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1 ively regulates genes that drive invasion of metastatic melanoma.
2 therapeutic Pin1-FOXM1 inhibitors to target metastatic melanoma.
3 linical benefit in a subset of patients with metastatic melanoma.
4 a novel potential therapy for patients with metastatic melanoma.
5 and normal DNA isolated from 8 patients with metastatic melanoma.
6 en proposed as a target for the treatment of metastatic melanoma.
7 tantially improved personalized treatment of metastatic melanoma.
8 us dosing) in the treatment of patients with metastatic melanoma.
9 d NPs have the highest potential in treating metastatic melanoma.
10 ts with BRAF Val600Lys/Glu mutation-positive metastatic melanoma.
11 pared with ipilimumab alone in patients with metastatic melanoma.
12 om an unselected population of patients with metastatic melanoma.
13 RNA abundance and survival of patients with metastatic melanoma.
14 ed with standard therapy in BRAF V600-mutant metastatic melanoma.
15 nvolving patients with ipilimumab-refractory metastatic melanoma.
16 igand, supporting a TIGIT/CD226 imbalance in metastatic melanoma.
17 se findings support a key role for CASC15 in metastatic melanoma.
18 udy, we seek to identify a gene signature of metastatic melanoma.
19 may be a novel approach for the treatment of metastatic melanoma.
20 lised treatment strategies for patients with metastatic melanoma.
21 essential for cell motility and invasion of metastatic melanoma.
22 gen 4, has shown promise in the treatment of metastatic melanoma.
23 o identify new therapeutic opportunities for metastatic melanoma.
24 2 (A-kinase anchor protein 12), AKAP12v2, in metastatic melanoma.
25 ntitumor responses in patients with advanced metastatic melanoma.
26 been shown to have complementary activity in metastatic melanoma.
27 roves overall survival (OS) in patients with metastatic melanoma.
28 ging by the AJCC criteria, and follow-up for metastatic melanoma.
29 HP vaccine was administered to patients with metastatic melanoma.
30 mproved overall survival among patients with metastatic melanoma.
31 ating that NLRP1 inflammasomes are active in metastatic melanoma.
32 ve remarkably improved the response rates of metastatic melanoma.
33 th factor (CTGF) as a therapeutic target for metastatic melanoma.
34 cribe a novel KIT mutation in a patient with metastatic melanoma.
35 ised trials that enrolled 4416 patients with metastatic melanoma.
36 ared with nevi, and was further increased in metastatic melanoma.
37 at offer improved survival for patients with metastatic melanoma.
38 pilimumab prolongs survival in patients with metastatic melanoma.
39 ls have shown an overall survival benefit in metastatic melanoma.
40 123)I-BZA2 for diagnosis of melanin-positive metastatic melanoma.
41 1 as a potential target for the treatment of metastatic melanoma.
42 acy for predicting survival in patients with metastatic melanoma.
43 ory effect on the progression of established metastatic melanoma.
44 therapy on overall survival in patients with metastatic melanoma.
45 as an effective therapy for the treatment of metastatic melanoma.
46 ediate long-term survival for a patient with metastatic melanoma.
47 lasting, clinical responses in patients with metastatic melanoma.
48 in expression was generally downregulated in metastatic melanoma.
49 ma, and almost completely absent in nevi and metastatic melanoma.
50 for the treatment of patients with BRAFV600 metastatic melanoma.
51 to 50% or more of patients with unresectable metastatic melanoma.
52 al response to vemurafenib in a patient with metastatic melanoma.
53 mediating antibody-induced immunotherapy of metastatic melanoma.
54 l viability, and suppressed tumorigenesis in metastatic melanoma.
55 umor regression in patients with BRAF(V600E) metastatic melanoma.
56 ated with vemurafenib for a BRAFV600-mutated metastatic melanoma.
57 for the CP regimen in first-line therapy of metastatic melanoma.
58 as well as 12 FNA samples from patients with metastatic melanoma.
59 nts an effective treatment for patients with metastatic melanoma.
60 al detachment during nivolumab treatment for metastatic melanoma.
61 w approved for patients with unresectable or metastatic melanoma.
62 which is routinely used at first therapy for metastatic melanoma.
63 served with the combination in patients with metastatic melanoma.
64 ctive, immune-based treatment strategies for metastatic melanoma.
65 roved the clinical outcomes of patients with metastatic melanoma.
66 cers, such as non-small-cell lung tumors and metastatic melanoma.
67 y benefits overall survival of patients with metastatic melanoma.
68 AMIGO2-PTK7 axis as a targetable pathway for metastatic melanoma.
69 of CDK4/6 inhibitor in highly proliferative metastatic melanoma.
70 (FUT1, FUT2) were identified as features of metastatic melanoma.
71 s major impact on the tumorigenic program of metastatic melanoma.
72 ilizer conjugate, has the potential to treat metastatic melanoma.
73 atic modules in monocytes and DCs from human metastatic melanoma.
74 om CombiDT in patients with BRAFi-refractory metastatic melanoma.
75 etastases, eruptive nevi, and epidermotropic metastatic melanoma.
76 h the CTLA4-blocking antibody ipilimumab for metastatic melanoma.
77 s coincided with the approval of IMLYGIC for metastatic melanoma.
78 identify new targets to improve treatment of metastatic melanoma.
79 yields sustained remissions in patients with metastatic melanoma.
80 n long-term survival of patients with widely metastatic melanoma.
81 al processes operate during the evolution of metastatic melanoma.
82 aged 18 years and older and had advanced or metastatic melanoma.
83 t promise in a variety of cancers, including metastatic melanoma.
84 on Cancer (AJCC) criteria and follow-up for metastatic melanoma.
85 y dysplastic nevi, as well as in primary and metastatic melanomas.
86 ber alterations and somatic mutations in 303 metastatic melanomas.
87 ate the ERK cascade, account for over 80% of metastatic melanomas.
88 diting enzyme ADAR1 is frequently reduced in metastatic melanomas.
89 rs may guide adjuvant therapies in stage III metastatic melanomas.
93 topic posterior pituitary gland), 5.melanin (metastatic melanoma), 6.lesions containing mineral subst
94 ere associated with poor OS in patients with metastatic melanoma after ipilimumab treatment but not v
95 agents have revolutionized the treatment of metastatic melanoma, allowing some subsets of patients t
96 2 inhibitor provides a survival advantage in metastatic melanoma, an effect that is increased when ad
98 on and NF-kappaB activity were suppressed in metastatic melanoma and enhanced in primary melanoma aft
99 oth patients had been heavily pretreated for metastatic melanoma and had multiple sites of intraperit
101 s identified as a key metabolic signature of metastatic melanoma and renal cancer, and metastatic cel
103 ts older than 18 years, with treatment-naive metastatic melanoma and whose tumour tissue was positive
104 ve patients with BRAF V600 mutation-positive metastatic melanoma, and approximately 20% were progress
105 n endothelial cell biology and angiogenesis, metastatic melanoma, and corneal epithelial cells; howev
106 by metastasis stage, previous treatment for metastatic melanoma, and Eastern Cooperative Oncology Gr
107 ecently approved for use in the treatment of metastatic melanoma, and nivolumab as well for non-small
108 were 18 years or older, had unresectable or metastatic melanoma, and progressed after ipilimumab, or
109 ment is a potential therapeutic strategy for metastatic melanoma, and that SODD, in particular, is a
110 s that have been introduced for treatment of metastatic melanoma are active against brain metastases
111 d vemurafenib-a BRAF inhibitor used to treat metastatic melanoma-are all recognized clinical photosen
113 h de novo meningitis caused by P. acnes with metastatic melanoma as the only identified risk factor f
114 samples from four murine xenograft models of metastatic melanoma, as well as 12 FNA samples from pati
115 rvival among patients with BRAF V600-mutated metastatic melanoma, at the cost of some increase in tox
116 tors (BRAFi) elicit therapeutic responses in metastatic melanoma, but alarmingly, also induce the for
117 rapy has emerged as a powerful treatment for metastatic melanoma, but efficacy is limited by an inhos
119 or, has pronounced activity in patients with metastatic melanoma, but its activity in patients with B
120 eads to prolonged responses in patients with metastatic melanoma, but the common mechanisms of primar
121 n mediate cancer regression in patients with metastatic melanoma, but whether this approach can be ap
122 siderable clinical benefit for patients with metastatic melanoma by inhibiting immune checkpoint acti
125 CR-free whole genome sequencing of a matched metastatic melanoma cell line (COLO829) and normal acros
126 performed a co-culture experiment with human metastatic melanoma cell line (SKMEL- 147) and immortali
127 ssion, we conducted a microarray on a highly metastatic melanoma cell line in which NFAT1 expression
129 e reduced by knocking down of NLRP1 in human metastatic melanoma cell lines 1205Lu and HS294T, indica
133 rast, here we show that exosomes from poorly metastatic melanoma cells can potently inhibit metastasi
135 nterference with\ Pin1 in BRAF(V600E)-driven metastatic melanoma cells impaired both FOXM1 activity a
136 interleukin (IL)-2 or IL-15], and could lyse metastatic melanoma cells in a highly efficient manner c
137 chanistically, overexpression of miR-200a in metastatic melanoma cells induces cell cycle arrest by t
138 Conversely, low microRNA-200a expression in metastatic melanoma cells results in higher levels of CD
139 that inducible expression of CD82 in highly metastatic melanoma cells significantly increased p21 ex
143 owed that by downregulating Rac signaling in metastatic melanoma cells, ICAT increased their invasive
144 h to maintain submicromolar PDT in pigmented metastatic melanoma cells, where the presence of melanin
145 nuclein promotes the survival of primary and metastatic melanoma cells, which is the exact opposite o
149 rmore, expression of p63 in both primary and metastatic melanoma clinical samples significantly corre
150 g Administration approval of vemurafenib for metastatic melanoma, clinicians should be aware of this
151 n was consistently decreased in invasive and metastatic melanoma, compared with nevi and melanoma in
156 A 62-year-old woman with V600E BRAF -mutant metastatic melanoma enrolled in a phase 1 trial of dabra
157 c characteristics remain stable in recurrent metastatic melanoma even after years and several recurre
158 of melanoma cells in freshly isolated human metastatic melanoma ex vivo and in three-dimensional-cul
167 ose Patients who are diagnosed with stage IV metastatic melanoma have an estimated 5-year relative su
168 s (TILs) that mediate complete regression of metastatic melanoma have been shown to recognize mutated
171 lymphocytes (TILs) can mediate regression of metastatic melanoma; however, TILs are a heterogeneous p
172 ether such particles can offer patients with metastatic melanoma improved prognoses for the future.
173 rapeutics directed against BRAF(V600)-mutant metastatic melanoma improves progression-free survival i
175 ients with BRAF inhibitor (BRAFi)-refractory metastatic melanoma in contrast to the higher response r
176 tration for the treatment of unresectable or metastatic melanoma in patients with Braf(V600E) mutatio
177 notherapy against multiple cancers including metastatic melanoma, in which ELN formation has been ass
179 zumab provides durable antitumor activity in metastatic melanoma, including complete response (CR) in
180 that inhibits uncontrolled neural crest and metastatic melanoma invasion and promotes collective mig
181 ed human melanoma cell proteolytic activity; metastatic melanoma is a highly aggressive and drug-resi
184 treatment of BRAF-unmutated unresectable or metastatic melanoma is a landmark for the development of
191 h minimal toxicity and that in patients with metastatic melanoma, it induces favorable immune respons
192 fic mAb, showed durable clinical efficacy in metastatic melanoma; its mechanism of action is, however
194 y outcomes in patients with BRAF V600-mutant metastatic melanoma (MM) who received BRAF inhibitor dab
196 + and CD8+ T lymphocytes in 57 patients with metastatic melanoma (MMel) with various sites of metasta
200 ma cells and low-passage cultures from human metastatic melanomas (MRA cells) results in increased ap
203 Among previously untreated patients with metastatic melanoma, nivolumab alone or combined with ip
204 We analysed samples from 46 patients with metastatic melanoma obtained before and during anti-PD-1
207 uced a paradigm shift in melanoma treatment: Metastatic melanoma, once considered incurable, can now
208 clinical responses in many cancers including metastatic melanoma, only a subset of patients has shown
209 ector clones has been reported in refractory metastatic melanoma patients after adoptive T-cell trans
210 s melanoma tissue correlate with survival of metastatic melanoma patients after dendritic cell (DC) v
211 angiogenic factors in MAPK inhibitor-treated metastatic melanoma patients and to correlate these chan
212 e form, which can be detected in the sera of metastatic melanoma patients but not in normal sera.
213 ay offer a new strategy for the treatment of metastatic melanoma patients harboring melanin-positive
214 data from a pilot trial in therapy-resistant metastatic melanoma patients show anti-tumor activity th
216 nalyzing longitudinal tumor biopsies from 17 metastatic melanoma patients treated with CPB therapies,
217 r combination BRAF and MEK inhibitor-treated metastatic melanoma patients using a multiplex chemokine
218 cell infiltration in primary tumors from 77 metastatic melanoma patients was quantified using the ra
219 redictor of survival after DC vaccination in metastatic melanoma patients who, on average, started th
224 criteria for participants included BRAF V600 metastatic melanoma, prior BRAFi monotherapy, measurable
225 D) ligand RAE-1beta, or when inoculated with metastatic melanoma, prostate carcinoma, or mammary carc
229 s with ipilimumab-naive or -treated advanced/metastatic melanoma received one of three dose regimens
235 ve trials in MMel.The clinical management of metastatic melanoma requires predictors of the response
236 CombiDT treatment in patients with BRAF V600 metastatic melanoma resistant to BRAFi monotherapy condu
237 ng tumor-infiltrating lymphocytes (TILs) for metastatic melanoma reveals a substantial subset that ex
238 d c-Myc proteins was significantly higher in metastatic melanoma samples as compared with that in pri
239 parameter flow cytometry on freshly isolated metastatic melanoma samples from 2 cohorts of 20 patient
242 significantly with patients presenting nodal metastatic melanoma, suggesting that targeting this path
243 mor-associated macrophages observed in human metastatic melanoma, supporting the concept that NLRC4 e
244 n of oncogenic BRAF mutations in primary and metastatic melanomas supports a linear model of clonal e
245 (PFS), and overall survival in patients with metastatic melanoma that has a BRAF(V600) mutation.
246 mised trials comparing treatment regimens in metastatic melanoma that included dacarbazine as the con
247 brain mass was resected and confirmed to be metastatic melanoma; the surgical bed was treated with s
250 is significantly upregulated in primary and metastatic melanoma tissues compared with melanocytes an
251 SPINT2 expression is significantly lower in metastatic melanoma tissues compared with those in early
253 e evaluated resistance mechanisms arising in metastatic melanoma to MAPK pathway kinase inhibitors as
255 our regressions in a subset of patients with metastatic melanoma treated with an anti-CTLA4 antibody
259 c and histone epigenetic analysis of patient metastatic melanoma tumors taken prior to checkpoint blo
260 conduct a prospective study of patients with metastatic melanoma undergoing ipilimumab treatment and
261 mpare the long-term outcome of patients with metastatic melanoma vaccinated with 6MHP to that of a gr
262 ession-free survival in cancer patients with metastatic melanoma, we developed a set of stochastic di
263 inical specimens of primary breast cancer or metastatic melanoma, we found a positive correlation bet
264 ls of immune checkpoint blockade therapy for metastatic melanoma, we found that tumor aneuploidy inve
266 d and metastatic lymph nodes performed in 39 metastatic melanomas, we found that blood markers were a
267 dacarbazine-controlled randomised trials of metastatic melanoma; we postulate that this association
270 which did not include metastases (except for metastatic melanoma which was a radiological suggestion
271 is study suggests that the late evolution of metastatic melanoma, which markedly turns an indolent di
272 ve oral chemotherapy agent for patients with metastatic melanoma who carry the BRAF V600E mutation.
273 man undergoing treatment with ipilimumab for metastatic melanoma who developed classic cutaneous find
274 n an exemplary clinical case: a patient with metastatic melanoma who developed disease recurrence fol
275 tudy reported the cases of two patients with metastatic melanoma who developed fatal myocarditis duri
276 phase I/II trial enrolling 63 patients with metastatic melanoma who did not receive vemurafenib nor
277 and relapsing lesions in four patients with metastatic melanoma who had had an initial objective tum
278 uble-blind study involving 142 patients with metastatic melanoma who had not previously received trea
280 ith BRAF(V600E)-mutant or BRAF(V600K)-mutant metastatic melanoma who received the approved dose of da
281 coreceptors PD-1 and Tim-3 in patients with metastatic melanoma who were administered tumor vaccines
282 lung cancer, colorectal liver metastases, or metastatic melanoma who were scanned for therapy monitor
283 al600Glu or Val600Lys mutant unresectable or metastatic melanoma who were treated with the combinatio
284 pulation of patients with BRAF(V600) mutated metastatic melanoma, who are more representative of rout
285 ients with an unusually prolonged history of metastatic melanoma, who developed a total of 26 recurre
287 rial, we randomly assigned 704 patients with metastatic melanoma with a BRAF V600 mutation to receive
288 sed phase 3 study in which 704 patients with metastatic melanoma with a BRAF Val600 mutation were ran
289 rvival in previously untreated patients with metastatic melanoma with BRAF V600E or V600K mutations,
290 rapies in patients with previously untreated metastatic melanoma with BRAF V600E or V600K mutations.
291 val in previously untreated patients who had metastatic melanoma with BRAF V600E or V600K mutations.
292 sessed vemurafenib in patients with advanced metastatic melanoma with BRAF(V600) mutations who had fe
295 complete regressions in 24% of patients with metastatic melanoma, with median survival > 3 years.
296 nant tumor in patients who do not succumb to metastatic melanoma within the first few posttreatment y
297 ed 418 previously untreated patients who had metastatic melanoma without a BRAF mutation to receive n
299 roves clinical outcomes in BRAF(V600)-mutant metastatic melanoma without brain metastases; however, t
300 ) represent promising therapeutic agents for metastatic melanoma, yet their mechanism of action remai
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