Cancer is a group of diseases characterized by unregulated cell growth and the invasion and spread of cells from the site of origin, or primary site, to other sites in the body. In normal cell growth, there is a finely controlled balance between growth promoting and growth restraining signals such that proliferation occurs only when required. The balance is tilted when increased cell numbers are required, for example during normal tissue turnover or during wound healing.

Differentiation of cells during normal process occurs in an ordered manner and proliferation ceases when no longer required. In tumor cells this process is disrupted, continued cell proliferation occurs and loss of differentiation may be found, and normal process of programmed cell death may no longer operate.

Tumor cells show a number of features which differentiate them from normal cells :

1. They are capable of secreting their own growth factors to stimulate their own proliferation, a process termed autocrine stimulation
2. Normal cells require contact with the surface in the extracellular environment to be able to grow whereas tumor cells are anchorage independent


3. Normal cells respond to the presence of other cells, and in culture will form a monolayer due to contact inhibition whereas tumor cells lack this and often grow over or under each other
4. Tumor cells are less adhesive than normal cells
5. Normal cells stop proliferating once they reach a certain density but tumor cells continue to proliferate

Most agents that cause cancer (carcinogens) are agents that cause alterations to the DNA sequence or mutations (mutagens). Thus, similarly to all genetic disease, cancer results from alterations in DNA. A large amount of evidence indicates that cancers arise from a single cell which has undergone mutation. Mutation in genes allows them to escape normal control on proliferation. The accumulation of mutations in cells over time represents a multi step process that underlies carcinogenesis. The requirement for an accumulation of mutations explains why there is an increased risk of cancer with age and why cancer has become more prevalent over the centuries as human lifespan has increased.

References:

1. Macdonald F, Ford C.H.J. Molecular biology of cancer. BIOS Scientific Publishers. 1997.
2. Pecorino L. Molecular biology of cancer : Mechanism, targets and therapeutics. Oxford University Press. 2005.