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1 portant environmental factor associated with malignant melanoma.
2 ors that may exhibit histologic overlap with malignant melanoma.
3 s occurred, representing 33% of all incident malignant melanoma.
4 c signaling in the majority of patients with malignant melanoma.
5 significantly reflects mutation frequency in malignant melanoma.
6 tor for CCL1, is strongly expressed by human malignant melanoma.
7 tial therapeutic strategies for treatment of malignant melanoma.
8 raging for applications in breast cancer and malignant melanoma.
9 stulated to contribute to the elimination of malignant melanoma.
10 L ULBP2 as strong prognostic marker in human malignant melanoma.
11 dramatic clinical responses in patients with malignant melanoma.
12 oH2A (mH2A) suppresses tumour progression of malignant melanoma.
13 forming the prognosis for many patients with malignant melanoma.
14 g established in vitro and in vivo models of malignant melanoma.
15 utical for treating patients with metastatic malignant melanoma.
16 V1 may function as an antimetastatic gene in malignant melanoma.
17 B-p53 interaction as a strategy for treating malignant melanoma.
18 several human malignancies, including human malignant melanoma.
19 n cancer, breast cancer, bladder cancer, and malignant melanoma.
20 (18)F-labeled probe for PET of MC1R-positive malignant melanoma.
21 nctions as a "lineage addiction" oncogene in malignant melanoma.
22 tion and restoring wild-type p53 function in malignant melanoma.
23 ients with macroscopic nodal metastases from malignant melanoma.
24 e cancer/testis Ag NY-ESO-1 in patients with malignant melanoma.
25 development of bortezomib and IFN-alpha for malignant melanoma.
26 H(Arg(11)) an ideal candidate for the PET of malignant melanoma.
27 ives rise to genomically unstable progeny in malignant melanoma.
28 invasive ductal carcinoma of the breast, and malignant melanoma.
29 nt, and has been described as an oncogene in malignant melanoma.
30 nevi represents an important risk factor for malignant melanoma.
31 ge and identify treatments for patients with malignant melanoma.
32 (PET) imaging would aid in the detection of malignant melanoma.
33 porter and chemoresistance mediator in human malignant melanoma.
34 cs and targeting therapies for patients with malignant melanoma.
35 be useful for the treatment of patients with malignant melanoma.
36 ignificant antitumor responses in a model of malignant melanoma.
37 play an important role in the progression of malignant melanoma.
38 a valuable prognostic tool for management of malignant melanoma.
39 l treatment of completely resected high-risk malignant melanoma.
40 lanocytic lesions, only some of which become malignant melanoma.
41 iptional inactivation of the RASSF1A gene in malignant melanoma.
42 y resected stage IIB and stage III cutaneous malignant melanoma.
43 , has been observed in highly aggressive and malignant melanoma.
44 recently been discovered as driver events in malignant melanoma.
45 ed as exposures, and the primary outcome was malignant melanoma.
46 on factor FOXM1 is elevated and activated in malignant melanoma.
47 y a combination of rFVIIa and factor F(X) in malignant melanoma.
48 thane extract of W. tinctoria leaves against malignant melanoma.
49 statistically significant increased risk of malignant melanoma.
50 valuated as a chemotherapeutic agent against malignant melanoma.
51 f a pathway implicated in the development of malignant melanoma.
52 for the H2A.Z isoform H2A.Z.2 as a driver of malignant melanoma.
53 RSK signaling and increased cell survival in malignant melanoma.
54 AC inhibition may thus be key to treating malignant melanoma.
55 ic agent for PET and radionuclide therapy of malignant melanoma.
56 nt aetiological factor in the development of malignant melanoma.
57 rgeted treatment strategies are required for malignant melanoma.
58 inding benzamide in patients with metastatic malignant melanoma.
59 e ionotropic glutamate receptors, GRIN2A, in malignant melanoma.
60 lecular determinants of cytoarchitecture, in malignant melanoma.
61 notropic glutamate receptor signaling has in malignant melanoma.
62 S100B is a prognostic marker for malignant melanoma.
63 sence and functional implications of IgG4 in malignant melanoma.
64 trategy for challenging environments such as 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 inhibited by Ca(2+)-binding S100 proteins in malignant melanomas.
71 breast cancers, 4/20 neuroblastomas and 4/15 malignant melanomas.
72 of recurrent low-grade gliomas and advanced malignant melanomas.
73 that this gene is epigenetically silenced in 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 oteins such as S100B are elevated in primary malignant melanoma and are used as markers for this and
87 imple, accurate, in vivo distinction between malignant melanoma and atypical nevi, and may lead to a
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
94 been used to treat patients with metastatic malignant melanoma and patients rendered disease-free vi
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
99 ngly implicated in the etiology of cutaneous malignant melanoma and the UV portion of the sunlight sp
101 inhibition of RAF is already established in malignant melanoma and under investigation in non-small-
103 thway), is highly expressed in primary human malignant melanomas and melanoma cell lines with activat
104 BRAF oncoprotein is mutated in about half of malignant melanomas and other cancers, and a kinase acti
105 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 to treat metastatic renal cell carcinoma and malignant melanoma, but its use is limited by the severe
121 p53 protein complex was discovered in C8146A malignant melanoma, but the consequences of this interac
122 es, has the potential for early detection of malignant melanoma by exploiting the sensitivity and hig
123 hat PDE5 inhibitors may increase the risk of malignant melanoma by negating newly identified brakes o
124 ell degranulation, but a deleterious role in malignant melanoma, by impeding IgG1-mediated anti-tumor
127 ukin (IL)-2, a T-cell cytokine used to treat malignant melanoma, can induce profound depression.
131 o have significant activity in the Sk-Mel-28 malignant melanoma cell line (IC(50) values of 1.10 and
132 proliferative action of eugenol in the human malignant melanoma cell line, WM1205Lu, showed that it a
133 play essential roles in the control of mouse malignant melanoma cell proliferation and/or anchorage-i
134 ase-dependent cell death in a panel of human malignant melanoma cells (A375, G361, LOX-IMVI) but not
135 oM) and five inhibited the growth of primary malignant melanoma cells (C8146A) at comparable concentr
137 FN5, SLFN11, SLFN12, SLFN13, and SLFN14), in malignant melanoma cells and primary normal human melano
139 exerts potent inhibitory activities against malignant melanoma cells in vitro and in vivo, but the m
141 in situ contain a high level of HDAC1/2 and malignant melanoma cells overexpress HDAC1/2/3 compared
142 Importantly, stable knockdown of SLFN5 in malignant melanoma cells resulted in increased anchorage
143 logic inhibition of class I HDACs sensitizes malignant melanoma cells to apoptosis following exposure
144 e impact of class I HDACs on the response of malignant melanoma cells treated with alkylating agents.
145 gest feasibility of apoptotic elimination of malignant melanoma cells using the quinone methide-deriv
146 tional capacity of normal human melanocytes, malignant melanoma cells, and metastatic melanoma cells
153 underlying the high prevalence of cutaneous malignant melanoma (CMM) in Parkinson disease (PD) are u
154 i (DN) is a strong risk factor for cutaneous malignant melanoma (CMM), and it frequently occurs in me
155 ion genes have been identified for cutaneous malignant melanoma (CMM), but they account for only appr
160 factor receptor (IGF1R) is overexpressed by malignant melanomas compared with benign naevi, and medi
161 sera obtained from a subset of patients with malignant melanoma, compared with healthy control indivi
164 tem cell phenotype-expressing tumor cells in malignant melanoma cultures and clinical melanomas.
165 bladder cancer, renal cell cancer (RCC), and malignant melanoma data in 635 adult (>18 years of age)
170 uired at the transition from benign nevus to malignant melanoma do not support telomere maintenance.
174 cancer antigens led to the recognition that malignant melanoma frequently evokes a host response.
180 f cell proliferation and drug sensitivity in malignant melanoma, holding translational potential for
181 Using tissue sections from patients with malignant melanoma, immunofluorescence studies for the p
182 between increased BMI and rectal cancer and malignant melanoma in men; postmenopausal breast, pancre
183 nt report, we evaluated the growth of B16F10 malignant melanoma in mice with a monocyte/macrophage-se
187 have shown great promise in the treatment of malignant melanoma in the last few years, with these dru
188 ion was associated with an increased risk of malignant melanoma in two cohorts of women and men.
189 this peptide was selectively exposed within malignant melanoma in vivo, whereas little if any was de
194 specific T cells in patients with metastatic malignant melanoma, indicating that the tumor-bearing st
196 erline the importance of molecularly defined malignant melanoma initiating cells for CSC-focused diag
199 identify a subpopulation enriched for human malignant-melanoma-initiating cells (MMIC) defined by ex
200 In patients at high risk for recurrence of malignant melanoma, interferon-alpha (IFN-alpha), a stim
208 sed on gene expression profiling showed that malignant melanoma is amenable to systemic treatment.
225 or obstacle in understanding the etiology of malignant melanoma is the lack of mouse models and trans
231 further evidence that molecular subtypes of malignant melanoma may develop along divergent pathways.
232 oma (BCC), squamous cell carcinoma (SCC), or malignant melanoma (MM) and comparative risk estimates o
233 gene is the most frequently mutated gene in malignant melanoma (MM) and papillary thyroid cancer (PT
234 A phase I study of patients with metastatic malignant melanoma (MM) and renal cell carcinoma (RCC) e
235 omplex formation with p53 ((Ca)S100B.p53) in malignant melanoma (MM) and restores p53 tumor suppresso
237 detection, dermatologists strive to diagnose malignant melanoma (MM) at the earliest possible stage.
244 Conditioned medium (CM) from metastatic malignant melanoma (MMM) cell lines attracted LEC migrat
246 , PNL-2, and Melan-A) confirmed diagnosis of malignant melanoma of the ciliary body with extraocular
250 ) lymphatic vessels were detected in 7 of 10 malignant melanomas of the ciliary body with extraocular
252 ther tumor lymphangiogenesis occurs in human malignant melanomas of the skin and whether the extent o
255 idal tumors clinically as benign nevi versus malignant melanomas on the basis of tumor size appear li
256 consecutive days to patients with metastatic malignant melanoma or metastatic renal cell cancer.
257 othripsis with poor outcome in patients with malignant melanomas (P = 0.0002) and provides a genetic
259 cal significance of our results, we analyzed malignant melanoma patient samples with or without brisk
263 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
283 n progenitor cells, is expressed in clinical malignant melanoma tumors and preferentially marks a sub
286 ific in vivo targeting of (18)F-FB-RMSH-1 to malignant melanoma was successfully achieved in preclini
287 mber of individuals with two or more primary malignant melanomas was not detected among the groups (P
289 node or in-transit metastasis from cutaneous malignant melanoma were randomly assigned to receive eit
291 ble for the induction of mammalian cutaneous malignant melanoma whereas UVA is ineffective even at do
292 olet light exposure, a known risk factor for malignant melanoma, whereas the uneven distribution of m
294 0201 patients at high risk for recurrence of malignant melanoma who received prolonged immunization w
295 to metastasize to the small bowel; however, malignant melanoma with metastatic spread to the appendi
296 al responses achieved by treating metastatic malignant melanoma with therapeutic modalities based on
297 and DGKI-BRAF fusion were identified in two malignant melanomas with a low mutational burden (number
298 or chromosome arm gains and losses, whereas malignant melanomas with poor prognosis harbored signifi
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