Why haven’t we been able to find a cure for cancer yet?
It’s a question that spontaneously arises whenever we hear of someone dying of cancer. The discovery of antibiotics and the invention of vaccines drastically reduced the number of deaths due to bacterial and viral diseases. These innovations, together with the general improvement of healthcare conditions, led to a significant extension of the average life span, revealing that in old age (in most cases) we are susceptible to different types of cancer. After cardio-circulatory system-related deaths (ischemic heart disease and stroke), cancer is the second leading cause of death worldwide. Although we are far from a definitive cure, cancer mortality has dropped dramatically over the years.
What are tumors?
A tumor arises when a cell of the organism undergoes a process of transformation, passing through a pre-cancerous stage to the stage of malignancy. A tumor cell begins to proliferate in an uncontrolled manner, ignoring signals that the body sends it to stop. It is therefore a different kind of disease than bacterial and viral infections.
Tumor causing factors can be grouped into: physical agents (ultraviolet and ionizing radiation), chemical agents (asbestos, cigarette smoke, etc.) and biological agents, such as viruses, bacteria and parasites (e.g. the papillomavirus can cause cervical cancer and combined hepatitis B and C are related to liver cancer). These agents cause a mutation, known as a driver mutation (or guide mutation), after which the process of malignant transformation begins.
If we know all these things, why haven’t we been able to find a cure for cancer yet?
For several reasons. First of all, because there are hundreds of different types of cancer, and you can not treat them all the same way. When we need to repair something at home, we choose tools depending on the damage, would anyone fix a leaky faucet with hammer and nails? There are hundreds of different types of cells in the human body, and each of these can give rise to a different type of cancer. Different illness, different care.
How do cancer cells differ from healthy cells?
The genome consists of a coding part and a non-coding part, which alternate in all the chromosomes. The coding part consists of genes, approximately 20,000 in the human genome (although not all are active), and each gene corresponds to a protein. Proteins are responsible for all functions in the cell. Some proteins are constantly present in the cell, while others are produced only when necessary. Proteins are only translated by something called “exons” (coding DNA segments), separated by non-coding segments called “introns”.
Based on the instructions received, a protein is generated by jumping or including one exon (one coding segment) rather than another. This is called “splicing”. Because of this, we understand now that there are different versions of the same protein. Once the protein is translated, it can still be further modified with some small “details” (even dozens!) which can affect its function; further increasing the complexity within the cell.
A mutation can affect a coding region or a specific splicing site of a gene, alter a post-translational modification, or be in a region that regulates how a protein functions (leading to too much or too little of the protein to be produced, altering the cellular processes).
So in this small example, you can see it is not possible to find “one total cure for cancer” because it would need to serve a different therapy for each different mutation that causes a specific tumor. And keep in mind that a mutation is not associated with a type of tumor; the same mutation can determine the onset of several types of tumors, depending on the type of cell in which it occurs.
How are cancer-driver mutations identified?
By sequencing a patients’ DNA. Recently, DNA sequencing techniques have improved dramatically, but we are far from offering DNA sequencing as a basic diagnostic tool, even if this seems to be the future direction. A major problem is that a DNA sequence varies significantly from one individual to another. This is called genetic variability, a very normal phenomenon that makes us different from one another. Because of this, it becomes difficult to determine which variation, among the thousands identified with sequencing, is responsible for the tumor. To do this, population studies are needed to analyze data from dozens of patients, but these are usually long and expensive studies.
So why are some tumors curable?
This is because the mutation that characterizes them has been identified several years ago. We are constantly collecting more and more information about tumors, testing new potential drugs, offering more efficient diagnostic services (remember that early diagnosis is the first step to defeat a tumor), and doing more prevention (stop smoking, drink less alcohol, exercise, eat more fruits and vegetables, and eat less red meat).
Thanks to the new information gathered through DNA sequencing, we are nowadays starting to consider tumor classifications based on the type of driver mutation, rather than on the organ they hit: to put it simply, if I have to fix a hole in the wall, I use plaster and a spatula, regardless of whether the hole is in the kitchen or in the bedroom. The possibility of treating different types of tumors with the same driver mutation using a unique drug is becoming real. In conclusion, we can say that the future is brighter than the present, at least when it comes to scientific research.
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