In 1761, Giovanni Morgagni of Padua was the first to do something that is now routine; he did autopsies to relate the patient’s illness to pathological findings after death. This research laid the foundation for scientific oncology, the study of cancer. A century later, the development of anesthesia allowed surgery to flourish, and classic cancer operations such as the radical mastectomy were developed.
By the middle of the 20th century, researchers found most of the things that caused cancer (carcinogens) cause genetic damage (mutations) that looked a lot like the mutations that could be inherited and could result in the same types of cancer if more mutations were introduced.
Now billions spent and millions have died, what do we not understand?
1. The problem is now that doctors can’t always tell the difference between lethal cancers that need treating and non-lethal cancers that don’t.
2. Sometimes, patients who seem to have been successfully treated for cancer can have the disease come back years or even decades later, often without warning. Some researchers believe that the cancer cells that were not killed by initial treatment can go to sleep, lying dormant before a new trigger of growth begins. What causes some cancer cells to go sleep, or where they hide when they’re asleep, is unknown. Scientists also don’t know for sure what wakes these cells up days or years later.
3. When cancer is detected early, treatment is more likely to be successful. But too often, cancers are diagnosed at a late stage when they’re much harder to treat. Human evaluation techniques and today’s detection capabilities are one of the biggest problems. Early detection at the cellular level and artificial intelligence as an evaluator of imagery and biomarkers is the future.
4. How do microbes (virus, bacteria, fungus) play a role in how cancers develop, their damage to DNA, and how the imbalance of microbes create mutated cells.
5. The relationship between cancer and proteins in cell communication pathways is still unknown. Today geneticists have deciphered how APOBEC, a protein that fights viral infections, becomes a dangerous mutagen when DNA replication goes awry. It takes advantage of a weakness in our DNA replication process to induce mutations in our genome.
6. The proteasome is a large protein complex responsible for the degradation of intracellular proteins, a process that requires metabolic energy. Proteasome is accountable for clearing away the “garbage” produced by cells. When the proteasome’s function is blocked, cells are overcome with their waste and die. Proteasomes are the cell’s protein recyclers. Proteins need to be destroyed for many reasons: they may be damaged, or they may be part of an invading virus, or they may not be required anymore.
7. Lifestyle factors creating mutagenesis and how these mechanisms cause cancer, it is more than toxicity. One example, being overweight is linked to 13 types of cancer.
8. The concept of an origin cancer being a single disease rather than multiple issues and multiple cancer cell types contributing to the original tumor. Each diagnosis and treatment needs to be personalized.
9. Cellular communication between cancer cells and our immune cells. Why does cancer have the ability to turn off our natural defenses?
10. Cancers can adapt and create resistance to treatments and reestablish its presence through a single cancer circulating stem cell.
There are many more answers to these questions and many more questions to answer.
The only hope we have to cure it is to understand it.