I am a 35 year old male with stage IV colon cancer

Joninmn
Joninmn Member Posts: 1
edited March 2014 in Colorectal Cancer #1
Hello. I was diagnosed with stage 4 colon cancer last January. Here is a quick breakdown of my experience:

Jan 16th: Diagnosed. Stage 4 with 3 mets on liver. My CEA was 11.

Jan 18th: I had 97% of my colon removed. I also had 33 lymph nodes taken out (3 out of 33 came back positive)

Jan 31st: Came home from the hospital

Feb 9th: Had my initial appointment with my oncologist. My CEA came in at 67.

Mar - May: Had my first 3 months of chemo. Each week, my CEA continued to drop. On May 31st, my CEA dropped down to 1.3

June 27th: I had a liver resection. My surgeon removed the 2 spots on my liver (the third spot was no where to be found).

Aug – Oct: I had another 3 months of chemo. My last session was on October 31st.

Nov 14th: I had another PET scan. The scan did not detect any evidence of disease.

Since May, my CEA has fluctuated between 0.9 and 1.2 Just today, my CEA came back at 1.4 I do not know if this is anything to be worried about. This is very interesting….last week, my liver specialist wanted to run some liver function tests. These tests all came back just fine. They also checked my CEA as well. This time, this particular doctor’s group used the Bayer method. This method’s normal range is 0-2.5 Under this test, my number came back at 0.5 (this was less than 10 days ago). The method that my oncologist uses calls for a normal range of 0-3. Since my 1.4 result came out of this higher range, I hope that I do not have anything to be worried about.

Thanks for your feedback,
Jon

Comments

  • KathiM
    KathiM Member Posts: 8,028 Member
    #2
    I was reassured that CEA can vary a bit between tests. Mine 'climbed' to its highest last time...1.2.....even in full stage 3 rectal cancer, mine was .7......

    I was told not to worry, and you know, I'm NOT! Neither should you, I think. I know, easier said than done...but I'm REALLY enjoying life again! It's been 2 years, 7 months NED for me....

    GREAT news on the liver function tests!!!

    Hugs, Kathi
  • Faith4Cure
    Faith4Cure Member Posts: 405 Member
    #3
    Those counts seem pretty low. I agree with Kathi, CEA tests can really fluctuate, and with those low counts I don't think it is cause to worry. I think you should celebrate being NED and enjoy the holidays!

    Faith
  • jerseysue
    jerseysue Member Posts: 624 Member
    #4
    Jeez when I was first dx my CEA was up over 300. My onc told me anything below a 5 is "normal". I'm a Stage IV since 4/05 and my CEA has been as low as 0 but I'm fighting to keep it down at this time. You sound like you are doing really well! Have a great Christmas and a Healthy New Year.
  • rmap59
    rmap59 Member Posts: 266
    #5
    Don't worry be happy!!! The CEA sounds good to me. Have a Merry Christmas and Happy New Year and keep the faith.
    Robin
  • Kanort
    Kanort Member Posts: 1,272 Member
    #6
    I agree with my fello semi-colons....your CEA will bounce around a bit. Your numbers are not worrisome, but actually very good. Enjoy your holidays and your wellness.

    Hugs,

    Kay
  • 2bhealed
    2bhealed Member Posts: 2,064 Member
    #7
    hi jon!

    Welcome to the Semi-colons. I assume you live in MN? I do.

    My tumor didn't give off a CEA so I have never had to worry about it. Seems to me that that has given me one less thing to worry about which has worked in my favor. It's a non issue. :-) So can't help you there. but I can tell you that I am a 6 year Stage 3 lymph pos colon cancer survivor having never done chemo. WOOHOO!

    that's great that you are NED (No Evidence of Disease)!

    Merry Christmas!

    peace, emily the juice chick
  • katienavs
    katienavs Member Posts: 88 Member
    #8
    Hi Jon,
    I know how you are feeling. CEA has always been an accurate indicator for me. It was 249 at diagnosis in June 2006 and as of two weeks ago it was 1.1. I was concerned about the 1.1 because that is up from 0.7 two months ago. I have been assured that this small jump means nothing and is within the normal deviation.
    I'm only 26 so I can also probably relate to a lot of the age related emotions you are having.
    Hang in there and put this small meaningless increase out of your mind for the holidays!
    Katie
  • Felixthecat
    Felixthecat Member Posts: 37
    #9
    Wishing you all the best and if all else fails, 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

    2006:Therapy of cancer by cytokines mediated by gene therapy approach.
    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16474432&dopt=Abstract
    • Gene therapy offers a new approach for treatment of cancer. Transfer of genes encoding immunostimulatory cytokines has been used with remarkable success to eliminate cancer in animals. However, clinical trials in patients with this strategy had limited efficacy. Therefore, improvement of gene transfer vector system is necessary. A hybrid viral vector, consisting of SFV replicon with either murine IL-12 or reporter LacZ gene, was constructed. This hybrid vector showed specificity and high level of expression in HCC both in vitro and in vivo. In a rat orthotropic liver tumor model, treatment of established tumors by the hybrid vector with mIL-12 gene resulted in a strong anti-tumor activity without accompanying toxicity. Subsequently, a helper-dependent adenovirus vectors containing a mifepristone (RU486) inducible system was constructed for controlled and liver-specific expression of human interleukin 12 (hIL-12) (HD-Ad/RUhIL-12) and mouse IL-12 (mIL-12) (HD-Ad/RUmIL-12). Data showed that high and sustained serum levels of hIL-12 could be attained by continuing administration of RU486 every 12 or 24 h. Repetitive induction of hIL-12 could be obtained over, at least, a period of 48 weeks after a single injection of HD-Ad/RUhIL-12. Treatment of liver metastases with of HD-Ad/RUmIL-12 plus RU846 resulted in complete tumor regression in all animals. Then, different cytokine genes were inserted into conditional replicative adenoviruses vectors (also called oncolytic adenovirus). Replication of adenovirus in tumor cells would kill tumor cells and release viruses, which infect surrounding tumor cells. The combination of cytopathic effect by oncolytic adenovirus and biological effect of transgene would exert strong antitumor activity. These new types of vectors may provide a potent and safe tool for cancer gene therapy.

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