2023-08-15 22:30:00
Why haven’t we cured cancer? After all, we’ve been to the moon, we’ve found “cures” for other deadly diseases. As a pandemic swept the world, scientists created vaccines at breakneck speed.
Despite decades of research and hundreds of billions of dollars dedicated to the search for curescancer remains an insidious disease that kills hundreds of thousands of people each year.
What is cancer? More than a disease, cancer is a constellation of more than 200 diseases. It has been linked to mutations in between 500 and 1,000 genes (of the 20,000 or more each person has). We are literally trying to tackle hundreds of different diseases and none of them are easy. Every cancer is different, and therein lies our first problem. In breast cancer alone, there are 20 to 30 different cancers (differentiated by their genetic mutations). Almost every patient has a different type disease that behaves differently in your body.
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This is the point where the moon analogy breaks down. We know what the moon is, where it is, how far away it is, what it is made of; it is a fixed target. Cancer is very different, we still don’t fully understand what it is or how it works. In terms of that metaphor, it would be like trying to fly to a thousand different moons in a thousand different places… and halfway to a moon, it might change shape or direction, or move to a different part of the sky.
For a long time, cancers have been categorized by the organ in which they first appear. Today, cancer subtypes are increasingly being described by their genetic or molecular markers. In breast cancerFor example, we might talk regarding mutations in the BRCA1 or BRCA2 genes.
Or we might talk regarding HER2-positive breast cancer, which expresses a protein called growth factor receptor 2 epidermal human and tends to be more aggressive than other types of breast cancer. These markers allow us to better define what we are fighting once morest.
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Scientists can now examine the “fingerprint” of a tumor. We can see up to six different types of cells melanoma in a tumor, and they’re all doing different things, mutating and growing at different rates, and potentially responding differently to potential treatments.
When I was a student, it was thought that one person’s melanoma was the same as another’s. But when we looked at the genome, we realized that that’s actually not the case at all.
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Despite everything, cancers have something in common: They are cells that have lost normal control of their growth.
The trillions of cells in our bodies have specific functions and follow a predictable cycle of growth, division, and death. We have all these complex control mechanisms that cause our cells to copy themselves only when they need to.
But with cancer, one of these cells ignore the controls incorporated from the body and multiplies uncontrollably. These uncontrolled cells can travel through the blood or lymphatic systems, nesting in tissues and flourishing there.
When cancer spreads, it is called metastatic. Doctors call the original tumor “primary” and secondary tumors metastasis. Pathologists talk regarding cancer grades (how aggressive it is) and stages of its development (how much is there and how far it has spread).
if cancer in one of his patients hasn’t spread yetwill use the word “treatment” from the beginning, because the whole intention of the treatment is curative. But for patients with metastatic cancer, they are more circumspect, explaining “we are treating your disease to prolong your life and to help you live as well as possible with cancer.”
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So it’s not just the cancer heterogeneity that makes it so difficult to treat, but also the cancer’s ability to adapt and evolve which means that even within a patient, cancer cells can be very different from one another. This means that while a medicine it might work on one part of the tumor, it might not work on another.
Added to this is the fact that cancer cells often have what is called “plasticity”. This means that the cells can easily switch from one type to anotherso even if they start out sensitive to a drug, they can change to a resistant form very quickly.
Given the cancer cells are our own cells, but slightly distorted, this makes them extremely difficult to identify and attack without damaging normal cells. Cancer cells are not an invasive species, they are not a bacterium or a virus, they are our own cells that have lost control of their proliferation. So what we’re really trying to do is find that little difference between a normal cell and a cancer cell, and it’s a really difficult task.
“We are trying to find a drug that attacks something that is almost identical to our own cells” (Daniel Gomez, researcher)
People often compare the search for a cure for cancer to the search for a cure for infectious diseases. But there are key differences.
A bacteria or a virus are completely different to us, so it is relatively easy to find a drug that attacks only that bacteria or virus and not our cells. But with cancer, we’re trying to find a drug that attacks something that’s almost identical to our own cells.
This is evident in the way drugs are developed. It’s relatively easy to make an antibiotic that will kill bacteria without killing us. But with cancer, the treatments are often drugs that kill both cancer cells and normal cells, which means they can be toxic.
Added to this is the fact that the body’s immune system often fights cancer treatments. Although the immune system can recognize and attack cancer in its early stages, once the cancer has become established, it often finds ways to evade the immune system.
Cancer, cure and treatments
Despite what has been said, there are great hopes and cancer treatment has evolved, and greatly, in recent decades. The surgery, chemotherapy and radiation therapy They are still the treatments of choice, but they are being performed more and more effectively and efficiently.
We also have hormone therapy, used for cancers that depend on certain hormones for their growth (breast, prostate) by blocking the production or action of these hormones.
We are in the era of precision medicine, where we hope to adapt treatments to the genetic profile of a patient and his tumor.
But this is not the only way that treatments are improving. There is also a move toward more personalized and less toxic treatments, and toward harnessing the body’s own immune system to fight cancer.
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In recent years, the immunotherapy, which uses the body’s immune system to attack cancer, has generated a lot of excitement. These treatments “train” the immune system to recognize and kill cancer cells.
In addition, there are targeted therapies (monoclonal antibodies) that attack specific changes in cancer cells. These therapies are different from standard chemotherapy, which targets all cells that are dividing rapidly. Targeted therapies are more like “smart bullets” that specifically target cancer cells.
As we learn more regarding individual cancers and how they work, and as our treatments become more sophisticated, there is hope that we may come to a point where that cancer is a chronic diseasesomething that people can live with for many years.
Conclusion: In summary, cancer is a complex, heterogeneous and constantly evolving disease. But with continued research and advances in medicine, there is hope that we can make cancer a manageable disease in the near future.
*Director of the Center for Molecular Oncology and Translational Medicine. National University of Quilmes
Former Director of the National Cancer Institute of Argentina; Conicet Senior Researcher.
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