...and I know this conflicts with the early indications of the Slamon trial. I think that the latest stats were different than the earlier ones.
Found what I read... and it was not Pegram, it was an interview with Dr. Burstein.
"DR BURSTEIN: The TOPO II issue, which has been discussed a lot since the BCIRG 006 data were presented in 2005, looks less relevant now with the 2006 data (Press 2005; Slamon 2006; [4.5, 4.6]).
The TOPO II gene is on human chromosome 17, not too far from the HER2/neu locus. In some cases of acquired HER2 gene amplification, you also have amplification of the TOPO II locus. TOPO II is a target of anthracyclines, and many people have suggested that TOPO II overexpression particularly identifies tumors that benefit from anthracyclines.
In the preliminary work from the BCIRG 006 trial that Dennis Slamon and Mike Press reported at the San Antonio meeting in 2005, they suggested that in TOPO II overexpressors, the anthracycline/ trastuzumab (AC
TH) arm was superior to the nonanthracycline/trastuzumab (TCH) arm. For the majority of tumors in which the TOPO II is not amplified, however, TCH was more or less equivalent to AC
TH (Press 2005). If in the aggregate they’re the same, it washes out the effects of the TOPO II test question. I believe if clinicians decide that they can use a nonanthracycline/
trastuzumab-based regimen, it doesn’t matter whether they perform the TOPO II testing.
In the 35 percent of cases in which the tumor was both HER2-positive and TOPO II-positive, the curves all track similarly, which is a puzzle (Slamon 2006)"
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