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Abstract
Renal cell tumors (RCT) collectively constitute the third most common type of genitourinary neoplasms, only surpassed by prostate and bladder cancer. They comprise a heterogeneous group of neoplasms with distinctive clinical, morphological, and genetic features. Epigenetic alterations are a hallmark of cancer cells and their role in renal tumorigenesis is starting to emerge. Aberrant DNA methylation, altered chromatin remodeling/histone onco-modifications and deregulated microRNA expression not only contribute to the emergence and progression of RCTs, but owing to their ubiquity, they also constitute a promising class of biomarkers tailored for disease detection, diagnosis, assessment of prognosis, and prediction of response to therapy. Moreover, due to their dynamic and reversible properties, those alterations represent a target for epigenetic-directed therapies. In this review, the current knowledge about epigenetic mechanisms and their altered status in RCT is summarized and their envisaged use in a clinical setting is also provided.
Highlights
Renal cell tumors (RCT) are the most common neoplasms of the kidney in adults, representing 2–3% of all non-cutaneous malignant neoplasms, ranking 14th in incidence for both genders, with a mortality rate of 1.6/100,000, worldwide (Ferlay et al, 2010)
hypoxia-inducible factors (HIF) upregulation is a feature of ccRCC, the regulation of histone methylation status, and of genetic expression, by Jumonji C (JmjC) histone demethylases might be another mechanism leading to epigenetic changes in RCC carcinogenesis
Both Jumonji domain containing 1A (JMJD1A) and Jumonji domain containing 2B (JMJD2B) were found to be elevated in a RCC cell line with VHL loss of function (Beyer et al, 2008), and the expression of JMJD1A was reported to be higher in RCC cancer tissue than in adjacent normal renal tissue, mainly in cancer cells surrounding blood vessels, suggesting that JMJD1A is involved in tumor angiogenesis (Guo et al, 2011)
Summary
Renal cell tumors (RCT) are the most common neoplasms of the kidney in adults, representing 2–3% of all non-cutaneous malignant neoplasms, ranking 14th in incidence for both genders, with a mortality rate of 1.6/100,000, worldwide (Ferlay et al, 2010). The development of such tools might have a relevant clinical impact, mainly if they would be based on non-invasive approaches (Scelo and Brennan, 2007) In this regard, cancerrelated genetic and/or epigenetic alterations might be used as biomarkers enabling the detection of cancerous cells in clinical samples, increasing the ability to identify tumors at their earliest stages (Esteller, 2008). Aberrant DNA methylation is probably the best characterized cancer-related epigenetic alteration and it is considered by some as one of the earliest events in the process of tumorigenesis (Feinberg et al, 2006) Those aberrations include both global and gene-specific hypomethylation as well as gene-specific CpG island promoter hypermethylation (Mulero-Navarro and Esteller, 2008; Sharma et al, 2010). Functional epigenomic approaches emerged as efficient strategies to identify genes whose expression was silenced by promoter methylation in RCC, through the identification of genes re-expressed after treatment with demethylating drugs in RCC cell lines and further validated in primary tumor samples
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