Mechanizmy obrony przeciwnowotworowej - przyczyny niepowodzeń

• Autorzy: Madej J.A. , Madej J.P.

Warianty tytułu

EN

Antitumor defense mechanisms: The causes of failures

• Języki publikacji: PL

Abstrakty

EN

Neoplastic transformation is accompanied, among others, by the inhibition of apoptosis. Four mechanisms that allow cells to avoid apoptosis are well known: loss of APAF1 (apoptosis-inducing factor 1), up-regulation of caspase inactivating apoptosis inhibitors, expression of FasL (Fas ligands) on the cell surface, and production of caspase 8 inhibiting protein (FLIP – FADD – like interleukin – 1β converting proteins). Moreover, the roles of RB1 and TP53 genes in the neoplastic process have been described. Tumor cells can show mutations of genes responsible for the expression of proteins regulating the cell cycle and of proteins controlling apoptosis, e.g. TP53 protein. Neoplastic cells seek to avoid not only apoptosis, but also necrosis, inflammatory cells, and the reaction of the immunological system. The types of neoplastic antigens, i.e. TSA (tumor specific antigens) and TAA (tumor associated antigens), as well as the possibilities of their recognition by the organism burdened with neoplasm, have been described. Furthermore, the mechanisms of weakening the immunological response by neoplastic cells and the role of inflammatory cells and inflammatory response in destroying neoplasms (mainly the cellbased response i.e. cells such as NK, LAK, Tc, Th, and macrophages) have been presented. Macrophages have received special attention because of the role of macrophages associated with tumors (e.g. mammary gland cancer in dogs) in causing an abnormal (non-canonical) course of the Wnt pathway. Paradoxically, the immune response sometimes promotes neoplastic growth by the so-called immune facilitation effect. After the first stage (i.e. the limitation of apoptosis), the necrosis of neoplastic cells and inflammatory infiltration occur, followed by unlimited neoplastic progression due to insufficient immunological anti-neoplastic cell reaction.

Słowa kluczowe

PL

nowotwory; transformacja nowotworowa; apoptoza; hamowanie apoptozy; martwica; odpowiedz immunologiczna; antygeny nowotworowe; odpowiedz przeciwnowotworowa

• Wydawca: -
• Czasopismo: Medycyna Weterynaryjna
• Rocznik: 2015
• Tom: 71
• Numer: 09
• Opis fizyczny: s.534-542,rys.,bibliogr.

Twórcy

autor

Madej J.A.

• Zakład Patomorfologii i Weterynarii Sądowej, Katedra Patologii, Wydział Medycyny Weterynaryjnej, Uniwersytet Przyrodniczy we Wrocławiu, ul.Norwida 31, 50-345 Wrocław

autor

Madej J.P.

• Zakład Histologii i Embriologii, Katedra Biostruktury i Fizjologii Zwierząt, Wydział Medycyny Weterynaryjnej, Uniwersytet Przyrodniczy we Wrocławiu, ul.Norwida 25/27, 50-375 Wrocław

Bibliografia

• 1. Blackburn E. H.: Switching and signaling at telomere. Cell 2001, 106, 661-670.
• 2. Chaffer C. L., Weinberg R. A.: Perspective on cancer cell metastasis. Science 2011, 331, 1559-1564.
• 3. Condeelis J., Pollard J. W.: Macrophages: obligate partners for tumor cell migration, invasion, and metastasis. Cell 2006, 124, 263-266.
• 4. Domagała W., Chosia M., Urasińska E.: Podstawy patologii. PZWL, Warszawa 2010.
• 5. Eichhorst S. T., Krammer P. H.: Derangement of apoptosis in cancer. Lancet 2001, 7, 358-345.
• 6. Gołąb J., Jakóbisiak M., Lasek W., Stokłosa T.: Immunologia. Wyd. Nauk. PAN, Warszawa 2007.
• 7. Hayes D. F., Smerage J. B.: Circulating tumor cells. Prog. Mol. Biol. Transl. Sci. 2010, 95, 95-112.
• 8. Kawiak J., Hoser G.: Niektóre mechanizmy immunologiczne w nowotworach. Immunoterapia nowotworów w modelach zwierzęcych oraz w klinice. Post. Biol. Kom. 2000, supl. 15, 27, 91-101.
• 9. Kawiak J., Zabel M. (pod red.).: Seminaria z cytofizjologii. Wyd. Med. Urban&Partner, Wrocław 2002.
• 10. Król M., Mucha J., Majchrzak K., Homa A., Bulkowska M., Majewska A., Gajewska M., Pietrzak M., Perszko M., Romanowska K., Pawłowski K., Manuali E., Hellemen E., Motyl T.: Macrophages mediate a switch between canonical and non-canonical Wnt pathways in canine mammary tumors. PLOS ONE. 2014, 9, 1-13.
• 11. Król M., Pawłowski K. M., Majchrzak K., Gajewska M., Majewska A., Motyl T.: Global gene expression profils of canine macrophages and canine mammary cancer cells grown as a co-culture in vitro. Vet. Rec. 8, 2012, 1-19.
• 12. Kumar V., Cotram R. S., Robbins S. L.: Robbins Patologia. Elsevier Urban&Partner, Wrocław 2007.
• 13. Logan C. Y., Nusse R.: The Wnt sygnaling pathway in development and disease. Annu. Rev. Cell Dev. Biol. 2004, 20, 781-810.
• 14. Madej J. A.: Extracellular matrix in tumours as a source of additional neoplastic lesions – a review. Bul. Vet. Inst. Pulawy 2014, 58, 1-9.
• 15. Marcus J., Popko B.: Galactolipids are molecular determinants of myelin development and axo-glial organization. Biochim. Biophys. Acta 2002, 1573, 406-413.
• 16. Mego M., Mari S. A., Cristofanilli M.: Molecular mechanisms of metastasis – clinical applications. Cancer Cell 2010, 7, 693-701.
• 17. Newman A. C., Hughes C. C. W.: Macrophages and angiogenesis: a role of Wnt signalig. Vascular Cell 2012, 4, 13-20.
• 18. Pająk B., Orzechowski A.: FLIP – przeciwnik, który może przegrać pojedynek w walce z czynnikiemi swoiście hamującymi translację. Post. Hig. Med. Dośw. 2005, 59, 104-149.
• 19. Pollard J. W.: Macrophages define the invasive microenvironment in breast cancer. J. Leukoc. Biol. 84, 2008, 623-630.
• 20. Reed J. C.: Mechanisms of apoptosis. Am. J. Pathol. 2000, 157, 1415-1421.
• 21. Roitt I., Brostoff J., Male D.: Immunologia. PZWL, Wyd. Słowiński Verlag. Warszawa 2000.
• 22. Sawicki W., Malejczyk J.: Histologia. PZWL, Warszawa 2012.
• 23. Silbernagl S., Lang F.: Taschenatlas Phatophysiologie. 3 ed., Georg Thiema Verlag K.G. Stuttgart, Germany 2009.
• 24. Silini A., Ghilardi C., Figini S., Sangalli A., Fruscio R., Dahse R., Pedley R. B., Giavazzi R., Bani M.: Regulator of G – protein signaling 5 (RGS5) protein: a novel marker of cancer vasculate elicited and sustained by the tumor’s proangiogenic microenviroment. Cell Mol. Life Sci. 2012, 7, 1167-1178.
• 25. Vineis P., Schatzkin A., Potter J. D.: Models of cancerogenesis: a overview. Carcinogenesis 2011, 31, 1703-1709.
• 26. Wang Y.: Wnt/Planer cell polarity signaling: a new paradigm for cancer therapy. Mol. Cancer Ther. 2009, 8, 2103-2109.
• 27. Xie K., Huang S.: Regulation of cancer metastasis by stress pathways. Clin. Exp. Metastasis 2003, 20, 31-43.
• 28. Zheng L., Lee W. H.: The retinoblastoma gene: a prototypic and multifunctional tumor suppresor. Exp. Cell Res. 2001, 264, 9-15.