Research

“Every man must decide whether he will walk in the light of creative altruism or in the darkness of destructive selfishness” Martin Luther King, Jr.

The healthy ageing human body

The human body is composed of billions of cells but only about 200 different cells types, like brain cells, muscle, blood etc. If we zoom into any of our tissues, we discover a hierarchy between cells, where the “boss” is the tissue stem cell (very few of them), and the soldiers are most cells that form the tissue mass. We could not live without either of them; it’s a perfect synergy.

Throughout our lives, some soldier cells become injured and die and the stem cell will start dividing to give rise to other soldier cells to replace them. It is very important to keep the tissue stem cell happy, protected and free to produce soldier cells whenever needed.

But as we age, the environment around the tissue stem cell becomes polluted; the walls are damaged, which slows down the ability of stem cells to regenerate the tissue, when challenged. This can lead to faster ageing and disease.

Ageing is the biggest risk for developing cancer, and about one in three of us will develop cancer at old age. Therefore, it would be a breakthrough if we could prevent it, rather than just treat it, which is very costly.

Could we stop cancer before it starts?

Cancer is generally understood to be not just one disease but hundreds of diseases, depending on the cancer type, and it is thought that mutations in the DNA sequence are what’s causing them. But recent research started to challenge this assertion. What is emerging recently is that tissues in old people are beaming with cancer-associated mutations, but only a few of us will develop cancer. Even if we develop cancer, only one of our many tissues will form a tumour. Why? The possibilities are enormous considering the significant amount of mutations found in all tissues in all people.

What is cellular transformation?

What is the moment a cell decides to turn against us form a tumour? We actually don’t know. We can only say that cells adopt specific behaviours, which can be measured, such as hiding from the immune system, uninhibited proliferation, independence from anchoring to neighbouring cells. Then there are the more complex changes, such as adapting metabolism to cancer specific needs, reorganising the nucleus and the proteins that protect DNA to a more open conformation etc. All of these can happen in the presence of a great diversity of genomic aberrations, ranging from very few mutations detected (in some childhood cancers) to a profoundly altered genomic sequence (melanoma).