HER2 Support Group Forums - View Single Post - Wanted to share my miracle Herceptin Story..

Lani · 09-27-2007, 11:05 PM

I attended the lecture this afternoon--interestingly this gentleman believes there are basically two types of tumors which have multiple subsets and that her2+ tumors usually fall within what HE calls the luminal group (vs the basal group)

Interestingly he said John Park of UCSF is working on characterizing Circulating tumor cells using gene expression profiling (ie, it could be done on a blood sample rather than a biopsy), but he feels the way CTCs are often separated out from a blood sample (using an epithelial cell marker such as EpCAM) may not produce a representative sample.

His work predicts that adding a second targetted therapy to one to which a cancer can become "resistant" is a smart move in a prophylactic fashion--in the case he showed he added an AKT inhibitor to an EGFR inhibitor which markedly improved its efficacy, but of the cell lines shown, the ones for which this worked best did not seem to be her2+ cell lines.

Interestingly, he showed that EGFR content of a breast tumor by IHC does not predict those for which an EGFR inhibitor like IRESSA might be most effective, and in this example SKBr3 and BT474 (Her2+er- and her2+er+ cell lines) were among the most sensitive to IRESSA treatment.

He is looking for biomarkers predicting efficacy of IRESSA and other inhibitors underdevelopment, many of which are years from approval. But
he is involved in a faster way to screen compounds, some already on the market and FDA approved, for efficacy against various cell lines and has 5 employees working full time testing 40 compounds against a whole slew of cell lines.

Go team!

09-27-2007, 11:05 PM	#6
Lani Senior Member Join Date: Mar 2006 Posts: 4,778	Natalie, an update I attended the lecture this afternoon--interestingly this gentleman believes there are basically two types of tumors which have multiple subsets and that her2+ tumors usually fall within what HE calls the luminal group (vs the basal group) Interestingly he said John Park of UCSF is working on characterizing Circulating tumor cells using gene expression profiling (ie, it could be done on a blood sample rather than a biopsy), but he feels the way CTCs are often separated out from a blood sample (using an epithelial cell marker such as EpCAM) may not produce a representative sample. His work predicts that adding a second targetted therapy to one to which a cancer can become "resistant" is a smart move in a prophylactic fashion--in the case he showed he added an AKT inhibitor to an EGFR inhibitor which markedly improved its efficacy, but of the cell lines shown, the ones for which this worked best did not seem to be her2+ cell lines. Interestingly, he showed that EGFR content of a breast tumor by IHC does not predict those for which an EGFR inhibitor like IRESSA might be most effective, and in this example SKBr3 and BT474 (Her2+er- and her2+er+ cell lines) were among the most sensitive to IRESSA treatment. He is looking for biomarkers predicting efficacy of IRESSA and other inhibitors underdevelopment, many of which are years from approval. But he is involved in a faster way to screen compounds, some already on the market and FDA approved, for efficacy against various cell lines and has 5 employees working full time testing 40 compounds against a whole slew of cell lines. Go team!