I haven't said much about the state of my health recently. About 6 weeks ago I was alerted to a sudden change when my CEA reading leapt from the previous plateau of 5.2 ng/ml to 9.3 ng/ml over a three week period. I had no doubt at the time that this was real and probably indicated that some residual cancer cells had gone through angiogenesis to get their own blood supply enroute to becoming tumours. After discussing the matter with my oncologist we decided to wait another two weeks for a second reading, and in the meantime consult with the Sydney team of David Morris and Winston Liau.That second reading, which I obtained last week, showed another rise to 14.3 ng/ml. You can see from the graph that the exponential growth represents a doubling period of three weeks, as fast as I have experienced during the rapid tumour growth phase of 2009.
My options are now somewhat limited. Given the early return of the disease, further peritonectomy/HIPEC surgery is not advised due to a likely poor prognosis. The full range of FDA-approved chemotherapy drugs shown to be effective in colorectal cancer, I have already sampled, namely Oxaliplatin, Capecitabine, Irinotecan and Avastin. The remaining drugs, Cetuximab and Panitumumab are only effective for KRAS gene wildtype (60% of the population), and sadly, I am mutant (40% of the population).
If the disease progresses at this rate, and based on experience in 2009/2010, I will have cm size tumours in a matter of 6 weeks, just about the time I had planned to fly with Miang to the UK to begin a 3 month sabbatical. Clearly we have some major issues to grapple with.
Next week I will have another PET-CT scan. If we can locate the site or sites of the tumour the potential for resection will be considered, a possibility, for example, if there were a single tumour acting as the source of the rising CEA. I have to say that this seems unlikely.
Interestingly, the rise in CEA started 3 weeks upon cessation of Capecitabine adjuvant chemotherapy. I could go back on to Capecitabine soon, or I could try hitting the cancer with the triple cocktail of Avastin/Irinotecan/Capecitabine, which caused a dramatic reduction to a plateau of 8 ng/ml, during 2010. But I am up against evolution and natural selection. All my new cancer cells have experienced those drugs before and it is not at all clear that they would respond a second time.
It's hard to find much good news here, but I am a master at seeing the silver lining in the clouds. I do have confidence in the CEA as a marker for the disease well in advance of radiological indication or physiological symptoms. That means we can at least track the responsiveness to treatments quite sensitively.
After our last discussions, my oncologist and I think the next step may be to try Capecitabine alone, to see if we can stabilise the disease for a while, to give Miang and me some time in the UK with the family. The triple cocktail can be kept in reserve for later use.
The future of cancer therapy is undoubtedly to be found in better understandings of the immune system, and how it can be assisted. My good friend Graham Legros, immunology expert and Director of the Malaghan Medical Research Institute, gave me a tutorial recently. One thing is clear. The immune system is immensely complex and its provocation may well produce beneficial effects. I am considering that, on the basis that I may be "n=1", worthless as medical evidence, but significant given my singular life.
More on that matter later no doubt.

I'm really sorry to hear that. Cancer is unremitting in its adaptation and evolution it would seem. I too have had a slowly creeping CEA over the past few months, with the most recent CT showing a change from 18 months of stable disease to slow growth in a single metastatic lymph node. News of progression is never what we want to hear.
ReplyDeleteThinking and praying for you.
Jared.