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1 a treatment group with a final diagnosis of mesothelioma).
2 n patients with previously treated malignant mesothelioma.
3 re also obtained for rare nasal melanoma and mesothelioma.
4 tients with PD-L1-positive malignant pleural mesothelioma.
5 tients with ASS1-deficient malignant pleural mesothelioma.
6 suppressor gene in pleural lesions preceding mesothelioma.
7 ducted investigating CPIs in lung cancer and mesothelioma.
8 s with previously treated advanced malignant mesothelioma.
9 to several cancers, in particular malignant mesothelioma.
10 signs of clinical activity in patients with mesothelioma.
11 ith a PI3K/mTOR dual inhibitor, GDC-0980, in mesothelioma.
12 specific and sensitive in immunostaining of mesothelioma.
13 for patients with advanced malignant pleural mesothelioma.
14 odesis, 87 assigned to VAT-PP) had confirmed mesothelioma.
15 eurodesis in patients with malignant pleural mesothelioma.
16 patients with extensive treatment-refractory mesothelioma.
17 iferation of merlin-deficient meningioma and mesothelioma.
18 ce, but also occurring as primary peritoneal mesothelioma.
19 FGFR1, FGF2, and FGF18 were overexpressed in mesothelioma.
20 SS1P is currently in clinical trials in mesothelioma.
21 ilica seemed to increase the risk of pleural mesothelioma.
22 ent of recurrent and/or unresectable pleural mesothelioma.
23 with exposure to asbestos from patients with mesothelioma.
24 ailable serum biomarker of malignant pleural mesothelioma.
25 ed persons as compared with 48 patients with mesothelioma.
26 rent age gradient were testicular cancer and mesothelioma.
27 ps and 1,026 patients with malignant pleural mesothelioma.
28 g to the development of diseases, especially mesothelioma.
29 aluated with respect to genotype and site of mesothelioma.
30 ivo against both epithelioid and sarcomatoid mesothelioma.
31 frequent genetic lesions in human malignant mesothelioma.
32 e target for therapeutic development against mesothelioma.
33 median survival of 27 months) for peritoneal mesothelioma.
34 is in an orthotopic mouse model of malignant mesothelioma.
35 or placebo in unresectable malignant pleural mesothelioma.
36 thetase 1 (ASS1)-negative cancers, including mesothelioma.
37 d eventual sporadic development of malignant mesothelioma.
38 th advanced ASS1-deficient malignant pleural mesothelioma.
39 helioma or RECIST version 1.1 for peritoneal mesothelioma.
40 improved PFS in patients with ASS1-deficient mesothelioma.
41 evelopment of a variety of tumours including mesotheliomas.
42 minantly associated with uveal melanomas and mesotheliomas.
43 pressor NF2, a frequent tumorigenic event in mesothelioma(10,11), rendered cancer cells more sensitiv
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
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
55 r clinical registration trials for malignant mesothelioma: amatuximab in the first-line setting and a
57 s with measurable advanced malignant pleural mesothelioma and disease progression after one or two pr
58 anisms underlying the long latency period of mesothelioma and driving carcinogenesis are unknown.
59 h unresectable epithelioid malignant pleural mesothelioma and ECOG performance status 0-1 were random
62 is mutated in several cancers, most notably mesothelioma and melanoma, where it is thought to promot
63 ciated cancers such as renal cell carcinoma, mesothelioma and meningioma, but not uveal melanoma.
66 ere associated with BAP1 syndrome, including mesothelioma and ocular/cutaneous melanomas, as well as
67 e tumor regression in patients with advanced mesothelioma and opens up the possibility that such an a
69 ising candidates for monitoring and treating mesothelioma and other mesothelin-expressing cancers.
72 d in many human cancers, including malignant mesothelioma and pancreatic, ovarian, and lung adenocarc
73 Recent publications, particularly the MARS (Mesothelioma and Radical Surgery) feasibility study by T
76 rs or older who had pathologically confirmed mesothelioma and were deemed fit enough to undergo trimo
77 with a family history of cancers other than mesothelioma, and 153 asbestos-exposed individuals witho
78 logies from 123 patients (69 lung cancer, 25 mesothelioma, and 29 extrathoracic primary malignancies)
79 ancer, 93 patients with effusions not due to mesothelioma, and 43 healthy controls), effusions (from
80 bestos-exposed individuals develop malignant mesothelioma, and because mesothelioma clustering is obs
81 ective and selective therapeutic strategy in mesothelioma, and identifies mitochondrial morphology as
82 ients each with adrenocortical carcinoma and mesothelioma, and one patient each with malignant gangli
83 th pleural effusion due to malignant pleural mesothelioma, and talc pleurodesis might be preferable c
84 P1) in two families with a high incidence of mesothelioma, and we observed somatic alterations affect
85 odermal origin, various types of carcinomas, mesotheliomas, and sarcomas as well as myeloid leukemias
86 dkn2a results in rapid, aggressive malignant mesotheliomas, and that deletion of Bap1 contributes to
93 inicopathologic characteristics of malignant mesotheliomas arising in these patients have not been es
96 urthermore, BAP1 mutation carriers developed mesothelioma at an earlier age that was more often perit
97 New biomarkers are needed to detect pleural mesothelioma at an earlier stage and to individualize tr
98 germline BAP1 mutations in 2 of 26 sporadic mesotheliomas; both individuals with mutant BAP1 were pr
99 re also seen in other cancers including some mesothelioma, breast cancer, colorectal carcinoma, melan
103 cohorts, but were identified in nine of 150 mesothelioma cases (6%) with a family history of cancer.
104 PrP(C) is observed in human Merlin-deficient mesothelioma cell line TRA and in human Merlin-deficient
106 tent anti-tumor cytotoxicity towards primary mesothelioma cell lines in vitro and an NCI-H226 xenogra
108 rmation, and G1 cell cycle arrest in several mesothelioma cell lines, accompanied by apoptosis induct
109 n human mesothelioma, we examined nine human mesothelioma cell lines, and found that four of nine sho
112 increased calretinin expression observed in mesothelioma cells and in certain colon cancer might be
113 maintenance of EphB4-expression in malignant mesothelioma cells and other IGF-II-secreting cancers (I
114 ted phage antibody display libraries on live mesothelioma cells and tissues following counterselectio
115 e that EphB4 protein expression in malignant mesothelioma cells depend upon a degradation rescue mech
116 data suggest that the malignant phenotype of mesothelioma cells depends on intact FGF signals, which
119 e we show that EphB4 expression in malignant mesothelioma cells is markedly decreased upon neutraliza
120 gether, our findings indicate that malignant mesothelioma cells rely on HMGB1, and they offer a precl
122 stablishes an autocrine circuit in malignant mesothelioma cells that influences their proliferation a
124 ependent growth of HMGB1-secreting malignant mesothelioma cells was inhibited in vitro by treatment w
125 ived primary metastatic breast cancer cells, mesothelioma cells, and lung cancer xenograft cells.
127 develop malignant mesothelioma, and because mesothelioma clustering is observed in some families, we
129 Human antibodies targeting all subtypes of mesothelioma could be useful to image and treat this dea
130 inogenesis during the long latency period of mesothelioma development and shows that CNT and asbestos
131 rt CNTs into the pleural cavity, the site of mesothelioma development, produced asbestos-like length-
132 3 wk) for the treatment of malignant pleural mesothelioma did not result in survival benefit in the p
134 ental models of diffuse malignant peritoneal mesothelioma (DMPM), a rapidly lethal disease, poorly re
135 ental models of diffuse malignant peritoneal mesothelioma (DMPM), a rare and rapidly fatal disease, p
136 a fibulin-3 levels can further differentiate mesothelioma effusions from other malignant and benign e
137 are in favor of an increased risk of pleural mesothelioma for subjects exposed to both asbestos and M
138 with stage I or II epithelioid and biphasic mesothelioma from 1,612 symptomatic or high-risk control
140 ian survival of only 12 weeks, and malignant mesotheliomas from these mice were consistently high-gra
142 , as well as other types of cancer including mesothelioma, glioma multiforme, breast, colorectal, ski
144 of non-small cell lung cancer and malignant mesothelioma, has adverse effects including neutropenia,
145 y of life in patients with malignant pleural mesothelioma have, to our knowledge, not been assessed i
146 bladder; brain and nervous system; thyroid; mesothelioma; Hodgkin lymphoma; non-Hodgkin lymphoma; mu
148 or Cdkn2a to drive development of malignant mesothelioma in approximately 20% of double-CKO mice, an
149 e to asbestos is required for development of mesothelioma in BAP1 mutation carriers are not known.
150 significantly increase the risk of malignant mesothelioma in genetically predisposed individuals carr
152 cant increase in the incidence of aggressive mesotheliomas in the two mouse models carrying clinicall
154 r Nf2 alone gave rise to few or no malignant mesotheliomas, inactivation of Bap1 cooperated with loss
167 notherapy in patients with malignant pleural mesothelioma is feasible, well-tolerated, and capable of
174 d cytotoxicity when cocultured with a murine mesothelioma line that stably expresses mesothelin.
175 ing that predisposition of Bap1(+/-) mice to mesothelioma may be facilitated, in part, by cooperation
176 highly significant for patients with pleural mesothelioma (median survival 7.9 y versus 2.4 y, P = 0.
177 .0012), but not for patients with peritoneal mesothelioma (median survival 8.2 y versus 5.4 y, P = 0.
179 creas, adrenocortical, small bowel, sarcoma, mesothelioma, melanoma, gastric, and germ cell tumors.
180 l, ovarian, endometrial and prostate cancer, mesothelioma, melanoma, leukemias, and osteosarcoma.
181 AP1) gene has been linked to uveal melanoma, mesothelioma, meningioma, renal cell carcinoma and basal
182 l relationship established between malignant mesothelioma (MM) and asbestos exposure, the exact mecha
183 We have generated mouse models of malignant mesothelioma (MM) based upon disruption of the Bap1, Nf2
189 ral, causes unprecedented rates of malignant mesothelioma (MM) mortality in some Turkish villages.
190 t of the micronutrient selenium on malignant mesothelioma (MM) progression, we cultured four differen
191 tabine plus cisplatin is active in malignant mesothelioma (MM), although single-arm phase II trials h
195 ring the progression of malignant peritoneal mesothelioma (MPeM), tumor nodules propagate diffusely w
196 nt mesothelial tissues and malignant pleural mesothelioma (MPM) cell lines as compared to benign tiss
198 rocedures in patients with malignant pleural mesothelioma (MPM) has been a widespread practice across
209 Hemithoracic IMPRINT for malignant pleural mesothelioma (MPM) is safe and has an acceptable rate of
210 tients with ASS1-deficient malignant pleural mesothelioma (MPM) or non-small-cell lung cancer (NSCLC)
212 AR1, F2R) on the growth of malignant pleural mesothelioma (MPM), using human MPM cells that lack or e
217 ancer-directed surgery for malignant pleural mesothelioma (MPM); however, it is unclear if these resu
218 to be highly expressed in malignant pleural mesotheliomas (MPM), was detected in serum using an elec
220 carriers were uveal melanoma (n = 60 [28%]), mesothelioma (n = 48 [22%]), cutaneous melanoma (n = 38
222 s were anal, biliary, cervical, endometrial, mesothelioma, neuroendocrine, salivary, small-cell lung,
223 9)m)Tc (((9)(9)m)Tc-M40) in murine models of mesothelioma of both epithelioid (M28) and sarcomatoid (
225 after injection, which was due to peritoneal mesothelioma, on the basis of tumor morphology and immun
228 olid Tumors (RECIST) version 1.0 for pleural mesothelioma or RECIST version 1.1 for peritoneal mesoth
230 uch as mesothelin, which is overexpressed in mesothelioma, ovarian, lung, breast, and pancreatic canc
231 d cancer target known to be overexpressed in mesothelioma, ovarian, lung, breast, and pancreatic canc
235 However, to date, we found that none of the mesothelioma patients carrying germline BAP1 mutations w
236 o accurately predict the overall survival of mesothelioma patients from whole-slide digitized images,
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
241 to measure serum mesothelin concentration in mesothelioma patients, indicating its potential use for
244 ssociation between pleural diffuse malignant mesothelioma (PDMM) and chest radiation for lymphoma.
246 anced, recurrent ovarian cancer or malignant mesothelioma received anetumab ravtansine at the maximum
249 tract metastases (PTMs) in malignant pleural mesothelioma remains controversial, and clinical practic
251 Research UK (CRUK/04/003), the June Hancock Mesothelioma Research Fund, and Guy's and St Thomas' NHS
253 lost in both spontaneous ovarian tumors and mesotheliomas, resulting in the loss of Bap1 expression.
257 A tissue microarray analysis of 198 human mesothelioma specimens showed that 33% of cases had redu
258 y population, because type of control group, mesothelioma stage, and histologic subtype significantly
259 s, cause-specific mortality was elevated for mesothelioma (standardized mortality ratio (SMR) = 2.85,
260 ting that mTOR activation is common in human mesothelioma, suggesting that it is a potential therapeu
261 NF2 tumors but not with malignant NF2 mutant mesotheliomas, suggesting that senescence may underlie t
262 icantly higher incidence of asbestos-induced mesothelioma than wild-type (WT) littermates (73% vs. 32
263 wide characterization of pathways altered in mesothelioma that could be potentially exploited to desi
264 bers into the pleural cavity of mice induces mesothelioma that exhibits common key pro-oncogenic mole
266 omparison of patients with and those without mesothelioma, the receiver-operating-characteristic curv
267 was to evaluate, in patients with malignant mesothelioma, the relationship between inherited loss-of
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 nirradiated tumors in a concomitant model of mesothelioma through systemic activation of cytotoxic T
272 lung cancer [NSCLC], small-cell lung cancer, mesothelioma, thymic epithelial tumours, and other pulmo
273 their use of a murine model of human pleural mesothelioma to explore potential factors that limit CAR
274 reported in patients with malignant pleural mesothelioma treated in a phase 1 study of vorinostat, w
276 f Foxp3(+) regulatory T cells (Tregs) in the mesothelioma tumor microenvironment after nonablative ol
277 ended survival and a 95-99% reduction in the mesothelioma tumor volume, in comparison with vehicle-tr
278 ealth Organization classification subdivides mesothelioma tumors into three histological types: epith
281 bined with cyclophosphamide in patients with mesothelioma was safe, the only side effect being modera
282 d a high incidence (22/26, 85%) of malignant mesotheliomas was observed in Bap1;Nf2;Cdkn2a (triple)-C
283 Using an orthotopic mouse model of pleural mesothelioma, we determined that relatively high doses o
284 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 ents with histologically confirmed malignant mesothelioma were evaluated for inherited mutations in t
288 women and 29 men) with unresectable pleural mesothelioma were treated with repetitive transarterial
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
296 r with any subtype of confirmed or suspected mesothelioma with pleural effusion, recruited from 12 ho
297 atment of mice with malignant ascites due to mesothelioma with rapamycin led to a marked reduction in
298 f Bap1, Nf2, and Cdkn2a result in aggressive mesotheliomas, with Bap1 loss contributing to tumorigene
300 tion in vivo reduced the growth of malignant mesothelioma xenografts in severe-combined immunodeficie