Molecular and Genetic Frontiers of Cancer Treatment

文:林辉扬医生

As Science discover more about genetics, newer technology allow oncologist to see the finer details of the micro-molecular and genetic structure of cancer cells, sprouting newer treatments that attack the rouge cells at it’s very core.

One of the hallmarks of cancer is the way the cells behave. Normally, cells grow and divide, forming new ones only to maintain the state of health. Old cells die and new cells take their place. However, sometimes a single cell may mutate in a way that results in uncontrolled and unorganised growth of one mass of cells with the destruction of other healthy functional cells. These disordered masses of cells are named cancer cells. They occur as a result of factors such as exposure to environmental toxins, dietary cancer-causing chemicals, excessive radiation or genetic predisposition.

Firstly, the network of chemical and molecular signals that maintain the cells in a constant state of healthy balance must be kept in fine balance. Once this is disrupted, the cells no longer divide normally or die when they should, resulting in cancer.

Cancer can also happen because of disruption in two types of genes. Proto-oncogenes are normal genes involved in cell growth and division. Abnormal changes in these lead to the creation of super cancer genes called oncogenes. These promote excessive and continuous cell growth and division. Tumour suppressor genes are normal genes that slow down cell growth and division. When a tumour suppressorgene malfunctions, autogrowth kicks in and cells may be unable to stop growing and dividing. Cells replicate themselves endlessly leading to the formation of a useless mass of tissue, known as a tumour.

The original cancerous cells can also induce other cells to behave abnormally by producing abnormal proteins. These proteins may be normal proteins produced in excessive amounts or abnormal proteins that stimulate cells into deregulated growth or function. Cancer occurs when abnormal proteins inside cells cause it to go into uninhibited growth, reproducing excessively and allowing those cells to live much longer than normal cells.

Because the cells in cancerous tumours are abnormal, they can also invade nearby organs and tissue and spread to other parts of the body.

Since this is all happening at a molecular and cellular level, the aim of today’s treatment regimens is to target, as accurately as possible, the specific molecules involved in the evolution of cancer.

Molecular treatment has changed the landscape of treatment. This is because in the quest to destroy cancer cells, the toxicities of cancer treatment can now be minimised while achieving greater benefits.

There are several major benefits to having more specific and molecule-targeted treatment. Namely, better prognosis, quality of life, tolerance to treatment, less side effects and longer survival.

Some of these treatments target specific cells which are abnormal, and attack them in different ways. They can, for instance, damage these cells directly, deliver anti-growth signals to them or halt the supply of nutrients to them by altering their blood supply lines. Such targeted cancer therapies basically disrupt cancer cell growth and division at various points during the development, growth, and spread of cancer. Many of these therapies involve proteins which are part of the signalling process. By blocking the signals that tell cancer cells to grow and divide uncontrollably, targeted therapies can stop the growth and division of cancer cells.

Other molecular treatments cause specific cancer cell apoptosis, which means cell death, by stimulating the signalling system that initiates natural cell ageing. Targeted cancer therapies at the molecular level allow doctors to increasingly tailor-make cancer treatments to individual patients. With more personalised strategies, fewer side effects, better quality of life and higher treatment effects can be attained. It is fortunate that these treatments are already being used widely, and will be used even more widely over time.