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jcavanaugh
Posts: 100
Joined: Mar 2004

Well, I knew this day would come. After 6 years, we have run out of drugs. We thought that Hopkins could help us but all they offered was a clinical trial. We really do not want this. I called Cancer Treatment Centers of America and spoke to a wonderful gentlemen who told me to go to ever major cancer treatment center in America if I had to because there is a lot of stuff out there besides clinical trials. He said that even drugs my dad has had some success with before can be delivered in a alternative way to help him now. He told me that people in similar situations came to them and they were able to put them in remission. Unfortunately, my parents are very stubborn. My mom worries about medicare and cost and my dad is not one to be aggressive when it comes to fighting this disease. I feel as if I am the only one fighting for him. I want them to pursue other institutions. My mom mentioned to the local oncologist that we had thought about going to M.D. Anderson and he said that there was nothing they could do for us (waste of time). How does he know? Any thoughts???

Jennifer

KathiM's picture
KathiM
Posts: 8077
Joined: Aug 2005

Jennifer,

In the final analysis, the old adage of 'lead a horse to water...' holds. The biggest weapon in the fight against cancer is the survivor's will to fight. I'm not saying to give up, but you MUST talk turkey to your dad about his desire to continue to fight. One memorable time I had, when I gave up, someone asked me if I was ready to lose....'WHAT?', I said....'Of course not...but I am just so tired!'. So I rested a bit, and fought again.

I must side with CTCA....it's amazing how little the cancer treatment world shares with each other!!!! ESPECIALLY the oncologists....and also look what happened recently when someone was told she had DAYS to live, that they were tapering off her drugs....and she is better than ever!

But, listen to you dad...ask the question...he may be done....I don't know....without his support in the fight, well, it's much harder to win....

Hugs, Kathi

valeriec's picture
valeriec
Posts: 350
Joined: Oct 2006

Jennifer,
I must agree with Kathi....talk "turkey" with your dad. See if he is still willing to fight. If he is, I have also heard of re-visiting chemos that have been used in the past and it actually working. In my mom's case, she was afraid and too tired to try the third line chemo, and she never did start it....I respected her choice to stop chemo, but that said, it was very hard. I, too, felt like at times I was the only one fighting for my mom, but as Kathi said, with out their support, it is much harder to win. Do I wish I could change things with my mom?? Sure, I do. But we all play the hand we were dealt and do the best we can. Please, have a heart to heart with both your parents. Stay strong for them.
Valerie

Felixthecat
Posts: 37
Joined: Dec 2007

The drug referred to below is only available via the FMFs Compassionate Use Program so if other treatments are unsuccessful you could contact them and try it. It is a hormone antagonist and quite well tolerated as meds go:

Their website link is:
http://feminist.org/rrights/compassionateuse.asp

2004: Effects of mifepristone on proliferation of human gastric adenocarcinoma cell line SGC-7901 in vitro.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15309708&itool=iconfft&query_hl=20&itool=pubmed_docsum
Mifepristone effectively inhibited the proliferation of PR-positive human gastric adenocarcinoma cell line SGC-7901 in vitro through multiple mechanisms, and may be a beneficial agent against human adenocarcinoma

2004: (Detailed article) Reversal of multidrug resistance in drug-resistant human gastric cancer cell line SGC7901/VCR by antiprogestin drug mifepristone
http://www.thymic.org/thypdf/biol/mif2.pdf

2004: Reversal of multidrug resistance in drug-resistant human gastric cancer cell line SGC7901/VCR by antiprogestin drug mifepristone
http://www.wjgnet.com/1007-9327/abstract_en.asp?v=10&f=1722
Mifepristone has potent reversal effect on MDR in SGC7901/VCR via inhibiting the function of MRP and P-gp, modulating the expression of Bcl-2 and Bax proteins, and enhancing the sensitivity to anticancer agent VCR

2004: Inhibitory effects of mifepristone on the growth of human gastric cancer cell line MKN-45 in vitro and in vivo.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15669177&itool=iconabstr&query_hl=20&itool=pubmed_docsum
Mifepristone exerts significant growth inhibitory effects on PR-positive human MKN-45 gastric cancer cells via multiple mechanisms, and may be a beneficial agent against the tumor.

2004: Effects of mifepristone on invasive and metastatic potential of human gastric adenocarcinoma cell line MKN-45 in vitro and in vivo.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15188494&dopt=
• “Mifepristone can effectively inhibit the invasive and metastatic potential of human gastric adenocarcinoma cell line MKN-45 in vitro and in vivo through inhibition of heterotypic adhesion to basement membrane, cell migration and angiogenesis.”

2003: Glucocorticoid Cotreatment Induces Apoptosis Resistance toward Cancer Therapy in Carcinomas1
http://cancerres.aacrjournals.org/cgi/content/full/63/12/3112

GCs are widely used in high doses in the therapy of leukemias and lymphomas and are also used as antiemetics or preservatives for normal cells during chemotherapy of solid tumors. In addition, GCs are among the most widely used anti-inflammatory drugs. In this study, we have shown that application of GCs renders certain tumors resistant or less susceptible to apoptosis after cancer therapy. This finding urges to carefully reconsider the widespread use of GCs in almost all treatment protocols for patients with solid cancers. In the clinical setting of cancer therapy, e.g., in antiemetic regimens, corticosteroids are usually given transiently to suppress acute side effects of cancer therapy. Although our experiments did not mimic precisely the clinical situation because we administered DEX daily to achieve steady-state levels, short-term exposure to DEX may nevertheless be sufficient to abrogate or diminish the efficacy of concomitant chemotherapy in cancer patients in vivo. This is suggested by our experiments where DEX was found to down-regulate basal and cisplatin-induced expression of apoptosis effectors within 24 h in vitro. Also, endogenous levels of GCs and those existing as a consequence of administered hormones may render solid tumors less susceptible to apoptosis after cancer therapy. The administration of steroid/receptor agonists such as RU486 might be beneficial before chemotherapy and radiotherapy to enhance cell death of solid tumor cells

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