Transcription
Many people say that it's impossible to treat cancer, but is that true? Today we'll talk about the treatment of chronic myeloid leukemia. So, can we treat cancer? The answer is: it depends. Some cancers are indeed very treatable thanks to breakthroughs in medicine. I talked about hematopoiesis before, but for chronic myeloid leukemia, these cells are increased in number.
Let's jump in a time capsule and go back in history, before the year 2000. How did we use to treat chronic myeloid leukemia? We used to treat it using interferon alpha, hydroxyurea, busulfan, and allogeneic stem cell transplant was a last resort because, as you know, it's difficult. But today, we have better stuff.
Fast forward to the future. Now we have some miraculous drugs called the tyrosine kinase inhibitors, or TKIs. These are indeed revolutionary. In my previous video on chronic myeloid leukemia, we talked about the pathogenesis: we have the Philadelphia chromosome, fusion gene, then fusion protein, which is a tyrosine kinase. How to block this protein? Use a tyrosine kinase inhibitor such as imatinib. Any drug that ends in "-nib" is a tyrosine kinase inhibitor. This is science called drug nomenclature. We have first generation, second generation, and third generation tyrosine kinase inhibitors. First generation: we have imatinib. Second generation, more potent: we have dasatinib, nilotinib, bosutinib. Third generation is ponatinib. Isn't that musical? There should be a music band called "Tinibs."
Currently, there are six FDA-approved drugs to treat CML. We have five tyrosine kinase inhibitors, and we have the sixth drug called masitinib. This masitinib is a protein synthesis inhibitor, more selective on BCR-ABL, while the TKIs are tyrosine kinase inhibitors, again selectively BCR-ABL. So, tyrosine kinase inhibitor, protein synthesis inhibitor. I've talked about the phases of chronic myeloid leukemia before, but for now, please remember you have the chronic phase, then accelerated phase, then the blast phase. So, imatinib can be used for all phases. Dasatinib, same thing, all phases. Nilotinib, all phases except for the blast phase or the blast crisis phase. Bosutinib, all phases except frontline therapy, which means you never use bosutinib as the first drug; you always try something before it. If they fail, you can switch to bosutinib. Ponatinib, same stuff, all phases except frontline. Masitinib, after two or more TKIs have failed. You try two or more of these. Last resort, you go to this one.
There are some special situations to treat chronic myeloid leukemia. What if the chronic myeloid leukemia is resistant to imatinib? Now you can use dasatinib or nilotinib. What if the CML has a certain type of mutation called T315I mutation? You can use ponatinib.
So let's summarize: treatment of chronic myeloid leukemia consists of the "Tinibs," tyrosine kinase inhibitors, right? If all of them failed and the sixth drug failed, go to good old allogeneic bone-marrow transplant. Again, there is a difference between autologous and allogeneic. Autologous means from the body to the same body, such as skin grafts; they take a piece of skin from you, put it on a different site on the same body. Allogeneic means between two bodies of the same species, from human to human. Xenogeneic means between different species. The way I remember it: when you talk to your friend over the phone, you say "hello," which is close to "allogeneic," or allogeneic, okay? Because you're talking to another human being, that's not yourself, right?
Because I'm a crazy person, I went to Philadelphia to talk about the Philadelphia chromosome. These videos are coming soon. Please subscribe to my channel and click the bell to get notified when these videos are available. Thank you so much for watching. I'll see you in the next video.