Clinical, Pathologic, and Imaging Features and Biological Markers of Uveal Melanoma

Rashid, Alia; Grossniklaus, Hans E.

doi:10.1007/978-1-62703-727-3_21

Cited by 11 publications

(6 citation statements)

References 120 publications

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“…Although major advances have been made in the diagnosis and therapy of uveal melanoma, the 5-year relative survival rate has not improved from 1973 to 2008, especially in patients with metastatic disease[ 7 ]. Since the molecular mechanisms of its aggressiveness remain not elucidated, no therapy is effective for metastatic uveal melanoma patients[ 8 , 9 ]. Therefore, understanding the crucial signals that contribute to the invasive and metastatic potential of uveal melanoma might help to identify novel therapies for uveal melanoma patients.…”

Section: Introductionmentioning

confidence: 99%

MiR-144 Inhibits Uveal Melanoma Cell Proliferation and Invasion by Regulating c-Met Expression

et al. 2015

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MicroRNAs (miRNAs) are a group endogenous small non-coding RNAs that inhibit protein translation through binding to specific target mRNAs. Recent studies have demonstrated that miRNAs are implicated in the development of cancer. However, the role of miR-144 in uveal melanoma metastasis remains largely unknown. MiR-144 was downregulated in both uveal melanoma cells and tissues. Transfection of miR-144 mimic into uveal melanoma cells led to a decrease in cell growth and invasion. After identification of two putative miR-144 binding sites within the 3' UTR of the human c-Met mRNA, miR-144 was proved to inhibit the luciferase activity inMUM-2B cells with a luciferase reporter construct containing the binding sites. In addition, the expression of c-Met protein was inhibited by miR-144. Furthermore, c-Met-mediated cell proliferation and invasion were inhibited by restoration of miR-144 in uveal melanoma cells. In conclusion, miR-144 acts as a tumor suppressor in uveal melanoma, through inhibiting cell proliferation and migration. miR-144 might serve as a potential therapeutic target in uveal melanoma patients.

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Section: Introductionmentioning

confidence: 99%

MiR-144 Inhibits Uveal Melanoma Cell Proliferation and Invasion by Regulating c-Met Expression

et al. 2015

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“…While iris melanomas are usually benign, ciliary body and choroidal melanomas can be highly metastatic [ 2 ]. Metastasis occurs by hematogenous spread and most commonly targets the liver [ 3 ]. Despite advances in the last three decades in the diagnosis of - and treatment options for - the primary tumor, we have unfortunately not witnessed a corresponding improvement in patient survival.…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-inducible factor 1 upregulation of both VEGF and ANGPTL4 is required to promote the angiogenic phenotype in uveal melanoma

et al. 2016

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PurposeExpression of the hypoxia-inducible factor (HIF)-1-regulated gene product, vascular endothelial growth factor (VEGF), correlates with tumor vascularity in patients with uveal melanoma (UM). While the relationship between HIF-1 and VEGF in cancer is well-studied, their relative contribution to the angiogenic phenotype in UM has not previously been interrogated. Here we evaluate the contribution of HIF-1, VEGF, and a second HIF-1-regulated gene product, angiopoietin-like 4 (ANGPTL4), to angiogenesis in UM.Experimental DesignUM cells were examined for expression of HIF-1α, VEGF, and ANGPTL4. Their contribution to the angiogenic potential of UM cells was assessed using the endothelial cell tubule formation and directed in vivo angiogenesis assays. These results were corroborated in tissue from UM animal models and in tissue from patients with UM.ResultsInhibition of VEGF partially reduced tubule formation promoted by conditioned medium from UM cells. Inhibition of ANGPTL4, which was highly expressed in hypoxic UM cells, a UM orthotopic transplant model, a UM tumor array, and vitreous samples from UM patients, inhibited the angiogenic potential of UM cells in vitro and in vivo; this effect was additive to VEGF inhibition.ConclusionsTargeting both ANGPTL4 and VEGF may be required for the effective inhibition of angiogenesis in UM.

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“…Uveal melanoma is the second most common form of melanoma and the most common primary intraocular malignant tumor in adults, with an incidence of about 1200–1500 new cases per year in the United States, accounting for 5%–6% of all cases of primary systemic melanoma [1–4]. Uveal melanoma is one of the most highly aggressive cancer and leada to metastatic death in up to half of patients despite successful local therapy [5, 6].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA dysregulation in uveal melanoma: a new player enters the game

Shen

et al. 2015

Oncotarget

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Uveal melanoma is the second most common form of melanoma and a predominant intraocular malignant tumor in adults. The development of uveal melanoma is a multistep process involving genetic and epigenetic alteration of proto-oncogenes and tumor-suppressor genes. Recent discoveries have shed a new light on the involvement of a class of noncoding RNA known as microRNAs (miRNAs) in uveal melanoma. A lot of miRNAs show differential expressions in uveal melanoma tissues and cell lines. Genes coding for these miRNAs have been characterized as novel oncogene and tumor-suppressor genes based on findings that these miRNAs control malignant phenotypes of uveal melanoma cells. Several studies have confirmed that dysregulation of miRNAs promotes cell-cycle progression, confers resistance to apoptosis, and enhances invasiveness and metastasis. Moreover, several miRNAs have also been shown to correlate with uveal melanoma initiation and progression, and thus may be used as biomarkers for early diagnosis and prognosis. Elucidating the biological aspects of miRNA dysregulation may help us better understand the pathogenesis of uveal melanoma and promote the development of miRNA directed-therapeutics against this disease.

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Clinical, Pathologic, and Imaging Features and Biological Markers of Uveal Melanoma

Cited by 11 publications

References 120 publications

MiR-144 Inhibits Uveal Melanoma Cell Proliferation and Invasion by Regulating c-Met Expression

MiR-144 Inhibits Uveal Melanoma Cell Proliferation and Invasion by Regulating c-Met Expression

Hypoxia-inducible factor 1 upregulation of both VEGF and ANGPTL4 is required to promote the angiogenic phenotype in uveal melanoma

MicroRNA dysregulation in uveal melanoma: a new player enters the game

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