Coralia Bleotu

By Coralia Bleotu and Gabriela Anton

Part of the book: Topics on Cervical Cancer With an Advocacy for Prevention

By Chifiriuc Mariana Carmen, Socolov Demetra, Moshin Veaceslav, Lazar Veronica, Mihaescu Grigore and Bleotu Coralia

Part of the book: Chlamydia

By Demetra Socolov, Coralia Bleotu, Nora Miron, Razvan Socolov, Lucian Boiculese, Mihai Mares, Sorici Natalia, Moshin Veaceslav, Anca Botezatu and Gabriela Anton

Part of the book: Chlamydia

By Gabriela Anton, Adriana Plesa, Coralia Bleotu, Anca Botezatu, Mariana Anton, Lorelei Irina Brasoveanu and Mihai Stoian

Part of the book: Oncogene and Cancer

By Coralia Bleotu, Demetra Socolov, Mariana Anton, Anca Botezatu, Adriana Plesa, Iulia Virginia Iancu, Lorelei Irina Brasoveanu, Gabriela Anton and Carmen Cristina Diaconu

Recent data on the cell deregulation that occurs during the progression to cancer underlines the cooperation between genetic and epigenetic alterations leading to a malignant phenotype. Unlike genetic alterations, the epigenetic changes do not affect the DNA sequence of the genes, but determine the regulation of gene expression acting upon the genome. Moreover, unlike genetic changes, epigenetic ones are reversible, making them therapeutic targets in various conditions in general and in cancer disease in particular. The term epigenetics includes a series of covalent modifications that regulate the methylation pattern of DNA and posttranslational modifications of histones. Gene expression can also be regulated at the posttranscriptional level by microRNAs (miRNAs), a family of small noncoding RNAs that inhibit the translation of mRNA to protein. miRNAs can act as ‘oncomiRs’, as tumor suppressors, or both. In this chapter, we will (1) summarize the current literature on the key processes responsible for epigenetic regulation: DNA methylation, histone modifications and posttranscriptional gene regulation by miRNAs; (2) evaluate aberrant epigenetic modifications as essential players in cancer progression; (3) establish the roles of microenvironment-mediated epigenetic perturbations in the development of gynecological neoplasia; (4) evaluate epigenetic factors involved in drug resistance.

Part of the book: Gynecologic Cancers

By Marinela Bostan, Mirela Mihaila, Camelia Hotnog, Coralia Bleotu, Gabriela Anton, Viviana Roman and Lorelei Irina Brasoveanu

A big challenge for a successful colon cancer treatment is the lack of eradication of the entire tumour cell population and consequent development of chemoresistance. Control of cell number from tissues and elimination of cells predisposed to malignant transformation, having an aberrant cell cycle or presenting DNA mutations, might be performed by a cellular ‘suicide’ mechanism — the programmed cell death, or apoptosis. Coordinated activation and execution of multiple subprograms are needed, added by a good knowledge of the basic components of the death machinery, besides their interaction to regulate apoptosis in a coordinated manner. Triggering apoptosis in target cells is a key mechanism by which chemotherapy promotes cell killing. Many anti‐cancer drugs act during physiological pathways of apoptosis, leading to tumour cell destruction. New therapeutic approaches in cancer induce tumour cells to undergo apoptosis and break the cancer cell resistance to apoptosis commands. Administrations of natural compounds that prevent induction, inhibit or delay the progression of cancer, or induce inhibition or reversal of carcinogenesis at a premalignant stage represent chemoprevention strategies. Several natural compounds have been shown to be promising based on their anti‐cancer effects and low toxicity; alternative approaches might be taken into account to obtain a stronger anti‐tumour response when lower concentrations of anti‐cancer drugs are used, and to diminish the undesirable side‐effects.

Part of the book: Colorectal Cancer