A three-gene expression signature model to predict clinical outcome of clear cell renal carcinoma

2008 ◽  
Vol 123 (5) ◽  
pp. 1126-1132 ◽  
Author(s):  
Masahiro Yao ◽  
Ying Huang ◽  
Koichi Shioi ◽  
Keiko Hattori ◽  
Takayuki Murakami ◽  
...  
2017 ◽  
Vol 474 (1) ◽  
pp. 159-161
Author(s):  
V. Yu. Bashmakov ◽  
T. M. Gorbacheva ◽  
A. V. Panevina ◽  
S. A. Solodskikh ◽  
I. P. Moshurov ◽  
...  

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e17078-e17078
Author(s):  
Saif Alimohamed ◽  
James I. Geller ◽  
Bruce Aronow

e17078 Background: The Cancer Genome Atlas project has become a leading source for data that has allowed the identification of a broad range of human cancer tumor types and subtypes and has revealed deep complexity with respect to the differentiation, or lack thereof, among human cancers. In particular, differential gene expression analyses have revealed a wealth of active oncogenic pathways, underlying gene mutation drivers, discriminative markers, and candidate therapeutic targets. Despite its rich composition, several factors have led to it not attaining the utility it would seem to offer. Methods: To study this, we dissected molecular subtypes in the TCGA and used the Pan-Kidney (n = 1022 samples) Portion within it to determine where obstacles seem to limit its utility. We re-clustered the renal carcinomas to create more appropriate histology annotations for these samples. The molecular subtypes were then found through K-means using differentially expressed known developmental regulators per histological annotation. After deriving these new annotations, the histology and molecular subtypes were compared to one another via T-test to generate gene modules that characterize these classes/subclasses. Results: We identified a number of factors that include inconsistent metadata attributes, apparent misclassification of histological subtypes, and molecular subtypes that do not match with that obtained by focused approaches to rederive principle subclasses. Our gene modules showed a molecular subtype of clear cell renal carcinoma that was enriched for vascular development and nephron development. In general, the clear cell renal carcinoma and papillary renal cell carcinoma cohorts both showed significant co-expression with atlases that were enriched for genes involved in kidney development. Conclusions: Our atlas highlights the limitations of the current TCGA atlas and provides another tool to capture the rich insights from the TCGA repository through the efforts explained above, highlighted by its use in kidney carcinoma.


2004 ◽  
Vol 171 (4S) ◽  
pp. 436-436 ◽  
Author(s):  
Hyung L. Kim ◽  
David B. Seligson ◽  
Nicolette Janzen ◽  
Matthew H. Bui ◽  
Robert A. Figlin ◽  
...  

Oncogene ◽  
2007 ◽  
Vol 26 (45) ◽  
pp. 6499-6508 ◽  
Author(s):  
J S P Yuen ◽  
M E Cockman ◽  
M Sullivan ◽  
A Protheroe ◽  
G D H Turner ◽  
...  

2021 ◽  
Vol 22 (3) ◽  
pp. 1342
Author(s):  
Aleksandra Cios ◽  
Martyna Ciepielak ◽  
Wanda Stankiewicz ◽  
Łukasz Szymański

The development of new technologies and industry is conducive to the increase in the number and variety of electromagnetic field (EMF) sources in our environment. The main sources of EMF are high-voltage lines, household appliances, audio/video devices, mobile phones, radio stations, and radar devices. In the growing use of electronic devices, scientists are increasingly interested in the effects of EMF on human health. Even though many studies on the effects of EMF have already been carried out, none of them has shown a significant effect on mammals, including humans. Moreover, it is not entirely clear how EMF influences cell behavior. The International Agency for Research on Cancer on 31 May 2011, classified PEM as a possible carcinogenic factor. This study aimed to investigate the effect of the electromagnetic field on morphological and functional changes in clear cell renal carcinoma. The research was carried out on in vitro cultures of four cell lines: HEK293, 786-O 769-P, and Caki1. The results of the research showed that the EMF of low frequency had a slight effect on the viability of cells. EMF, which induced cell arrest in the G1 phase, increased the number of early apoptotic cells and decreased the number of viable cells in the 786-O line. EMF did not affect the proliferation and viability of HEK293 cells. Extreme low-frequency EMF (ELF-EMF) also showed an inhibitory effect on the migration and metastatic properties of clear cell kidney cancer cells. Moreover, shortly after the end of ELF-EMF exposure, significant increases in ROS levels were observed in all tested cell lines. As part of the work, it was shown that low-frequency EMF shows an inhibitory effect on the proliferation of primary cancer cells, diminishing their migratory, invasive, and metastatic abilities. It also increases the apoptosis of cancer cells and the amount of reactive oxygen species. Based on the results of our research, we want to point up that the effect of ELF-EMF depends on a specific metabolic state or at a specific stage in the cell cycle of the cells under study.


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