Today was another day of truth, in a way. I had an appointment with the oncologist who will be looking after me after the trainee doctor who was responsible for me up to now left to continue her training in a different hospital. The topic of conversation was the PET-CT scan from last Wednesday and the conclusion we can draw for the continuation of my therapy.
First off, the scan confirmed what the CT scan a week before had already indicated. The tumors in my lung and liver have grown a bit. Nothing dramatic, but clearly visible. The tumor in one of the lymph nodes looked similar to before. There were a few new tumors in the pulmonary pleurae, which are bags of cells that surround the lungs. All of the tumors are metabolically active.
None of this is good news, but it’s not exactly unexpected and didn’t shock me. The progression was to be expected, in particular after knowing the results of the CT scan. I can even see positive aspects. The progression is slow. It’s not as if I’m going to die within the next half year. The metastases in the peritoneum haven’t returned. My condition is stable, even though stable means stably deteriorating.
When discussing the CT scan with my previous doctor, I got the feeling that she had given up. She didn’t really talk about possible downstream therapies. Instead, it was all about stopping chemo because it’s not doing anything. This is not my approach. The new doctor is more to my liking.
As others have done before, he ruled out anything but chemotherapy. Radiation therapy makes no sense because the cancer is delocalized. Surgery makes no sense for the same reason and because new metastases are still appearing. I need to stop the growth of the cancer before anything else can be cut out of me.
So chemotherapy it is. Here, the doctor is going with my suggestion of changing the antibody. Instead of antibodies against VEGF (vascular endothelial growth factor), he will try to treat me with an antibody against EGFR (epidermal growth factor receptor). Why do I write try? EGFR antibodies are known to work against cancers without mutations in KRAS. Recent results have shown that they might also work in cancers with my particular KRAS mutation. These results are not clinical studies, and EGFR hasn’t been approved as a drug against my cancer.
The doctor will make the case to my insurance provider that the EGFR antibody should be covered but cautioned that they might say no because it’s experimental. This sounds like something I would expect from the US health system, which is frequently represented as ruthless or even predatory – though I never experienced it as such. I’m a bit surprised I experience this in Switzerland. You might say an insurance company can simply not pay for all treatments a doctor might want to try. On the other hand, why is the doctor (in this case supported by the joint opinion of the hospital cancer board) not the one who makes decisions on treatments?
If the insurance company says now, the doctor will ask the maker of the antibody to give us a few batches for free. This sounded like the most normal thing to do. Go figure. The antibody would be used together with the chemotherapy I’ve just stopped. This was not the doctor's idea, but Flucha and I convinced him. He didn’t have an answer to our questions of what was wrong with continuing chemotherapy.
If the antibody doesn’t become available, there are two alternative chemotherapies. Both are oral, which means I’ve got to swallow pills throughout the day instead of going to the hospital for infusions. One is trifluridine, which I had already discussed with the doctor in Zurich. He wasn’t convinced this would be of much help. The other is Regorafenib, a tyrosine kinase inhibitor that, according to Wikipedia, has achieved an average added survival of 1.5 months and isn’t even on the market in Germany because the agency that makes such decisions resolved that the potential benefit of the drug wasn’t high enough to justify the cost. This is what my doctor wants to try first if we can’t get the EGFR antibody.
None of this sounds good. To get my mind off these things, I asked the doctor a few questions related to the immune system that arose after my previous post. What’s up with my T cells and why wouldn’t a PD-1 antibody that prevents tumor cells from inhibiting killer cells be a good idea? There’s apparently nothing wrong with my immune system. It’s just that tumor cells are difficult targets for immune cells. Immunotherapy works best when tumor cells have mutations in certain DNA damage repair proteins. In these cases, the tumor cells present bits of DNA on their surface that helps T cells recognize them. I don’t have any of these mutations. My cancer cells look as if coated with Teflon. Immune cells with pass them by without stopping.
What we didn’t talk about were vitamin C and fasting and methadone. To strengthen my arsenal in this increasingly difficult fight, I will contact the clinic by Lake Constance that accompanies patients during long periods of fasting. Maybe they’re willing to infuse me with copious amounts of vitamin C. I’d pay for that. The other hope is the clinical study in Ulm that evaluates the use of methadone. It started in March. At some point they must have preliminary results.
The two most conventional chemotherapies have failed to rein in my cancer. This is nothing to celebrate, but it’s also no cause for despair. There are a lot of things to try before giving up becomes an option. I can’t wait to continue the fight.
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