Gene Expression Profiling Separates Chromophobe Renal Cell Carcinoma from Oncocytoma and Identifies Vesicular Transport and Cell Junction Proteins as Differentially Expressed Genes

2006 ◽  
Vol 12 (23) ◽  
pp. 6937-6945 ◽  
Author(s):  
Stephen Rohan ◽  
Jiangling J. Tu ◽  
Jean Kao ◽  
Piali Mukherjee ◽  
Fabien Campagne ◽  
...  
2021 ◽  
Author(s):  
Hamed Ishaq Khouja ◽  
Ibraheem Mohammed Ashankyty ◽  
Leena Hussein Bajrai ◽  
PK Praveen Kumar ◽  
Mohammad Amjad Kamal ◽  
...  

Abstract Micro-abstract: Using the publicly available datasets, we have investigated the list of critical pathways and the genes which appear to be clinically highly significant in case of renal cell carcinoma. ARHGAP6, TGM4, CD248, SLC13A3, EPO, PARD6A, CLCA2, UBE2S, ERAL1, FGFR1, MRVI1, DYNC1I2, CDCA7 are among the top ranked genes which appeared highly significant in terms of patient survival.Clinical practice points: Using the publicly available datasets, we have investigated the gene expression profiling for renal cell carcinoma. In the previous work, it has been focused on selected genes and pathways. Here, we have investigated the list of critical pathways and the genes which appear to be clinically highly significant in case of renal cell carcinoma. ARHGAP6, TGM4, CD248, SLC13A3, EPO, PARD6A, CLCA2, UBE2S, ERAL1, FGFR1, MRVI1, DYNC1I2, CDCA7 are among the top ranked genes which appeared highly significant in terms of patient survival. These genes leads to potential alteration in PI3K-Akt, Foxo, endocytosis, MAPK, tight junction, cytokine-cytokine receptor interaction pathways. Our work will help in diagnosing the renal cell carcinoma patients because here, we have presented the differentially expressed genes, their inferred pathways, and the clinical impact of the selective genes. Since, our finding is from overall perspective including clinical relevance so this study will help in future for diagnostic also.Background: Cancer is among the highly complex disease and renal cell carcinoma is the sixth-leading cause of cancer death. In order to understand complex diseases such as cancer, diabetes and kidney diseases, high-throughput data are generated at large scale and it has helped in the research and diagnostic advancement. However, to unravel the meaningful information from such large datasets for comprehensive and minute understanding of cell phenotypes and disease pathophysiology remains a trivial challenge and also the molecular events leading to disease onset and progression are not well understood. Methods: With this goal, we have collected gene expression datasets from publicly available dataset which are for two different stages (I and II) for renal cell carcinoma.Results and conclusion: In this work, we have applied computational approach to unravel the differentially expressed genes, their networks for the enriched pathways. Based on our results, we conclude that among the most dominantly altered pathways for renal cell carcinoma, are PI3K-Akt, Foxo, endocytosis, MAPK, Tight junction, cytokine-cytokine receptor interaction pathways and the major source of alteration for these pathways are MAP3K13, CHAF1A, FDX1, ARHGAP26, ITGBL1, C10orf118, MTO1, LAMP2, STAMBP, DLC1, NSMAF, YY1, TPGS2, SCARB2, PRSS23, SYNJ1, CNPPD1, PPP2R5E. In terms of clinical significance, there are large number of differentially expressed genes which appears to be playing critical roles in survival.


2001 ◽  
Vol 11 (11) ◽  
pp. 1861-1870 ◽  
Author(s):  
Judith M. Boer ◽  
Wolfgang K. Huber ◽  
Holger Sültmann ◽  
Friederike Wilmer ◽  
Anja von Heydebreck ◽  
...  

2012 ◽  
Vol 1 (2S) ◽  
Author(s):  
Kyle A. Furge ◽  
Karl Dykema ◽  
David Petillo ◽  
Michael Westphal ◽  
Zhongfa Zhang ◽  
...  

Using high-throughput gene-expression profiling technology, we can now gaina better understanding of the complex biology that is taking place in cancer cells. This complexity is largely dictated by the abnormal genetic makeup ofthe cancer cells. This abnormal genetic makeup can have profound effectson cellular activities such as cell growth, cell survival and other regulatory processes. Based on the pattern of gene expression, or molecular signatures of the tumours, we can distinguish or subclassify different types of cancers according to their cell of origin, behaviour, and the way they respond to therapeuticagents and radiation. These approaches will lead to better molecularsubclassification of tumours, the basis of personalized medicine. We have, todate, done whole-genome microarray gene-expression profiling on several hundredsof kidney tumours. We adopt a combined bioinformatic approach, based on an integrative analysis of the gene-expression data. These data are used toidentify both cytogenetic abnormalities and molecular pathways that are deregulatedin renal cell carcinoma (RCC). For example, we have identified the deregulationof the VHL-hypoxia pathway in clear-cell RCC, as previously known,and the c-Myc pathway in aggressive papillary RCC. Besides the more commonclear-cell, papillary and chromophobe RCCs, we are currently characterizingthe molecular signatures of rarer forms of renal neoplasia such ascarcinoma of the collecting ducts, mixed epithelial and stromal tumours, chromosomeXp11 translocations associated with papillary RCC, renal medullarycarcinoma, mucinous tubular and spindle-cell carcinoma, and a group of unclassified tumours. Continued development and improvement in the field of molecular profiling will better characterize cancer and provide more accurate diagnosis, prognosis and prediction of drug response.


2006 ◽  
Vol 98 (1) ◽  
pp. 205-216 ◽  
Author(s):  
JON A.J. LOVISOLO ◽  
BARBARA CASATI ◽  
LIBERO CLERICI ◽  
ERMINIO MARAFANTE ◽  
ALDO V. BONO ◽  
...  

BMC Urology ◽  
2004 ◽  
Vol 4 (1) ◽  
Author(s):  
Louis S Liou ◽  
Ting Shi ◽  
Zhong-Hui Duan ◽  
Provash Sadhukhan ◽  
Sandy D Der ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (11) ◽  
pp. e0165718 ◽  
Author(s):  
Mohammed I. Khan ◽  
Anna M. Czarnecka ◽  
Sławomir Lewicki ◽  
Igor Helbrecht ◽  
Klaudia Brodaczewska ◽  
...  

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