Postby GrouseMan » Thu Sep 08, 2016 9:28 pm
In my wife's case no, her oncologist has not suggested Lonsurf/TAS-102. I doubt that he knows much about it. Its not commonly used in the US yet. It seems to be much more common in Japan. Its just another cytotoxic drug that has broad systemic reactions effecting normal as well as cancerous cells. It just effects the cancer cells more because they need more raw materials to reproduce as rapidly as they do compared to normal cells. Its one of these chemical compounds that messes up the cell because it looks chemically speaking very much like Uracil a natural building block that all cells use. But since its slightly different when the cell trys to use 5-FU or the similar compounds found as part of TAS-102 drug - its messes up the synthesis of DNA and HOPEFULLY these messed up cancerous cells undergo apoptosis and are destroyed. Same thing happens in normal cells, but because they don't replicate/proliferate as rapidly sometime the damage to normal cells is lessened, but there still is damage to normal cells. We call this class of anticancer drugs Antimetabolites. So - I don't expect a big advantage switching from one Anti-metabolite drug to another, as likely the same mechanism that resulted in resistance to 5-FU will also quickly apply to Tipiracil (chemical name: 5-Chloro-6-[(2-imino-1-pyrrolidinyl)methyl]-2,4(1H,3H)-pyrimidinedione) and Trifluridine (Chemical Name: 1-[4-hydroxy-5-(hydroxymethyl)oxolan-2-yl]-5- (trifluoromethyl) pyrimidine-2,4-dione) which in combination make up TAS-102. 5-FU chemical name is: 5-Fluoro-1H,3H-pyrimidine-2,4-dione. Notice anything similar in the names? These chemical compounds have a lot in common and would be expected to be metabolized by cells very similarly.
Avastin, is a Monoclonal Anti-body that binds to VEGFA, a protein that is involved in signaling via the VEGFr receptor. By binding the protein it turns off this kinase signaling pathway. Again, normal cells interact some what with Avastin, but less so because they are NORMALLY not producing excess amounts of VEGF family of Proteins, like cancer cells do. Oxaliplatin and Irrinotecan are called DNA binders. The bind to DNA and mess up its ability to replicate. These binders usually result in a non viable cell as It can't now properly undergo replication. Though there are mechanisms by which cells can attempt to correct these situations during the replication cycle - again we hope the toxic cell killing property effects rapidly reproducing cells as opposed to normal ones again. But as you all know having taking these two drugs - there are bad side effects and that is because of their effects on normal cells, nit just the cancerous ones!
So should my wife's Oncolgist suggest TAS 102, I would want to know specifically what his rational for using it was. He would have to convince me of its merits over 5-FU.
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