[chrisy]

combined with my brains leaking out of my ears because of information overload!

There was so much great information again this year at SABCS. This year the symposium was also sponsored by the AACR (the cancer researchers group) so there was an increased focus on the "basic science" aspects - which I can best explain as research gaining understanding of the "how" and "why" cells function as they do.

Generally, there is again a growing trend and discussion on learning how to identify the factors which contribute to a specific cancer's behavior, then use that knowledge to find ways to "personalize" therapy based on each individual's situation. The main goal of this is to select treatments that you know will WORK for a person - thus not wasting energy, money, hair, and anxiety throwing one size fits all therapy at people.

The most talked about application of this was a presentation by Jenny Chang, looking at the differences in how herceptin and tykerb work - they both target her2 but via different mechanisms. The conclusion of her study:

Conclusions: Activation of PI3 kinase pathway is associated with trastuzumab but not lapatinib resistance. Lapatinib may affect signalling through the Ras/Raf/MAPK/ERK pathway, inhibiting cell division. Low PTEN expression was not associated with lapatinib resistance, and may explain the clinical efficacy of lapatinib in trastuzumab-resistant patients, supporting clinical trials for the combination of both agents.

The implication of this is that they will be someday be able to determine who will benefit from which drug, and target herceptin to some, lapatinib to others. There will be head to head trials of lapatinib vs. herceptin in adjuvant settings coming soon to validate this.