Creme de la creme - Gina. I printed this and put it in my keeper file so in 20 years, I can fax it back to you and say "see, see - I told you that you posted incredible emails that printed to 4 sheets".
There is no resistance to Herceptin. I agree with this. I also agree that there are some dose dependent aspects to Herceptin - especially much more so in metastatic disease where there is tumor load (versus the adjuvant - early breast cancer setting). However, after my first loading dose, I wore heavy clothes, shoes, coat, purse and book bag. Nobody caught on. (No I don't get that much extra but my new (and much more observant onc) did comment that I lost 8 lbs in 6 weeks (I didn't but "I did"). Now I am really on the 6mg/kg dose every three weeks (and another reason why I started the first 12 as weeklies - "really putting on the weight" during these 12). Now I am what I am on the every three week. But, one is not getting that much more "weighing" 12-15 lbs more.
Again - resistance - part is the increasing tumor load versus the herceptin dose (and your description is perfect). Another is that life (even life we want to die) finds a way. What I mean is the downregulation of Her2 and the upregulation of - you name it - ER, PR, Her 1, EGFR, Her 3, Her 4 and all others that we know and don't know. Therefore, there is no Her2 to tag or very little (especially for a weakening immune system to find). Hence - during new recurrences, get your tumor tested again and make sure it hasn't dramatically changed!!! Or of course is that some cells have lots of Her2 receptors and some have just alittle bit. You kill the ones with lots and the only ones left to reproduce are the ones with less (or something else that's different that effects proliferation rate - Darwinism at its finest (another fav topic of mine)).
Also - how does Herceptin work? I think like you said - tagged cells are destoryed by the immune system. I also think it could work by tagging the receptors so they can't bind with the growth hormone and grow out of control. The growth receptor mechanism is blocked. However, the cell does not die - it dies a natural death. The question is when. I think sometimes the time was near anyway. But if it is a young cancer cell, it may hang around a long time and the tagging of herceptin is a surface phenomenon (remember - I sell surfactants for living an acronym for surface active agents) and surfaces interacting with one another is not a permanent situation. How long does the surface interaction occur? It is key and lock but is the fit tight? Is the fit tighter for you than for me (because of genetic and biochemical makeup?) Is it tight if I keep my omega 3/6 in balance, eat tumeric with vitamin C, without vitamin C (is this why Herceptin works better for some than others - the fit is tighter - there is less migration from the cell surface? I am just playing devils advocate here but I think you know what I mean. Or just that Herceptin comes off the surface before the immune system finds it to destory it with the cancer cell still attached?
Neulasta - I took Leukine during dense dosing because it boosts the macrophages (monocytes and dendrites too) and has protective effects on the lymphs (see
www.leukine.com) Someone once told me that Neulasta might actually be proven to do more harm than good one day. But the oncs love it because they want to see the neutrophils and they are heavily entertained by Amgen. I am not a proponent of neulasta (or procrit either).
Well, Gina, the Hungarian enthusiasm has been lit this afternoon. Certainly, I will think of more later as I am at work now and want to maintain employment.
Bestest regards
Becky