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>AA said: Deb: As I understand it, TOPO IIA testing doesn't require a fresh sample, and someone did post recently that a test for it has been approved... You know quite a bit about the process behind clinical trials, and I am wondering whether it would provide reasonably important information to collect a representative group of those of us who "missed out" on traztuzumab and test us to get more of an idea how relevant TOPO IIa testing actually is?
I don't know, AA. If Slamon is correct, it would mean that at least in countries where Herceptin is available, topoIIa status is a moot point (ie: not relevant at all). He uses it only to make his case that anthracyclines have no place in current treatment, when he shows that the stats that appeared to show an increased benefit of anthracycline for all breast cancer, or even for all HER2+ breast cancer, were not truly showing it for all. They were reflecting a large increased benefit for topoIIa+ cancers and none at all for the rest. The increased benefit in that small group was strong enough, however, to skew the stats for all. And at that time, we didn't even know the subgroup existed. (I wonder how many other subgroups we'll learn of over time - that we don't have a clue about today).
I wondered if there might be some link between topoIIA+ and response to Herceptin, since there seemed to be no subgroup of Slamon's cited studies where there was an additional benefit for an anthracycline with Herceptin, even though we know that only about 1/2 of HER2+ cancer responds to Herceptin. So in that 1/2 that doesn't respond, shouldn't we see 1/3 of that 1/2 (1/6 of all HER2+, if it's randomly associated) who did get an additional benefit from the anthracycline? Maybe it's too small a group to show significance, or maybe being topoIIa+ has something to do with Herceptin response? I'm sure that they looked at that, so the answer must be - no association between topoIIa status and Herceptin response.
I wish that I knew more about clinical trials. NBCC has a Project LEAD course on clinical trials, held every two years, and I think it begins in early November. Is anyone on this list attending?
> AA: Wouldn't it also help in deciding whether (or not) to do other therapies? Wouldn't it also provide some insight into whether there are HER2 positives who both did not get trastuzumab AND are not Topo II and have not recurred?
As I said above, I don't think that it has any relevance, if Slamon is correct. Again, most any information about those who didn't get Herceptin is now moot, in our country at least. I would be interesting to those of us who didn't get it, but the information would have no practical application. That also applies to discussions of "late" trastuzumab. Science has moved on (and left you and me in the dust).
I'm curious (if you don't my telling us) why you did not take your onc up on the offer to do late Herceptin? Was it cost? Or some other hesitation?
I'm not sure what you're asking when you ask for technical information about why trastuzumab works better with a chemo. You mean the biological/cellular explanation? I don't know. It would involve one of those complex growth pathway diagrams that make my head hurt. And as far as synergy, I don't know that they do understand the phenomenon at cellular level - they are simply able to measure it from clinical observation. But I could be wrong.
Do you remember in the movie, Slamon/Connick said something about Herceptin being able to keep disease stable but not able to shrink it? Maybe that's why it's better with a chemo? Most of the targeted therapies (Avastin, Tykerb) seem to work better, or work only, with a chemo. I don't know the answers. But the questions are interesting.
Debbie Laxague
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