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1 apy in 10 patients with anti-PD-1-refractory metastatic melanoma.
2 al detachment during nivolumab treatment for metastatic melanoma.
3 w approved for patients with unresectable or metastatic melanoma.
4 which is routinely used at first therapy for metastatic melanoma.
5 served with the combination in patients with metastatic melanoma.
6 ctive, immune-based treatment strategies for metastatic melanoma.
7 cers, such as non-small-cell lung tumors and metastatic melanoma.
8 y benefits overall survival of patients with metastatic melanoma.
9 AMIGO2-PTK7 axis as a targetable pathway for metastatic melanoma.
10 CI, ipilimumab, in 2011 for the treatment of metastatic melanoma.
11 of CDK4/6 inhibitor in highly proliferative metastatic melanoma.
12 (FUT1, FUT2) were identified as features of metastatic melanoma.
13 ilizer conjugate, has the potential to treat metastatic melanoma.
14 om CombiDT in patients with BRAFi-refractory metastatic melanoma.
15 etastases, eruptive nevi, and epidermotropic metastatic melanoma.
16 h the CTLA4-blocking antibody ipilimumab for metastatic melanoma.
17 s coincided with the approval of IMLYGIC for metastatic melanoma.
18 identify new targets to improve treatment of metastatic melanoma.
19 yields sustained remissions in patients with metastatic melanoma.
20 y untreated BRAF V600-mutant unresectable or metastatic melanoma.
21 al processes operate during the evolution of metastatic melanoma.
22 aged 18 years and older and had advanced or metastatic melanoma.
23 on Cancer (AJCC) criteria and follow-up for metastatic melanoma.
24 ively regulates genes that drive invasion of metastatic melanoma.
25 public whole-exome sequencing (WES) data for metastatic melanoma.
26 therapeutic Pin1-FOXM1 inhibitors to target metastatic melanoma.
27 linical benefit in a subset of patients with metastatic melanoma.
28 a novel potential therapy for patients with metastatic melanoma.
29 and normal DNA isolated from 8 patients with metastatic melanoma.
30 en proposed as a target for the treatment of metastatic melanoma.
31 tantially improved personalized treatment of metastatic melanoma.
32 us dosing) in the treatment of patients with metastatic melanoma.
33 d NPs have the highest potential in treating metastatic melanoma.
34 ts with BRAF Val600Lys/Glu mutation-positive metastatic melanoma.
35 in BRAF(V600) mutation-positive advanced or metastatic melanoma.
36 pared with ipilimumab alone in patients with metastatic melanoma.
37 om an unselected population of patients with metastatic melanoma.
38 RNA abundance and survival of patients with metastatic melanoma.
39 ed with standard therapy in BRAF V600-mutant metastatic melanoma.
40 nvolving patients with ipilimumab-refractory metastatic melanoma.
41 igand, supporting a TIGIT/CD226 imbalance in metastatic melanoma.
42 FPE specimens through RNA gene expression in metastatic melanoma.
43 se findings support a key role for CASC15 in metastatic melanoma.
44 may be a novel approach for the treatment of metastatic melanoma.
45 lised treatment strategies for patients with metastatic melanoma.
46 essential for cell motility and invasion of metastatic melanoma.
47 gen 4, has shown promise in the treatment of metastatic melanoma.
48 o identify new therapeutic opportunities for metastatic melanoma.
49 nal and potentially impactful treatments for metastatic melanoma.
50 2 (A-kinase anchor protein 12), AKAP12v2, in metastatic melanoma.
51 ntitumor responses in patients with advanced metastatic melanoma.
52 been shown to have complementary activity in metastatic melanoma.
53 roves overall survival (OS) in patients with metastatic melanoma.
54 ging by the AJCC criteria, and follow-up for metastatic melanoma.
55 HP vaccine was administered to patients with metastatic melanoma.
56 mproved overall survival among patients with metastatic melanoma.
57 ve remarkably improved the response rates of metastatic melanoma.
58 th factor (CTGF) as a therapeutic target for metastatic melanoma.
59 cribe a novel KIT mutation in a patient with metastatic melanoma.
60 ised trials that enrolled 4416 patients with metastatic melanoma.
61 ared with nevi, and was further increased in metastatic melanoma.
62 at offer improved survival for patients with metastatic melanoma.
63 pilimumab prolongs survival in patients with metastatic melanoma.
64 ls have shown an overall survival benefit in metastatic melanoma.
65 rst-line treatment in patients with advanced metastatic melanoma.
66 has led to a sea change in the treatment of metastatic melanoma.
67 ic potential of targeting this axis to treat metastatic melanoma.
68 l death receptor 1 therapy in a patient with metastatic melanoma.
69 mbrolizumab in patients with unresectable or metastatic melanoma.
70 ed nanoparticles have the potential to treat metastatic melanoma.
71 care for patients with BRAF V600E/K-mutated metastatic melanoma.
72 n in serum may serve as a novel biomarker of metastatic melanoma.
73 ate the clinical effect of targeting CDC7 in metastatic melanoma.
74 e checkpoint inhibitors for the treatment of metastatic melanoma.
75 roved the clinical outcomes of patients with metastatic melanoma.
76 s major impact on the tumorigenic program of metastatic melanoma.
77 atic modules in monocytes and DCs from human metastatic melanoma.
78 n long-term survival of patients with widely metastatic melanoma.
79 t promise in a variety of cancers, including metastatic melanoma.
80 udy, we seek to identify a gene signature of metastatic melanoma.
81 ating that NLRP1 inflammasomes are active in metastatic melanoma.
82 r patients with advanced-ie, unresectable or metastatic-melanoma.
83 rs may guide adjuvant therapies in stage III metastatic melanomas.
84 y dysplastic nevi, as well as in primary and metastatic melanomas.
85 ber alterations and somatic mutations in 303 metastatic melanomas.
86 rom The Cancer Genome Atlas are misdiagnosed metastatic melanomas.
87 ate the ERK cascade, account for over 80% of metastatic melanomas.
91 h improved overall survival in patients with metastatic melanoma, a growing challenge of drug resista
92 ere associated with poor OS in patients with metastatic melanoma after ipilimumab treatment but not v
93 agents have revolutionized the treatment of metastatic melanoma, allowing some subsets of patients t
94 2 inhibitor provides a survival advantage in metastatic melanoma, an effect that is increased when ad
95 /2, which has been approved for treatment of metastatic melanoma and anaplastic thyroid cancer in pat
96 novel framework using a published dataset of metastatic melanoma and find biological insights from th
97 oth patients had been heavily pretreated for metastatic melanoma and had multiple sites of intraperit
99 s identified as a key metabolic signature of metastatic melanoma and renal cancer, and metastatic cel
100 dose interleukin-2 (IL-2) is active against metastatic melanoma and renal cell carcinoma, but treatm
101 ve patients with BRAF V600 mutation-positive metastatic melanoma, and approximately 20% were progress
102 n endothelial cell biology and angiogenesis, metastatic melanoma, and corneal epithelial cells; howev
103 by metastasis stage, previous treatment for metastatic melanoma, and Eastern Cooperative Oncology Gr
104 ecently approved for use in the treatment of metastatic melanoma, and nivolumab as well for non-small
105 were 18 years or older, had unresectable or metastatic melanoma, and progressed after ipilimumab, or
106 s that have been introduced for treatment of metastatic melanoma are active against brain metastases
107 d vemurafenib-a BRAF inhibitor used to treat metastatic melanoma-are all recognized clinical photosen
108 h de novo meningitis caused by P. acnes with metastatic melanoma as the only identified risk factor f
109 ticles into C57/BL6 albino mice bearing lung metastatic melanoma at the dose of 20 mg/kg 4 times a we
110 rvival among patients with BRAF V600-mutated metastatic melanoma, at the cost of some increase in tox
113 tors (BRAFi) elicit therapeutic responses in metastatic melanoma, but alarmingly, also induce the for
114 rapy has emerged as a powerful treatment for metastatic melanoma, but efficacy is limited by an inhos
116 or, has pronounced activity in patients with metastatic melanoma, but its activity in patients with B
117 atly improved the prognosis of patients with metastatic melanoma, but resistance to these therapeutic
118 eads to prolonged responses in patients with metastatic melanoma, but the common mechanisms of primar
119 a subset of patients with BRAF(V600)-mutated metastatic melanoma by increasing the frequency of long-
120 siderable clinical benefit for patients with metastatic melanoma by inhibiting immune checkpoint acti
124 CR-free whole genome sequencing of a matched metastatic melanoma cell line (COLO829) and normal acros
125 performed a co-culture experiment with human metastatic melanoma cell line (SKMEL- 147) and immortali
126 ssion, we conducted a microarray on a highly metastatic melanoma cell line in which NFAT1 expression
128 e reduced by knocking down of NLRP1 in human metastatic melanoma cell lines 1205Lu and HS294T, indica
132 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 chanistically, overexpression of miR-200a in metastatic melanoma cells induces cell cycle arrest by t
137 Conversely, low microRNA-200a expression in metastatic melanoma cells results in higher levels of CD
138 that inducible expression of CD82 in highly metastatic melanoma cells significantly increased p21 ex
141 owed that by downregulating Rac signaling in metastatic melanoma cells, ICAT increased their invasive
142 nuclein promotes the survival of primary and metastatic melanoma cells, which is the exact opposite o
146 n was consistently decreased in invasive and metastatic melanoma, compared with nevi and melanoma in
148 ent transcriptional silencing in primary and metastatic melanoma consistent with a tumor suppressor f
153 c characteristics remain stable in recurrent metastatic melanoma even after years and several recurre
154 of melanoma cells in freshly isolated human metastatic melanoma ex vivo and in three-dimensional-cul
160 ose Patients who are diagnosed with stage IV metastatic melanoma have an estimated 5-year relative su
161 s (TILs) that mediate complete regression of metastatic melanoma have been shown to recognize mutated
165 ased targeted therapies for the treatment of metastatic melanoma hold promise but responses are often
166 eted therapies achieve long-term survival in metastatic melanoma; however, new treatment strategies a
167 lymphocytes (TILs) can mediate regression of metastatic melanoma; however, TILs are a heterogeneous p
168 ted genomic DNA from the AGTR1 CpG island in metastatic melanoma implying that AGTR1 encodes a tumour
169 rapeutics directed against BRAF(V600)-mutant metastatic melanoma improves progression-free survival i
171 enrolled 15 patients with BRAF(V600)-mutated metastatic melanoma in a first-in-human clinical trial o
172 ients with BRAF inhibitor (BRAFi)-refractory metastatic melanoma in contrast to the higher response r
174 notherapy against multiple cancers including metastatic melanoma, in which ELN formation has been ass
176 zumab provides durable antitumor activity in metastatic melanoma, including complete response (CR) in
177 that inhibits uncontrolled neural crest and metastatic melanoma invasion and promotes collective mig
178 ed human melanoma cell proteolytic activity; metastatic melanoma is a highly aggressive and drug-resi
181 treatment of BRAF-unmutated unresectable or metastatic melanoma is a landmark for the development of
187 fic mAb, showed durable clinical efficacy in metastatic melanoma; its mechanism of action is, however
188 68.8; interquartile range, 58.4 to 77.0) and metastatic melanomas (MFI, 87.5; interquartile range, 77
189 t blockade (ICB) of PD-1 and CTLA-4 to treat metastatic melanoma (MM) has variable therapeutic benefi
190 y outcomes in patients with BRAF V600-mutant metastatic melanoma (MM) who received BRAF inhibitor dab
192 + and CD8+ T lymphocytes in 57 patients with metastatic melanoma (MMel) with various sites of metasta
198 Among previously untreated patients with metastatic melanoma, nivolumab alone or combined with ip
199 We analysed samples from 46 patients with metastatic melanoma obtained before and during anti-PD-1
200 rotein and mRNA expression in paired primary/metastatic melanoma or colorectal cancer cells than thos
201 ector clones has been reported in refractory metastatic melanoma patients after adoptive T-cell trans
202 s melanoma tissue correlate with survival of metastatic melanoma patients after dendritic cell (DC) v
203 ostoperative lymphatic exudate and plasma of metastatic melanoma patients after lymphadenectomy and f
204 angiogenic factors in MAPK inhibitor-treated metastatic melanoma patients and to correlate these chan
205 e form, which can be detected in the sera of metastatic melanoma patients but not in normal sera.
206 ay offer a new strategy for the treatment of metastatic melanoma patients harboring melanin-positive
208 data from a pilot trial in therapy-resistant metastatic melanoma patients show anti-tumor activity th
209 nalyzing longitudinal tumor biopsies from 17 metastatic melanoma patients treated with CPB therapies,
210 r combination BRAF and MEK inhibitor-treated metastatic melanoma patients using a multiplex chemokine
211 cell infiltration in primary tumors from 77 metastatic melanoma patients was quantified using the ra
212 redictor of survival after DC vaccination in metastatic melanoma patients who, on average, started th
213 s of PTX3 were found in tissues and blood of metastatic melanoma patients, and in BRAF inhibitor-resi
218 criteria for participants included BRAF V600 metastatic melanoma, prior BRAFi monotherapy, measurable
219 D) ligand RAE-1beta, or when inoculated with metastatic melanoma, prostate carcinoma, or mammary carc
220 th inflammation-attenuating glycoprotein non-metastatic melanoma protein B (GPNMB) signaling in human
223 s with ipilimumab-naive or -treated advanced/metastatic melanoma received one of three dose regimens
224 Despite emergence of new systemic therapies, metastatic melanoma remains a challenging and often fata
231 ve trials in MMel.The clinical management of metastatic melanoma requires predictors of the response
232 BRAF inhibitors like vemurafenib in treating metastatic melanoma, resistance has emerged through "par
233 CombiDT treatment in patients with BRAF V600 metastatic melanoma resistant to BRAFi monotherapy condu
234 d c-Myc proteins was significantly higher in metastatic melanoma samples as compared with that in pri
235 parameter flow cytometry on freshly isolated metastatic melanoma samples from 2 cohorts of 20 patient
237 significantly with patients presenting nodal metastatic melanoma, suggesting that targeting this path
238 mor-associated macrophages observed in human metastatic melanoma, supporting the concept that NLRC4 e
239 n of oncogenic BRAF mutations in primary and metastatic melanomas supports a linear model of clonal e
240 (PFS), and overall survival in patients with metastatic melanoma that has a BRAF(V600) mutation.
241 may represent a novel therapeutic target in metastatic melanoma, the most lethal form of skin cancer
242 brain mass was resected and confirmed to be metastatic melanoma; the surgical bed was treated with s
245 SPINT2 expression is significantly lower in metastatic melanoma tissues compared with those in early
246 e evaluated resistance mechanisms arising in metastatic melanoma to MAPK pathway kinase inhibitors as
249 our regressions in a subset of patients with metastatic melanoma treated with an anti-CTLA4 antibody
255 c and histone epigenetic analysis of patient metastatic melanoma tumors taken prior to checkpoint blo
256 conduct a prospective study of patients with metastatic melanoma undergoing ipilimumab treatment and
257 s in the systemic treatment of patients with metastatic melanoma using immune checkpoint and tyrosine
258 a-based immunotherapeutic strategies against metastatic melanoma, using a genetically engineered mous
259 mpare the long-term outcome of patients with metastatic melanoma vaccinated with 6MHP to that of a gr
260 ession-free survival in cancer patients with metastatic melanoma, we developed a set of stochastic di
261 inical specimens of primary breast cancer or metastatic melanoma, we found a positive correlation bet
262 K5 knockout mice and a mouse model of highly metastatic melanoma, we found that CDK5 is dispensable f
263 ls of immune checkpoint blockade therapy for metastatic melanoma, we found that tumor aneuploidy inve
265 d and metastatic lymph nodes performed in 39 metastatic melanomas, we found that blood markers were a
266 dacarbazine-controlled randomised trials of metastatic melanoma; we postulate that this association
268 ve oral chemotherapy agent for patients with metastatic melanoma who carry the BRAF V600E mutation.
269 man undergoing treatment with ipilimumab for metastatic melanoma who developed classic cutaneous find
270 n an exemplary clinical case: a patient with metastatic melanoma who developed disease recurrence fol
271 tudy reported the cases of two patients with metastatic melanoma who developed fatal myocarditis duri
272 phase I/II trial enrolling 63 patients with metastatic melanoma who did not receive vemurafenib nor
273 and relapsing lesions in four patients with metastatic melanoma who had had an initial objective tum
274 uble-blind study involving 142 patients with metastatic melanoma who had not previously received trea
276 ith BRAF(V600E)-mutant or BRAF(V600K)-mutant metastatic melanoma who received the approved dose of da
277 ected population-based cohort of adults with metastatic melanoma who started therapy with pembrolizum
278 ds: We analyzed 60 consecutive patients with metastatic melanoma who underwent (18)F-FDG PET/CT scans
279 coreceptors PD-1 and Tim-3 in patients with metastatic melanoma who were administered tumor vaccines
280 lung cancer, colorectal liver metastases, or metastatic melanoma who were scanned for therapy monitor
281 al600Glu or Val600Lys mutant unresectable or metastatic melanoma who were treated with the combinatio
282 pulation of patients with BRAF(V600) mutated metastatic melanoma, who are more representative of rout
283 ients with an unusually prolonged history of metastatic melanoma, who developed a total of 26 recurre
285 rial, we randomly assigned 704 patients with metastatic melanoma with a BRAF V600 mutation to receive
287 hird of the patients who had unresectable or metastatic melanoma with a BRAF V600E or V600K mutation.
288 sed phase 3 study in which 704 patients with metastatic melanoma with a BRAF Val600 mutation were ran
291 rvival in previously untreated patients with metastatic melanoma with BRAF V600E or V600K mutations,
292 rapies in patients with previously untreated metastatic melanoma with BRAF V600E or V600K mutations.
293 val in previously untreated patients who had metastatic melanoma with BRAF V600E or V600K mutations.
295 In the current study, 103 patients with metastatic melanoma with rare, activating non-V600E/K BR
296 complete regressions in 24% of patients with metastatic melanoma, with median survival > 3 years.
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