Postby GrouseMan » Sun Nov 11, 2018 11:11 am
The KRAS mutation itself does NOT rule out the use of Avastin which is an Antiangiogenic MAB. It interacts with VEGF-A and prevents solid tumors from recruiting the development of blood vessels to provide a food supply if you will. The KRAS mutation is not involved with the VEGF, FGF, PDGF pathway, but instead with the EGFr ERB2, 3, and 4 path ways. So although those papers indicate that it use in KRAS mutant cases may not have improved overall survival in these cases. It is not counter indicated, and when used with FOLFOX and FOLFIRI has been shown to have some benefit.
Good luck in your journey
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