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← Return to New biomarker Claudin 18.2
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Hello markymarkfl,
I believe I read from a post on another topic that your biomarker is decreasing now, and that's great!
After beginning GAC in January, my biomarker (CA19-9) is decreasing so that it went from 3840 (just prior to 1st treatment) to 141, though it hasn't been measured for a few weeks now. Additionally, my recent MRI showed that 1 lesion on my liver is no longer visible, and the other has decreased in size. The soft tissue around the hepatic artery/celiac trunk and within the abdominal peritoneum are "stable"; so with this information my oncologist wants to keep me on the GAC regimen. According to my dr. (Wainberg), the treatment for the CLDN18.2 protein has proven successful for gastric cancer, so the clinical trials at UCLA (largest study on west coast) are to test if it will work for pancreatic cancer, also. Since the GAC is working, my dr. did feel inclined to take me off something that is working for something where the result is unknown. However, since we all know that chemo has its shelf limit, I going to ask if I can at least do the test to see if I have the CLDN18.2 protein, and then when GAC no longer is effective, I'm ready to go for this clinical trial. I also saw your post on the KRAS12-D, and I'm very interested in the study that may be forthcoming in 2-3 yrs. - Oh, well! I also have the ATM and KRAS12-D mutations and was reading today in simple words that ATM accelerates KRAS12-D carcinogenesis. There may be some ATM clinical trials out there (I'm just not very good at retrieving the info for what, when, etc.); it's something I'll consider once the GAC wears down. At the start of my journey, I knew very little about this disease (even though my dad had it over 23 years ago); however, the research regarding pancreatic cancer I feel is exploding right now and there may be a "cure" in my lifetime. What I know now is that with my 3 mutations (TP53 being the other), the chances of this spreading for me were 100%, even though only 1 lymph node was impacted. Please keep providing your fantastic graphs and links and info., as we are all helping each other by sharing this information!
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Good thinking and good planning on your part!
My CA19-9 is only down a few points since resuming full-dose GAC after two reduced doses and one missed dose, but at least that reversed the upward trend. New data coming in two weeks...
Interesting news in my mutation department: We've known all along about my germline ATM mutation. When docs finally sent my 1.5-year old Whipple tissue to Tempus last month, it reported the KRAS G12D mutation. But, we also just sent new blood to Guardant, which reported a CHEK2 mutation but nothing on KRAS (despite reporting that it checks for "amplifications of this gene.")
It makes me wonder if Whipple got all the tissue with KRAS mutations. You'd think if that were an advantageous mutation and Whipple didn't get it all, that my recurrence would be flooded with KRAS by now. On the other hand, it may simply be that the tissue test was significantly more sensitive than the blood test.
On the other hand, CHEK2 was not reported in my two previous Guardant blood tests, and that one seems to correlate somewhat with chemo resistance in the literature and with my imaging/CA19 relapse.
It leaves me confused as to whether the best clinical trial for me should target ATM, KRAS, or CHEK2.