Genes that can beat cancer

At the beginning, there’s one single cell with which there’s something wrong. At the end, a giant tumor that can kill its host. What determines whether a mutated cell takes this particular path? And how can we prevent it?

There are many reasons why a normal, healthy cell becomes a cancer cell. It could be a common mistake, called a mutation, which are quite common in the process of cell division. In so-called replication, the process by which the DNA of the parent cell is used to create another cell that should be identical, a random change occurs. However, mutations can also be triggered by other influences, whether physical (e.g. radioactivity), chemical (environmental toxins), free radicals or viral infection. The result is a cell that not only loses its shape and structure, but above all is unable to communicate properly with its environment.

On the other hand, this alone does not mean that a person will get cancer. With the huge number of cells in our body that divide repeatedly, mistakes like this are commonplace. The critical issue is whether the body will allow this particular cell to continue to divide.

When cells commit suicide

The body has many mechanisms that allow it to prevent the development of a malignant tumour.

The immune system – our body’s immune cells are quite efficient at finding mutated cells that could become the basis for a tumour and then destroying them. A weakened immune system therefore increases the risk of cancer.

Apoptosis – this word refers to the ability that cells have encoded in them. If a serious mistake is made, they destroy themselves – they simply commit a kind of cell suicide. But if the apoptosis process is disrupted, the damaged cell can continue to divide.

Proliferation control – a healthy cell divides only when it receives a signal from the outside to do so. This signal lasts only for a limited time, so the division process remains under control. However, mutant cells often disrupt the communication with the environment, which takes place in the form of cell signalling. For example, the signal to divide may not be correctly terminated, so the cell does not continue to proliferate. This leads to so-called proliferation, or rapid, uncontrolled division, which leads to the formation of a tumour.

Telomere shortening – at the end of chromosomes (i.e. the structures in which DNA is stored) are parts called telomeres. Although these do not carry any genetic information, they are very important for regulating the functioning of cells. Every time they divide, they shorten, and if there is nothing left to shorten, they enter a so-called senescent state, when they can no longer divide. Scientists consider this process to be a protection against malignant growth, because too many divisions increase the likelihood of errors. The problem can arise if the gene for making the enzyme telomerase is activated in large numbers. This is switched off in most body cells, but if it is switched on, telomeres are restored. The cell becomes virtually immortal.

Turn on the right genes

If all of the above mechanisms are working in the body, the likelihood of developing a tumour is very low. However, once any of them are disturbed, the risk increases sharply. Certain genes in our DNA play a very important role.

Those that are related to the development of cancer fall into two basic categories:

• Proto-oncogenes – these are genes that promote tumour growth. For example, they often produce excessive amounts of growth-promoting proteins and therefore cause proliferation.
• Tumour suppressor genes – these are genes that suppress tumour formation, for example, by promoting apoptosis (a typical example is the p53 or bcl-2 gene).

The key question is to what extent these genes are active, i.e. to what extent the epigenetic reactions that switch these genes off or on are taking place. Thus, the ideal situation is when tumour suppressor genes are switched on and proto-oncogenes are switched off.

Increased levels of inflammatory processes in the relevant area also play a very important role in the development of certain types of cancer, such as colon cancer.

How fast (and if at all) a given tumour grows is then determined by the so-called angioneogenesis, or the formation of new blood vessels. While the tumour is still small, its cells receive nutrition from their immediate surroundings. But as it grows, the cells further from the surface no longer receive nutrients. A prerequisite for further growth is therefore the establishment of its own vascular supply. Thus, if angiogenesis is suppressed, the tumour can literally starve.

The activity of these genes is determined to a very high degree by a set of lifestyle and environmental influences called epigenetic factors. Experts estimate that up to 80% of all cancers are lifestyle-related.

Nutrition plays a major role here – some of its components promote tumour development (for example, excessive consumption of saturated fats), while many nutrients have a direct positive epigenetic effect. Smoking, obesity, long-term stress and many environmental pollutants also increase the risk of cancer, while regular exercise has a positive effect.

Useful dietary supplements

There are many natural substances that have direct anticancer effects (mainly due to epigenetic effects). Here is a small selection divided according to the principle on which they work.

Support of apoptosis: curcumin, boswellia, EGCG, quercetin, OPC

Proliferation control: astaxanthin (can reduce proliferation by up to 40% in breast cancer), curcumin, boswellia, pomegranate, genistein, quercetin, OPC

Deactivation of telomerase gene: EGCG

Limiting angioneogenesis: pomegranate, quercetin, OPCs

Detoxification of carcinogens: astaxanthin (promotes the production of enzymes to break down carcinogenic compounds)

Immunity support: astaxanthin, chicory (great source of probiotics), curcumin