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The evolution of cancer is mathematical, which is why the disease changes shape and resists treatments

2023-02-19 13:36:16Lifestyle SHKRUAR NGA ANDREW FEINBERG

The evolution of cancer is mathematical, which is why the disease changes shape

Cancer is often described as a disease that originates from genetic mutations, which cause cells to divide in an uncontrolled manner and invade other parts of the body. But the spread of cells away from their origin is in some cases a normal process. The embryo is found in the uterus during early pregnancy. Immune cells spread from lymph nodes to sites of infection to attack invading bacteria. And the germ cells migrate to where the gonad will be during early human development. Cancer is not a uniform disease.

Rather, it is a disease of phenotypic plasticity, which means that tumor cells can change from one form or function to another. This includes reverting to a less stable state and losing their normal function, which can lead to resistance to treatment or completely changing their cell type, a process that facilitates metastasis.

In addition to direct changes in the DNA of a person with cancer, one of the main drivers of cancer progression is where and when the DNA is activated. If the latter carries the "words" that express individual genes, then epigenetics is the "grammar" of the genome, what tells those genes whether or not they should be activated in a given tissue.

Although all tissues in the body have nearly the same DNA sequence, they can all perform different functions because of chemical and structural modifications that change which genes are activated and how they do so. This "epigenome" can be influenced by environmental exposures such as diet, adding a new dimension to how researchers understand a patient's vectors of health beyond the DNA code inherited from parents.

I'm a cancer researcher, and my lab at Johns Hopkins University studies how changes between normal tissues are controlled by an epigenetic code, and how that code breaks down in cancer. In our recently published study, Yale University colleague Andre Levchenko and I describe a new approach to understanding cancer persistence by combining epigenetics with mathematics.

We think that the concept of stochasticity can shed light on why cancers metastasize and become resistant to treatments. Stochasticity is a mathematical concept that refers to the idea that the randomness of steps in a process affects the predictability of its outcome.

Albert Einstein once studied the movement of particles suspended in a liquid or gas through this concept. Researchers can apply this concept to study the spread, resistance and evolution of Covid-19, the behavior of stock markets, and almost any game inside a casino.

A key way to measure the stochasticity of a process is entropy, which quantifies the degree of uncertainty in an outcome. For example, a fair coin toss has an entropy of 1, or low information, because there is no way to predict whether the coin toss will be heads or tails.

But a rigged coin toss has zero entropy, or much information, since the outcome is already known, and no new information will be gained by tossing the coin.

Researchers can use entropy to measure the amount of informational noise in the field of telecommunications.

While incorporating the concepts of stochasticity and entropy into biology, it allows researchers to better understand phenotypic plasticity in cancer. Experimental and computational biologists are using entropy to understand the underlying randomness in how cells are internally organized, respond to environmental signals, and mature and form tissues.

Stochasticity in epigenetics is very important to how cancer evolves. For example, a condition called Barrett's Esophagus occurs when healthy cells in the esophagus develop characteristics similar to those of normal cells in the intestine, which can eventually lead to esophageal cancer.

This is caused by random progressive changes in the epigenetic code, and this change occurs faster after a certain threshold is reached. The stochastic nature of these epigenetic changes also leads to increased entropy in the functioning of these genes and their progression to cancer.

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

Scientists are now beginning to identify regions of the genome that mediate stochasticity in cancer. A study that has not yet been peer-reviewed found that entropy is related to how chromosomes physically compact into the nucleus, another key epigenetic mechanism for controlling gene activity in cancer.

However, there is a connection between entropy and aging. My colleagues and I discovered that human aging is associated with an increase in epigenetic entropy in sun-damaged skin. Parts of the genome that have high entropy experience further loss of epigenetic information in sun-exposed skin, which can lead to cancer. Recently, researchers have identified DNA damage in mice as a cause of this age-related entropy. Thus, if epigenetic entropy increases with aging and is related to DNA damage, it may help explain why cancer risk increases significantly with age.

By identifying how epigenetic entropy causes cancer, scientists may be able to better detect cancer in its early stages, and create drugs that reduce entropy and thus reduce the risk of tumors spreading and resisting treatment./world .co.uk


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