Two Approaches to Cancer Development
Authors:
J. Šmardová 1,2; J. Koptíková 3
Authors place of work:
Ústav patologie, LF MU a FN Brno
1; Ústav experimentální biologie, PřF MU, Brno
2; Institut biostatistiky a analýz, LF a PřF MU, Brno
3
Published in the journal:
Klin Onkol 2016; 29(4): 259-266
Category:
Přehled
doi:
https://doi.org/10.14735/amko2016259
Summary
Background:
The somatic mutation theory explaining the process of carcinogenesis is generally accepted. The theory postulates that carcinogenesis begins in a first renegade cell that undergoes gradual transformation from a healthy to a fully malignant state through the accumulation of genetic and epigenetic “hits”. This theory focuses specifically on mutations and genetic aberrations, and their impact on cells. It considers tumors as populations of sick cells that lose control of their own proliferation. The theory was put forward by Robert Weinberg and Douglas Hanahan, and is the predominant view in current cancer biology. By contrast, the tissue organization field theory proposed by Carlos Sonnenschein and Ana Soto considers loss of physiological structure and function by a tissue as key events in tumor development. According to this theory, tumors arise at a tissue rather than at a cellular level. It is based on a presumption that proliferation status, rather than quiescence, is the default position of cells in multicellular organisms.
Aim:
The article aims to provide answers to following questions: Are the views of proponents of the somatic mutation theory (the reductionists) and proponents of the tissue organization field theory (the organicists) incompatible and incommensurable, even when the mainstream of tumor biology has shifted its attention from tumor cells toward the tumor microenvironment? Where to find a third interconnecting systemic approach? Is it useful to be aware of the controversy between reductionists and organicists? What this awareness contributes to? How do these alternative views influence practical oncology and tumor biology in general?
Conclusion:
Whether the true position is held by reductionists or organicists is unimportant. What is important is to be aware of the existence of these two concepts because this knowledge makes the way we think about tumor origin and development, and how we set up and interpret our experiments, more precise.
Key words:
carcinogenesis – mutation – cell – tissues – cell proliferation – cell quiescence
This study was supported by grant of Internal Grant Agency of the Czech ministry of Health No. NT/13784-4/2012.
The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study.
The Editorial Board declares that the manuscript met the ICMJE recommendation for biomedical papers.
Submitted:
29. 7. 2015
Accepted:
27. 4. 2016
Zdroje
1. Weinberg RA. Oncogenes, tumor suppressor genes, and cell transformation: trying to put it all together. In: Brugge J, Curran T, Harlow E et al (eds). Origin of human cancer: a comprehensive review. New York: Cold Spring Harbor Laboratory Press 1991: 1– 13.
2. Weinberg RA. Coming full circle – from endless complexity to simplicity and back again. Cell 2014; 157(1): 267– 271. doi: 10.1016/ j.cell.2014.03.004.
3. Hanahan D, Weinberg RA. The hallmarks of cancer. Cell 2000; 100(1): 57– 70.
4. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell 2011; 144(5): 646– 674. doi: 10.1016/ j.cell.2011.02.013
5. Malaterre C. Organicism and reductionism in cancer research: towards a systemic approach. Int Stud Philos Sci 2007; 21(1): 57– 73.
6. Weinberg AR. Jediná odrodilá buňka. Jak vzniká rakovina. Praha: Academia 2003.
7. Sonnenschein C, Soto AM. Are times a ’changing’ in carcinogenesis? Endocrinology 2005; 146(1): 11– 12.
8. Sonnenschein C, Soto AM. The society of cells: cancer and control of cell proliferation. New York: Springer-Verlag 1999.
9. Stewart TA, Mintz B. Successful generations of mice produced from an established culture line of euploid teratocarcinoma cells. Proc Natl Acad Sci U S A 1981; 78(10): 6314– 6318.
10. Soto AM, Sonnenschein C. The somatic mutation theory of cancer: growing problems with the paradigm? Bioessays 2004; 26(10): 1097– 1107.
11. Soto AM, Sonnenschein C. Emergentism as a default: cancer as a problem of tissue organization. J Biosci 2005; 30(1): 103– 118.
12. Soto AM, Sonnenschein C. One hundred years of somatic mutation theory of carcinogenesis: is it time to switch? Bioessays 2014; 36(1): 118– 120. doi: 10.1002/ bies.201300160.
13. Maffini MV, Soto AM, Calabro JM et al. The stroma as a crucial target in mammary gland carcinogenesis. J Cell Sci 2003; 117(8): 1495– 1502.
14. Dolberg DS, Bissell MJ. Inability of Rous sarcoma virus to cause sarcomas in the avian embryo. Nature 1984; 309(5968): 552– 556.
15. Weaver VM, Petersen OW, Wang F et al. Reversion of the malignant phenotype of human breast cells in three-dimensional culture and in vivo by integrin blocking antibodies. J Cell Biol 1997; 13(1): 231– 245.
16. Nelson CM, Bissell MJ. Of extracellular matrix, scaffolds, and signaling: tissue architecture regulates development, homeostasis, and cancer. Annu Rev Cell Dev Biol 2006; 22: 287– 309.
17. LaBarge MA, Petersen OW, Bissell MJ. Of microenvironments and mammary stem cells. Stem Cell Rev 2007; 3(2): 137– 146.
18. Ghajar CM, Bissell MJ. Extracellular matrix control of mammary gland morphogenesis and tumorigenesis: insights from imaging. Histochem Cell Biol 2008; 130(6): 1105– 1118. doi: 10.1007/ s00418-008-0537-1.
19. Bissell MJ, Inman J. Reprogramming stem cell is microinvironmental task. Proc Natl Acad Sci U S A 2008; 105(41): 15637– 15638. doi: 10.1073/ pnas.0808457105.
20. Weigelt B, Bissell MJ. Unraveling the microenvironmental influnces on the normal mammary gland and breast cancer. Semin Cancer Biol 2008; 18(5): 311– 321. doi: 10.1016/ j.semcancer.2008.03.013.
21. Spencer VA, Xu R, Bissell MJ. Gene expression in the third dimension: ther ECM-nucleus connection. J Mammary Gland Biol Neoplasia 2010; 15(1): 65– 71. doi: 10.1007/ s10911-010-9163-3.
22. Bissell MJ, Hines WC. Why don’t we get more cancer? A proposed role of the microinvorement in restraining cancer progression. Nat Med 2011; 17(3): 320– 329. doi: 10.1038/ nm.2328.
23. Klausner RD. The fabric of cancer cell biology – weaving together the strands. Cancer Cell 2002; 1(1): 3– 10.
24. Hanahan D, Coussens LM. Accessories to the crime: functions of cells recruited to the tumor microenvironment. Cancer Cell 2012; 21(3): 309– 322. doi: 10.1016/ j.ccr.2012.02.022.
25. Polyak K, Weinberg RA. Transition between epithelial and mesenchymal states: acquisition of malignant and stem cell traits. Nat Rev Cancer 2009; 9(4): 265– 272. doi: 10.1038/ nrc2620.
26. Tam WL, Weinberg RA. The epigenetics of epithelial-mesenchymal plasticity in cancer. Nat Med 2013; 19(11): 1438– 1449.
27. Gupta PB, Chaffer CL, Weinberg RA. Cancer stem cells:mirage or reality? Nat Med 2009; 15(9): 1010– 1012. doi: 10.1038/ nm0909-1010.
28. Pattabiraman DR, Weinberg RA. Tackling the cancer stem cells – what chalenges do they pose? Nat Rev Drug Discov 2014; 13(7): 497– 512. doi: 10.1038/ nrd4253.
29. Chaffer CL, Weinberg RA. How does multistep tumori-genesis really proceed? Cancer Discov 2015; 5(1): 22– 24. doi: 10.1158/ 2159-8290.CD-14-0788.
30. Sonnenschein C, Soto AM. Somatic mutation theory of carcinogenesis: why it should be dropped and replaced. Mol Carcinogenesis 2000; 29(4): 205– 211.
31. Sonnenschein C, Soto AM. Theories of carcinogenesis: an emerging perspective. Semin Cancer Biol 2008; 18(5): 372– 377. doi: 10.1016/ j.semcancer.2008.03.012.
32. Kenny PA, Lee GY, Bissell MJ. Targeting the tumor microenvironment. Front Biosci 2010; 12: 3468– 3474.
33. Folkman J, Hahnfeldt P, Hlatky L. Cancer: looking outside the genome. Nat Rev Mol Cell Biol 2000; 1(1): 76– 79.
34. NOVA [homepage on the Internet]. Cancer warrior [cited 2015 June 1]. Available from: http://www.pbs.org/wgbh/nova/cancer/program.html .
35. Feinberg AP. Epigenetic stochasticity, nuclear structure and cancer: the implications for medicine. J Int Med 2014; 276(1): 5– 11. doi: 10.1111/ joim.12224.
36. Timp W, Feinberg AP. Cancer as a dysregulated epigenome allowing cellular growth advanatge at the expense of the host. Nat Rev Cancer 2013; 13(7): 497– 510. doi: 10.1038/ nrc3486.
37. Rodríguez-Paredes M, Esteller M. Cancer epigenetics reaches mainstream oncology. Nat Med 2011; 17(3): 330– 339. doi: 10.1038/ nm.2305.
38. Chlapek P, Chovanová S, Sláviková V et al. Mikroprostředí nádoru – možnost výzkumu v podmínkách in vitro. Klin Onkol 2014; 27 (Suppl): S48– S52.
Štítky
Detská onkológia Chirurgia všeobecná OnkológiaČlánok vyšiel v časopise
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