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julierene · 09-06-2006, 07:39 PM

One of the BIG things that aren't in this are :

1. What chemo/treatment are these women on?

Another BIG PROBLEM is that everyone has a different biology and genetic makeup that makes their cancer cells respond differently to the different treatments. I would make 1 assumption from this study. High CTC's are only indicitating poor survival because they aren't finding the targeted therapies that work for these women.

Once the CTC cell lands, they take on different charachteristics that are more easily combatable for targeted therapies to work. Right now, doctors don't have very good ideas for what drugs work best for people. We have a handful of things we can test for like HER2 and hormone status, but not everyone responds the same even if they have the same markers. It's a big puzzle - STILL. CTC's I have heard are the traveling cancer cells in the blood. High levels of CTC's just mean that the disease isn't under control YET. If you have a treatment that works great for you, you can potentially go back to it later down the line. I responded so well to Herceptin/Carboplatin/Taxol that he wants to use it if I am NED for over a year and a half. My PET was completely clear after only 3 months. My CA 27/28 went from 12 at that point when I was clear, to 9 just 3 months later. This treatment worked REALLY well for me. BUT... I can almost guarantee I had a high level CTC before I started the treatment. I had a Stage 2a that was supposedly clear everything - but the CTC probably is why it traveled. I wish I had that test before to try to have the chance to lower the numbers. But I hear that doctors have theorized that CTC's are in a "stem cell kind of state". During that state, it's hard for the chemo to work because it's not a "fast dividing cell at that point". It only becomes a fast dividing cell when it lands. So don't get freaked, just work on finding a treatment that gives good results on your PET scans.

Tykerb just came out with some really exciting news, have you looked into getting onto a trial with that? What a novel idea of fighting HER2 inside the cell while Herceptin is fighting the outside receptors!!!

http://www.clinicaltrials.gov/ct/sho...225758?order=2 Check this one out.

Hang in there! Julie

09-06-2006, 07:39 PM	#11
julierene Senior Member Join Date: Dec 2005 Location: Illinois Posts: 327	One of the BIG things that aren't in this are : 1. What chemo/treatment are these women on? Another BIG PROBLEM is that everyone has a different biology and genetic makeup that makes their cancer cells respond differently to the different treatments. I would make 1 assumption from this study. High CTC's are only indicitating poor survival because they aren't finding the targeted therapies that work for these women. Once the CTC cell lands, they take on different charachteristics that are more easily combatable for targeted therapies to work. Right now, doctors don't have very good ideas for what drugs work best for people. We have a handful of things we can test for like HER2 and hormone status, but not everyone responds the same even if they have the same markers. It's a big puzzle - STILL. CTC's I have heard are the traveling cancer cells in the blood. High levels of CTC's just mean that the disease isn't under control YET. If you have a treatment that works great for you, you can potentially go back to it later down the line. I responded so well to Herceptin/Carboplatin/Taxol that he wants to use it if I am NED for over a year and a half. My PET was completely clear after only 3 months. My CA 27/28 went from 12 at that point when I was clear, to 9 just 3 months later. This treatment worked REALLY well for me. BUT... I can almost guarantee I had a high level CTC before I started the treatment. I had a Stage 2a that was supposedly clear everything - but the CTC probably is why it traveled. I wish I had that test before to try to have the chance to lower the numbers. But I hear that doctors have theorized that CTC's are in a "stem cell kind of state". During that state, it's hard for the chemo to work because it's not a "fast dividing cell at that point". It only becomes a fast dividing cell when it lands. So don't get freaked, just work on finding a treatment that gives good results on your PET scans. Tykerb just came out with some really exciting news, have you looked into getting onto a trial with that? What a novel idea of fighting HER2 inside the cell while Herceptin is fighting the outside receptors!!! http://www.clinicaltrials.gov/ct/sho...225758?order=2 Check this one out. Hang in there! Julie __________________ Jan04: Bilateral Mastectomy at age 28 Initial DX: Left Breast: IDC 2cm, Grade 3, HER2+3, 0 Nodes +, ER/PR-. Right Breast: Extensive DCIS ER-/PR+; Stage 1-2a Feb04-Apr04: 4 AC, dose dense Aug 04: 4 Taxotere Dec 05: Bone and Liver METS; Stage 4. Carboplatin/Taxol/Herceptin. DX with Li-Fraumeni Syndrome Apr 06: NED, maintenance Herceptin Apr 07: CA1503=14; masses in liver; Xeloda/Tykerb Nov 07: NED, Tykerb maintenance Sept 08: Liver mets again, on Tykerb/Xeloda again, CA=19 and 27 Nov 08: Progression, Tykerb/Gemzar, CA=25 Dec 08: Progression, Herceptin/Navelbine, CA=40, 57, and 130 Jan 09: Progression in bone, recession in liver, Herceptin/Carbo/Abraxane CA=135 June 09: CA27/29=24, chemo break Sept 09: Progression, CA=24, waiting on clinical trial (4 weeks no treatment) Nov 09: now have brain mets, trial "on hold", getting 14 WBR treatments starting 11/2/09 Dec 09: possible start on p53 trial Last edited by julierene; 09-06-2006 at 07:54 PM..