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Solving the Cancer Mystery That Devastated My Family

Known commonly as p53, it is a tumor suppressor gene with the power to block potentially cancerous cells from becoming malignant. But when mutated, p53 loses its cancer-fighting ability, dramatically increasing the chances of cancer. It has since become the most studied gene in the human body, so important that it has been dubbed the “guardian of the genome.” The mutation is so pernicious that 50% of people who inherit it develop cancer by age 40, versus about 5% for the overall population. More than 90% of people with the mutation get cancer in their lifetime.

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Articles of Interest

Cancer Stemness: p53 at the Wheel

The tumor suppressor p53 maintains an equilibrium between self-renewal and differentiation to sustain a limited repertoire of stem cells for proper development and maintenance of tissue homeostasis. Inactivation of p53 disrupts this balance and promotes pluripotency and somatic cell reprogramming.

Comparing the Role of the p53 Gene and Telomerase Enzyme in ‘Accelerated Aging Due to Cancer’: A Literature Review

Aging is defined as progressive physiological alterations in an organism that lead to senescence. In response to stress, when proliferative-competent cells undergo permanent, irreversible growth arrest (like replicative dividing limit, oncogene activation, oxidative stress, or deoxyribonucleic acid (DNA) damage), it is termed as cellular senescence. Biomarkers p53, telomerase, and other inflammatory cytokines have a vital link with senescence, and directed use of these markers might be useful in manipulating cancer and the aging process.

Drugging p53 in cancer: one protein, many targets

Mutations in the TP53 tumour suppressor gene are very frequent in cancer, and attempts to restore the functionality of p53 in tumours as a therapeutic strategy began decades ago. However, very few of these drug development programmes have reached late-stage clinical trials, and no p53-based therapeutics have been approved in the USA or Europe so far. This is probably because, as a nuclear transcription factor, p53 does not possess typical drug target features and has therefore long been considered undruggable.

Geneticists Found the 'Master Tumor Suppressor' That Stops Cancer in Elephants

Elephants’ genomes possess 20 copies of a tumor suppressing gene called P53, new research shows.

p53 : The Most Frequently Altered Gene in Human Cancers

t seems nearly impossible for a normal cell to become a cancer cell unless it inactivates the p53 network. Our current understanding of this network has come from diverse lines of investigation, many initiated by serendipitous findings that only later converged into a coherent picture. This story provides insights into the nature of cancer, as well as the nature of scientific progress.

p53: The Gene that Cracked the Cancer Code

All of us have lurking in our DNA a most remarkable gene: it is known simply as p53 and its job is to protect us from cancer. p53: The Gene that Cracked the Cancer Code tells the story of the discovery of the gene and of medical science’s mission to unravel its mysteries and get to the heart of what happens in our cells when they turn cancerous. When all is well, this gene constantly scans our cells to ensure that when they grow and divide as part of the routine maintenance of our bodies, they do so without mishap.

The history of p53

The history of p53 and the various interpretations of its function in cells serves as an example of how scientific paradigms can influence research fields. It also offers some interesting lessons for young scientists in search of a rewarding research topic.

The p53 tumor suppressor protein

The p53 gene has been mapped to chromosome 17. In the cell, p53 protein binds DNA, which in turn stimulates another gene to produce a protein called p21 that interacts with a cell division-stimulating protein (cdk2). When p21 is complexed with cdk2 the cell cannot pass through to the next stage of cell division. Mutant p53 can no longer bind DNA in an effective way, and as a consequence the p21 protein is not made available to act as the 'stop signal' for cell division. Thus cells divide uncontrollably, and form tumors.

What’s the Point of Finding Cancer Mutations?

Here’s an honest question: What is the point of knowing that a gene called KRAS is mutated in many colorectal cancers? Or knowing that p53 is mutated in several types of cancer? Or knowing any of the hundreds of genetic mutations that appear in tumor cells across the land? Unless you work in an academic or industry laboratory, what is the use of knowing the genetic mutation responsible for a cancer? For almost every known cancer mutation, there is no drug to match it with.