HER2 Support Group Forums - View Single Post - anthracyclines to become an adjuvant chemo of the past?

dlaxague · 09-21-2008, 03:58 PM

Your second link didn't work for me. The first one talked of anthracyclines in the absence of Herceptin, as nearly as I could tell from the abstract. And Slamon agrees with that, although he breaks it down further into HER+ AND topo2a+. But now that Herceptin is a standard part of adjuvant treatment for HER2+ bc - even for HER+ and topoIIa+ cancers, anthracylines do not appear to offer additional benefit over Herceptin and a nonanthracyline chemo (TCH for example).

The more that they find and break down these subgroups, the more they are finding that regimens that appeared to offer an advantage to all do not, after all, offer an advantage to many. They offer an advantage to one small subgroup but it's such a strong advantage that in the larger, less-specific group, it appeared to offer an advantage, either because they didn't break it down into subgroups, or more often, because they did not (at that time) even know that the subgroups existed. Does that make sense?

Debbie Laxague

PS: So a question has occurred to me and I haven't let it sit long enough to digest whether it makes sense. Does it make sense to you? "So – we already know that Herceptin “works” for only about half of all HER2+ cancers, for reasons yet unknown (right?). It would not be unreasonable to think that some percentage of those who do not respond to Herceptin would still be Topo2a positive and so alhough they missed Herceptin’s benefit, they could still reap an anthracycline’s improvement in DFS or OS. But it doesn’t look like that’s true, in the studies cited. Is that because we’re getting into such small subgroups that the n’s just aren’t large enough? Or is there some relationship between Topo2a overexpression and Herceptin response?"

09-21-2008, 03:58 PM	#14
dlaxague Senior Member Join Date: May 2006 Posts: 221	to chicagoetc Your second link didn't work for me. The first one talked of anthracyclines in the absence of Herceptin, as nearly as I could tell from the abstract. And Slamon agrees with that, although he breaks it down further into HER+ AND topo2a+. But now that Herceptin is a standard part of adjuvant treatment for HER2+ bc - even for HER+ and topoIIa+ cancers, anthracylines do not appear to offer additional benefit over Herceptin and a nonanthracyline chemo (TCH for example). The more that they find and break down these subgroups, the more they are finding that regimens that appeared to offer an advantage to all do not, after all, offer an advantage to many. They offer an advantage to one small subgroup but it's such a strong advantage that in the larger, less-specific group, it appeared to offer an advantage, either because they didn't break it down into subgroups, or more often, because they did not (at that time) even know that the subgroups existed. Does that make sense? Debbie Laxague PS: So a question has occurred to me and I haven't let it sit long enough to digest whether it makes sense. Does it make sense to you? "So – we already know that Herceptin “works” for only about half of all HER2+ cancers, for reasons yet unknown (right?). It would not be unreasonable to think that some percentage of those who do not respond to Herceptin would still be Topo2a positive and so alhough they missed Herceptin’s benefit, they could still reap an anthracycline’s improvement in DFS or OS. But it doesn’t look like that’s true, in the studies cited. Is that because we’re getting into such small subgroups that the n’s just aren’t large enough? Or is there some relationship between Topo2a overexpression and Herceptin response?"