Cancer is associated with pain suffering and early death. In the eyes of most people a diagnosis of cancer is equal to a death sentence. Scientists and doctors have been trying to diagnose cancer early with a view to treating it early and they have been remarkably successful at it.
Presently, life expectancy of patents diagnosed early (stage 1) is as good as the healthy individual because many of the interventions are effective. Recent advances in genetics have greatly assisted in the understanding of cancers and treatments.
In this article I am writing about chromosome 17, particularly gene p53. In 1979 researchers found the location of gene 53 to be on chromosome 17. They further deduced that this gene (p53) regulated the cell cycle. In the undamaged cell gene p53 had a role in maintaining cell cycle, maintaining healthy metabolic processes and cell regeneration. In other words it kept the cell healthy and young.
Scientists noted that when the cell became damaged gene p53 suspended its activities and this resulted in "unregulated growth”. The unregulated growth resulted in formation of tumors because the cell with damaged DNA divided, the damaged DNA was replicated and each daughter cell"s cycle was also unrestrained. This is how a cancer cell initiates, basically.
Li-Fraumeni Syndrome
Further evidence of the important role of p53 gene (chromosome 17) comes from mutation studies. The p53 gene is a tumour suppressor gene. When it is active it stops the formation of tumors. So if a person inherits only one functional copy of the p53 gene from his/her parents this person with haploid number of genes is predisposed to cancers.
This type of person will usually develop several independent tumors in a variety of tissues in early adulthood and often die at a very early age. Patients who have only the haploid of gene p53 are said to suffer from Li-Fraumeni syndrome. Health individuals usually have diploid genes, one set from the male parent and one set from the female parent.
Uncontrolled Protein synthesis
In the normal cell p53 protein binds DNA. This bound DNA stimulates another gene to produce a protein called p21 which interacts with a cell division-stimulating protein (cdk2). When p21 is bound to cdk2 the cell cannot pass through to the next stage of cell division. Studies show that mutant p53 gene cannot bind DNA in an effective manner. Consequently the p21 protein cannot act as the "stop signal" for cell division. Thus cells divide uncontrollably, and form tumors.
Help with unravelling the molecular mechanisms of cancerous growth has come from the use of mice as models for human cancer. Powerful and new genetic knockout techniques have been used to study the functions of many genes. A large amount of information now exists on many aspects of the p53 gene's normal function and mutant expression in human cancers. This knowledge is now clarifying the important role in the patho physiology of human cancers. It is now clear that p53 is just one component of a network of events that culminate in tumor formation.
Scientists have now taken this research one step further. They produced mice with more p53 genes in the hope of finding a cure for cancer. They found that these mice with more p53 gent stayed younger longer and did not develop any cancer. So they concluded that this gene must have a role in “maintaining youth and preventing cancer”. More studies will need to be done to conclusively show this to be the case in mankind.
In my article published about six months ago I had stated that human death is not sudden. It is a gradual process which begins around puberty and slowly our body cells die. An individual dies when a critical mass of cells is unable to sustain body processes. (You may read my previous artical).
In summary it is fair to state that if an individual wishes to have a long life then he/she must look after cellular health in the hope of keeping more cells alive longer. We kill many of our body cells during high risk activities, alcohol consumption, drug use/abuse, and exposure to extreme weather. Consumption of fatty foods and resultant obesity are also seen as high risk activities in this context.
This research is good. For application in is not good because I
do not know the everyday application of this chromosome and how to increase or reduce its activity.
Can you try and make things a little simpler so that an ordinary person can undersand and apply the scientific findings.