Part of the book: Topics on Cervical Cancer With an Advocacy for Prevention
Part of the book: Chlamydia
High‐risk human papillomavirus (HPV) genotypes infection associates with cervical dysplasia and carcinogenesis. hr‐HPV transforming potential is based on E6 and E7 viral oncoproteins actions on cellular proteins. A persistent infection with hr‐HPV leads to progression from precursor lesions to invasive cervical cancer inducing changes in host genome and epigenome. Pathogenesis and development of cancer associated with both genetic and epigenetic defects alter transcriptional program. An important role for malignant transformation in HPV‐induced cervical cancer is played by epigenetic changes that occur in both viral and host genome. Furthermore, there are observations demonstrating that oncogenic viruses, once they integrated into host genome, become susceptible to epigenetic alterations made by host machinery. Epigenetic regulation of viral gene expression is an important factor in HPV‐associated disease. Gene expression control is complex and involves epigenetic changes: DNA methylation, histone modification, and non‐coding RNAs activity. Persistent infection with hr‐HPV can cause viral DNA integration into host genome attracting defense mechanisms such as methylation machinery. In this chapter, we aim to review HPV infection role in chromatin modification/remodeling and the impact of HPV infection on non‐coding RNAs in cervix oncogenesis. The reversible nature of epigenetic alterations provides new opportunities in the development of therapeutic agents targeting epigenetic modification in oncogenesis.
Part of the book: Human Papillomavirus
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
Despite being a “silent epidemic” disease, chronic kidney disease (CKD) is considered one of the major causes of mortality, together with its main complication, the cardiovascular disease, which contributes to the poor prognosis of these patients. Inflammation has been recognized as an essential part of CKD and is closely linked to cardiovascular complications. The identification of novel biomarkers using omics technologies is rapidly advancing and could improve the early detection in renal diseases. Omics approaches, including proteomics, could provide novel insights into disease mechanisms, identifying at the same time accurate inflammatory biomarker panels with an essential role in disease monitoring and follow-up. Recent advances highlight the gut microbiota as an important source of inflammation in kidney diseases. An increasing body of evidence reveals the cross talk between microbiota and host in CKD; in addition, gut dysbiosis may represent an underappreciated cause of inflammation and subsequently could lead to malnutrition, accelerated cardiovascular disease and CKD progression. This chapter discusses the relationship between inflammation and CKD and highlights the novel approaches regarding microbiota involvement in CKD pathology, as well as their potential to facilitate improving the quality of life.
Part of the book: Chronic Kidney Disease