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"How" does relapse occur?

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  • "How" does relapse occur?

    I'm curious to know how the body relapses with TC, even 5 or more years after diagnosis and "all clear". What is the exact mechanism?

    Are there some lingering micro-metastases? I wonder how such secondary tumours appear out of nowhere. Does cancer flick some kind of "switch" in the body?
    100% classical seminoma (I-A, RTI). Surveillance (no adjuvant therapy). 4 years all-clear and hoping for many more.

  • #2
    I have an answer for you, but I'm headed out the door. I'll amend this post with the response once I get home and get the kid settled in.
    "Life moves pretty fast; if you don't stop and look around once in a while, you could miss it." -Ferris Bueller
    11.22.06 -Dx the day before Thanksgiving
    12.09.06 -Rt I/O; 100% seminoma, multifocal; Stage I-A; Surveillance; Six years out! I consider myself cured.

    Comment


    • #3
      Great question Chris!! I've often wondered how cancer can lay "dormant" for years in some cases and then just start up as if from no where. Look forward to your reply Fed.

      Cheers

      Mike
      approx. 28 April 08 - Noticed lump
      23 June 08 - Diagnosed (Yep! Left it 2 months!)
      30 June 08 - R I/O (NSGCT 90% EC Stage 1)
      28 July 08 - Start 2XBEP
      3 Sept 08 - Finished chemo

      Comment


      • #4
        I've had the same question wondering around in my head. Fred I am looking forward to your answer, and thanks for sharing this information with us.
        Aug 08 Left I/O. HCG 645, LDH 364, AFP 2.2
        Classic seminoma tumor size 5.5x 4.5 cm
        Stage pT1s
        On surveillance
        April 11 Left implant surgery
        Enlarged lymph node and rising markers 8-11
        Radiation to lymph nodes 12-11
        On surveillance

        Comment


        • #5
          As promised

          OK, I'll try not to use too much geek jargon.

          Metastasis is the sequence of steps that enable individual cells from a primary tumor to colonize other regions in the body. In general, metastases are responsible for the vast majority (>90%) of cancer fatalities because it is these growths that wreak havoc at other organ sites. Metastasis involves very complex steps, but essentially, once the primary tumor is established, localized invasion and growth leads to intravasation of individual cells (what we know around here as vascular or lymphatic invasion). Circulation is really a very hostile environment for individual cancer cells because the hydrodynamic shear forces in capillaries can tear the cells to pieces. Also, without stromal support (i.e. an anchor where they can feed), they can die of starvation. Sometimes individual cancer cells survive this hostile environment by recruiting an entourage of platelets to "escort" them through circulation. At some point, the cancer cells end up lodged in a capillary unable to move. If it doesn't die off, the cell may extravasate (leave the blood vessel) and set up shop in a foreign tissue, thus establishing a micrometastasis. Most of the times these don't survive, but if for some reason, the growth acquires the ability to colonize, then it can grow and proliferate forming a secondary growth.

          The most difficult part of this cascade is colonization. In fact, colonization is the most inefficient step in the process because the cancer cell growth must adapt to an environment that is likely very different from the site where it first appeared. Moreover, these growths start as single cells (or many individual cells that intravasate in a single file). A tumor that is about the size of a pea contains about 1 billion cells, so you can imagine how difficult it would be to find a micrometastasis consisting of just a few hundred cells in a human. Of course, this process takes a long time because it depends on many, many factors including the speed of cell division and the ability to anchor and survive. If a cell is relatively indolent and slow-growing (such as a seminoma or the US definition of a teratoma), then you can expect a successful met to take a while to get established -if at all. Other more rapidly growing and invasive cancers (such as choriocarcinoma or melanoma) are better at this.
          Last edited by Fed; 11-11-08, 10:00 PM.
          "Life moves pretty fast; if you don't stop and look around once in a while, you could miss it." -Ferris Bueller
          11.22.06 -Dx the day before Thanksgiving
          12.09.06 -Rt I/O; 100% seminoma, multifocal; Stage I-A; Surveillance; Six years out! I consider myself cured.

          Comment


          • #6
            WOW, that was very informative. It is indeed amazing how the human body works. Thanks Fed.
            Diag. 08/20/08
            Left I/O 08/22/08
            NSGCT (100% EC); Stage IA
            Adjuvant 1xBEP 10/27/08

            Comment


            • #7
              You know, I'm so damned proud to have a little Brother who is so smart, I really don't mind you wanted to be an elf
              I Love ya Lil' Bro,
              Mark
              I Love My Pack!

              sigpic

              Comment


              • #8
                WOW!!! Thanks Fed!

                Mike
                approx. 28 April 08 - Noticed lump
                23 June 08 - Diagnosed (Yep! Left it 2 months!)
                30 June 08 - R I/O (NSGCT 90% EC Stage 1)
                28 July 08 - Start 2XBEP
                3 Sept 08 - Finished chemo

                Comment


                • #9
                  Thanks Fed, this makes great sense to me and I can now understand how chemo can be used as an adjuvant therapy to drastically reduce the chances of relapse.

                  I still find it incredible that some forms of TC can relapse 10 years later! Mind you, we are used to knowing that pre-cancerous cells can also take years to develop into cancer so I guess that we should not be surprised that many processes in cancer can indeed take years at a time before they can be detected visually or by scans.

                  Cancer is obviously bad but it is also fascinating in many ways. This is why I don't view my own TC as "evil". I simply accept it for what it is and this has helped me a lot coming to terms with it.
                  100% classical seminoma (I-A, RTI). Surveillance (no adjuvant therapy). 4 years all-clear and hoping for many more.

                  Comment


                  • #10
                    Thanks for the succinct and clear explanation, Fed! This is probably one of the best overviews I've seen. What's still remarkable to me is how indolent (I kept thinking "lazy") seminoma is. My oncologist has mentioned seeing relapse out to ten years post-IO and has me on a surveillance schedule that goes out to twenty years. While the rate of relapse declines over time (I imagine it follows a Poisson distribution), it's nevertheless remarkable just how slow seminoma can be.
                    TC1: 1996, right orchiectomy, seminoma stage I 3.5 cm mass, radiation therapy (peri-aortic & pelvic 27.3 Gy)
                    TC2: 2008, left orchiectomy, seminoma stage IA 5 cm mass, left & right prostheses, AndroGel TRT, surveillance at MSKCC

                    Comment


                    • #11
                      Originally posted by ukboyuk View Post
                      Cancer is obviously bad but it is also fascinating in many ways.
                      This is exactly what drew me to the field in the first place. Now, though, it's personal .
                      Originally posted by ukboyuk View Post
                      This is why I don't view my own TC as "evil". I simply accept it for what it is and this has helped me a lot coming to terms with it.
                      To me, cancer is just a "normal" product of ordinary metabolism. It highlights the imperfections in all living things. In the end, it is what it is.
                      "Life moves pretty fast; if you don't stop and look around once in a while, you could miss it." -Ferris Bueller
                      11.22.06 -Dx the day before Thanksgiving
                      12.09.06 -Rt I/O; 100% seminoma, multifocal; Stage I-A; Surveillance; Six years out! I consider myself cured.

                      Comment


                      • #12
                        Hi Fed,
                        Thanks for the info. I too was wondering how reoccurence happens. So, is non-seminoma fast growing?
                        ~Mary Ann
                        CaregiverSon Josh 23yr Dx 3/5/08 IIIC NonSeminoma affected lung, kidney liver back & tumor/clots in vena cava & celiac artery 3/7/08 L I/O 3/30/08 PostOp surgery 4XEP (VP16 & Cisplatin) 3/12-5/25 LDH > 5000 & AFP 145 (3/5 pre-op) LDH 563 & AFP 4 (5/26 after 4Xchemo) off blood thinners 3/18/09 Surveillance per Dr E 8/4/08 *1/2012 ALL CLEAR!

                        Self 1/29/09 dx thyroid cancer metastasized to right lung 2/10 thyroid removd 4/17 rx RA131 5/11/10 &7/16/10. 1/12survellience

                        Comment


                        • #13
                          Originally posted by mahalomom View Post
                          So, is non-seminoma fast growing?
                          Embryonal carcinoma and choriocarcinoma certainly are, and because of this, relapses involving these cell types show up early (within 2 years). Yolk sac and teratoma are slower, but no less dangerous.
                          "Life moves pretty fast; if you don't stop and look around once in a while, you could miss it." -Ferris Bueller
                          11.22.06 -Dx the day before Thanksgiving
                          12.09.06 -Rt I/O; 100% seminoma, multifocal; Stage I-A; Surveillance; Six years out! I consider myself cured.

                          Comment


                          • #14
                            Interesting how a slower growing cancer leaves a longer remission "sentence" to live/cope with.
                            100% classical seminoma (I-A, RTI). Surveillance (no adjuvant therapy). 4 years all-clear and hoping for many more.

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