Three categories of genes are known to play an important role in the genesis of cancer. These are oncogenes, tumour suppressor genes and mutator genes.
Oncogenes are produced by mutations in the pre-existing normal genes, known as proto-oncogenes. Oncogenes remain harmless in a cell until they are activated by mutations. The activated oncogenes produce abnormal proteins including growth factors and cellular growth factor receptors, which induce unregulated rapid multiplication of the cell leading to genesis of cancer. So far, more than thirty oncogenes have been identified, which include: ras family of oncogenes (found in about 50 per cent cases of the human cancer); c-myc oncogene (associated with Burkitt’s lymphoma); N-myc oncogene (associated with neuroblastoma); and HER-2/neu oncogene (associated with the breast and the ovarian cancers). Oncogenes possess tumour specificity, i.e. activation of a particular oncogene causes a specific cancer. Researchers believe that at least three oncogenes must get activated (mutated) in a cell before it becomes malignant.
Tumour suppressor genes, on the other hand, inhibit the genesis of cancer by producing regulatory proteins, which suppress cellular proliferation. If mutation occurs in a tumour suppressor gene, it may lose its tumour suppressing action, leading to unregulated proliferation of the cell. The most important tumour suppressor gene, known so far, is the p53 gene that suppresses uncontrolled proliferation of the cell as well as triggers apoptosis (programmed cell death). The p53 gene is found to be mutated in about 50 per cent cases of the human cancer. Other tumour suppressor genes include: Rb gene (associated with retinoblastoma and osteosarcoma); Ret gene (associated with the endocrine cancer); WT-1 gene (associated with Wilm’s tumour); NF-1 gene (associated with neurofibromatosis type-1); NF-2 gene (associated with neurofibromatosis type-2); APC and DCC genes (associated with the colon cancer). It has been observed that the tumour suppressor genes show better tumour specificity as compared to the oncogenes.
Mutator genes are another category of genes whose job is to repair the damaged DNA. If mutation occurs in a mutator gene, it may lead to accumulation of the damaged DNA that eventually affects oncogenes and tumour suppressor genes, thus leading to genesis of cancer. Hereditary nonpolyposis colon cancer (HNPCC) is caused by mutations in one of the five mutator genes, known so far.
Benign & Malignant Tumours
When a living cell in the body loses control over the cell division, it starts multiplying at a much faster rate, losing all restraints and controls, often forming a mass known as tumour (neoplasm), which may be benign or malignant in character. A benign tumour is usually encapsulated and grows in size at one site. It remains within the tissue of its origin and does not spread to other parts of the body. A benign tumour can be completely removed by surgery.
On the other hand, a malignant tumour invades adjacent tissues and spreads (metastasis) to distant parts of the body through various routes including blood vessels and lymphatic channels. Some benign tumours have the tendency to become malignant. The following changes may be observed when a benign tumour becomes malignant.
Rapid growth of the tumour .
Increased vascularity of the tumour.
Fixation of the tumour.
Metastasis of the tumour.
Although tumours are basically divided into benign and malignant tumours, but the concept of this classification appears to be too rigid. It has been observed that there exists a third group of tumours that invade locally but do not metastasise. These are called intermediate tumours, which include adenoma of the bronchus, mixed salivary tumour, carcinoid tumour and the basal cell carcinoma.
Attributes Of Cancer
Cancer has different forms in different tissues but there are some common biological properties of the cancerous cells, which include unrestrained cell division, lack of cell maturation, loss of normal cellular functions and invasive behaviour of the cells. The four major attributes that differentiate a cancerous cell from a normal cell are clonality, autonomy, anaplasia and metastasis.
Clonality: A cancerous cell multiplies to form a clone of cancerous cells.
Autonomy: Cancerous cells are not regulated by the normal biochemical and physical forces of the body.
Anaplasia: Cancerous cells do not possess cellular differentiation and functions.
Metastasis: Cancerous cells can grow in other tissues and organs of the body.
Dr. S.P. Kaushal
Sino Vedic Cancer Clinic