity against established AB12 malignant mesothelioma tumors using an immune-mediated m
148 ows promise in an ongoing clinical trial for malignant mesothelioma using direct pleural infusion.
149 ensity loss of heterozygosity analysis of 46 malignant mesotheliomas, using 26 polymorphic microsatel
151 O mice, and a high incidence (22/26, 85%) of malignant mesotheliomas was observed in Bap1;Nf2;Cdkn2a
154 imary tumor specimens and cell lines from 50 malignant mesotheliomas were examined for loss of hetero
155 and is present in the serum of patients with malignant mesothelioma, which could negatively affect th
156 ents with unresectable pleural or peritoneal malignant mesothelioma who had progressed after one or t
157 ival for patients with pleural or peritoneal malignant mesothelioma who have progressed following pla
158 nt that might be beneficial to patients with malignant mesothelioma who have progressed on first-line
159 GB1 inhibition in vivo reduced the growth of malignant mesothelioma xenografts in severe-combined imm
160 strongly associated with the development of malignant mesothelioma, yet the mechanistic basis of thi