Postby GrouseMan » Fri Feb 15, 2019 5:06 pm
His tumors over express EGFr according to this. So its over producing the receptor and EGF protein around slips into it and turns it on. Its a driver of tumor growth. Thus inhibition of EGFr slows growth. If they use Erbitux it will work for a while and likely well. But eventually Erbitux starts to fail usually because the tumor finds another way to turn the EGFr receptor on by over producing closely related proteins that will also activate similar closely related ErbB's that take over the driving of growth. It doesn't require a mutation. Just extra copies. But there have been studies that show that when Erbitux fails one can quit it for a while and the tumor will revert back to becoming sensitive to it again or other similar small molecule inhibitors of EGFr. The new generation of EGFr inhibitors not only work against over expression but some also work on the mutant variants and the additional ErbB's. There are more drugs approved against EGFr for use in Lung Cancer than Colon cancer, but they should work in colon cancer as well if one can do Erbitux the others are likely to be effective also.
Here is some information about Erbitux:
https://en.wikipedia.org/wiki/CetuximabHere is some information about the EGFr (ErbB's)s:
https://en.wikipedia.org/wiki/Epidermal ... r_receptorHere is a representative example of a Third Generation EGFr inhibitor I was involved in developing:
https://en.wikipedia.org/wiki/Dacomitinibhttps://www.vizimpro.com/Good Luck
GrouseMan
DW 53 dx Jun 2013
CT mets Liver Spleen lung. IVb CEA~110
Jul 2013 Sig Resct
8/13 FolFox,Avastin 12Tx mild sfx, Ongoing 5-FU Avastin every 3 wks.
CEA: good marker
7/7/14 CT Can't see the spleen Mets.
8/16/15 CEA Up, CT new abdominal mets. Iri, 5-FU, Avastin every 2 wks.
1/16 Iri, Erbitux and likely Avastin (Trial) CEA going >.
1/17 CEA up again dropped from Trial, Mets growth 4-6 mm in abdomen
5/2/17 Failed second trial, Hospitalized 15 days 5/11. Home Hospice 5/26, at peace 6/4/2017