The “classic” view of molecular oncology indicates that cancer is a genetic disease involving tumor suppressor and oncogenic proteins. However, in the recent years, it has been demonstrated that small regulatory non-coding RNAs (ncRNAs) named microRNAs (miRNAs) are involved in human tumorigenesis, thus revealing a new layer in the molecular architecture of human cancer. Gene expression studies revealed that hundreds of miRNAs are deregulated in cancer cells and functional studies clarified that miRNAs are involved in all the molecular and biological processes that drive tumorigenesis. Here, we summarize the recent advances in miRNA involvement in human cancer and illustrate the benefits of using these knowledge for medical practice. New diagnostic classifiers based on miRNAs will soon be available for medical practitioners and, even more importantly, miRNAs may become novel anti-cancer tools.

microRNAs and cancer – new paradigms in molecular oncology

NEGRINI, Massimo;
2009

Abstract

The “classic” view of molecular oncology indicates that cancer is a genetic disease involving tumor suppressor and oncogenic proteins. However, in the recent years, it has been demonstrated that small regulatory non-coding RNAs (ncRNAs) named microRNAs (miRNAs) are involved in human tumorigenesis, thus revealing a new layer in the molecular architecture of human cancer. Gene expression studies revealed that hundreds of miRNAs are deregulated in cancer cells and functional studies clarified that miRNAs are involved in all the molecular and biological processes that drive tumorigenesis. Here, we summarize the recent advances in miRNA involvement in human cancer and illustrate the benefits of using these knowledge for medical practice. New diagnostic classifiers based on miRNAs will soon be available for medical practitioners and, even more importantly, miRNAs may become novel anti-cancer tools.
2009
Negrini, Massimo; Nicoloso, M.; Calin, G. A.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/534398
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