"The role of next-generation sequencing to determine appropriateness of anti-PD1/PD-L1 therapy needs further investigation, but has shown promise in predicting response and survival in melanoma and urothelial carcinoma."
> 50% of melanomas progress with enriched "AXL-high" populations, and because AXL is linked to de-differentiation and invasiveness avoiding an "AXL-high relapse" is desirable.
<b>Conclusion:</b> In conclusion, rapamycin suppresses angiogenesis and lymphangiogenesis in melanoma by blocking the mTOR signal pathway and subsequently downregulating the expression of VEGF-A/VEGFR-2 and VEGF-C/VEGFR-3.
<b>Conclusion:</b> In conclusion, rapamycin suppresses angiogenesis and lymphangiogenesis in melanoma by blocking the mTOR signal pathway and subsequently downregulating the expression of VEGF-A/VEGFR-2 and VEGF-C/VEGFR-3.
<b>Conclusion:</b> The non-toxic radiopharmaceuticals <sup>131</sup>I-IITM and <sup>211</sup>At-AITM are useful high-precision TRT agents that can be used to target the oncoprotein mGluR1 for melanoma therapy.
<b>Conclusion:</b> These results indicate that PSMA expression in nonprostatic tumors may not be limited to the endothelium but may also include solid tumor tissue of nonprostatic cancers including melanoma and SCLC.
<b>Conclusion:</b> These results suggest that haspin can be considered as a viable anti-melanoma target, and that concomitant inhibition of haspin and MEK activities with small molecules could represent a novel therapeutic strategy with improved efficacy for treatment of melanoma.
<b>Conclusions:</b> In this study, we suggest that bone metastasis in melanoma might be related to AL118506.1 and its role in regulating thrombospondin 2 and T follicular helper cells.
<b>Methods:</b> We used branched polyamidoamine (PAMAM) dendrimers as scaffold for melanoma specific gp100 synthetic long peptides and the common DC-SIGN and Langerin ligand Lewis Y (Le<sup>Y</sup>), to create multivalent glyco-dendrimers with varying molecular weights for investigating dual DC-SIGN and Langerin targeting.
<b>Methods:</b> We used branched polyamidoamine (PAMAM) dendrimers as scaffold for melanoma specific gp100 synthetic long peptides and the common DC-SIGN and Langerin ligand Lewis Y (Le<sup>Y</sup>), to create multivalent glyco-dendrimers with varying molecular weights for investigating dual DC-SIGN and Langerin targeting.
<b>Purpose:</b> Checkpoint kinase 1 inhibitors (CHEK1i) have single-agent activity <i>in vitro</i> and <i>in vivo</i> Here, we have investigated the molecular basis of this activity.<b>Experimental Design:</b> We have assessed a panel of melanoma cell lines for their sensitivity to the CHEK1i GNE-323 and GDC-0575 <i>in vitro</i> and <i>in vivo</i> The effects of these compounds on responses to DNA replication stress were analyzed in the hypersensitive cell lines.<b>Results:</b> A subset of melanoma cell lines is hypersensitive to CHEK1i-induced cell death <i>in vitro</i>, and the drug effectively inhibits tumor growth <i>in vivo</i> In the hypersensitive cell lines, GNE-323 triggers cell death without cells entering mitosis.
<b>Purpose:</b> BRAF inhibitors are clinically active in patients with advanced BRAF<sup>V600</sup>-mutant melanoma, although acquired resistance remains common.
<b>Purpose:</b> c-KIT overexpression is well recognized in cancers such as gastrointestinal stromal tumors (GIST), small cell lung cancer (SCLC), melanoma, non-small cell lung cancer (NSCLC), and acute myelogenous leukemia (AML).
<b>Purpose:</b> Pembrolizumab monotherapy, ipilimumab monotherapy, and pegylated interferon alfa-2b (PEG-IFN) monotherapy are active against melanoma and renal cell carcinoma (RCC).
<b>Purpose:</b> Polyinosinic-polycytidylic acid-poly-l-lysine carboxymethylcellulose (poly-ICLC), a synthetic double-stranded RNA complex, is a ligand for toll-like receptor-3 and MDA-5 that can activate immune cells, such as dendritic cells, and trigger natural killer cells to kill tumor cells.<b>Patients and Methods:</b> In this pilot study, eligible patients included those with recurrent metastatic disease in whom prior systemic therapy (head and neck squamous cell cancer and melanoma) failed.
<b>Purpose:</b> To examine the relationship between immune activity, PD-L1 expression, and tumor cell signaling, in metastatic melanomas prior to and during treatment with targeted MAPK inhibitors.<b>Experimental Design:</b> Thirty-eight tumors from 17 patients treated with BRAF inhibitor (<i>n</i> = 12) or combination BRAF/MEK inhibitors (<i>n</i> = 5) with known PD-L1 expression were analyzed.
<b>Purpose:</b> To examine the relationship between immune activity, PD-L1 expression, and tumor cell signaling, in metastatic melanomas prior to and during treatment with targeted MAPK inhibitors.<b>Experimental Design:</b> Thirty-eight tumors from 17 patients treated with BRAF inhibitor (<i>n</i> = 12) or combination BRAF/MEK inhibitors (<i>n</i> = 5) with known PD-L1 expression were analyzed.
<i>In vivo</i> administration of IAP antagonists and α-GalCer resulted in increased IFNγ and IL-2 production from iNKT cells and decreased tumor burden in a mouse model of melanoma lung metastasis.