Widespread Immunity to Breast and Prostate Cancers is Predicted by a Novel Model that also Determines Sporadic and Hereditary Susceptible Population Sizes

I. Kramer

Mathematical Modelling of Natural Phenomena (2010)

  • Volume: 5, Issue: 3, page 134-164
  • ISSN: 0973-5348

Abstract

top
Natural immunity to breast and prostate cancers is predicted by a novel, saturated ordered mutation model fitted to USA (SEER) incidence data, a prediction consistent with the latest ideas in immunosurveillance. For example, the prevalence of natural immunity to breast cancer in the white female risk population is predicted to be 76.5%; this immunity may be genetic and, therefore, inherited. The modeling also predicts that 6.9% of White Females are born with a mutation necessary to cause breast cancer (the hereditary form) 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 susceptible to developing breast cancer (the sporadic form). The modeling determines the required number of ordered mutations for a cell to become cancerous as well as the mean time between consecutive mutations for both the sporadic and hereditary forms of the disease. The mean time between consecutive breast cancer mutations was found to vary between 2.59 - 2.97 years, suggesting that such mutations are rare events and establishing an upper bound on the lifetime of a breast cell. The prevalence of immunity to breast cancer 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% for Whites, 50.5% for Blacks, 77.7% for Asians, and 78.6% for Indians. It is of paramount importance to delineate the mechanism underlying immunity to these cancers.

How to cite

top

Kramer, I.. "Widespread Immunity to Breast and Prostate Cancers is Predicted by a Novel Model that also Determines Sporadic and Hereditary Susceptible Population Sizes." Mathematical Modelling of Natural Phenomena 5.3 (2010): 134-164. <http://eudml.org/doc/197709>.

@article{Kramer2010,
abstract = {Natural immunity to breast and prostate cancers is predicted by a novel, saturated ordered mutation model fitted to USA (SEER) incidence data, a prediction consistent with the latest ideas in immunosurveillance. For example, the prevalence of natural immunity to breast cancer in the white female risk population is predicted to be 76.5%; this immunity may be genetic and, therefore, inherited. The modeling also predicts that 6.9% of White Females are born with a mutation necessary to cause breast cancer (the hereditary form) 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 susceptible to developing breast cancer (the sporadic form). The modeling determines the required number of ordered mutations for a cell to become cancerous as well as the mean time between consecutive mutations for both the sporadic and hereditary forms of the disease. The mean time between consecutive breast cancer mutations was found to vary between 2.59 - 2.97 years, suggesting that such mutations are rare events and establishing an upper bound on the lifetime of a breast cell. The prevalence of immunity to breast cancer 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% for Whites, 50.5% for Blacks, 77.7% for Asians, and 78.6% for Indians. It is of paramount importance to delineate the mechanism underlying immunity to these cancers.},
author = {Kramer, I.},
journal = {Mathematical Modelling of Natural Phenomena},
keywords = {cancer incidence; mutation model; immunity; sporadic; hereditary; pathways; proto-oncogene; immunosurveillance; cell lifetime},
language = {eng},
month = {4},
number = {3},
pages = {134-164},
publisher = {EDP Sciences},
title = {Widespread Immunity to Breast and Prostate Cancers is Predicted by a Novel Model that also Determines Sporadic and Hereditary Susceptible Population Sizes},
url = {http://eudml.org/doc/197709},
volume = {5},
year = {2010},
}

TY - JOUR
AU - Kramer, I.
TI - Widespread Immunity to Breast and Prostate Cancers is Predicted by a Novel Model that also Determines Sporadic and Hereditary Susceptible Population Sizes
JO - Mathematical Modelling of Natural Phenomena
DA - 2010/4//
PB - EDP Sciences
VL - 5
IS - 3
SP - 134
EP - 164
AB - Natural immunity to breast and prostate cancers is predicted by a novel, saturated ordered mutation model fitted to USA (SEER) incidence data, a prediction consistent with the latest ideas in immunosurveillance. For example, the prevalence of natural immunity to breast cancer in the white female risk population is predicted to be 76.5%; this immunity may be genetic and, therefore, inherited. The modeling also predicts that 6.9% of White Females are born with a mutation necessary to cause breast cancer (the hereditary form) 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 susceptible to developing breast cancer (the sporadic form). The modeling determines the required number of ordered mutations for a cell to become cancerous as well as the mean time between consecutive mutations for both the sporadic and hereditary forms of the disease. The mean time between consecutive breast cancer mutations was found to vary between 2.59 - 2.97 years, suggesting that such mutations are rare events and establishing an upper bound on the lifetime of a breast cell. The prevalence of immunity to breast cancer 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% for Whites, 50.5% for Blacks, 77.7% for Asians, and 78.6% for Indians. It is of paramount importance to delineate the mechanism underlying immunity to these cancers.
LA - eng
KW - cancer incidence; mutation model; immunity; sporadic; hereditary; pathways; proto-oncogene; immunosurveillance; cell lifetime
UR - http://eudml.org/doc/197709
ER -

References

top
  1. I. Kramer. 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. 
  2. I. Kramer. 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. 
  3. 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.  
  4. A. G. Knudson, Jr.Mutation and cancer: statistical study of retinoblastoma. Proc. Nat. Acad. Sci., USA, 68 (1971), No. 4, 820-823.  
  5. S. H. Friend, R. Bernards, S. Rogelj, R. A. Weinberg, J. M. Rapaport, D. M. Albert, T. P. Dryja. A human DNA segment with properties of the gene that predisposes to retinoblastoma and osteosarcoma. Nature, 323 (1986), 643-646. 
  6. A. T. Yeung, B. B. Patel, X.-M. Li, S. H. Seeholzer, R. A. Coudry, H. S. Cooper, A. Bellacosa, B. M. Boman, T. Zhang, S. Litwin, E. A. Ross, P. Conrad, J. A. Crowell, L. Kopelovich, A. Knudson. One-hit effects in cancer: altered proteome of morphologically normal colon crypts in familial adenomatous polyposis. Cancer Research, 68 (2008), 7579-7586. 
  7. S. Monfardini, E. Vaccher, G. Pizzocaro. Unusual malignant tumors in 49 patients with HIV infection. AIDS, 3 (1989), 449-452. 
  8. S.C. Remick. Non-AIDS-defining cancers. Hematol Oncol Clin North Am., 10 (1996), 1203-1213. 
  9. C. Smith, S. Lilly, K.P. Mann. AIDS-related malignancies. Ann. Med., 30 (1998), 323-344. 
  10. T.P. Cooley. Non-AIDS-defining cancer in HIV-infected people. Hematol Oncol Clin North Am., 17 (2003), 889-899. 
  11. S.M. Mbulaiteye, R.J. Biggar, J.J. Goedert. Immune deficiency and risk for malignancy among persons with AIDS. J Acquir Immune Defic Syndr., 32 (2003), 527-533. 
  12. M. Frish, R.J. Biggar, E.A. Engels. AIDS-Cancer Match Registry Study Group Association of cancer with AIDS-related immunosuppression in adults. JAMA, 285 (2001), 1736-1745. 
  13. F. Stephen Hodi, S. Granter, J. Antin. Withdrawal of immunosuppression contributing to the remission of malignant melanoma: a case report. Cancer Immunity, 5 (2005), 7. 
  14. N.F. Crum. Increased risk of prostate cancer among HIV-infected men. Contagion, Vol 2 (2005), No. 2, 66-70.  
  15. W.G. Nelson, A.M. De Maizo, W.B. Issacs. Mechanisms of disease: prostate cancer. N Engl J Med, 349 (2003), 366-381. 
  16. E.A. Platz, A.M. De Maizo. Epidemiology of inflammation and prostate cancer. J Urol, 171 (2004), S36-S40. 
  17. A.M. De Maizo, V.L. Marchi, J.L. Epstein. Proliferative inflammatory atrophy of the prostate: implications for prostatic carcinogenesis. Am J Pathol, 155 (1999), 1985-1992. 
  18. F. Steven Hodi, S. Granter, J. Antin. Withdrawal of immunosuppression contributing to the remission of malignant melanoma: a case report. Cancer Immunity, 5 (2005), 7. 
  19. J. Ruvinsky. Are You Immune to Cancer?.DISCOVER, 27 (2006), No. 8.  
  20. H. Davies. Mutations of the BRAF gene in human cancer. Nature, 417 (2002), 949-54. 
  21. M.S. Brose, P. Volpe, M. Feldman, M. Kumar, I. Rishi. BRAF and RAS mutations in human lung cancer and melanoma. Cancer Res., 62 (2002), No. 23, 6997-7000. 
  22. K.L. Novik, J.J. Spinelli, A.C. Macarthur, K. Shumansky, P. Sipahimalani, A. Lai, J.M. Conners, R.D. Gascovne, R.P. Gallagher, A.B. Brooks-Wilson. Genetic variation in H2AFX contributes to risk of non-Hodgkin lymphoma. Cancer Epidemiol Biomarkers Prev, 16 (2007), No. 6,1098-106.  
  23. H. Li, Y. Gu, B. Hukku, D.G. McLeod, T.K. Hei, J.S. Rhim. Malignant transformation of human benign prostate epithelial cells by high linear energy transfer alpha-particles. Int J. Oncol., 31 (2007), No. 3, 537-44. 
  24. P. Lichtenstein, N.V. Holm, P.K. Verkasalo, A. Iliadou, J. Kaprio, M. Koskenvuo, E. Pukkala, A. Skytthe, K. Hemminiki,. 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. 
  25. 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.]  
  26. A. Vecchione, F. Gottardo, L.G. Gomella, B. Wildemore, M. Fassan, E. Bragantini, F. Pagano, R. Baffa. Molecular genetics of prostate cancer: clinical translational opportunities. J Exp Clin Cancer Res, 26 (2007), No. 1, 25-37. 
  27. T.M. Lane, J.C. Strefford, R.J. Yanez-Munoz, P. Purkis, E. Forsythe, T. Nia, J. Hines, Y.L. Lu, R.T. Oliver. Identification of a recurrent t(4;6) chromosome translocation in prostate cancer. J Urol, 177 (2007), No. 5, 1907-12.  
  28. O. Saramaki, T. Visakorpi. Chromal aberrations in prostate cancer. Front Biosci, 12 (2007), 3287-301. 
  29. I.M. Berguin, Y. Min, B. Wu, J. Wu, D. Perry, J.M. Cline, M.J. Thomas, T. Thornberg, G. Kulik, A. Smith, I.J. Edwards, R. DÕAgnostino, H. Zhang, H. Wu, J.X. Kang, Y.Q. Chewn. Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids. J Clin Invest, 117 (2007), No. 7, 1866-75. 
  30. 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.  
  31. N. Yamamoto, H. Suyama, N. Yamamoto, N. Ushijima. Immunotherapy of metastatic breast cancer patients with vitamin D-binding protein-derived macrophage activating factor (GcMAF). Int. J. Cancer, 122 (2008), 461-467. 
  32. N. Yamamoto, H. Suyama, N. Yamamoto. Immunotherapy for Prostate Cancer with Gc Protein-Derived Macrophage-Activating Factor, GcMAF. Translational Oncology, 1 (2008), No. 2, 65-72. 
  33. N. Yamamoto. 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. 
  34. N. Yamamoto, M. Ueda. Pathogenic significance of acetylgalactosaminidase activity found in the hemagglutinin of influenza virus. Microbes and Infection, 7 (2005), No. 4, 674-681. 
  35. 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.  
  36. G.P. Dunn, L.J. Old, R.D. Schreiber. The Immunobiology of Cancer Immunosurveillance and Immunoediting. Immunity, 21 (2004), 137-148. 
  37. G.P. Dunn, A.T. Bruce, H. Ikeda, L.J. Old, R.D. Schreiber. Cancer immunoediting: from immunosurveillance to tumor escape. Nature immunology, 3 (2002), 991-998. 
  38. G.P. Dunn, C.M. Koebel, R.D. Schreiber. Interferons, immunity, and cancer immunoediting. Nat Rev Immunol., 6 (2006), No. 11, 836-48. 
  39. Q. Zhihai, T. Blankenstein. A cancer immunosurveillance controversy. Nature Immunology, 5 (2004), 3-4. 
  40. L. Zitvogel, A. Tesniere, G. Kroemer. Cancer despite immunosurveillance: immunoselection and immunosubversion. Nat Rev Immunol., 6 (2006), No. 10, 715-27. 
  41. A.E. Germenis, V. Karanikas. Immunoepigenetics: the unseen side of cancer immunoediting. Immunol Cell Biol., 85 (2007), No. 1, 55-9. 
  42. B.A. Inman, X. Frigola, H. Dong, E.D. Kwon. Costimulation, coinhibition and cancer. Curr Cancer Drug Targets, 7 (2007), No. 1, 15-30. 
  43. C. Greenman. Patterns of somatic mutation in human cancer genomes. Nature, 446 (2007), 153-158. 
  44. P. Armitage, R. Doll. The age distribution of cancer and a multi-stage theory of carcinogenesis. British Journal of Cancer, 8 (1954), No. 1, 1-12. 
  45. F. Pompei, R. Wilson. The age distribution of cancer; the turnover at old age. Health and Environmental Risk Assessment, 7 (2001), No. 6, 1619-50.  
  46. P. Armitage, R. Doll. A Two-Stage Theory of Carcinogenesis in Relation to the Age Distribution of Human Cancer. Br. J. Cancer, 11 (1957), No. 2, 161-169. 
  47. S. Moolgavkar, A. Knudson. (1981). Mutation and cancer: a model for human carcinogenesis. J. Natl. Cancer Inst., 66, No. 6, 1037-1052.  
  48. S.H. Moolgavkar, A. Dewanji, D.J. Venzon. (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.  
  49. S.H. Moolgavkar, E.G. Luebeck. (1990). Two-event model for carcinogenesis: biological, mathematical, and statistical considerations. Risk Anal., 10, No. 2, 323-341.  
  50. W.F. Heidenreich, E.G. Luebeck, S.H. Moolgavkar. (1997). Some properties of the hazard function of the two-mutation clonal expansion model. Risk Anal., 17, No. 3, 391-399.  
  51. E.G. Lueback, S.H. Moolgavkar. Multistage carcinogenesis and the incidence of colorectal cancer. PNA, 99 (2002), No. 23, 15095-15100. 

NotesEmbed ?

top

You must be logged in to post comments.

To embed these notes on your page include the following JavaScript code on your page where you want the notes to appear.

Only the controls for the widget will be shown in your chosen language. Notes will be shown in their authored language.

Tells the widget how many notes to show per page. You can cycle through additional notes using the next and previous controls.

    
                

                
Note: Best practice suggests putting the JavaScript code just before the closing </body> tag.