A few types of cancer in non-humans have been found to be caused by the tumor cells themselves. This phenomenon is seen in Sticker’s sarcoma, also known as canine transmissible venereal tumor.[7] The closest known analogue to this in humans is individuals who have developed cancer from tumors hiding inside organ transplants.

 Molecular biology

Cancers are caused by a series of mutations. Each mutation alters the behavior of the cell somewhat.

 Carcinogenesis, which means the initiation or generation of cancer, is the process of derangement of the rate of cell division due to perturbations in normal cellular regulatory processes. Molecular biology, the study of genetics using modern techniques such as gene cloning, seeks to explain the etiology of cancer in terms of the genetic changes that underlie cancer.

 It is impossible to tell the initial cause for any specific cancer. However, with the help of molecular biological techniques, it is possible to characterize the mutations or chromosomal aberrations within a tumor, and rapid progress is being made in the field of predicting prognosis based on the spectrum of mutations in some cases. For example, some tumors have a defective p53 gene. Changes in the sequence of this gene, known as mutations, are associated with a poor prognosis in many different cancer patients, since those tumor cells are less likely to go into apoptosis or programmed cell death when damaged by therapy. Telomerase mutations remove additional barriers, extending the number of times a cell can divide. Other mutations enable the tumor to grow new blood vessels to provide more nutrients, or to metastasize, spreading to other parts of the body.

 In order for cells to fail to regulate normal growth and division, [[genes] which regulate cell growth must be damaged. The two key concepts of the molecular biology approach to cancer pathogenesis are encompassed by the oncogene and thetumor suppressor gene. Oncogenes are genes which are normally inactive, but when activated can promote cell growth and mitosis, a process of cell division. Tumor suppressor genes, on the other hand, are usually active in the normal cell, and usually discourage cell growth, or temporarily halt cell division in order to carry out DNA repair after DNA damage. Damage to tumor suppressor genes is often observed in the development of malignancies. Typically, a series of several mutations to these genes are required before a normal cell transforms into a cancer cell.

 Oncogenes

 Oncogenes promote cell growth through a variety of ways. Many can produce hormones, a “chemical messenger” between cells which encourage mitosis, the effect of which depends on the signal transduction of the receiving tissue or cells. In other words, when a hormone receptor on a recipient cell is stimulated, the signal is conducted from the surface of the cell to the cell nucleus to effect some change in gene transcription regulation at the nuclear level. Some oncogenes are part of the signal transduction system itself, or the signal receptors in cells and tissues themselves, thus controlling the sensitivity to such hormones. Oncogenes often produce mitogens, or are involved in transcription of DNA in protein synthesis, which creates the proteins and enzymes responsible for producing the products and biochemicals cells use and interact with.

 Mutations in proto-oncogenes, which are the normally quiescent counterparts of oncogenes, can modify their expression and function, increasing the amount or activity of the product protein. When this happens, the proto-oncogenes become oncogenes, and this transition upsets the normal balance of cell cycle regulation in the cell, making uncontrolled growth possible. The chance of cancer cannot be reduced by removing proto-oncogenes from the genome, even if this were possible, as they are critical for growth, repair and homeostasis of the organism. It is only when they become mutated that the signals for growth become excessive.

 Ras oncogene

 One of the first oncogenes to be defined in cancer research is the ras oncogene. Mutations in the Ras family of proto-oncogenes (comprising H-Ras, N-Ras and K-Ras) are very common, being found in 20% to 30% of all human tumours.[8] Ras was originally identified in the Harvey sarcoma virus genome, and researchers were surprised that not only was this gene present in the human genome but that, when ligated to a stimulating control element, could induce cancers in cell line cultures.[9]