There are different treatments to fight off cancer. They can be either ‘classical’ or ‘targeted’, depending on the tumour’s DNA profile. Sometimes a patient is offered a combination of treatments.
Communication between patients and their doctor is essential: the final decision belongs to the patient.
Surgery removes either the whole tumour or part of it. Radiotherapy uses radiation to destroy cancer cells while chemotherapy uses drugs to kill them.
Most of the time, ‘classical’ chemotherapy blocks cell division. The drugs that are commonly used target not only cancer cells but also healthy cells in the process of division – this is what causes side effects such as a decrease in white cells or the loss of hair.
Drugs used in precision medicine target altered proteins – or defective biological processes – found specifically in cancer cells.
More than one hundred drug molecules are used for treating cancer.
These molecules target one hundred different proteins.
By 2030, it is estimated that 500 new drug molecules will be available.
By accumulating mutations in their DNA, cancer cells either produce numerous altered proteins or overexpress others. Consequently, many biological processes are defective.
It is estimated that several hundred proteins, when altered, are involved in the development of cancer.
Every patient is unique and each cancer is unique.
Researchers can sometimes offer patients tailored treatment by determining which mutations are present and which proteins have been altered – or which biological processes are defective – in their cancer cells.
GOALS:
1. address the root causes of the disease by specifically blocking the defective biological processes in the cancer cells, thereby destroying them;
2. avoid resistance to treatment and limiting side effects;
3. bypass healthy cells so as to limit side effects.
1. TARGETING ALTERED PROTEINS
Certain mutations activate proteins involved in cell division, such as the EGFR, BRAF, MEK (MEK1) and ERK proteins.
There are drugs that specifically inhibit altered proteins found only in cancer cells.
When a drug and an altered protein interact, the cancer cells die because they need the altered proteins to survive.
2. TARGETING OVEREXPRESSED PROTEINS
Certain mutations increase the expression of some proteins in cancer cells.
One well-known example is the overexpression of proteins that are able to induce the formation of blood vessels which serve to transit nutrients and oxygen cancer cells need to survive.
Drugs that target these ‘angiogenic’ proteins – such as the VEGF protein for example – hinder blood vessel development, gradually starving and stifling the cancer cells until they die.
3. TARGETING NETWORKS OF ALTERED PROTEINS
Sometimes, there is no established drug known to specifically target a given altered protein. However, a different drug may be able to target another protein which, itself, interacts with the altered protein, thereby interrupting the dysfunctional process.
In the example below, the KRAS protein is part of a network of proteins involved in transmitting a signal that regulates cell division. When the KRAS protein is altered by a mutation, it becomes overactive thus amplifying the signal and the cells divide non-stop.
No established drug is yet known to specifically target the altered KRAS protein. However, if a drug can target a protein downstream of the KRAS protein – i.e. MEK or ERK – then transmission of the defective signal is blocked. Consequently, the cancer cells cannot divide anymore and tumour growth is checked.
4. AVOIDING RESISTANCE TO TREATMENT
Mutations can sometimes modify the actual pouch of an altered protein into which a given drug would usually insert itself. In such a case, the drug cannot interact with the protein.
Such mutations cause resistance to treatment.
When this happens, it is paramount to adapt treatments accordingly in order to avoid side effects caused by treatments that have become useless.
Immunotherapy has joined targeted chemotherapy in the realm of strategic therapies.
The aim of immunotherapy is to urge a patient’s immune system to turn against cancer cells of its own accord.
Our immune system usually attacks cancer cells. However, certain cancer cells accumulate mutations which help them acquire all sorts of strategies to shun our immune system.
Certain mutations cause the expression of proteins on the surface of cancer cells. These proteins stop the immune system from attacking the cancer cells (like the PD-L1 protein for example).
Patients can be given treatments that specifically target these proteins thus restoring the correct function of their immune system which will eliminate the cancer cells itself.