ABSTRACT
For several years, epidemiologists believed that age, genetic inheritance, living lifestyle, tobacco consumption and inflammation are the causes of several well-defined cancers; this limits the amount of incorporation of any new factors, other causative agents or bacterial infection that could contribute to cancer. Helicobacter pylori were identified as a causative agent of gastric cancers in landmark studies in the early 1990s, resulting in a seismic shift toward the link between pathogenic bacterial infection and human cancer. A rising number of researchers have found that systemic inflammation, such as the connections between H. pylori and stomach cancer, Streptococcus anginosus and esophageal cancer, is responsible for cancer morbidity and death. Another oral bacterium, Porphyromonas gingivalis, has been linked to the onset and development of oral cancer. Streptococcus bovis is related to lung cancer. A bacterial infection affects the carcinogenesis process either directly or indirectly. Bacteria can cause cancer in three ways: by causing chronic inflammation, activating anti-apoptotic activity and generating carcinogenic chemicals. A series of genetic changes transfigure a normal cell into a tumor cell which incorporates numerous reasons for causing cancer. In cancer patients, bacterial infections are a major cause of morbidity and mortality. Different people react differently to different malignancies, which can complicate the interaction between cancer and bacteria. Bacteria's importance in terms of diversity in their interactions with humans, as well as their components that influence carcinogenesis, has made them a significant element in defining the human state in health and illness. The discovery of bacterial involvement and influence in cancer formation may give a new path and therapeutic strategy to cancer prevention. In this chapter, we'll look at how bacterial DNA integration damages host DNA, alters gene expression profiles and leads to a wide range of cancers in humans.
