Share this post on your profile with a comment of your own:

Successfully Shared!

View on my Profile
Back to Homepage

Cancer – Targeted Therapy Explained

September 10, 2021


With targeted therapy, though, we can find things that were very aggressive at one time and all of a sudden attack it and it changes the game. So one example is CML, chronic myeloid leukemia. That was tough. There was a translocation, which means the chromosomes got switched up in a mutation, 922. And that thing would make these leukemic cells grow really fast. Well, guess what? We were able to find a way to knock that process off, which is why now people live for years with CML. In addition, when cancers have two ways to grow fast, they either have an on switch that says, grow, grow, grow, grow, or they have ways to say this signal usually tells me to stop and die, but it’s not going to work. Those grow grow, grow signals, we have so many, like so many. EGFR, c-kit, KRAS, all these little molecular proteins and stuff that we realize make cells grow.

Your cancer, you specifically, regardless of the type, can have it in any one of those mutations. And that’s what makes cancer difficult to cure. But if you can find one where EGFR, in lung cancer, adenocarcinoma, that thing tells the lung cancer to grow, grow, grow, grow, grow. Well, guess what? We discovered the EGFR protein, and now you can take an oral pill to attack it. Total game changer. My wife had a 92 year old patient, lung cancer all over her body. They said, why get a biopsy? She’s 92. Through the blood, she checked to see if she had an EGFR mutation, which is about 8% of adenocarcinoma. She did. Started an oral pill. All the cancer melted away. Gained another 50 pounds back, she’s traveling the world. So when we can identify these things and target it specifically, it’s a big game changer. If it can’t cure it, it can actually minimize the amount of tumor and cancer significantly. The same thing happened with what’s called HER2 positive breast cancer. That was a very scary, aggressive breast cancer to have. Because that HER2 receptor proliferated. Again, it’s an on switch, and, oh my gosh, how do we stop this? Wow. We found a target for HER2. And now you can stop and block and hold down that process significantly. So it’s a silver bullet of sorts, but it takes identifying the mechanism.

Send this to a friend