Ayok: What I have learned so far

The article I found most intresting to read was Lee and Bernstein's "P53 mutations increaces resistance to ionizing radiation."

The P53 gene is thought to play an important role in neoplastic development. It is thought to function as a cell cycle marker after irradiation, suggesting that mutant forms of p53 gene significantly increaces cellular resistance to a variety of hemtapoietic cell lineages(p53-2,p53-3,pL53-2). Researchers believe that p53 acts in a dominant negative manner to suppress the activity of the wild type p53 protein. Wild type p53 has been postulated to play a role in DNA repair. In this particular article, transgenic mice expressing mutant alleles of p53 were used to measure the resistance of hematopoietic cells to radition. to assess the effects of the mutant allele, the ability of radiatioon to prevent colony formation of cancer cells in a variety of tissues were observed(spleen, liver, lung, thymus). Results showed that mice that were hemizygous or either transgene showed no abnormatlities but infactt ad high incidence of lymphiod tumors. This research depicted how radiation can effect the activiny of mutant forms of p53 which interm effects how succesful radiation is in treating cancer. After addition research, I unearthed some intersting facts about the P53 gene.

Intresting facts

1. If a person inherits only one functional copy of the p53 gene from their parents, they are predisposed to cancer and usually develop several independent tumors in a variety of tissues in early adulthood, a condition known as Li-Fraumeni syndrome.

2. How cancer starts?
When there is DNA damage, the p53 gene suspends the cell cycle until the damage can be repaired. If there is a mutation in p53, the cell cycle continues unrestrained and reproduces the damaged DNA, leading to uncontrolled cell proliferation and cancer tumors. Cancer develops as a result of the cell with damaged DNA dividing, the damaged DNA being replicated and passed to each newly produced daughter cell.

3. p53 becomes activated in response to a variety of factors which include but is not limited to DNA damage (induced by either UV, IR or chemical agents,such as hydrogen peroxide). Other inducive factors are ribonucleotide depletion and deregulated oncogene expression. This activation is marked by two major events. Firstly, the half-life of the p53 protein is increased drastically, leading to a quick accumulation of p53 in stressed cells. Secondly, a conformational change forces p53 to take on an active role as a transcription regulator.