ABSTRACT
Cancer can be broadly described as the result of genetic and other changes that lead to alterations in normal cellular function. še e›ect of these alterations is unlimited growth and expansion that occurs both locally and at distant sites within the body. It is estimated that in 2010, 1,529,560 new cases of cancer will be diagnosed in the United States, with 562,340 deaths [1]. Any individual can develop cancer, but the risk increases with age. še majority of all cancers occur sporadically, and only 5% are hereditary, although enhanced risk for some cancers may be familial. A variety of causes can contribute to malignant transformation and the development of a tumor. šese can include genetic changes that either actively contribute to the development of cancer when altered (oncogenes) or lead to cancer when their protective e›ect is removed (tumor suppressor genes). In addition, nongenetic causes can also accelerate tumor progression, including exposure to carcinogens and other mutagenic agents, as well as chronic in§ammation and some infectious agents, including hepatitis B virus, human papilloma virus, and human immunodeœciency virus (HIV). še development of cancer is also in§uenced by the normal cells surrounding the tumor cells, as the tumor cells interact with such “stromal” cells to create conditions that are favorable for their continued growth and survival. Once tumors reach a critical size, this interaction with the “tumor microenvironment” enables the tumors to coopt the process of normal blood vessel development resulting in the formation of new blood vessels to further feed the tumor in a process known as angiogenesis.
