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I love speculation. I'm not sure I follow the reasoning on this one, though. When we talk of circulation to tumors, aren't we usually talking about the actual network of blood vessels, rather than the number of red or white cells within them? I think that is two completely different things going on. For example, that article recently posted about surgery perhaps stimulating mets talked about angiogenesis (making a network of blood vessels to support tumor growth).
It will be interesting to see when they look closer at what's going on with the Procrit information whether the outcomes relate to actual levels of red blood cells achieved after its administration, or to dose of the med(s), or to something else altogether. The suggestion that its safer when tthe target Hgb is below 12 does lend support to the theory that AA proposed.
Just anecdotally, my Hgb is pretty high, it didn't take too hard a hit during treatment (no procrit), and I'm NED at 6 years out. I got LOTS of neupogen, however. Neupogen and Nuelasta are sort of the same drug, btw - both made by Amgen. Neulasta is the long-acting one, given once each cycle. Neupogen is the older version given daily for varying periods. I wonder now if that isn't the better choice, as probably not everyone needs the mega dose of Nuelasta and could get by with just one or two Neupogen injections, which could perhaps be safer. Perhaps. Maybe. So much to know.
As long as we're speculating and letting our mind wander - there has been discussion of treating lymphedema with vascular endothelial growth factors which might stimulate growth of new lymphatic pathways to make up for the ones lost to axillary surgery. But the question there is could that also stimulate cancer growth (perhaps as removing a tumor does)? Perhaps. Maybe.
And lastly, more speculation and rambling: As long term data emerge on the use of blood cell stimulants of all types, I wonder about myelodysplasias in the long term. We know that chemo increases risk of leukemia, but could the blood cell stimulants (I'm too lazy to look up the technical terms, sigh) contribute to this also? Again an anecdote: I have a friend who was diagnosed and treated for a relatively friendly breast cancer last fall (lumpectomy and rads only). Routine lab work during this time revealed thrombocytosis (too many platelets). I'll omit the discussion of that disease but it resulted in a referral to Stanford's bone marrow transplant program and the physician that she saw there first assumed that her condition (which will eventually require BMT) was secondary to treatment for breast cancer. That was not the case for her, but I wonder, since he quickly made that assumption, how many times he does see bone marrow failure post breast cancer chemo, and if anyone's looking at the incidence of that related to the different kinds of chemo, and also to the use of blood cell stimulants. The scenario for my friend's condition is that initially (now), her bone marrow is running amok, producing too much, but that over time this will lead to failure and no production (hence the need for BMT). Hmm. That's sort of what Nuepogen and Procrit do - cause production to run amok, right? Again, just speculation.
Debbie Laxague
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