1. Cell growth not regulated by external signals. This is autonomous cell growth.

2. The capacity to invade tissues, and metastasis to distant sites.

Cancer is genetic disease. The level of its expression is always a single cell. Besides those heritable cancers, most cancers are caused by mutations that occur in somatic cells. They are caused by intrinsic errors in DNA replication or are induced by carcinogen exposure. The malignant phenotype is acquired only after 5 to 10 mutations.

Cancer is most common in tissues with rapid turnover, especially those exposed to environmental carcinogens, and whose proliferation is regulated by hormones. Thus, environmental factors exert potent effects on gene expression of target cells. The set of signals received by a particular cell leads to the activation of particular sets of transcription factors. The pattern of gene expression determine whether a cell will divide, differentiate or die.

For a cancer to arise, mutations must affect a variety of pathways. Apoptosis is averted by mutations in p53 pathway. The expression of telomerase is a common feature in cancers. Over expression of growth factors and receptors is frequently detected.

Many potential therapeutic agents are in clinical development based on our concepts of tumour cell biology. They include the development of growth factor and growth facte receptor antagonists, inhibitors of phosphoryl transfer to block key kinases, selective inhibitors of PKC, P13K, phopholipase C, farnesyl transferase inhibitors that block the insertion of Ras into the membrane, mutant versions of protein s such as Ras and p53 that may make the cell vulnerable to immunologic attack if employed as a vaccine and inhibitors of angiogenesis or the steps in metastasis that may limit tumour growth and prevent its spread.

Based on these principles it seem that suitable combination of inhibitors will be required to improve antitumour effects.