Fundamental paradox of survival determinism: the ur-etiology disease paradigm

Theory in Biosciences - Tập 132 - Trang 65-71 - 2012
Pavle Krsmanovic1
1Functional Architecture of the Cell (B065), German Cancer Research Centre (DKFZ), Heidelberg, Germany

Tóm tắt

Following a common practice in medicine, biomedical researches tend to view various disease conditions as direct results of preceding, disease-causing events. Such events are commonly those that could have been previously detected and which have given the history of studies of particular diseases, been previously recognized as playing an important role in an onset and/or progression of the disease in question. Although such practice is justified from the very principles of experimental investigation and scientific observation, it comes short of finding the fundamental causes behind these disease conditions. This manuscript proposes a different view to the origin of some types of diseases as well as some other biological phenomena. Namely, the focus of the concept relates to a notion of survival determinism, proposed to have been in the very core of evolution of primordial organisms. Thereby, as various disease models are discussed in the light of the proposed mechanisms for adaptation, they could be seen as relicts of the early evolutionary history of life on Earth.

Tài liệu tham khảo

Brown DR (2001) Microglia and prion disease. Microsc Res Tech 54:71–80 Brown DR, Schmidt B, Groschup MH, Kretzschmar HA (1998) Prion protein expression in muscle cells and toxicity of a prion protein fragment. Eur J Cell Biol 75(1):29–37 Clevers H (2011) The cancer stem cell: premises, promises and challenges. Nat Med 17(3):313–319 De Meyer GRY, Martinet W (2009) Autophagy in the cardiovascular system. BBA 1793:1485–1495 Duesberg P, Li R, Rasnick D, Rausch C, Willer A, Kraemer A, Yerganian G, Hehlmann R (2000) Aneuploidy precedes and segregates with chemical carcinogenesis. Cancer Genet Cytogenet 119:83–93 Feinberg AP, Ohlsson R, Heinkoff S (2006) The epigenetic progenitor origin of human cancer. Nat Rev Genet 7:21–33 Halestrap AP (2006) Calcium, mitochondria and reperfusion injury: a pore way to die. Biochem Soc Trans 34(2):232–237 Khemiri A, Jouenne T, Cosette P (2008) Presence in Legionella pneumophila of a mammalian-like mitochondrial permeability transition pore? FEMS Microbiol Lett 278:171–176 King CR, Lemmer J, Campbell JR, Atkins AR (1978) Osteosarcoma in a patient with Hutchinson–Gilford progeria. J Med Genet 15:481–484 Kono T, Yayoi O, Wu Q et al (2004) Birth of parthenogenic mice that can develop to adulthood. Nature 428(22):860–864 Koshland DE Jr (2002) The seven pillars of life. Science 295:2215–2216 Krsmanovic P (2011) Ontological hypothesis of the cancer etiology: discord between cells’ survival determinism and their disposition to biological altruism. Med Hypotheses 77(3):389–400 Maloyan A, Sanbe A, Osinska H, Westfall M, Robinson D, Imahashi K, Murphy E, Robbins J (2005) Mitochondrial dysfunction and apoptosis underlie the pathogenic process in alpha-B-crystallin desmin-related cardiomyopathy. Circulation 112(22):3451–3461 Mittwoch U (1978) Parthenogenesis. J Med Genet 15(3):165–168 Paulin D, Li Z (2004) Desmin: a major intermediate filament protein essential for the structural integrity and function of muscle. Exp Cell Res 301(1):1–7 Perng MD, Su M, Wen SF, Li R, Gibbon T, Prescott AR, Brenner M, Quinlan RA (2006) The Alexander disease-causing glial fibrillary acidic protein mutant, R416W, accumulates into Rosenthal fibers by a pathway that involves filament aggregation and the association of αB-crystallin and HSP27. Am J Hum Genet 79:197–213 Pollard JW (2004) Tumour-educated macrophages promote tumour progression and metastasis. Nat Rev Cancer 4:71–78 Prokocimer M, Davidovich M, Nissim-Rafinia M, Wiesel-Motiuk N, Bar DZ, Barkan R, Meshorer E, Gruenbaum Y (2009) Nuclear lamins: key regulators of nuclear structure and activities. J Cell Mol Med 13(6):1059–1085 Shalev SA, De Sandre-Giovannoli A, Shani AA, Levy N (2007) An association of Hutchinson–Gilford progeria and malignancy. Am J Med Genet A 143A(16):1821–1826 Slotkin RK, Martienssen R (2007) Transposable elements and the epigenetic regulation of the genome. Nat Rev Genet 8(4):272–285 Stevens LC, Varnum DS (1974) The development of teratomas from parthenogenetically activated ovarian mouse eggs. Dev Biol 37(2):369–380 Tang Y, Chen Y, Jiang H, Nie D (2010) Promotion of tumor development in prostate cancer by progerin. Cancer Cell Int 10:47 Wang J, Fan HC, Behr B, Quake SR (2012) Genome-wide single-cell analysis of recombination activity and de novo mutation rates in human sperm. Cell 150:402–412 Weisleder N, Taffet GE, Capetanaki Y (2004) Bcl-2 overexpression corrects mitochondrial defects and ameliorates inherited desmin null cardiomyopathy. PNAS 101(3):769–774