StDrogo wrote:I'm a bit confused about the relevance of your response.....CEA and CA 19-9 ought to be particularly sensitive for such a substantial mass if this were cancer . .
[CEA/CA199]...only if the tissues are certain types
of CRC or gastrointestinal cancer, AND communicate well to the blood. Also some met locations don't report well. This is why we cast the net broader on the non-specific panels analyzed with respect to a prior cancer or CRC diagnosis (compared with specialized med papers). We would also consider a liquid biopsy, if available, for finding more specific hits in a tight situation with unknown disease process or id. Your wife presents differently than most, I'm not clear how normalized her health and panels were following surgeries. There is the possibility it might be relatively "benign", a new primary, CUPS or another mystery. Different doctors or papers may also reflect particular experience treating off different markers. I'm not clear whether you had Kras genetic test results.
As time goes by, cell populations and/or expressions can change. We hit repeatedly at marker shifts or anomalies to suppress or remove them, as much as some preconception of the proper cancer treatment. A lot of people get thrown off by changes to a single marker trying to cling to prior methods and formulas that worked before, often with no formal options or trials available. On chemo, MCV changes have been distinctive for us too.
Timing and multiple adjuncts are factors with immune processes; recruitable high WBC seems preferable to depressed WBC and factions that remain unrecruited. The published perioperative with CIM are for metastatic spread prevention under particular conditions with some subtleties and exclusions. The published 3 week post op data seemed brittle to me. I have to say my bias is for longer, stronger pre-op with cumulative mild "good" molecules with multiple anti-inflammatory treatments, "natural" and not. We try to pick up many small improvements for both diagnostics and treatment chemistry where these capabilities interact beneficially.
PSK we use based on beneficial WBC and RBC changes that occurred with responses at two dose levels, as well as using CEA as a predictive marker for PSK benefit, based on published statistical associations with CRC treatment.
Our initial pre-op use of vitamin D3 (11,000 --> 17,000 iu) was based on concern about repletion (later validated), and enhancements, tempered by caution and supplies on hand. Our later
, higher dosage use of megavitamin D3 (and its supportive adjuncts) was not based on deficiency, it was based on the recommendations of a UCSF endocrinologist who tracked research and unusual reports across a century for vitamin D on immune responses including cancer, and his subsequent clinical experience.
On many supplements that are debated, like curcumin, I allow that there may be secondary processes, like extra transport routes, that are poorly documented. I've seen this issue ignored (or inadequately described) several times when I know there are extra transport considerations, or "interesting" human data.
Some shrinkage/necrosis responses are fast, some play out over a year or two; best marked by scans or biopsy too.