On the Earl of Essex

Tumour‐Induced Angiogenesis: A Review

“…The mutated cells have a proliferative advantage over neighbouring, healthy cells and are able to form a growing mass. The reason for this advantage is not necessarily an increase in the proliferation rate, but may, in some cases, be a decrease in the cell death rate (King, 1996). For example, one of the key functions of tumour7 suppressor genes such as p53 is to induce apoptosis (programmed cell death) in damaged cells (Santini et al, 2000).…”

“…For example, one of the key functions of tumour7 suppressor genes such as p53 is to induce apoptosis (programmed cell death) in damaged cells (Santini et al, 2000). Loss of p53, the most commonly mutated gene in human tumour cells (Santini et al, 2000), thus allows propagation of damaged DNA (King, 1996).…”

“…Figure 1 shows schematically the difference between a benign and a malignant tumour; only a malignant tumour constitutes a cancer. In this case, surgery is not guaranteed to be successful because the tumour does not possess a well defined boundary and the presence of a single mutated cell could be enough to regenerate the tumour colony (King, 1996). Departure of mutated cells from the primary site represents the transition from in situ to invasive growth and is a key event in cancer progression.…”

“…Indeed, it is often said that cancer is not, in reality, one disease, but a class of different diseases with the common features of excessive cell proliferation and tissue invasion (King, 1996). It is the combination of these features that makes cancer so dangerous: a single mutated cell which does not have a proliferative disorder is harmless; likewise, a population of abnormally proliferating cells that does not invade surrounding tissue is easily treatable (Alberts et al, 1994).…”

“…The existence of the quiescent layer presents a problem for treatments, such as chemotherapy, that are based on the intravenous administration of an agent that is toxic to proliferating cells (King, 1996). The proliferating rim may be eradicated, but the cells underneath will not be affected and will emerge from quiescence to become proliferating cells (Sutherland, 1988).…”