The evolution of cancer is mathematical, so the disease changes shape, and it is subject to treatment

Cancer is often described as a disease derived from genetic mutations that force cells to separate in an uncontrolled way and invade other parts of the body. But the spread of cells away from their origins is in some cases a normal process. The embryo is found in the womb during early pregnancy. Imune cells spread from lymph nodes to infections to attack invading bacteria. And brain cells migrate to where the goads will be during the early human development. Cancer is not a uniform disease.

Rather, it is a disease of phenotypical plasticity, which means that tumoral cells can vary from one form or function to another. This includes becoming less stable and losing their normal function, which can bring resistance to treatment or completely changing the type of their cells, the process that facilitates metastase.

In addition to direct changes in the DNA of a man with cancer, one of the leading drivers of cancer progress is that the country and the time when DNA is activated. If the latter carries “the words” that express individual genes, then the epigenetic is “grmatic”e genome, what it tells those genes whether to activate in a given tissue.

Although all body tissues have almost the same DNA sequences, they can all perform different functions because of chemical and structural modifications that change which genes are activated and how they do so. This “negenome” can be influenced by environmental exposures such as food diet, adding a dimension to how researchers understand patient health vectors beyond the parental DNA code.

I'm a cancer researcher and my lab at John Hopkins University, studies how differences between normal tissue, are controlled by an epigenetic code, and how this code breaks down in the case of cancer. In our recently published study, colleague Andre Levchenko from Yale University and I describe a new approach to understanding the sustainability of cancer by combining epigenetics with math.

We think that the concept of desertity can shed light on why cancers suffer metastases and become resistant to treatment. Stocasticity is a mathematical concept that refers to the idea that the chance of steps in a process affects the predictability of its outcome.

Albert Einstein once studied through this concept the movement of particles suspended into a fluid or gas. Researchers can apply this concept to study the spread, resistance, and evolution of Covid-19, bringing scholarships, and almost every game within a casino.

A key way to measure the essence of a process is enthropia, which determines the degree of uncertainty in one result. For example, an honest currency jump has a 1, or low information, because there's no way of predicting whether the currency drop will be head or tail.

But a trick throw of the coin has a zero or a lot of information, as the result is already known, and no new information will be gained by dropping the coin.

Researchers may use enthropine to measure the amount of information noise in the telecommunication field.

While the inclusion of the concepts of desertity and enthropy in biology, it enables researchers to better understand fentropic plasticity in cancer. experimental biologists and computer biologists are using enthropin to understand the basic coincidence in the way cells are organized from inside, react to environmental signals, and mature and form tissues.

Epigenetics is very important for the way cancer evolves. For example, a condition called Ezophagu Barrett occurs when healthy esophagus cells develop characteristics similar to those that normally have intestine cells, which can eventually lead to esophagus cancer.

This is caused by progressive random changes in the epigenetic code, and this change takes place sooner after reaching a certain threshold. The extreme nature of these epigenetic changes also leads to increased enthropia in the functioning of these genes and in their progress towards cancer.

Epigenetics is the reason why twins who share exactly the same gene can develop in completely different ways. By measuring the activity of genes and the epigenetic changes of individual cells, biologists and mathematicians can compare enthropin in cancer cells with normal cells that surround them.

Scientists have now begun to identify the genome regions that mediate desertity in cancer. A study that has not yet been revised by colleagues found that enthropy relates to the way chromosomes are physically compressed into the nucleus, another key epigenetic mechanism for controlling genes in cancer.

Meanwhile, there is a connection between enthropy and aging. My colleagues and I discovered that human aging is associated with an increase in epigenetic enthusiasm in the skin damaged by the sun. The parts of the genome that have high enthropics experience further loss of epigenetic information in the sun - exposed skin, which can lead to cancer. Recently, researchers have identified DNA damage to rats as a cause for this age-related entropy. So, if epigenetic efficiency grows in aging and is related to DNA damage, it can help explain why the risk of cancer increases significantly with age.

By identifying how epigenetic epithropy causes cancer, scientists may be able to detect cancer better in its early stages and develop drugs that educate enthropy and thus reduce the risk of spreading tumors and resistance to treatment. / “