(Baseline subject: I was poking around looking for any natural possibilities to mimic Gefilitnib/Erlonitib in the Folica stuff.)
The Folica patents were categorically saying “must be a non-natural EGF-R inhibitor” and I had believed that at the time. I once read something suggesting that the natural EGF-R inhibiting substances we were talking about at the time were also inhibiting WNT action. I assumed that was a good enough reason (although probably not the only reason) for Folica ruling out anything but the drugs. When we were talking about all this a year or two ago, I had been more focused on the EGF-R angle and less on the WNT angle than the mood has been lately.
Recently I was surfing around for Tyrosine Kinase inhibitors (TK inhibition seems to be the front-page therapueutical reason for docs to prescribe Gefilitnib & Erlonitnib to cancer patients) and started reading about Genistein. Genistein inhibits TK. There is even some moderate discussion of its effects on cancer cells like Gefilitnib & Erlonitib.
Now I’m trying to make heads or tails of what this might mean in regards to WNT signalling. They’re mucking around with several of our usual suspects (WNT 5a & 7a, DKK-1, etc):
» (Baseline subject: I was poking around looking for any
» natural possibilities to mimic Gefilitnib/Erlonitib in the Folica
» stuff.)
»
»
» The Folica patents were categorically saying “must be a non-natural EGF-R
» inhibitor” and I had believed that at the time. I once read something
» suggesting that the natural EGF-R inhibiting substances we were talking
» about at the time were also inhibiting WNT action. I assumed that was a
» good enough reason (although probably not the only reason) for Folica
» ruling out anything but the drugs. When we were talking about all this a
» year or two ago, I had been more focused on the EGF-R angle and less on the
» WNT angle than the mood has been lately.
»
»
»
» Recently I was surfing around for Tyrosine Kinase inhibitors (TK
» inhibition seems to be the front-page therapueutical reason for docs to
» prescribe Gefilitnib & Erlonitnib to cancer patients) and started reading
» about Genistein. Genistein inhibits TK. There is even some moderate
» discussion of its effects on cancer cells like Gefilitnib & Erlonitib.
»
»
» Now I’m trying to make heads or tails of what this might mean in regards
» to WNT signalling. They’re mucking around with several of our usual
» suspects (WNT 5a & 7a, DKK-1, etc):
»
» http://www.fasebj.org/cgi/content/meeting_abstract/22/1_MeetingAbstracts/885.10
Apparently I know a LOT less than you about the WNT signalling and the “usual suspects,” but I like following Elaine Fuchs research which involves WNT signalling. I think I remember reading WNT regulates beta catenin activity. In conjuction with TCF3 and TCF4, beta catenin sends the signal for stem cells in the bulge to create a new hair follicle.
What are these other “usual suspects” believed to do in the hair business?
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