julierene
03-22-2006, 10:40 PM
Maybe this topic would be better in a new thread - cause the other one was SO long...
The topic is why Herceptin becomes Ineffectiveness in people it was previously effective.
1) Haven't the studies shown that MORE Herceptin gives the same results as the current dosages without increasing effectiveness?
2) Why not make the theory that the tumor cells have capabilities of "learning"? I used the term loosely though, because I don't think cancer cells are necessarily smart - but maybe just survive out of 'natural selection'.
Cancer isn't just one type of cell replicating itself over and over. It's a product of an immune system that fails to recognize a damaged cell. My left breast had er-/pr- grade 3, IDC. My right breast had er+/pr- moderately differentiated DCIS. When I found out about that, I was like how? How could I be er-/pr- in one breast and er+/pr- in the other? It wasn't about the cancer... It was about my immune systems inability to recognize bad cells. Our normal cells are constantly learning how to overcome viruses and all sorts of stuff. The immune system seems smart when it comes to foreign attack (in a lot of cases). But when it comes to our own body malfunction, it struggles - especially when our genetics aren't perfect.
We already know that cells have a LOT of receptors on their surface. HER2/neu is just one of them. But for those of us who are HER2+++, that's great right? Think about this made up example for a minute:
I would think Herceptin Ineffectiveness is a mechanism where those tumor cells (in their active state) whose cell surface makeup has a few more IGF-IR receptors, survive and replicate after Herceptin has blocked all of the HER2 receptors on its surface. Even though the HER2 receptors are plugged, the immune system doesn't necessarily kill the cell. For many of us, the chemotherapy is what goes in and kills all the fast dividing cells. Just because the receptors are blocked, doesn't mean the cell is dead.
Those cells that have almost all HER2 receptors are killed (while in their active state), because chemo comes in and recognizes it as a fast dividing cell. While on Herceptin alone, the stuff that's maybe got some IGF-IR receptors - could live (if not in their active state, maybe while in their inactive state. I am on the side of the fence of oncology theory that believe cancer cells 'hide' while in their stem cell slowly dividing state - which is why they evade chemotherapy). As those cells live, I think more are replicated with 'possibly' more of those type of IGF-IR receptors. As all the HER2 receptors start to disappear (because those cancer cells were killed - either because they had no receptors left or the chemo killed them) - we get cancer cells that continue to divide - even while taking Herceptin. <Maybe the HER2/neu receptors are being blocked, but the IGF-IR unblocked receptors allow the cell to survive and divide?>
Is it plausible?
<I used IGF-IR just because it's a hot topic and I can't remember all the other ones abbreviations>
The topic is why Herceptin becomes Ineffectiveness in people it was previously effective.
1) Haven't the studies shown that MORE Herceptin gives the same results as the current dosages without increasing effectiveness?
2) Why not make the theory that the tumor cells have capabilities of "learning"? I used the term loosely though, because I don't think cancer cells are necessarily smart - but maybe just survive out of 'natural selection'.
Cancer isn't just one type of cell replicating itself over and over. It's a product of an immune system that fails to recognize a damaged cell. My left breast had er-/pr- grade 3, IDC. My right breast had er+/pr- moderately differentiated DCIS. When I found out about that, I was like how? How could I be er-/pr- in one breast and er+/pr- in the other? It wasn't about the cancer... It was about my immune systems inability to recognize bad cells. Our normal cells are constantly learning how to overcome viruses and all sorts of stuff. The immune system seems smart when it comes to foreign attack (in a lot of cases). But when it comes to our own body malfunction, it struggles - especially when our genetics aren't perfect.
We already know that cells have a LOT of receptors on their surface. HER2/neu is just one of them. But for those of us who are HER2+++, that's great right? Think about this made up example for a minute:
I would think Herceptin Ineffectiveness is a mechanism where those tumor cells (in their active state) whose cell surface makeup has a few more IGF-IR receptors, survive and replicate after Herceptin has blocked all of the HER2 receptors on its surface. Even though the HER2 receptors are plugged, the immune system doesn't necessarily kill the cell. For many of us, the chemotherapy is what goes in and kills all the fast dividing cells. Just because the receptors are blocked, doesn't mean the cell is dead.
Those cells that have almost all HER2 receptors are killed (while in their active state), because chemo comes in and recognizes it as a fast dividing cell. While on Herceptin alone, the stuff that's maybe got some IGF-IR receptors - could live (if not in their active state, maybe while in their inactive state. I am on the side of the fence of oncology theory that believe cancer cells 'hide' while in their stem cell slowly dividing state - which is why they evade chemotherapy). As those cells live, I think more are replicated with 'possibly' more of those type of IGF-IR receptors. As all the HER2 receptors start to disappear (because those cancer cells were killed - either because they had no receptors left or the chemo killed them) - we get cancer cells that continue to divide - even while taking Herceptin. <Maybe the HER2/neu receptors are being blocked, but the IGF-IR unblocked receptors allow the cell to survive and divide?>
Is it plausible?
<I used IGF-IR just because it's a hot topic and I can't remember all the other ones abbreviations>