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1 ted with clinical PD-L1 expression scores in malignant melanoma.
2 nt aetiological factor in the development of malignant melanoma.
3 rgeted treatment strategies are required for malignant melanoma.
4 Dermal invasion is a hallmark of malignant melanoma.
5 inding benzamide in patients with metastatic malignant melanoma.
6 e ionotropic glutamate receptors, GRIN2A, in malignant melanoma.
7 notropic glutamate receptor signaling has in malignant melanoma.
8 S100B is a prognostic marker for malignant melanoma.
9 ression of precursor melanocytic lesions and malignant melanoma.
10 sence and functional implications of IgG4 in malignant melanoma.
11 trategy for challenging environments such as malignant melanoma.
12 portant environmental factor associated with malignant melanoma.
13 ors that may exhibit histologic overlap with malignant melanoma.
14 s occurred, representing 33% of all incident malignant melanoma.
15 c signaling in the majority of patients with malignant melanoma.
16 tor for CCL1, is strongly expressed by human malignant melanoma.
17 tial therapeutic strategies for treatment of malignant melanoma.
18 raging for applications in breast cancer and malignant melanoma.
19 monly used to treat patients with metastatic malignant melanoma.
20 stulated to contribute to the elimination of malignant melanoma.
21 L ULBP2 as strong prognostic marker in human malignant melanoma.
22 dramatic clinical responses in patients with malignant melanoma.
23 oH2A (mH2A) suppresses tumour progression of malignant melanoma.
24 g established in vitro and in vivo models of malignant melanoma.
25 utical for treating patients with metastatic malignant melanoma.
26 V1 may function as an antimetastatic gene in malignant melanoma.
27 B-p53 interaction as a strategy for treating malignant melanoma.
28 several human malignancies, including human malignant melanoma.
29 n cancer, breast cancer, bladder cancer, and malignant melanoma.
30 (18)F-labeled probe for PET of MC1R-positive malignant melanoma.
31 nctions as a "lineage addiction" oncogene in malignant melanoma.
32 tion and restoring wild-type p53 function in malignant melanoma.
33 ients with macroscopic nodal metastases from malignant melanoma.
34 e cancer/testis Ag NY-ESO-1 in patients with malignant melanoma.
35 lic activity in many cancer types, including malignant melanoma.
36 development of bortezomib and IFN-alpha for malignant melanoma.
37 H(Arg(11)) an ideal candidate for the PET of malignant melanoma.
38 ives rise to genomically unstable progeny in malignant melanoma.
39 invasive ductal carcinoma of the breast, and malignant melanoma.
40 nt, and has been described as an oncogene in malignant melanoma.
41 nevi represents an important risk factor for malignant melanoma.
42 ge and identify treatments for patients with malignant melanoma.
43 (PET) imaging would aid in the detection of malignant melanoma.
44 porter and chemoresistance mediator in human malignant melanoma.
45 cs and targeting therapies for patients with malignant melanoma.
46 be useful for the treatment of patients with malignant melanoma.
47 ignificant antitumor responses in a model of malignant melanoma.
48 play an important role in the progression of malignant melanoma.
49 recently been discovered as driver events in malignant melanoma.
50 AC inhibition may thus be key to treating malignant melanoma.
51 lecular determinants of cytoarchitecture, in malignant melanoma.
52 significantly reflects mutation frequency in malignant melanoma.
53 forming the prognosis for many patients with malignant melanoma.
54 lanocytic lesions, only some of which become malignant melanoma.
55 ed as exposures, and the primary outcome was malignant melanoma.
56 on factor FOXM1 is elevated and activated in malignant melanoma.
57 y a combination of rFVIIa and factor F(X) in malignant melanoma.
58 thane extract of W. tinctoria leaves against malignant melanoma.
59 statistically significant increased risk of malignant melanoma.
60 valuated as a chemotherapeutic agent against malignant melanoma.
61 f a pathway implicated in the development of malignant melanoma.
62 for the H2A.Z isoform H2A.Z.2 as a driver of malignant melanoma.
63 RSK signaling and increased cell survival in malignant melanoma.
64 ic agent for PET and radionuclide therapy of malignant melanoma.
65 des a genetic approach to predict outcome in malignant melanomas.
66 rst description of chromothripsis in primary malignant melanomas.
67 xpressed by both benign melanocytes and many malignant melanomas.
68 ism of regulation of MITF in melanocytes and malignant melanomas.
69 (also known as BRAF) are found in 50-70% of malignant melanomas.
70 breast cancers, 4/20 neuroblastomas and 4/15 malignant melanomas.
71 inhibited by Ca(2+)-binding S100 proteins in malignant melanomas.
72 that this gene is epigenetically silenced in malignant melanomas.
73 underwent enucleation surgery for choroidal malignant melanomas.
74 or the regulation of MITF in melanocytes and malignant melanomas.
75 ion (V600E) is found in more than 50% of all malignant melanomas.
76 as pain, inflammation, airway diseases, and malignant melanomas.
77 95% CI 1.19-1.30), rectum (1.14, 1.07-1.22), malignant melanoma (1.32, 1.24-1.40), breast (1.17, 1.15
78 s (24/32), basal cell carcinomas (30/31) and malignant melanomas (15/15), and provide evidence for a
79 5 sebaceous cell carcinomas [31.25%], and 4 malignant melanomas [25%]) were included in the study.
81 me in cell replication, were investigated in malignant melanoma, a cancer with a paucity of effective
82 chromatin that suppresses the development of malignant melanoma, a highly intractable cutaneous neopl
84 whereas an increased incidence was found for malignant melanoma among both men (SIR = 1.09) and women
86 imple, accurate, in vivo distinction between malignant melanoma and atypical nevi, and may lead to a
87 In NICD(OE-HEC) mice, hepatic metastasis of malignant melanoma and colorectal carcinoma was signific
88 HRH receptors in surgical specimens of human malignant melanoma and evaluated the effects of AN-207 i
89 fter diagnosis with 10 patients who survived malignant melanoma and had a median disease-free surviva
90 and the role of miRNA in the pathogenesis of malignant melanoma and identify biomarkers of metastasis
92 EF-hand proteins that has been implicated in malignant melanoma and neurodegenerative conditions such
93 ve revolutionized the clinical management of malignant melanoma and now offer hope to patients with a
95 ase may have broad applications for treating malignant melanoma and potentially other cancer types.
98 eoplastic syndrome associated with cutaneous malignant melanoma and the presence of autoantibodies th
100 into the tumor suppressive role of PARK2 in malignant melanoma and uncover a novel mechanism for the
101 inhibition of RAF is already established in malignant melanoma and under investigation in non-small-
102 thway), is highly expressed in primary human malignant melanomas and melanoma cell lines with activat
103 BRAF oncoprotein is mutated in about half of malignant melanomas and other cancers, and a kinase acti
104 n to evidence of multiple GISTs, lentigines, malignant melanoma, and an angioleiomyoma were identifie
106 use is associated with an increased risk of malignant melanoma, and whether any increase in risk is
107 utations occur in approximately 70% of human malignant melanomas, and a single hyperactivating V600E
108 EK-ERK pathway is deregulated in over 90% of malignant melanomas, and targeting MEK as a central kina
109 ng antibodies to augment T-cell responses to malignant melanoma are at an advanced stage; however, li
112 lignant melanoma in situ (MMIS) and invasive malignant melanoma are rising in the United States, but
113 , we report 4 cases of orbital recurrence of malignant melanoma as a late complication of biopsy and/
114 man and murine melanoma cell lines, in human malignant melanoma, as well as in metastatic melanoma in
115 rospectively evaluated the risk of cutaneous malignant melanoma associated with citrus consumption.
120 p53 protein complex was discovered in C8146A malignant melanoma, but the consequences of this interac
121 es, has the potential for early detection of malignant melanoma by exploiting the sensitivity and hig
122 hat PDE5 inhibitors may increase the risk of malignant melanoma by negating newly identified brakes o
123 ell degranulation, but a deleterious role in malignant melanoma, by impeding IgG1-mediated anti-tumor
125 ukin (IL)-2, a T-cell cytokine used to treat malignant melanoma, can induce profound depression.
126 gh response rates and profound regression of malignant melanomas carrying BRAF(V600E) mutations.
130 o have significant activity in the Sk-Mel-28 malignant melanoma cell line (IC(50) values of 1.10 and
131 proliferative action of eugenol in the human malignant melanoma cell line, WM1205Lu, showed that it a
132 play essential roles in the control of mouse malignant melanoma cell proliferation and/or anchorage-i
133 ase-dependent cell death in a panel of human malignant melanoma cells (A375, G361, LOX-IMVI) but not
135 FN5, SLFN11, SLFN12, SLFN13, and SLFN14), in malignant melanoma cells and primary normal human melano
138 exerts potent inhibitory activities against malignant melanoma cells in vitro and in vivo, but the m
139 BRAF and that block paradoxical signaling in malignant melanoma cells occurring through this drug tar
140 in situ contain a high level of HDAC1/2 and malignant melanoma cells overexpress HDAC1/2/3 compared
141 Importantly, stable knockdown of SLFN5 in malignant melanoma cells resulted in increased anchorage
142 logic inhibition of class I HDACs sensitizes malignant melanoma cells to apoptosis following exposure
143 e impact of class I HDACs on the response of malignant melanoma cells treated with alkylating agents.
144 gest feasibility of apoptotic elimination of malignant melanoma cells using the quinone methide-deriv
145 tional capacity of normal human melanocytes, malignant melanoma cells, and metastatic melanoma cells
152 underlying the high prevalence of cutaneous malignant melanoma (CMM) in Parkinson disease (PD) are u
153 i (DN) is a strong risk factor for cutaneous malignant melanoma (CMM), and it frequently occurs in me
154 ion genes have been identified for cutaneous malignant melanoma (CMM), but they account for only appr
158 factor receptor (IGF1R) is overexpressed by malignant melanomas compared with benign naevi, and medi
159 sera obtained from a subset of patients with malignant melanoma, compared with healthy control indivi
162 tem cell phenotype-expressing tumor cells in malignant melanoma cultures and clinical melanomas.
163 bladder cancer, renal cell cancer (RCC), and malignant melanoma data in 635 adult (>18 years of age)
168 uired at the transition from benign nevus to malignant melanoma do not support telomere maintenance.
169 ka (Oryzias latipes), that overexpresses the malignant melanoma driver gene xmrk, a mutant egfr gene,
172 w, we focus on the role of RAC1 signaling in malignant melanoma, emphasizing recent advances that des
179 f cell proliferation and drug sensitivity in malignant melanoma, holding translational potential for
180 Using tissue sections from patients with malignant melanoma, immunofluorescence studies for the p
181 between increased BMI and rectal cancer and malignant melanoma in men; postmenopausal breast, pancre
182 nt report, we evaluated the growth of B16F10 malignant melanoma in mice with a monocyte/macrophage-se
186 have shown great promise in the treatment of malignant melanoma in the last few years, with these dru
187 ion was associated with an increased risk of malignant melanoma in two cohorts of women and men.
188 this peptide was selectively exposed within malignant melanoma in vivo, whereas little if any was de
193 erline the importance of molecularly defined malignant melanoma initiating cells for CSC-focused diag
196 identify a subpopulation enriched for human malignant-melanoma-initiating cells (MMIC) defined by ex
197 In patients at high risk for recurrence of malignant melanoma, interferon-alpha (IFN-alpha), a stim
205 sed on gene expression profiling showed that malignant melanoma is amenable to systemic treatment.
228 further evidence that molecular subtypes of malignant melanoma may develop along divergent pathways.
229 oma (BCC), squamous cell carcinoma (SCC), or malignant melanoma (MM) and comparative risk estimates o
230 gene is the most frequently mutated gene in malignant melanoma (MM) and papillary thyroid cancer (PT
231 A phase I study of patients with metastatic malignant melanoma (MM) and renal cell carcinoma (RCC) e
232 omplex formation with p53 ((Ca)S100B.p53) in malignant melanoma (MM) and restores p53 tumor suppresso
233 detection, dermatologists strive to diagnose malignant melanoma (MM) at the earliest possible stage.
240 Conditioned medium (CM) from metastatic malignant melanoma (MMM) cell lines attracted LEC migrat
244 onal nominally significant associations with malignant melanoma, multiple myeloma, oral cancer, and e
245 , PNL-2, and Melan-A) confirmed diagnosis of malignant melanoma of the ciliary body with extraocular
249 ) lymphatic vessels were detected in 7 of 10 malignant melanomas of the ciliary body with extraocular
254 idal tumors clinically as benign nevi versus malignant melanomas on the basis of tumor size appear li
255 consecutive days to patients with metastatic malignant melanoma or metastatic renal cell cancer.
256 othripsis with poor outcome in patients with malignant melanomas (P = 0.0002) and provides a genetic
258 cal significance of our results, we analyzed malignant melanoma patient samples with or without brisk
262 with histologically documented metastasized malignant melanoma received a single dose of 235 +/- 62
271 ss is associated with a higher percentage of malignant melanoma samples with non-brisk host responses
272 suppressor activity in cancer cells such as malignant melanoma, so a search for small molecules that
274 expressed in a very high percentage of human malignant melanoma specimens and can be used for targete
275 ivation of BRAF is a frequent event in human malignant melanomas suggesting that BRAF-dependent signa
277 in and beta-catenin as two of the markers of malignant melanoma that were down-regulated in Panx1-KD
278 mparative genomic hybridization (aCGH) to 20 malignant melanomas that showed, despite comparable conv
280 ion and the possible clinical implication on malignant melanoma therapy with temozolomide and other a
284 n progenitor cells, is expressed in clinical malignant melanoma tumors and preferentially marks a sub
288 ific in vivo targeting of (18)F-FB-RMSH-1 to malignant melanoma was successfully achieved in preclini
289 mber of individuals with two or more primary malignant melanomas was not detected among the groups (P
291 node or in-transit metastasis from cutaneous malignant melanoma were randomly assigned to receive eit
293 olet light exposure, a known risk factor for malignant melanoma, whereas the uneven distribution of m
295 0201 patients at high risk for recurrence of malignant melanoma who received prolonged immunization w
296 to metastasize to the small bowel; however, malignant melanoma with metastatic spread to the appendi
297 al responses achieved by treating metastatic malignant melanoma with therapeutic modalities based on
298 and DGKI-BRAF fusion were identified in two malignant melanomas with a low mutational burden (number
299 or chromosome arm gains and losses, whereas malignant melanomas with poor prognosis harbored signifi