clinical trial

i just completed that trial last month! i did it at providence hospital in portland, oregon. i think there are eleven participating hospitals in the country and that was the closest one to me. i had to go up there every month for four months for injections. i was randomized into the half of the study where the vaccine was coupled with my own dendritic cells. this means that a month before the first injection they used leukopheresis to take a lot of my white blood cells and they "matured" them in a lab making them super effective dendritic cells. they then mixed that with the vaccine and gave it to me through an injection in my leg once a month for four months. there are possible side effects but i never felt any of them. i always felt just fine afterward. only thing was a site reaction, my leg would turn red and hard where they did the injection.
i am happy to talk to you more about this trial over the site email.
the reason i was so happy to participate in the trial is that i didn't want to quit fighting the battle. i was able to get to NED from stage iv and wanted to do as much as possible to keep the cancer from coming back. i really hope this trial helps!!!!

zhguo48 said:

Hi, Katienavs,
Thank you so much for your kind reply that is exactly what I want know. I will go to MD Anderson in Houston to take a part of this trial after the holidays. They told me that I need to be screend/examed before they make sure that I am indeed qualified for this trial. Your message made me feel much more comfortable about this cancer vaccine. I was concerned a lot about its potential benefit v.s. side effect, as well as if it is worth of the long distance traveling (8-hour driving).
I would be more than happy to keep in touch with you via e-mail. I will let you know when I get back for Houston.

it was far for me too, i had to fly up there from sacramento. i think it was so worth it though. good luck and please keep in touch! i would love to hear how it goes and hear what the oncologist at MD Anderson tells you to compare with what the oncologist at Providence told me.

Another drug you could try. 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