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  • Can TC be passed from Father to son?

    Is there any connection that if a father has TC then the son is more likely? I have heard that there is no family connection for TC, but I wanted to ask the experts here. Is my son more likely to get TC since my husband has it or are his chances the same as any young man?

    Also...I am wondering if anyone here that got TC also had a hernia? Boyce had a hernia since birth and had it repaired in his 20's. In his 30's he got TC...same side as the herina. Our doctor said there was zero connection...but I still wonder.

    Margaret
    Co-survivor with husband Boyce, Diagnosed 7-11-06, orchiectomy right testicle on 7-12-06- Stage 3A: Mixed germ cell tumor with inguinal seminomatous and kartotypic carcinoma. One tumor over 10 cm, second tumor 4 cm, Chemo 4xBEP: Bi-lateral RPLND Dec 2006, nerve sparing but left sterile.
    Current DVT
    Current testosterone replacement therapy, Testim.

    "You must abandon the life you planned, to live the life that was meant for you" ~wisdom I have learned from my family on this forum

  • #2
    I have a first cousin who also had TC, he was cured by his I/O at 19 years old- now at 38 he will ride with me in the challange. I'm hoping to get him to register into the forum.

    I've asked the docs about passing it along to my son- I never really got a good firm answer on that, just to keep aware.

    Joe
    Stage III. Embryonal Carcinoma, Mature Teratoma, Choriocarcinoma.
    Diagnosed 4/19/06, Right I/O 4/21/06, RPLND 6/21/06, 4xEP, All Clear 1/29/07, RPLND Incisional Hernia Surgery 11/24/08, Hydrocelectomy and Vasectomy 11/23/09.

    Please see a physician for medical advice!

    My 2013 LiveSTRONG Site
    The 2013 Already Balders

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    • #3
      Originally posted by Margaret
      Is there any connection that if a father has TC then the son is more likely? I have heard that there is no family connection for TC, but I wanted to ask the experts here. Is my son more likely to get TC since my husband has it or are his chances the same as any young man?
      There are studies underway trying to see if there is such a connection, but it is unlikely to be the case. It turns out that the majority of cancers do not have a hereditary component (there are exceptions; some types of breast cancer, for example, can be caused by a genetic defect that can be inherited). The origin of cancer cells is mostly due to reactions of DNA with products of normal metabolism. In the case of TC, it seems that most of the mutations that lead to pathogenesis arise in utero, and for some reason, they "wake up" and give rise to the disease.

      Originally posted by Margaret
      Also...I am wondering if anyone here that got TC also had a hernia? Boyce had a hernia since birth and had it repaired in his 20's. In his 30's he got TC...same side as the herina. Our doctor said there was zero connection...but I still wonder.
      I agree with the doc. Cancer cells arise from genetic changes, and traumas (such as a hernia) are incapable of causing changes at the DNA level.

      Hope this helps out. Fire away if you have any other questions!
      "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.

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      • #4
        From what i remember, i was told that there was a possibility that it could be genetic. They told me to make sure my brother got checked out on a regular basis because of that.
        Diagnosed 10/03/03
        I/O 10/15/03
        RPLND 1/21/04
        Completed the Boston Marathon 4/19/05
        Completed the Boston Marathon 4/17/06
        Baby Riley born on 3/29/09

        2012 Livestrong Challenge Web page

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        • #5
          I have read a lot of stuff online that says if you have had cancer you are more likely to have cancer again than someone that has never had it. What exactly do they mean by this? Our we more likely to get another type of cancer than someone who has never had caner?
          May 2000 I/O 100% Emb. Carc./June 2000 RPLND, 1 Node with Micro Involvement/ July 2000 1xBEP, 1xEP

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          • #6
            Originally posted by Fed
            There are studies underway trying to see if there is such a connection, but it is unlikely to be the case. It turns out that the majority of cancers do not have a hereditary component (there are exceptions; some types of breast cancer, for example, can be caused by a genetic defect that can be inherited). The origin of cancer cells is mostly due to reactions of DNA with products of normal metabolism. In the case of TC, it seems that most of the mutations that lead to pathogenesis arise in utero, and for some reason, they "wake up" and give rise to the disease.
            Have to disagree with you here, Fed. My husband had TC at 35 and my son at 29. My husband had risk factors, my son, none, except that his father had TC. Too much of a coincidence for it to be otherwise. There are others on the forum who had uncles and grandfathers with TC. To think that my mother-in-law and I had the same dynamics happening "in utero" with no genetic component would be bizarre. If you have a son, you should be vigilent. I wish we were. Dianne
            Last edited by Fed; 06-25-07, 08:50 PM. Reason: closed quote tags
            Spouse: I/O 8/80; embryonal, seminoma, teratoma; RPLND 9/80 - no reoccurrence - HRT 8/80; bladder cancer 11/97; reoccurrence: 4X
            Son: I/O 11/04; embryonal, teratoma; VI; 3XBEP; relapse 5/08; RPLND 6/18/08 - path: mature teratoma

            Comment


            • #7
              Originally posted by jaybird
              I have read a lot of stuff online that says if you have had cancer you are more likely to have cancer again than someone that has never had it. What exactly do they mean by this? Our we more likely to get another type of cancer than someone who has never had caner?
              I too have wondered about this JayBird...I have heard that all of us have cancer cells in our bodies...some grow and some don't. Since my husband's grew, then will cancer be more prone in other areas of his body...I have no idea?? I have also heard...but have not confirmed, that his risks of cancer in other areas is higher due to the 4 rounds of BEP. I hope this is not true, but I have read some things that lead me to believe this is the case. I do ask our doc to scan him often enough to check him but not too much because of the risks involved with too many scans. I am going to do more research so I will be more informed as to what to look out for in the future.
              Co-survivor with husband Boyce, Diagnosed 7-11-06, orchiectomy right testicle on 7-12-06- Stage 3A: Mixed germ cell tumor with inguinal seminomatous and kartotypic carcinoma. One tumor over 10 cm, second tumor 4 cm, Chemo 4xBEP: Bi-lateral RPLND Dec 2006, nerve sparing but left sterile.
              Current DVT
              Current testosterone replacement therapy, Testim.

              "You must abandon the life you planned, to live the life that was meant for you" ~wisdom I have learned from my family on this forum

              Comment


              • #8
                I wonder myself Robert. TC is so rare compared to other cancers...yet both Boyce and his childhood friend that grew up together got it. Johnny lost his battle, Boyce is beating it. We often wonder if one day in the future the headlines will read "Now confirmed, AquaFresh toothpaste is what is giving everyone cancer" ...you know...something silly that we are using or doing that if we had only known, we could have prevented.
                Co-survivor with husband Boyce, Diagnosed 7-11-06, orchiectomy right testicle on 7-12-06- Stage 3A: Mixed germ cell tumor with inguinal seminomatous and kartotypic carcinoma. One tumor over 10 cm, second tumor 4 cm, Chemo 4xBEP: Bi-lateral RPLND Dec 2006, nerve sparing but left sterile.
                Current DVT
                Current testosterone replacement therapy, Testim.

                "You must abandon the life you planned, to live the life that was meant for you" ~wisdom I have learned from my family on this forum

                Comment


                • #9
                  The National Cancer Institute says, "Brothers of men with a history of testicular cancer are at increased risk of testicular cancer. They are 8 to 10 times more likely to develop testicular cancer than are men who do not have a brother with testicular cancer. Men with a father who has had testicular cancer are 4 times more likely to develop testicular cancer than men who do not have a father with a history of testicular cancer."
                  Scott, [email protected]
                  right inguinal orchiectomy 6/5/2003 > nonseminoma, stage I > surveillance > L-RPLND 6/24/2005 for recurrence, suspected teratoma but found seminoma, stage II > chylous ascites until 9/2005 > surveillance and "all clear" since


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                  • #10
                    Originally posted by Mom
                    Have to disagree with you here, Fed. My husband had TC at 35 and my son at 29. My husband had risk factors, my son, none, except that his father had TC. Too much of a coincidence for it to be otherwise. There are others on the forum who had uncles and grandfathers with TC.
                    I agree that it is a coincidence, but one cannot make a generalization from a single case -or from all of the ones in the Forum, for that matter. So far I have not seen a single paper that makes the connection between a gene and TC, and I won't buy it until such a link is established. A link of this sort that has been established is the case of BRCA1/2 and breast cancer, but this still accounts for a very small percentage of those cancers. Most of the evidence is based on statistics, and while that is adequate for the evaluation of propensities towards the disease, it hardly proves that there is a genetic link.

                    Originally posted by Mom
                    To think that my mother-in-law and I had the same dynamics happening "in utero" with no genetic component would be bizarre.
                    By in utero I meant the "time frame" in which it happens (i.e. during gestation), not that it was a consequence of the local environment. Proof of this is the existence of extragonadal germ cell tumors. The reason some people have mediastinal or retroperitoneal primaries is because they are "planted" during the development of the fetus (i.e. cells left behind).

                    Originally posted by Mom
                    If you have a son, you should be vigilent. I wish we were.
                    My take on this is if you are a guy, you should be vigilant anyways.

                    I hope this clears up my take on the situation. On a similar vein, I am trying to get a hold of a lecture recently given by Dr. David Nathan, the former president of Dana-Farber. He recently wrote a book for the general public on the evolution of cancer therapies, and he gave a video lecture to everyone at DFCI last week. It was fantastic, and it addresses issues relevant to the origin of cancer and how people are trying to figure out how this monstrosity comes to be. I am waiting to hear from Dr. Nathan's office to see if I can post it here in the Forum. Stay tuned.
                    "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


                    • #11
                      Originally posted by Robert2112
                      Why does someone who never smokes, get lung cancer, and a person who smoke 100 packs a day doesn't?
                      Funny you bring this particular circumstance to light. When I started working at DFCI 4 years ago, I was collaborating with a postdoc (my current boss) who was being trained at the time by Stan Korsmeyer. Stan was the guy that discovered that a majority of cancer cells survive because they lose the ability to detect errors in their metabolism that signal a damaged cell to die, a process called "apoptosis". This seminal discovery was mentioned consistently as worthy of a Nobel Prize. In mid-2004, Stan developed non-small cell lung carcinoma, and he died in March of 2005. The man never smoked a cigarette in his life.

                      There are certainly many factors that come into play in the transformation of a normal cell into a cancer cell. Like I mentioned above, normal cellular metabolism, in particular oxidative processes like digestion and the like, can produce toxic species. Likewise, other exogenous factors can cause damage, with tobacco smoke and gamma rays from the sun being the most common culprits. DNA is prone to oxidation, and such oxidative processes can lead to mutations. A large percentage of human DNA is "junk", meaning that it doesn't really encode anything, so mutations in these areas won't cause any discernible damage. When the mutations start piling up, cancer may develop. If you notice, the vast majority of cancer patients are older (just go to any cancer ward, and you'll see what I mean), and this is because they have been exposed to the by-products of metabolism and other environmental factors for a longer period of time.

                      Why is there a rise in TC? Who knows... I've wondered that myself: what incident caused my seminoma to "wake up" and start doing its thing. There's no way for me to know, and realistically, I will likely never know why this happened. I hate to say it (because this is about the most non-scientific argument you'll here from my end), but it is what it is. It would be torture to be dwelling on that thought and personally, as a scientist, I would be "driving myself nut" if I did.

                      I know this answer might be unsatisfactory (in fact, it's hardly an answer), but there's just so much we don't know that I am trying to be cautions making any generalizations.
                      "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
                        There's an article on this page of our site that should probably be removed. The TCRC says, "There are a number of articles on the Internet discussing the discovery of a testicular cancer gene in 2000. Unfortunately, it was later shown that this finding was caused by a problem with the data set in the analysis. When that error was corrected, the evidence for the testicular cancer gene disappeared."
                        Last edited by Scott; 06-25-07, 09:54 PM.
                        Scott, [email protected]
                        right inguinal orchiectomy 6/5/2003 > nonseminoma, stage I > surveillance > L-RPLND 6/24/2005 for recurrence, suspected teratoma but found seminoma, stage II > chylous ascites until 9/2005 > surveillance and "all clear" since


                        Your donation funds Livestrong services for people facing cancer now. Please sponsor my ride!

                        Comment


                        • #13
                          Familial testicular cancer: Interest in genetic testing among high-risk family member

                          I posted this to the research library a while back. The study is ongoing. I believe Huckchef (Brian) some others mentioned being involved or wanting to be. Other published studies suggest a possible link, but nothing that really backs it up. For Dianne (Mom) with a husband and son hit by this, it's hard to think it's chance. I think it's too early in the game to make a call, but my husband was cautioned to warn his twin about being extra attentive. Time and a whole lot of data will hopefully clarify, but I agree with Fed that regardless of genetics, every guy should pay attention to the "boys".



                          Genet Med. 2006 Dec;8(12):760-770.
                          Familial testicular cancer: Interest in genetic testing among high-risk family members.Peters JA, Vadaparampil ST, Kramer J, Moser RP, Court LJ, Loud J, Greene MH.
                          1 Clinical Genetics Branch (CGB), Division of Cancer Epidemiology and Genetics (DCEG), National Cancer Institute (NCI), National Institutes of Health (NIH), DHHS, Rockville, Maryland; 2 Department of Interdisciplinary Oncology, College of Medicine, University of South Florida, Tampa, Florida; 3 Division of Cancer Control and Special Populations (DCCPS), NCI, NIH, DHHS, Rockville, Maryland; 4 Currently at Caldera Pharmaceuticals, Los Alamos, New Mexico.

                          PURPOSE:: This study is part of an ongoing National Cancer Institute multidisciplinary, etiologically-focused, cross-sectional study of Familial Testicular Cancer (FTC). The current report targets interest in clinical genetic testing for susceptibility to FTC. METHODS:: Demographics, knowledge, health beliefs, and psychological and social factors were evaluated as covariates related to interest in genetic testing. RESULTS:: The majority (66%) of 229 participants (64 affected men, 66 unaffected men, and 99 women) from 47 multiple-case FTC families expressed interest in having a genetic test within 6 months, should such a test become available. Interest was similar among the three subgroups mentioned above. Worries about insurance discrimination based on genetic test results were associated with a significantly lower interest in testing. Alternatively, participants were more likely to be interested in genetic testing if they were younger and had higher levels of family support, a physician's recommendation supporting testing, cancer distress, and a need for information to inform the health care of their children. CONCLUSIONS:: This study reveals social and relationship factors that FTC survivors and their relatives considered important when contemplating the use of new genetic technologies. This is the first study describing hypothetical interest in genetic testing for familial testicular cancer.
                          Retired moderator. Husband, left I/O 16Dec2005, stage I seminoma with elevated b-HCG, no LVI, RTx15 (25Gy). All clear ever since.

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                          • #14
                            I probably should have said "pro-active" instead of "vigilant." I just don't believe in coincidences of this nature. I don't have the education or the knowledge in this area, but I do have the wisdom.
                            Spouse: I/O 8/80; embryonal, seminoma, teratoma; RPLND 9/80 - no reoccurrence - HRT 8/80; bladder cancer 11/97; reoccurrence: 4X
                            Son: I/O 11/04; embryonal, teratoma; VI; 3XBEP; relapse 5/08; RPLND 6/18/08 - path: mature teratoma

                            Comment


                            • #15
                              Originally posted by Scott
                              There's an article on this page of our site that should probably be removed. The TCRC says, "There are a number of articles on the Internet discussing the discovery of a testicular cancer gene in 2000. Unfortunately, it was later shown that this finding was caused by a problem with the data set in the analysis. When that error was corrected, the evidence for the testicular cancer gene disappeared."
                              Ahhhh Scott, you edited your post faster than I could post a more recent and contradictory study...below.


                              Hum Mol Genet. 2006 Feb 1;15(3):443-51. Epub 2006 Jan 11. Links
                              Genome-wide linkage screen for testicular germ cell tumour susceptibility loci.Crockford GP, Linger R, Hockley S, Dudakia D, Johnson L, Huddart R, Tucker K, Friedlander M, Phillips KA, Hogg D, Jewett MA, Lohynska R, Daugaard G, Richard S, Chompret A, Bonaïti-Pellié C, Heidenreich A, Albers P, Olah E, Geczi L, Bodrogi I, Ormiston WJ, Daly PA, Guilford P, Fosså SD, Heimdal K, Tjulandin SA, Liubchenko L, Stoll H, Weber W, Forman D, Oliver T, Einhorn L, McMaster M, Kramer J, Greene MH, Weber BL, Nathanson KL, Cortessis V, Easton DF, Bishop DT, Stratton MR, Rapley EA.
                              Genetic Epidemiology Division, Cancer Research UK Clinical Centre, St James's University Hospital, Leeds,UK.

                              A family history of disease is a strong risk factor for testicular germ cell tumour (TGCT). In order to identify the location of putative TGCT susceptibility gene(s) we conducted a linkage search in 237 pedigrees with two or more cases of TGCT. One hundred and seventy-nine pedigrees were evaluated genome-wide with an average inter-marker distance of 10 cM. An additional 58 pedigrees were used to more intensively investigate several genomic regions of interest. Genetic linkage analysis was performed with the ALLEGRO software using two model-based parametric analyses and a non-parametric analysis. Six genomic regions on chromosomes 2p23, 3p12, 3q26, 12p13-q21, 18q21-q23 and Xq27 showed heterogeneity LOD (HLOD) scores of greater than 1, with a maximum HLOD of 1.94 at 3q26. Genome-wide simulation studies indicate that the observed number of HLOD peaks greater than one does not differ significantly from that expected by chance. A TGCT locus at Xq27 has been previously reported. Of the 237 pedigrees examined in this study, 66 were previously unstudied at Xq27, no evidence for linkage to this region was observed in this new pedigree set. Overall, the results indicate that no single major locus can account for the majority of the familial aggregation of TGCT, and suggests that multiple susceptibility loci with weak effects contribute to the disease.
                              Retired moderator. Husband, left I/O 16Dec2005, stage I seminoma with elevated b-HCG, no LVI, RTx15 (25Gy). All clear ever since.

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