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Widespread Immunity to Breast and Prostate Cancers is Predictedby a Novel Model that also Determines Sporadic and Hereditary Susceptible PopulationSizes

Published online by Cambridge University Press:  28 April 2010

I. Kramer
I. Kramer*
Affiliation:
Physics Department, University of Maryland Baltimore County
*
* E-mail: [email protected]
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Abstract

Natural immunity to breast and prostate cancers is predicted by a novel, saturatedordered mutation model fitted to USA (SEER) incidence data, a prediction consistent withthe latest ideas in immunosurveillance. For example, the prevalence of natural immunity tobreast cancer in the white female risk population is predicted to be 76.5%; this immunitymay be genetic and, therefore, inherited. The modeling also predicts that 6.9% of WhiteFemales are born with a mutation necessary to cause breast cancer (the hereditaryform) and, therefore, are at the highest risk of developing it. By contrast,16.6% of White Females are born without any such mutation but are nonetheless susceptibleto developing breast cancer (the sporadic form). The modeling determinesthe required number of ordered mutations for a cell to become cancerous as well as themean time between consecutive mutations for both the sporadic and hereditary forms of thedisease. The mean time between consecutive breast cancer mutations was found to varybetween 2.59 - 2.97 years, suggesting that such mutations are rare events and establishingan upper bound on the lifetime of a breast cell. The prevalence of immunity to breastcancer is predicted to be 79.7% in Blacks, 86.5% in Asians, and 85.8% in Indians.Similarly, the prevalence of immunity to prostate cancer is predicted to be 67.4% forWhites, 50.5% for Blacks, 77.7% for Asians, and 78.6% for Indians. It is of paramountimportance to delineate the mechanism underlying immunity to these cancers.

Keywords

cancer incidencemutation modelimmunitysporadichereditarypathwaysproto-oncogeneimmunosurveillancecell lifetime
Type
Research Article
Information
Mathematical Modelling of Natural Phenomena , Volume 5 , Issue 3: Mathematical modeling in the medical sciences , 2010 , pp. 134 - 164
Copyright
© EDP Sciences, 2010

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References

Kramer, I.. Evidence that natural immunity to breast cancer and prostate cancer exists in the majority of their risk populations is predicted by a novel, inherently saturated, ordered mutation model . Computational and Mathematical Methods in Medicine, 9 (2008), No. 1, 1-26.CrossRefGoogle Scholar
Kramer, I.. What triggers transient AIDS in the acute phase of HIV infection and chronic AIDS at the end of the incubation period?: A model analysis of HIV infection from the acute phase to chronic AIDS stage . Computational and Mathematical Methods in Medicine, 8 (2007), No. 2, 125-151.CrossRefGoogle Scholar
I. Kramer. Calculating the number of people with Alzheimer disease in any country using saturated mutation models of brain cell loss that also predict widespread natural immunity to the disease. Computational and Mathematical Methods in Medicine, Oct. 5, 2009.
Knudson, A. G. Jr. Mutation and cancer: statistical study of retinoblastoma . Proc. Nat. Acad. Sci., USA, 68 (1971), No. 4, 820-823. CrossRefGoogle ScholarPubMed
Friend, S. H., Bernards, R., Rogelj, S., Weinberg, R. A., Rapaport, J. M., Albert, D. M., Dryja, T. P.. A human DNA segment with properties of the gene that predisposes to retinoblastoma and osteosarcoma . Nature, 323 (1986), 643-646.CrossRefGoogle ScholarPubMed
Yeung, A. T., Patel, B. B., Li, X.-M., Seeholzer, S. H., Coudry, R. A., Cooper, H. S., Bellacosa, A., Boman, B. M., Zhang, T., Litwin, S., Ross, E. A., Conrad, P., Crowell, J. A., Kopelovich, L., Knudson, A.. One-hit effects in cancer: altered proteome of morphologically normal colon crypts in familial adenomatous polyposis . Cancer Research, 68 (2008), 7579-7586.CrossRefGoogle ScholarPubMed
Monfardini, S., Vaccher, E., Pizzocaro, G.. Unusual malignant tumors in 49 patients with HIV infection . AIDS, 3 (1989), 449-452.CrossRefGoogle ScholarPubMed
Remick, S.C.. Non-AIDS-defining cancers . Hematol Oncol Clin North Am., 10 (1996), 1203-1213.CrossRefGoogle ScholarPubMed
Smith, C., Lilly, S., Mann, K.P.. AIDS-related malignancies . Ann. Med., 30 (1998), 323-344.CrossRefGoogle ScholarPubMed
Cooley, T.P.. Non-AIDS-defining cancer in HIV-infected people . Hematol Oncol Clin North Am., 17 (2003), 889-899.CrossRefGoogle ScholarPubMed
Mbulaiteye, S.M., Biggar, R.J., Goedert, J.J.. Immune deficiency and risk for malignancy among persons with AIDS . J Acquir Immune Defic Syndr., 32 (2003), 527-533.CrossRefGoogle ScholarPubMed
Frish, M., Biggar, R.J., Engels, E.A.. AIDS-Cancer Match Registry Study Group Association of cancer with AIDS-related immunosuppression in adults . JAMA, 285 (2001), 1736-1745.CrossRefGoogle Scholar
Stephen Hodi, F., Granter, S., Antin, J.. Withdrawal of immunosuppression contributing to the remission of malignant melanoma: a case report . Cancer Immunity, 5 (2005), 7.Google ScholarPubMed
Crum, N.F.. Increased risk of prostate cancer among HIV-infected men . Contagion, Vol 2 (2005), No. 2, 66-70. Google Scholar
Nelson, W.G., De Maizo, A.M., Issacs, W.B.. Mechanisms of disease: prostate cancer . N Engl J Med, 349 (2003), 366-381.CrossRefGoogle Scholar
Platz, E.A., De Maizo, A.M.. Epidemiology of inflammation and prostate cancer . J Urol, 171 (2004), S36-S40.CrossRefGoogle ScholarPubMed
De Maizo, A.M., Marchi, V.L., Epstein, J.L.. Proliferative inflammatory atrophy of the prostate: implications for prostatic carcinogenesis . Am J Pathol, 155 (1999), 1985-1992.CrossRefGoogle Scholar
Steven Hodi, F., Granter, S., Antin, J.. Withdrawal of immunosuppression contributing to the remission of malignant melanoma: a case report . Cancer Immunity, 5 (2005), 7.Google Scholar
Ruvinsky, J.. Are You Immune to Cancer?. DISCOVER, 27 (2006), No. 8. Google Scholar
Davies, H.. Mutations of the BRAF gene in human cancer . Nature, 417 (2002), 949-54.CrossRefGoogle ScholarPubMed
Brose, M.S., Volpe, P., Feldman, M., Kumar, M., Rishi, I.. BRAF and RAS mutations in human lung cancer and melanoma . Cancer Res., 62 (2002), No. 23, 6997-7000.Google ScholarPubMed
Novik, K.L., Spinelli, J.J., Macarthur, A.C., Shumansky, K., Sipahimalani, P., Lai, A., Conners, J.M., Gascovne, R.D., Gallagher, R.P., Brooks-Wilson, A.B.. Genetic variation in H2AFX contributes to risk of non-Hodgkin lymphoma . Cancer Epidemiol Biomarkers Prev, 16 (2007), No. 6,1098-106. CrossRefGoogle ScholarPubMed
Li, H., Gu, Y., Hukku, B., McLeod, D.G., Hei, T.K., Rhim, J.S.. Malignant transformation of human benign prostate epithelial cells by high linear energy transfer alpha-particles . Int J. Oncol., 31 (2007), No. 3, 537-44.Google ScholarPubMed
Lichtenstein, P., Holm, N.V., Verkasalo, P.K., Iliadou, A., Kaprio, J., Koskenvuo, M., Pukkala, E., Skytthe, A., Hemminiki, K.,. Environmental and heritable factors in the causation of cancer - analyses of cohorts of twins from Sweden, Denmark, and Finland . N Engl J Med, 343 (2000), No. 2, 78-85.CrossRefGoogle Scholar
R.K. Nam, W.W. Zhang, D.A. Loblaw, L.H. Klotz, J. Trachtenberg, M.A. Jewett, A. Stanimirovic, T.O. Davies, A. Toi, V. Venkateswaran, L. Sugar, K.A. Siminovitch, S.A. Naroid. A genome-wide association screen identifies regions on chromosomes 1q25 and 7p21 as risk loci for sporatic prostate cancer. Prostate Cancer Prostatic Dis., 2007 Sep 18, to be published.]
Vecchione, A., Gottardo, F., Gomella, L.G., Wildemore, B., Fassan, M., Bragantini, E., Pagano, F., Baffa, R.. Molecular genetics of prostate cancer: clinical translational opportunities . J Exp Clin Cancer Res, 26 (2007), No. 1, 25-37.Google ScholarPubMed
Lane, T.M., Strefford, J.C., Yanez-Munoz, R.J., Purkis, P., Forsythe, E., Nia, T., Hines, J., Lu, Y.L., Oliver, R.T.. Identification of a recurrent t(4;6) chromosome translocation in prostate cancer . J Urol, 177 (2007), No. 5, 1907-12. CrossRefGoogle Scholar
Saramaki, O., Visakorpi, T.. Chromal aberrations in prostate cancer . Front Biosci, 12 (2007), 3287-301.CrossRefGoogle Scholar
Berguin, I.M., Min, Y., Wu, B., Wu, J., Perry, D., Cline, J.M., Thomas, M.J., Thornberg, T., Kulik, G., Smith, A., Edwards, I.J., DÕAgnostino, R., Zhang, H., Wu, H., Kang, J.X., Chewn, Y.Q.. Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids . J Clin Invest, 117 (2007), No. 7, 1866-75.CrossRefGoogle Scholar
N. Yamamoto, M. Ueda. Therapeutic Efficacy of Vitamin D-binding Protein (Gc Protein)-derived Macrophage Activating Factor (GcMAF) for Prostate and Breast Cancers. 12th International Congress of immunology and 4th Annual Conference of FOCIS, Montreal, Canada, July 18-23, 2004.
Yamamoto, N., Suyama, H., Yamamoto, N., Ushijima, N.. Immunotherapy of metastatic breast cancer patients with vitamin D-binding protein-derived macrophage activating factor (GcMAF) . Int. J. Cancer, 122 (2008), 461-467.CrossRefGoogle Scholar
Yamamoto, N., Suyama, H., Yamamoto, N.. Immunotherapy for Prostate Cancer with Gc Protein-Derived Macrophage-Activating Factor, GcMAF . Translational Oncology, 1 (2008), No. 2, 65-72.CrossRefGoogle ScholarPubMed
Yamamoto, N.. Pathogenic significance of acetylgalactosaminidase Activity found in the Envelope Glycoprotein gp160 of Human Immunodeficiency Virus Type 1 . AIDS Research and Human Retroviruses, 22 (2006), No. 3, 262-271.CrossRefGoogle ScholarPubMed
Yamamoto, N., Ueda, M.. Pathogenic significance of acetylgalactosaminidase activity found in the hemagglutinin of influenza virus . Microbes and Infection, 7 (2005), No. 4, 674-681.CrossRefGoogle ScholarPubMed
N. Yamamoto, M. Ueda. Eradication of HIV by Treatment of HIV-infected/AIDS Patients with Vitamin D-binding Protein Derivative. 12th International Congress of immunology and 4th Annual Conference of FOCIS, Montreal, Canada, July 18-23, 2004.
Dunn, G.P., Old, L.J., Schreiber, R.D.. The Immunobiology of Cancer Immunosurveillance and Immunoediting . Immunity, 21 (2004), 137-148.CrossRefGoogle ScholarPubMed
Dunn, G.P., Bruce, A.T., Ikeda, H., Old, L.J., Schreiber, R.D.. Cancer immunoediting: from immunosurveillance to tumor escape . Nature immunology, 3 (2002), 991-998.CrossRefGoogle ScholarPubMed
Dunn, G.P., Koebel, C.M., Schreiber, R.D.. Interferons, immunity, and cancer immunoediting . Nat Rev Immunol., 6 (2006), No. 11, 836-48.CrossRefGoogle ScholarPubMed
Zhihai, Q., Blankenstein, T.. A cancer immunosurveillance controversy . Nature Immunology, 5 (2004), 3-4.Google Scholar
Zitvogel, L., Tesniere, A., Kroemer, G.. Cancer despite immunosurveillance: immunoselection and immunosubversion . Nat Rev Immunol., 6 (2006), No. 10, 715-27.CrossRefGoogle ScholarPubMed
Germenis, A.E., Karanikas, V.. Immunoepigenetics: the unseen side of cancer immunoediting . Immunol Cell Biol., 85 (2007), No. 1, 55-9.CrossRefGoogle ScholarPubMed
Inman, B.A., Frigola, X., Dong, H., Kwon, E.D.. Costimulation, coinhibition and cancer . Curr Cancer Drug Targets, 7 (2007), No. 1, 15-30.CrossRefGoogle ScholarPubMed
Greenman, C.. Patterns of somatic mutation in human cancer genomes . Nature, 446 (2007), 153-158.CrossRefGoogle ScholarPubMed
Armitage, P., Doll, R.. The age distribution of cancer and a multi-stage theory of carcinogenesis . British Journal of Cancer, 8 (1954), No. 1, 1-12.CrossRefGoogle Scholar
Pompei, F., Wilson, R.. The age distribution of cancer; the turnover at old age . Health and Environmental Risk Assessment, 7 (2001), No. 6, 1619-50. CrossRefGoogle Scholar
Armitage, P., Doll, R.. A Two-Stage Theory of Carcinogenesis in Relation to the Age Distribution of Human Cancer . Br. J. Cancer, 11 (1957), No. 2, 161-169.CrossRefGoogle ScholarPubMed
Moolgavkar, S., Knudson, A.. (1981). Mutation and cancer: a model for human carcinogenesis . J. Natl. Cancer Inst., 66, No. 6, 1037-1052. CrossRefGoogle ScholarPubMed
Moolgavkar, S.H., Dewanji, A., Venzon, D.J.. (1988). A stochastic two-stage model for cancer risk assessment: I. The hazard function and the probability of tumor . Risk Anal., 8, No. 3, 383-392. CrossRefGoogle ScholarPubMed
Moolgavkar, S.H., Luebeck, E.G.. (1990). Two-event model for carcinogenesis: biological, mathematical, and statistical considerations . Risk Anal., 10, No. 2, 323-341. CrossRefGoogle ScholarPubMed
Heidenreich, W.F., Luebeck, E.G., Moolgavkar, S.H.. (1997). Some properties of the hazard function of the two-mutation clonal expansion model . Risk Anal., 17, No. 3, 391-399. CrossRefGoogle ScholarPubMed
Lueback, E.G., Moolgavkar, S.H.. Multistage carcinogenesis and the incidence of colorectal cancer . PNA, 99 (2002), No. 23, 15095-15100.CrossRefGoogle Scholar