Saldaña-García MR, Saldaña-García C

Idioma: Español
Referencias bibliográficas: 38
Paginas: 219-222
Archivo PDF: 584.28 Kb.

RESUMEN

Los linfomas no Hodgkin (LNH) pertenecen a un grupo heterogéneo de neoplasias del sistema inmune, predomina el tipo de células B que representa más del 90% de los casos. El Rituximab (RTX) es un anticuerpo anti-CD20 monoclonal quimérico (ratón/humano) creado mediante Ingeniería Genética, que se ha utilizado con resultados muy alentadores en pacientes con recaída o refractarios al tratamiento de LNH de células B de bajo grado y en pacientes con recaída en etapas III/IV de linfoma folicular. Sus mecanismos de acción guardan relación con la apoptosis, la inhibición de factores de transcripción Map-quinasa, p38, el factor nuclear kappa-beta (NF-κ B), Sp-1, inhibición de genes de supervivencia de la familia Bcl-2 o YY1 que participan en la expresión del ligando de Fas. El RTX es capaz de inducir citotoxicidad dependiente del complemento y citotoxicidad celular dependiente de anticuerpos. Recientemente se postula su probable utilidad en enfermedades autoinmunes.

REFERENCIAS (EN ESTE ARTÍCULO)

1. Zelenetz A.D., et al., Non-Hodgkin's Lymphomas. J Natl Compr Canc Netw. 9(5): p. 484-560.

2. Jaffe ES, et al, World Health Organization classification of neoplastic diseases of the hematopoietic and lymphoid tissues. A progress report. Am J Clin Pathol, 1999. 111(1 Suppl 1): p. S8-12.

3. Vega MI, et al, Rituximab (chimeric anti-CD20) sensitizes B-NHL cell lines to Fas-induced apoptosis. Oncogene 2005; 24(55): p. 8114-27.

4. Alexander DD, et al, The non-Hodgkin lymphomas: a review of the epidemiologic literature. Int J Cancer, 2007. 120 Suppl 12: p. 1-39.

5. INEGI, 2007.

6. Solís-Poblano JC, C.-d.A.M.d.l.L., Pegfilgrastim en el tratamiento del linfoma no Hodgkin. Informe sobre cinco casos. GAMO Vol. 9 Núm. 3, mayo – junio 201, 2010.

7. Fisher RI, et al, Comparison of a standard regimen (CHOP) with three intensive chemotherapy regimens for advanced non-Hodgkin's lymphoma. N Engl J Med, 1993. 328(14): p. 1002-6.

8. Czuczman MS, et al, Rituximab in combination with CHOP or fludarabine in low-grade lymphoma. Semin Oncol, 2002. 29(1 Suppl 2): p. 36-40.

9. Mathe G, et al, BCG in cancer immunotherapy: experimental and clinical trials of its use in treatment of leukemia minimal and or residual disease. Natl Cancer Inst Monogr, 1973. 39: p. 165-75.

10. Mathe G, et al, Follow-up of the first (1962) pilot study of active immunotherapy of acute lymphoid leukaemia: a critical discussion. Biomedicine, 1977. 26(1): p. 29-35.

11. Hernandez-Flores G, et al, In vitro induction of apoptosis in acute myelogenous and lymphoblastic leukemia cells by adriamycine is increased by pentoxifylline. Presse Med 39(12): p. 1330-1.

12. Dominguez-Rodriguez JR, et al, In vivo inhibition by antioxidants of adriamycin-induced apoptosis in murine peritoneal macrophages. Anticancer Res 2001. 21(3B): p. 1869-72.

13. Bravo-Cuellar A, et al, Sensitization of cervix cancer cells to Adriamycin by Pentoxifylline induces an increase in apoptosis and decrease senescence. Mol Cancer. 9: p. 114.

14. Bravo-Cuellar A, et al, In vivo modification of adriamycin-induced apoptosis in L-5178Y lymphoma cell-bearing mice by (+)-alpha-tocopherol and superoxide dismutase. Cancer Lett, 2005. 229(1): p. 59-65.

15. Elmore S. Apoptosis: a review of programmed cell death. Toxicol Pathol, 2007. 35(4): p. 495-516.

16. Shi Y. Caspase activation, inhibition, and reactivation: a mechanistic view. Protein Sci, 2004. 13(8): p. 1979-87.

17. Green DR and Kroemer G. Pharmacological manipulation of cell death: clinical applications in sight? J Clin Invest, 2005. 115(10): p. 2610-7.

18. Ashwell JD, et al. Coming to terms with death: apoptosis in cancer and immune development. Immunol Today, 1994. 15(4): p. 147-51.

19. Kroemer G, et al, The biochemistry of programmed cell death. FASEB J, 1995. 9(13): p. 1277-87.

20. Packham G. and Stevenson Bodyguards and assassins: Bcl-2 family proteins and apoptosis control in chronic lymphocytic leukaemia. Immunology, 2005. 114(4): p. 441-9.

21. Schinoni MI, Parana R, and Cavalcante D. Apoptosis and progression of hepatic fibrosis in hepatitis C patients. Braz J Infect Dis, 2006. 10(2): p. 117-21.

22. Lawen A, Apoptosis-an introduction. Bioessays, 2003. 25(9): p. 888-96.

23. Vega MI, et al, Rituximab-mediated cell signaling and chemo/immunosensitization of drug-resistant B-NHL is independent of its Fc functions. Clin Cancer Res, 2009. 15(21): p. 6582-94.

24. Reff ME, et al. Depletion of B cells in vivo by a chimeric mouse human monoclonal antibody to CD20. Blood, 1994. 83(2): p. 435-45.

25. Seymour JF. New treatment approaches to indolent non-Hodgkin's lymphoma. Semin Oncol, 2004. 31(1 Suppl 2): p. 27-32.

26. Czuczman MS, et al. Treatment of patients with low-grade B-cell lymphoma with the combination of chimeric anti-CD20 monoclonal antibody and CHOP chemotherapy. J Clin Oncol, 1999. 17(1): p. 268-76.

27. Stashenko P, et al. Characterization of a human B lymphocyte-specific antigen. J Immunol, 1980. 125(4): p. 1678-85.

28. Tedder TF, McIntyre G, and Schlossman SF. Heterogeneity in the B1 (CD20) cell surface molecule expressed by human B-lymphocytes. Mol Immunol, 1988. 25(12): p. 1321-30.

29. Wines BD, et al, The IgG Fc contains distinct Fc receptor (FcR) binding sites: the leukocyte receptors Fc gamma RI and Fc gamma RIIa bind to a region in the Fc distinct from that recognized by neonatal FcR and protein A. J Immunol, 2000. 164(10): p. 5313-8.

30. Vega MI, et al. Rituximab-induced inhibition of YY1 and Bcl-xL expression in Ramos non-Hodgkin's lymphoma cell line via inhibition of NF-Κ B activity: role of YY1 and Bcl-xL in Fas resistance and chemoresistance, respectively. J Immunol, 2005. 175(4): p. 2174-83.

31. Vega MI, et al. Rituximab inhibits p38 MAPK activity in 2F7 B NHL and decreases IL-10 transcription: pivotal role of p38 MAPK in drug resistance. Oncogene, 2004. 23(20): p. 3530-40.

32. Pedersen IM, et al. The chimeric anti-CD20 antibody rituximab induces apoptosis in B-cell chronic lymphocytic leukemia cells through a p38 mitogen activated protein-kinase-dependent mechanism. Blood, 2002. 99(4): p. 1314-9.

33. Johnson P. and Glennie The mechanisms of action of rituximab in the elimination of tumor cells. Semin Oncol, 2003. 30(1 Suppl 2): p. 3-8.

34. Sinha BK, et al. Enzymatic activation and binding of adriamycin to nuclear DNA. Cancer Res, 1984. 44(7): p. 2892-6.

35. Maheo K, et al. Differential sensitization of cancer cells to doxorubicin by DHA: a role for lipoperoxidation. Free Radic Biol Med, 2005. 39(6): p. 742-51.

36. Arkfeld DG. The potential utility of B cell-directed biologic therapy in autoimmune diseases. Rheumatol Int, 2008. 28(3): p. 205-15.

37. Linker RA, Kieseier BC, and Gold R. Identification and development of new therapeutics for multiple sclerosis. Trends Pharmacol Sci, 2008. 29(11): p. 558-65.

38. Waubant E, Spotlight on anti-CD20. Int MS J, 2008. 15(1): p. 19-25.