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1  a treatment group with a final diagnosis of mesothelioma).
2 th advanced ASS1-deficient malignant pleural mesothelioma.
3 for patients with advanced malignant pleural mesothelioma.
4 odesis, 87 assigned to VAT-PP) had confirmed mesothelioma.
5 eurodesis in patients with malignant pleural mesothelioma.
6 patients with extensive treatment-refractory mesothelioma.
7 iferation of merlin-deficient meningioma and mesothelioma.
8 ce, but also occurring as primary peritoneal mesothelioma.
9 FGFR1, FGF2, and FGF18 were overexpressed in mesothelioma.
10      SS1P is currently in clinical trials in mesothelioma.
11 ilica seemed to increase the risk of pleural mesothelioma.
12 ent of recurrent and/or unresectable pleural mesothelioma.
13 with exposure to asbestos from patients with mesothelioma.
14 ailable serum biomarker of malignant pleural mesothelioma.
15 ed persons as compared with 48 patients with mesothelioma.
16 rent age gradient were testicular cancer and mesothelioma.
17 thetase 1 (ASS1)-negative cancers, including mesothelioma.
18 ps and 1,026 patients with malignant pleural mesothelioma.
19 g to the development of diseases, especially mesothelioma.
20 d for imaging and therapy of all subtypes of mesothelioma.
21 XL inhibitors warrant clinical evaluation in mesothelioma.
22  is presently undergoing phase II testing in mesothelioma.
23 helioma or RECIST version 1.1 for peritoneal mesothelioma.
24  expressed from VSV as a novel treatment for mesothelioma.
25  nanotubes may cause pleural fibrosis and/or mesothelioma.
26 ion for asbestos in the induction of pleural mesothelioma.
27  therapy in stage I to III malignant pleural mesothelioma.
28 ys in lung adenocarcinoma when compared with mesothelioma.
29 improved PFS in patients with ASS1-deficient mesothelioma.
30 ising results for the treatment of malignant mesothelioma.
31 n patients with previously treated malignant mesothelioma.
32 re also obtained for rare nasal melanoma and mesothelioma.
33 tients with PD-L1-positive malignant pleural mesothelioma.
34 tients with ASS1-deficient malignant pleural mesothelioma.
35 suppressor gene in pleural lesions preceding mesothelioma.
36 ducted investigating CPIs in lung cancer and mesothelioma.
37 s with previously treated advanced malignant mesothelioma.
38 d eventual sporadic development of malignant mesothelioma.
39  to several cancers, in particular malignant mesothelioma.
40  signs of clinical activity in patients with mesothelioma.
41 ith a PI3K/mTOR dual inhibitor, GDC-0980, in mesothelioma.
42  specific and sensitive in immunostaining of mesothelioma.
43 evelopment of a variety of tumours including mesotheliomas.
44 ignificantly higher in patients with pleural mesothelioma (105+/-7 ng per milliliter in the Detroit c
45 in-3 levels in plasma (from 92 patients with mesothelioma, 136 asbestos-exposed persons without cance
46 rt) than in asbestos-exposed persons without mesothelioma (14+/-1 ng per milliliter and 24+/-1 ng per
47 ) than in patients with effusions not due to mesothelioma (212+/-25 and 151+/-23 ng per milliliter, r
48  controls), effusions (from 74 patients with mesothelioma, 39 with benign effusions, and 54 with mali
49 ignificantly higher in patients with pleural mesothelioma (694+/-37 ng per milliliter in the Detroit
50              In patients suspected of having mesothelioma, a positive blood test for mesothelin at a
51 d clinical trial, the Arginine Deiminase and Mesothelioma (ADAM) study, was conducted between March 2
52 mice had a significantly higher incidence of mesothelioma after exposure to very low doses of asbesto
53 ophylactic radiotherapy in all patients with mesothelioma after large-bore thoracic interventions is
54 s, thereby increasing the risk of developing mesothelioma after minimal exposure.
55 r clinical registration trials for malignant mesothelioma: amatuximab in the first-line setting and a
56 ng HMGB1, may decrease the risk of malignant mesothelioma among asbestos-exposed cohorts.
57                    AXL inhibition suppressed mesothelioma anchorage-independent growth, with reductio
58 inactivating mutations of BAP1 predispose to mesothelioma and certain other cancers.
59 s with measurable advanced malignant pleural mesothelioma and disease progression after one or two pr
60 anisms underlying the long latency period of mesothelioma and driving carcinogenesis are unknown.
61  can be challenging, with differentiation of mesothelioma and lung adenocarcinoma emblematic of this
62 al trials for the treatment of patients with mesothelioma and lung cancer.
63  is mutated in several cancers, most notably mesothelioma and melanoma, where it is thought to promot
64 ciated cancers such as renal cell carcinoma, mesothelioma and meningioma, but not uveal melanoma.
65            A significant association between mesothelioma and MW exposure was observed after adjustme
66  in widespread use for first line therapy of mesothelioma and non-small cell lung cancer.
67 ere associated with BAP1 syndrome, including mesothelioma and ocular/cutaneous melanomas, as well as
68 e tumor regression in patients with advanced mesothelioma and opens up the possibility that such an a
69 sed for development of new therapies against mesothelioma and other cancers that show loss of the 9p2
70 or suppressor gene predispose individuals to mesothelioma and other cancers.
71 ising candidates for monitoring and treating mesothelioma and other mesothelin-expressing cancers.
72 s critical for the pathogenesis of malignant mesothelioma and other NF2-related malignancies are not
73 thelin is an emerging cell surface target in mesothelioma and other solid tumors.
74 d in many human cancers, including malignant mesothelioma and pancreatic, ovarian, and lung adenocarc
75 PP in the context of trimodal therapy in the Mesothelioma and Radical Surgery (MARS) feasibility stud
76  Recent publications, particularly the MARS (Mesothelioma and Radical Surgery) feasibility study by T
77 itary cancer syndrome with increased risk of mesothelioma and uveal melanoma.
78 ted cancer syndrome that is characterized by mesothelioma and uveal melanoma.
79 rs or older who had pathologically confirmed mesothelioma and were deemed fit enough to undergo trimo
80 er-related genes were studied in 158 pleural mesotheliomas and 18 normal pleura.
81 echanisms associated both with regression of mesotheliomas and with VSV-mediated virotherapy, and tha
82  with a family history of cancers other than mesothelioma, and 153 asbestos-exposed individuals witho
83 ancer, 93 patients with effusions not due to mesothelioma, and 43 healthy controls), effusions (from
84 bestos-exposed individuals develop malignant mesothelioma, and because mesothelioma clustering is obs
85 umors such as lymphomas, sarcoma, hepatomas, mesothelioma, and gastrointestinal stromal tumor.
86 ective and selective therapeutic strategy in mesothelioma, and identifies mitochondrial morphology as
87  epigenetic profiles of lung adenocarcinoma, mesothelioma, and nonmalignant pulmonary tissues (n = 28
88 th pleural effusion due to malignant pleural mesothelioma, and talc pleurodesis might be preferable c
89 was expressed at higher levels in epithelial mesothelioma, and the level of this miR could segregate
90 he potential to be a prognostic biomarker in mesothelioma, and validation of these findings as well a
91 P1) in two families with a high incidence of mesothelioma, and we observed somatic alterations affect
92 odermal origin, various types of carcinomas, mesotheliomas, and sarcomas as well as myeloid leukemias
93 PD-1/PD ligand 1 blockade in lung cancer and mesothelioma are being conducted.
94 ter efficacy than monotherapies in malignant mesothelioma are ongoing.
95               Non-small-cell lung cancer and mesothelioma are thoracic malignancies, which in their a
96     New therapeutic strategies for malignant mesothelioma are urgently needed.
97                                    Malignant mesotheliomas are highly aggressive tumors usually cause
98                         Cardiac sarcomas and mesotheliomas are the most lethal PMCTs, with 1-, 3-, 5-
99 inicopathologic characteristics of malignant mesotheliomas arising in these patients have not been es
100                                 Furthermore, mesotheliomas arose at an accelerated rate in Bap1(+/-)
101 urthermore, BAP1 mutation carriers developed mesothelioma at an earlier age that was more often perit
102  New biomarkers are needed to detect pleural mesothelioma at an earlier stage and to individualize tr
103 n 8 of 9 mesothelioma cell lines and 6 of 12 mesothelioma biopsies, including each of 12 mesothelioma
104  germline BAP1 mutations in 2 of 26 sporadic mesotheliomas; both individuals with mutant BAP1 were pr
105 re also seen in other cancers including some mesothelioma, breast cancer, colorectal carcinoma, melan
106            We developed a new mouse model of mesothelioma by bladder or intraperitoneal injection of
107  siRNA or with ABT-737 in ovarian, lung, and mesothelioma cancer cells.
108                  Furthermore, an analysis of mesothelioma cancer data using SS-RPMM, revealed at leas
109  cohorts, but were identified in nine of 150 mesothelioma cases (6%) with a family history of cancer.
110 in THP-1 macrophages and the MSTO-211H human mesothelioma cell line independently of LPS priming.
111 PrP(C) is observed in human Merlin-deficient mesothelioma cell line TRA and in human Merlin-deficient
112 L10) mRNA and protein production in the AB12 mesothelioma cell line using a pharmacological inhibitor
113 e, one targeted to mesothelin expressed by a mesothelioma cell line, and one using an adenovirus-expr
114 lyzed by a custom miR platform, along with 9 mesothelioma cell lines and 3 normal mesothelial lines.
115 s expressed and activated strongly in 8 of 9 mesothelioma cell lines and 6 of 12 mesothelioma biopsie
116  of FGFs and their receptors was analyzed in mesothelioma cell lines and tissue specimens.
117 -frame deletion of exon 10, and six of seven mesothelioma cell lines expressed the AXL ligand, growth
118 tent anti-tumor cytotoxicity towards primary mesothelioma cell lines in vitro and an NCI-H226 xenogra
119 nsient expression of ETS-2 and PU.1 cDNAs in mesothelioma cell lines resulted in an increase in the p
120  prognosis, and overexpression of the miR in mesothelioma cell lines resulted in significantly decrea
121             Analysis of a panel of malignant mesothelioma cell lines reveals a strong correlation bet
122                                              Mesothelioma cell lines were established, which showed l
123 rmation, and G1 cell cycle arrest in several mesothelioma cell lines, accompanied by apoptosis induct
124 n human mesothelioma, we examined nine human mesothelioma cell lines, and found that four of nine sho
125 o a more sarcomatoid phenotype in subsets of mesothelioma cell lines.
126 ectrometry to characterize RTK activation in mesothelioma cell lines.
127  increased calretinin expression observed in mesothelioma cells and in certain colon cancer might be
128 data suggest that the malignant phenotype of mesothelioma cells depends on intact FGF signals, which
129                                              Mesothelioma cells from Bap1(+/-) mice showed biallelic
130        However, normal mesothelial cells and mesothelioma cells from Bap1(+/-) mice showed downregula
131 gether, our findings indicate that malignant mesothelioma cells rely on HMGB1, and they offer a precl
132                                    Malignant mesothelioma cells strongly expressed HMGB1 and secreted
133 stablishes an autocrine circuit in malignant mesothelioma cells that influences their proliferation a
134                                 Furthermore, mesothelioma cells that lack BAP1 are sensitive to EZH2
135 ation of ETS family transcription factors in mesothelioma cells through the mitogen-activated protein
136 ependent growth of HMGB1-secreting malignant mesothelioma cells was inhibited in vitro by treatment w
137 nd HER2 expression in NCI-H226 and MSTO-211H mesothelioma cells.
138  develop malignant mesothelioma, and because mesothelioma clustering is observed in some families, we
139 he interim analysis of the malignant pleural mesothelioma cohort.
140   Human antibodies targeting all subtypes of mesothelioma could be useful to image and treat this dea
141 inogenesis during the long latency period of mesothelioma development and shows that CNT and asbestos
142 rt CNTs into the pleural cavity, the site of mesothelioma development, produced asbestos-like length-
143           The vast majority of patients with mesothelioma die of their disease within 3 years.
144 urthermore, they reveal that merlin-negative mesotheliomas display unregulated mTORC1 signaling and a
145 ental models of diffuse malignant peritoneal mesothelioma (DMPM), a rapidly lethal disease, poorly re
146 ental models of diffuse malignant peritoneal mesothelioma (DMPM), a rare and rapidly fatal disease, p
147 a fibulin-3 levels can further differentiate mesothelioma effusions from other malignant and benign e
148 omatic AXL mutations were not found, but all mesotheliomas expressed an alternatively spliced AXL tra
149 are in favor of an increased risk of pleural mesothelioma for subjects exposed to both asbestos and M
150  with stage I or II epithelioid and biphasic mesothelioma from 1,612 symptomatic or high-risk control
151 ing and test sets--accurately differentiated mesothelioma from lung adenocarcinoma over 99% of the ti
152                           Unlike in WT mice, mesotheliomas from Bap1(+/-) mice did not require homozy
153 , as well as other types of cancer including mesothelioma, glioma multiforme, breast, colorectal, ski
154 or cancer therapy, but their significance in mesothelioma has remained largely undefined.
155  of non-small cell lung cancer and malignant mesothelioma, has adverse effects including neutropenia,
156 y of life in patients with malignant pleural mesothelioma have, to our knowledge, not been assessed i
157  bladder; brain and nervous system; thyroid; mesothelioma; Hodgkin lymphoma; non-Hodgkin lymphoma; mu
158                                           In mesothelioma, immunotherapies being investigated include
159 e to asbestos is required for development of mesothelioma in BAP1 mutation carriers are not known.
160 significantly increase the risk of malignant mesothelioma in genetically predisposed individuals carr
161 doses of asbestos, doses that rarely induced mesothelioma in wild-type mice.
162 owed significant therapy against AB12 murine mesotheliomas in the context of both local and locoregio
163 cant increase in the incidence of aggressive mesotheliomas in the two mouse models carrying clinicall
164          Notably, we also observed malignant mesotheliomas in two Bap1-mutant mice, but not in any wi
165                            Malignant pleural mesothelioma incidence continues to rise, with few avail
166 matic alterations affecting BAP1 in familial mesotheliomas, indicating biallelic inactivation.
167 regate a largely surgically treated group of mesotheliomas into good or bad prognosis categories.
168                                              Mesothelioma is a fatal tumor of the pleura and is stron
169                            Malignant pleural mesothelioma is a highly aggressive cancer with poor pro
170                              Human malignant mesothelioma is an aggressive and highly lethal cancer t
171                                    Malignant mesothelioma is an aggressive cancer largely associated
172                            Malignant pleural mesothelioma is an aggressive malignancy characterized b
173                                              Mesothelioma is an aggressive malignancy generally assoc
174                                              Mesothelioma is an asbestos-associated and notoriously c
175                                              Mesothelioma is diagnosed in approximately 2500 patients
176 notherapy in patients with malignant pleural mesothelioma is feasible, well-tolerated, and capable of
177    The prognosis for patients diagnosed with mesothelioma is generally poor, and currently available
178 d differentiation of lung adenocarcinoma and mesothelioma is highly accurate, informs on the distinct
179                               Development of mesothelioma is linked mainly to asbestos exposure, but
180     Moreover, major epigenetic regulation of mesothelioma is mediated by hsa-miR-29c* and was shown t
181 erspective on where the clinical research in mesothelioma is moving.
182 ating checkpoint blockade in lung cancer and mesothelioma is provided.
183 ldwide, but its capacity to induce malignant mesothelioma is still debated.
184                                    Malignant mesothelioma is strongly associated with asbestos exposu
185                                 However, why mesothelioma is the predominate malignancy in some BAP1
186 d cytotoxicity when cocultured with a murine mesothelioma line that stably expresses mesothelin.
187 ing that predisposition of Bap1(+/-) mice to mesothelioma may be facilitated, in part, by cooperation
188 d malignant tumor types, including malignant mesothelioma, melanoma, and kidney carcinoma.
189 AP1) gene has been linked to uveal melanoma, mesothelioma, meningioma, renal cell carcinoma and basal
190 ivirus-mediated short hairpin RNA suppressed mesothelioma migration and cellular proliferation due to
191 l relationship established between malignant mesothelioma (MM) and asbestos exposure, the exact mecha
192 ne map genomic imbalances in human malignant mesothelioma (MM) cell lines derived from primary tumors
193                                    Malignant mesothelioma (MM) is a relatively rare but devastating t
194                                    Malignant mesothelioma (MM) is an aggressive malignancy, highly re
195                                    Malignant mesothelioma (MM) is an aggressive tumor with no treatme
196 ral, causes unprecedented rates of malignant mesothelioma (MM) mortality in some Turkish villages.
197                                    Malignant mesothelioma (MM) of pleura is an aggressive and highly
198 t of the micronutrient selenium on malignant mesothelioma (MM) progression, we cultured four differen
199 tabine plus cisplatin is active in malignant mesothelioma (MM), although single-arm phase II trials h
200 development and chemoresistance of malignant mesothelioma (MM), an aggressive asbestos-associated tum
201                                    Malignant mesothelioma (MM), is an intractable disease with limite
202 le to accelerated asbestos-induced malignant mesothelioma (MM).
203 ring the progression of malignant peritoneal mesothelioma (MPeM), tumor nodules propagate diffusely w
204 nt mesothelial tissues and malignant pleural mesothelioma (MPM) cell lines as compared to benign tiss
205                            Malignant pleural mesothelioma (MPM) is a deadly disease that occurs in 2,
206                            Malignant pleural mesothelioma (MPM) is a highly aggressive and generally
207                            Malignant pleural mesothelioma (MPM) is a highly aggressive tumor with poo
208                            Malignant pleural mesothelioma (MPM) is an aggressive cancer that is commo
209                            Malignant pleural mesothelioma (MPM) is an aggressive cancer that occurs m
210                            Malignant pleural mesothelioma (MPM) is an aggressive human cancer and miR
211                            Malignant pleural mesothelioma (MPM) is an aggressive neoplasm associated
212                            Malignant pleural mesothelioma (MPM) is an aggressive thoracic cancer with
213                      Human malignant pleural mesothelioma (MPM) is considered a rare tumor, but recen
214   Hemithoracic IMPRINT for malignant pleural mesothelioma (MPM) is safe and has an acceptable rate of
215 tients with ASS1-deficient malignant pleural mesothelioma (MPM) or non-small-cell lung cancer (NSCLC)
216  exomes (n = 103) from 216 malignant pleural mesothelioma (MPM) tumors.
217               Treatment of malignant pleural mesothelioma (MPM) with Ranpirnase (Onconase) results in
218 AR1, F2R) on the growth of malignant pleural mesothelioma (MPM), using human MPM cells that lack or e
219 e treatment of epithelioid malignant pleural mesothelioma (MPM).
220 as first-line treatment of malignant pleural mesothelioma (MPM).
221 ancer-directed surgery for malignant pleural mesothelioma (MPM); however, it is unclear if these resu
222  to be highly expressed in malignant pleural mesotheliomas (MPM), was detected in serum using an elec
223                            Malignant pleural mesotheliomas (MPMs) often show CDKN2A and NF2 inactivat
224 carriers were uveal melanoma (n = 60 [28%]), mesothelioma (n = 48 [22%]), cutaneous melanoma (n = 38
225 ylation profiles in a case series of pleural mesotheliomas (n = 23).
226 .8%), followed by lymphomas (n=150, 27%) and mesotheliomas (n=44, 8%).
227 9)m)Tc (((9)(9)m)Tc-M40) in murine models of mesothelioma of both epithelioid (M28) and sarcomatoid (
228 after injection, which was due to peritoneal mesothelioma, on the basis of tumor morphology and immun
229 olid Tumors (RECIST) version 1.0 for pleural mesothelioma or RECIST version 1.1 for peritoneal mesoth
230 , and 54 with malignant effusions not due to mesothelioma), or both.
231  anti-MCAM scFv and found that it recognizes mesothelioma organotypic xenografts in vivo.
232 uch as mesothelin, which is overexpressed in mesothelioma, ovarian, lung, breast, and pancreatic canc
233 nd phosphorylated c-Met expression levels in mesothelioma patient samples; these data suggest a stron
234       Accordingly, HMGB1 levels in malignant mesothelioma patient sera were higher than that found in
235 ation profiles are independent predictors of mesothelioma patient survival.
236  However, to date, we found that none of the mesothelioma patients carrying germline BAP1 mutations w
237    Collectively, these findings suggest that mesothelioma patients presenting with a family history o
238 ncidence and associated clinical features in mesothelioma patients with a family history of cancer ha
239 ned the germline BAP1 mutation status of 150 mesothelioma patients with a family history of cancer, 5
240 ited improved long-term survival compared to mesothelioma patients without BAP1 mutations.
241 to measure serum mesothelin concentration in mesothelioma patients, indicating its potential use for
242 seen with exosomes from pleural effusions of mesothelioma patients.
243 esected tumor, and FNA were analyzed from 13 mesothelioma patients.
244 ssociation between pleural diffuse malignant mesothelioma (PDMM) and chest radiation for lymphoma.
245  other cancers may also be involved and that mesothelioma predominates upon asbestos exposure.
246 inability to forecast outcomes for malignant mesothelioma prevents clinicians from providing aggressi
247 netic and global epigenetic dysregulation in mesothelioma, rather than a discrete, local coordination
248          Ten patients with malignant pleural mesothelioma received metronomic cyclophosphamide and de
249 tract metastases (PTMs) in malignant pleural mesothelioma remains controversial, and clinical practic
250 asbestos and suggest that high penetrance of mesothelioma requires such environmental exposure.
251  Research UK (CRUK/04/003), the June Hancock Mesothelioma Research Fund, and Guy's and St Thomas' NHS
252          Moreover, late diagnosis means that mesothelioma research is commonly focused on end-stage d
253  lost in both spontaneous ovarian tumors and mesotheliomas, resulting in the loss of Bap1 expression.
254                                 In end-stage mesothelioma, silencing of p16/Ink4a is sustained and de
255                               In addition to mesothelioma, some BAP1 mutation carriers developed uvea
256    A tissue microarray analysis of 198 human mesothelioma specimens showed that 33% of cases had redu
257 y population, because type of control group, mesothelioma stage, and histologic subtype significantly
258 s, cause-specific mortality was elevated for mesothelioma (standardized mortality ratio (SMR) = 2.85,
259 ting that mTOR activation is common in human mesothelioma, suggesting that it is a potential therapeu
260 or and MET, has been described in subsets of mesothelioma, suggesting that TKs might represent therap
261 NF2 tumors but not with malignant NF2 mutant mesotheliomas, suggesting that senescence may underlie t
262 6 as the surface antigen bound by one of the mesothelioma-targeting scFvs using a novel cloning strat
263 icantly higher incidence of asbestos-induced mesothelioma than wild-type (WT) littermates (73% vs. 32
264 wide characterization of pathways altered in mesothelioma that could be potentially exploited to desi
265 bers into the pleural cavity of mice induces mesothelioma that exhibits common key pro-oncogenic mole
266                In small cell lung cancer and mesothelioma, the efficacy of checkpoint inhibition has
267 omparison of patients with and those without mesothelioma, the receiver-operating-characteristic curv
268                         Except for malignant mesotheliomas, the role of NF2 mutation or inactivation
269 bestos-induced inflammatory lesions precedes mesothelioma; this results in silencing of Cdkn2a (Ink4a
270 g to the death of more than one patient were mesothelioma (three [1%] patients in the tremelimumab gr
271              Immunohistochemical analysis of mesothelioma tissue microarrays confirmed that MCAM is w
272 their use of a murine model of human pleural mesothelioma to explore potential factors that limit CAR
273  reported in patients with malignant pleural mesothelioma treated in a phase 1 study of vorinostat, w
274 ate of the major clinical trials that impact mesothelioma treatment in the resectable and unresectabl
275 g a novel therapeutic approach for malignant mesothelioma treatment.
276 by both epithelioid and sarcomatous types of mesothelioma tumor cells in situ but not by normal mesot
277 ended survival and a 95-99% reduction in the mesothelioma tumor volume, in comparison with vehicle-tr
278 iated regression of large vascularized flank mesothelioma tumors in NOD/scid/gammac(-/-) mice.
279    A training set of 44 and a test set of 98 mesothelioma tumors were analyzed by a custom miR platfo
280 quamous cell carcinoma (HNSCC) tumors and 23 mesothelioma tumors.
281  mouse model to assess its susceptibility to mesothelioma upon chronic exposure to asbestos.
282 gnancies in their lifetime, mostly malignant mesothelioma, uveal melanoma, and so on.
283 bined with cyclophosphamide in patients with mesothelioma was safe, the only side effect being modera
284   Using an orthotopic mouse model of pleural mesothelioma, we determined that relatively high doses o
285 SC2 loss was a common genetic event in human mesothelioma, we examined nine human mesothelioma cell l
286 tients with PD-L1-positive malignant pleural mesothelioma were enrolled from 13 centres in six countr
287  women and 29 men) with unresectable pleural mesothelioma were treated with repetitive transarterial
288                               No spontaneous mesotheliomas were seen in unexposed Bap1(+/-) mice foll
289  receptor c-Met are both highly expressed in mesotheliomas, where they protect cells from apoptosis a
290 sent in the serum of patients with malignant mesothelioma, which could negatively affect the response
291 help to identify individuals at high risk of mesothelioma who could be targeted for early interventio
292 unresectable pleural or peritoneal malignant mesothelioma who had progressed after one or two previou
293 s of patients with histocytologically proven mesothelioma who had undergone large-bore pleural interv
294 In a comparison of patients with early-stage mesothelioma with asbestos-exposed persons, the sensitiv
295 r with any subtype of confirmed or suspected mesothelioma with pleural effusion, recruited from 12 ho
296 atment of mice with malignant ascites due to mesothelioma with rapamycin led to a marked reduction in
297  mesothelioma biopsies, including each of 12 mesotheliomas with spindle-cell histology.
298 nhibited cell migration and proliferation in mesotheliomas with strong AXL activation.
299 ons and aberrant BAP1 expression in sporadic mesotheliomas without germline mutations.
300 tion in vivo reduced the growth of malignant mesothelioma xenografts in severe-combined immunodeficie

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