What they are doing is simply looking at how well their Hh antagonist (inhibitor) is working. For example, is it penetrating the tumor? How well is it absorbed? Does the inhibitor shrink part of the tumor? If so how much is left. With talking to friend, one of the assays they are looking at is how effective does the current Hh antagonist shut down the pathway? In the case of the Hh pathway they are actually looking at Gli/ptch expression.

If it shuts down the pathway (by observing ptch/Gli expression), then there are two options?
1) Up the frequency, prolong the duration, or formulate a new cream to up the concentration.
2) Pick a new Hh antagonist the will be more potent and shorten duration of treatment.

Or even a combo of numbers 1 and 2.

If it doesn’t shut down the pathway on BCC then:
1) Pick a new Hh antagonist that might be able to
2) Scrap the BCC program and move into solid tumors.

So depending on the tumor biology of the Hh antagonist will determine what their options are.

Also remember, Genentech and Curis are betting on BCC being DEPENDENT on the Hh pathway. Animal models say yes, human BCC samples suggest.

My honest guess would be that because it didn’t work 100% of the time on the 7 patients, they will either up the frequency of application or pick a new more potent inhibitor. I don’t think they would want to prolong the treatment because BCC is essentially already curable. This is my biased answer.

Here is a movie about transcription @
http://www.pathway2curis.com/viewtopic.php?p=211#211

In our pathway the transcription factor is Gli, Gli causes RNA polymerase to activate target genes that can cause cancer.