It would be fair to say that my body failed me. Despite the reasonably good care I took of it and without any familial predisposition, it let a few cells loose, letting them proliferate in my gut and then, when this had reached its limit, run wild inside me. Now it’s out of control. This sounds like the beginning of an exciting story, but without people, no one will read it.
It would be unfair to say that my doctors failed me, but that’s certainly one way of looking at it. They failed to treat my disease successfully. But maybe it wasn’t them. Maybe blame has to go to chemotherapy, which didn’t manage to stop the growth of the rogue cells inside me. Again, this is an abstract concept that’s not going to make a good story. I could take a few steps back and say the scientists in pharmaceutical companies failed me because they haven’t come up with a therapy that’s efficacious against my particular cancer.
There are many ways of attributing blame. None of them does me any good. It’s much better to mobilize the scientific education I enjoyed and dig into the literature to see if there’s anything that might be of use to me, anything that might be done differently to avoid having to expect a different result with the same approach. This is not an idea that has recently come to me. Over the last six months, I have downloaded a few dozen papers with intriguing titles, but outside the reports on clinical studies of the effect of polysaccharide K, I haven’t read any. This is now changing.
By utter chance, I noticed a paper about “A systems mechanism for KRAS mutant allele-specific responses to targeted therapy”. I do have a mutation in KRAS. Targeted therapy surely sounds better than hitting the body with a broadly acting inhibitor of RNA and DNA synthesis, such as 5-fluorouracil.
The abstract was even better than the title:
“Agents inhibiting the epidermal growth factor receptor (EGFR) benefit many colorectal cancer (CRC) patients, with the general exception of those whose tumor includes a KRAS mutation.”
Consistent with my KRAS mutation, I received antibodies against vascular endothelial growth factor (VEGF) and not EGFR. This is also planned for the second chemo run. However, the abstract continues,
“among the various KRAS mutations, that which encodes the G13D mutant protein (KRASG13D) behaves differently; for unknown reasons, KRASG13D CRC patients benefit from the EGFR-blocking antibody cetuximab.”
I do have the G13D mutation.
Why am I not getting cetuximab? This is a question for my doctor. It might not be approved for use in my case, and the original clinical trial (ten years old by now) showed a depressingly small effect, but it’s worth a try. At this point, anything is worth a try.
The question for another post is what KRAS is, why KRASG13D behaves differently from wild type and the other oncogenic mutations, and why it would be susceptible to EGFR inhibition in contrast to any of the other mutations. I’m bailing out here because it’s late, the post is already long enough, and I’m not sure anyone would want to read what will follow.
The next post will be scientific, a journal club if you will, demonstrating my understanding of what goes on with KRAS and why. This is my fate. I need to know the background. So far, I’ve given cancer papers a wide berth, but this can’t be justified anymore. I need to take my health into my own hands, at least the theoretical aspect. Bear with me.
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