Cancer results from abnormal cellular growth. It is considered to be benign when localised in situ while it is defined to be malign and metastatic when it is invasive and spreads inside the body through blood or lymphatic vessels. Cancer progression can be interpreted as an evolutionary process, as we discuss in Section 2.1. In spite of the increasing knowledge gained on the molecular mechanisms involved in the deregulation of cancer cells, such as the identification of many oncogenes and oncosuppressors (discussed in Section 2.2), many open questions still exist about the origin of cancer cells. In Section 2.3, we introduce a key oncosuppressor gene which is of fundamental importance for cancer development: P53, also known as the “guardian of the genome.” While important oncogenes and oncosuppressors clearly exist, cancer involves a multitude of different genes requiring an integrative data-based approach (Section 2.4).

Another important issue that is still under investigation is the presence of a subpopulation of more aggressive cancer cells, usually described as cancer stem cells (Section 2.5) (CSCs). The molecular aspects related to the capability of cancer cells to receive nutrients from the environment through existing vessels, and the ability of the same cancer cells to induce vessel formation (angiogenesis), are two critical aspects of the biology of cancer that we illustrate in Section 2.6. Furthermore, in Section 2.7, we illustrate the spread of cancer cells inside the body in the metastatic process. All together these aspects will be discussed here, combining biological and physical viewpoints. In this perspective, the cancer ecosystem is the combination of physical forces and biochemical ingredients. Finally, the new diagnostic tools for the identification of a cancer cell are also discussed and critically reviewed (Section 2.8).

Cancer Origin and Evolution

It is now commonly accepted that cancer is the consequence of random mutations in cells. This general idea dates back to the pioneering observations of chromosomal abnormalities in cancer made by Boveri at the beginning of the twentieth century (Boveri, 1903). The concept gained further traction with the discovery, made by Muller in the twenties, that ionizing radiation is mutagenic (Muller, 1930). In the forties, Berenblum and Shubik discovered that chemical carcinogenesis was described by two stages: initiation by carcinogens and promotion by other chemicals (Berenblum and Shubik, 1949).