Abstract
In this review we summarize the results of studies employing high-throughput methods of profiling of HPV-associated cervical intraepithelial neoplasia (CIN) and squamous cell cervical cancers at key intracellular regulatory levels to demonstrate the unique identity of the landscape of molecular changes underlying this oncopathology, and to show how these changes are related to the 'natural history' of cervical cancer progression and the formation of clinically significant properties of tumors. A step-wise character of cervical cancer progression is a morphologically well-described fact and, as evidenced by genome-wide screenings, it is indeed the consistent change of the molecular profiles of HPV-infected epithelial cells through which they progressively acquire the phenotypic hallmarks of cancerous cells. In this sense, CIN/cervical cancer is a unique model for studying the driving forces and mechanisms of carcinogenesis. Recent research has allowed definition of the whole-genome spectrum of both random and regular molecular alterations, as well as changes either common to processes of carcinogenesis or specific for cervical cancer. Despite the existence of questions that are still to be investigated, these findings are of great value for the future development of approaches for the diagnostics and treatment of cervical neoplasms.
Highlights
Owing to contemporary high-throughput techniques for biomedical data sampling and analysis, any state of the cell-from physiological ‘norm’ to pathology-can be described as a set of molecular profiles that constitute its overall molecular-genetic ‘portrait’
Cervical cancer (CeCa) is an example of oncopathology, for which the whole continuum of carcinogenesis, from the earliest stages-cervical intraepithelial neoplasia (CIN) of grades 1, 2, 3, as well as microinvasive cancer, have been described in sufficient detail relying on morphological criteria
In this review we summarize the results of studies employing methods of profiling of human papillomavirus (HPV)-associated CIN and squamous cell CeCa at the genome, epigenome, transcriptome, and proteome levels to demonstrate the unique identity of changes in the molecular-genetic ‘portrait’ of this oncopathology, and to show how these changes are related to the ‘natural history’ of CeCa progression and the formation of clinically significant properties of the tumor
Summary
Owing to contemporary high-throughput techniques for biomedical data sampling and analysis, any state of the cell-from physiological ‘norm’ to pathology-can be described as a set of molecular profiles (genome, transcriptome, epigenome, proteome, metabolome) that constitute its overall molecular-genetic ‘portrait’. In this review we summarize the results of studies employing methods of profiling of HPV-associated CIN and squamous cell CeCa at the genome, epigenome, transcriptome, and proteome levels to demonstrate the unique identity of changes in the molecular-genetic ‘portrait’ of this oncopathology, and to show how these changes are related to the ‘natural history’ of CeCa progression and the formation of clinically significant properties of the tumor.
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