Pathology of Uveal Melanoma: Histological Parameters and Patient Prognosis

2003 ◽  
pp. 421-440
Keyword(s):  
Uveal Melanoma ◽  
Patient Prognosis

Higher Percentage of FISH-Determined Monosomy 3 and 8q Amplification in Uveal Melanoma Cells relate to Poor Patient Prognosis

2012 ◽  
Vol 53 (6) ◽  
pp. 2668 ◽  
Author(s):  
Thomas van den Bosch ◽  
Jackelien G. M. van Beek ◽  
Jolanda Vaarwater ◽  
Robert M. Verdijk ◽  
Nicole C. Naus ◽  
...  
Keyword(s):  
Uveal Melanoma ◽  
Melanoma Cells ◽  
Poor Patient ◽  
Monosomy 3 ◽  
Patient Prognosis

scholarly journals Association Between High Immune Activity and Worse Prognosis in Uveal Melanoma and Low-Grade Glioma in TCGA Transcriptomic Data

2021 ◽  
Author(s):  
Hitoshi Matsuo ◽  
Takashi Kamatani ◽  
Yu Hamba ◽  
Keith A. Boroevich ◽  
Tatsuhiko Tsunoda
Keyword(s):  
Uveal Melanoma ◽  
Immune Activation ◽  
Low Grade Glioma ◽  
Low Grade ◽  
Mesenchymal Transition ◽  
Immune Activity ◽  
Cancer Types ◽  
Patient Prognosis ◽  
Endothelial Mesenchymal Transition ◽  
Worse Prognosis

Abstract Background: Immune status in the tumor microenvironment is an important determinant of cancer progression and patient prognosis. Although a higher immune activity is often associated with a better prognosis, this trend is not absolute and differs across cancer types. We aimed to give insights into why some cancers do not show better survival despite higher immunity by assessing the relationship between different biological factors, including cytotoxicity, and patient prognosis in various cancer types using RNA-seq data collected by The Cancer Genome Atlas.Results: Results showed that a higher immune activity was associated with worse prognosis in patients with uveal melanoma and low-grade glioma, which are cancers of immune-privileged sites. In these cancers, epithelial or endothelial mesenchymal transition and inflammatory state as well as immune activation had notably negative correlation with patient prognosis. Further analysis using additional single-cell data of uveal melanoma and glioma revealed that epithelial or endothelial mesenchymal transition was mainly induced in retinal pigment cells or endothelial cells that comprise the blood-retinal and blood-brain barriers, which are unique structures of the eye and central nervous system, respectively. Inflammation was mainly promoted by macrophages, and their infiltration increased significantly in response to immune activation. Furthermore, we found the expression of CCL5 was strongly correlated with immune activity and associated with bad prognosis, particularly in these cancers, suggesting that CCL5 is a potential molecular target for therapeutics.Conclusions: Epithelial or endothelial mesenchymal transition is associated with a bad prognosis. This suggests that inflammation loosens the structures of the blood barrier and causes further infiltration of immune cells, which may result in a feedback loop of additional inflammatory effects leading to runaway conditions.

Abstract #1010: Uveal Melanoma Masquerading as A Nontoxic Multinodular Goiter

2015 ◽  
Vol 21 ◽  
pp. 194-195
Author(s):  
Rokshana Thanadar ◽  
Uzma Siddiqui ◽  
Marie Lithgow ◽  
Runhua Hou
Keyword(s):  
Uveal Melanoma ◽  
Multinodular Goiter

Uveal melanoma metastatic risk based on comprehensive genetic testing

2020 ◽  
pp. 178-179
Author(s):  
V.A. Yarovaya ◽  
◽  
A.A. Yarovoy ◽  
A.R. Zaretsky ◽  
L.V. Chudakova ◽  
...  
Keyword(s):  
Genetic Testing ◽  
Uveal Melanoma ◽  
Metastatic Risk

TAp73 opposes tumor angiogenesis by promoting hypoxia-inducible factor 1α degradation

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Cancer Progression ◽  
Hypoxia Inducible Factor ◽  
Tumor Hypoxia ◽  
Human Lung Cancer ◽  
Regulatory Subunit ◽  
Patients With Cancer ◽  
Hypoxia Inducible Factor 1 ◽  
Chemically Induced ◽  
Induced Tumors ◽  
Patient Prognosis

Tumor hypoxia and hypoxia-inducible factor 1 (HIF-1) activationare associated with cancer progression. Here, we demonstrate thatthe transcription factor TAp73 opposes HIF-1 activity through anontranscriptional mechanism, thus affecting tumor angiogenesis.TAp73-deficient mice have an increased incidence of spontaneousand chemically induced tumors that also display enhanced vascularization.Mechanistically, TAp73 interacts with the regulatory subunit(α) of HIF-1 and recruits mouse double minute 2 homolog intothe protein complex, thus promoting HIF-1α polyubiquitination andconsequent proteasomal degradation in an oxygen-independentmanner. In human lung cancer datasets, TAp73 strongly predictsgood patient prognosis, and its expression is associated with lowHIF-1 activation and angiogenesis. Our findings, supported by invivo and clinical evidence, demonstrate a mechanism for oxygenindependentHIF-1 regulation, which has important implicationsfor individualizing therapies in patients with cancer.

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