The Colon Club

Hi all. Asking for some input. I have been on Keytruda exclusively since early this year and things have been going well. Extrahepatic lesions (supraclavicular, paraaortic) have gone. Liver lesions have shrunk and are PET negative. I have been gaining weight and am asymptomatic save for extreme dry mouth.

Yesterday I received the results of my PET/CT which showed a new small dot light up in segment VIII of my liver on PET. The same area however showed no structural lesion on the CT part of the scan.

Could this be progression or pseudoprogression? If Keytruda isnt working then why are all the other lesions still gone? Seeing my onc this week. I am in the process of planning SIRT so hopefully it can address that but not sure if they can hit something that cant be detected on CT. Should I stop Keytruda or add something like Avastin on top of it?

plastikos wrote:Hi all. Asking for some input. I have been on Keytruda exclusively since early this year and things have been going well. Extrahepatic lesions (supraclavicular, paraaortic) have gone. Liver lesions have shrunk and are PET negative. I have been gaining weight and am asymptomatic...

That sounds like an impressive, fine result!

Yesterday I received the results of my PET/CT which showed a new small dot light up in segment VIII of my liver on PET. The same area however showed no structural lesion on the CT part of the scan.

Possibly highly active tissue, microscopic cancer cells or not, and too small to image on CT but a quasar with FDG sugar added. We use that property against targetable cancer cells and some kinds of inflammation.

Could this be progression or pseudoprogression?
If Keytruda isnt working then why are all the other lesions still gone?

Biological heterogeneity, a new mutant or primary, perhaps local and transport differences to different sites, inflammation, or other artifact. We never have had a silver bullet that simply knocked out all sites. We have run across molecular indications of cancer heterogeneity several times now. We have had to pick the sites or types off one-by-one, while beating and holding down general activity and metastatic process. The peritoneum by massive provoked immune reaction and surgical clean up; lung thingies on metronomic immunochemo; then para-aortic LNs by intensified immunochemo and surgery, several liver objects on immunochemo intensified with more/different off-label adjuncts in different years; micromets and variable markers by actively modulated maintenance.

Should I stop Keytruda or add something like Avastin on top of it?

If Keyruda is working nicely on most sites, I'd be reluctant to stop that. I try to intensify or broaden the cancer attack with something bad for some kinds of cancer lines, but good or indifferent to the normal cells. This is an area where the extra markers, blood panels and attention to details are so handy. If CEA has gone down to baseline but AFP and/or CA19-9 are doubling, we can add mild or healthful adjuncts that are more likely to drive down cells related to those markers.

I have no knowledge of Keytruda, but what we did to stop a marker rise, was to scour for drug interactions, start at the low side of therapeutic doses for some targeted, nonstandard add-ons and escalate; or start full dose for some milder items, and monitor the expanded blood work. We even upped sample frequency to every 7-10-14 days, until seriously driving down one or more markers. Then our art was to do intensified immunochemo as close to the surgerical Art as possible, as reflected in various literature, not the standard defaults. There are differences between hours, days and weeks with different regimens and situations.

If only one tumor seems to not be responding it is possible it has mutated a defense to pembrolizumab.

I'm glad you are getting good results and are felling well!