How tumors develop: the key role of genetic changes

The discovery could revolutionize cancer treatment

Cancer, this is how it develops: the important role of genetic changes

Discovery could revolutionize cancer treatments

Every year, in Italy, Rocky Diagnosis changes the lives of hundreds of thousands of people.Consider the Italian Statistics 2025 report, the new cases of malignant tumors are around 390 thousand per year, the new cases of the European average.

This picture, made of significant progress but still impressive numbers, clearly shows how crucial it is to understand not only how a tumor originates, but especially how it develops over time and why it becomes resistant to treatment in many cases.It is precisely at this central hub that new international research is focused, which is destined to change the way cancer development is interpreted.

How does the tumor develop?

For years, the evolution of cancer has been largely explained as a random process caused by unpredictable mutations. New research published in the journal Nature Communications shows that tumor development follows a set of genetic rules associated with changes in the number of chromosomes in cells.Noemi Andor, Moffitt Cancer Center and Research Institute in Tampa, Florida, and author of the study.

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Because chromosomes are more important than individual mutations

When we talk about cancer, we often think of mutations that affect single "key" genes.In reality, during the growth of a tumor, cells much more often encounter large-scale errors in the division of DNA, resulting in the loss or gain of entire chromosomes.These changes, known as "chromosomal instability", mean that genetically very different cells coexist in the same tumor.It is as if the tumor were not a uniform mass, but a veritable ecosystem of cell populations that compete, adapt and change over time.

The difference with individual genetic mutations is important: each chromosome contains hundreds or thousands of genes, so when a cell gains or loses one, it simultaneously changes the function of the entire genetic network, affecting growth, differentiation, and response to stress.This mechanism allows tumors to make rapid evolutionary leaps, increasing internal diversity and the chance that some cells will survive treatment.However, these changes are not always beneficial: the same chromosomal structure can improve survival in a certain genetic condition and be detrimental in another.It is precisely this state of dependence that makes it difficult to predict the development of cancer.Only by looking at how cells change over time and what arrangement is chosen can it be understood that some tumors adapt successfully while others meet the limits of evolution.

Alpha-K: A tool for reading evolution over time

To overcome the limited understanding of what the chromosomal structure gives priority to the life of the tumor, the research team of alfa-k, a new computer tool, which is different from traditional methods, which only holds "snapshots" of the tumor at one time, Alfa-K studies the evolution of an individual over time, following how they gain or lose all the chromosomes not as a way of increasing chromosomes but as a way of Tumor development.The cells.Thanks to this information, Alfa-K builds real "fitness landscapes", maps that show which chromosomal changes are beneficial to the life of the cell and, instead, weaken it.

This method allows us to measure the quality of hundreds of thousands of different chromosome configurations. It explains why some evolutionary trajectories are preferred over others.In other words, ALFA-K is not only to describe the tumor. But it also helps us to predict how the tumor will change and change. This opens the way for targeted and aggressive treatment.

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Genome duplication: a strategy for survival

One of the most surprising things the study revealed is whole-genome duplication, a phenomenon where a tumor cell copies all its chromosomes and copies its entire inheritance.This process is not just a random error: it is a real evolutionary strategy.its life.ALFA-K was able to measure this "buffer" effect, showing that there is a threshold beyond which gene duplication is acceptable from an evolutionary perspective.

In other words, the phenomenon is neither random nor universal: only under certain conditions it gives tumor cells a real advantage, helping them survive and adapt faster.This discovery transforms a long-observed event from a simple biological curiosity into a predictable and measurable mechanism that is useful for understanding tumor development and why certain cells become more aggressive or resistant to treatments.

What a change to heal

The implications of these findings go beyond basic research.Understanding the rules that guide the evolution of tumor chromosomes can help doctors better interpret repeat biopsies.and identify signs of dangerous evolutionary change.When looking at it in perspectiveThis approach can help us choose treatment strategies that can predict drug resistance after it occurs.Rather than chasing it after it happens, Andor points out that the long-term goal is to move oncology from identifying tumors to predicting their behavior.Not only are we targeting cancer.But it also limits their ability to adapt and survive.A paradigm shift that could pave the way to a cureIn countries like ItalyThe cancer burden remains high despite advances.Understanding and predicting tumor evolution may be one of the keys to making more targeted and effective treatments.