Here's some of the more scientific bits I promised for those that are curious. (My apologies to any researchers in this field if I get the finer points wrong here. Feel free to correct me if I've got something wrong.) No apologies for the length of this post. I find all of this truly fascinating, and it helps me to know that even if I can't control this, there definitely are still scientific reasons for how it's happening. 

Within a type like lung cancer, there are several subtypes. Specifically my genetic testing shows that my Non-Small Cell Lung Cancer is due to a mutation in the EGFR genes. Even more specifically in my DNA there's a  exon 21 L858R point mutation. Researchers don't have all the answers yet, but huge progress has been made in understanding what each mutation does, and gives a fighting chance at redirecting it. This is how it breaks down for me.

EGFR is Epidermal Growth Factor Receptor.  These receptors are found in a lot of our elastic cells; lungs, skin, sebaceous glands, gastrointestinal, and others. EGFR is basically a protein but also the instructions for how to handle proteins in cell growth. Remember way back when you had biology class and they showed strands of DNA splitting and then zippering up to create new cells? That's part of what EGFR does. With a mutation here, instead of copying a cell once and resting, it goes into overdrive, and keeps reproducing.  Unfortunately as it copies, it copies that mutation, so the second cell also is also broken and multiplying more quickly than regularly. This then creates tumors such as the one in my chest, or free cells that float out to the lymph nodes and become metastases. 

The medication I take is a TKI, a tyrosine kinase inhibitor. TKIs slow down this replication by blocking that protein receptor. Blocking it, makes it unable to copy, so slows down the cancer. The med tries to find and block only the mutant EGFRs but it gets confused some times. So It does have the side effect of blocking the receptors even in non cancerous cells. That causes lots of gastrointestinal upset, and at times causes really dry skin patches, or that super fun cancer rash face. I'm learning to deal with the side effects, and my oncology team is helping to medicate when needed so I can stay on this med. It's also much more manageable than the old style chemo which sought to kill all growing cells. 

The med that I'm on has been the most successful in keeping things stable. In oncology terms it has the best PFS (progression free survival) rate for this cancer. But cells, cancer cells in particular are "smart." Or at least they are optimized for survival. One of the ways my mutants are optimized is with that exon 21 L858R mutation. It creates kind of a spur on that DNA replication.

For whatever reason when this spur is seen, these cancer cells are much more likely to cross the blood-brain barrier. That's problematic. The barrier is good at keeping most "bad guys" out, but it also keeps the good guys out. So medications are less effective.  Luckily Tagrisso is one that can sometimes cross, and that's the reason for doubling it, to flood the spinal cord with as much of those blockers as possible. Whatever manages to get into the cerebrospinal fluid gets washed around the brain and spine multiple times. So all those little cancer cells can land on a nerve or area of the brain and grow. Right now we know it's caused swelling in the meninges which is the spongy layer around the brain, so luckily I don't have many neurological symptoms other than mild headaches from time to time.  Eventually it may lead to more traditional effects like dizziness, nausea, and body weakness. This eventually triggers the body's natural dying process that you'd see from any disease. 

Here's the topics where more research is needed and hopefully where it's focused. 1. We're not sure what mechanism causes this mutation. Best guess is environmental/chemical like radon, or lifestyle factors.  2. We know EGFR+ lung cancer happens more in younger than average people, in women and never smokers. We are not sure why yet. Knowing may give insights into prevention. 3.  TKIs still have a high toxicity which can cause heart, vision, liver problems, increased pneumonia or lung impacts (similar to Covid's cytokine storms). Ideally a formula can be found that is effective but not as toxic to other areas. 4. Tagrisso is a 3rd generation TKI drug that help exon 21 L858 and another mutation exon 19 deletions. Small tweaks may lead to 4th gen that are even more effective at stopping these mutations completely, or that addresses additional mutations.