Clinical and laboratory features of different types of interferon therapy classic Ph-negative myeloproliferative neoplasms



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Abstract

Chronic myeloproliferative neoplasms are a group of disorders characterized by clonal disturbance of pluripotent bone marrow stem cells, leading to an excessive increase in hematopoietic cells that retain the ability to differentiate. Modern screening techniques have made changes to the current view of the epidemiology of myeloproliferative neoplasms. Recently, more and more researches are found with the median age below 50 years, and sometimes less than 40 years. This circumstance determines the need to improve therapy with the use of interferon-а. A new stage in the treatment of myeloproliferative neoplasms is the use of pegylated forms of interferon. A feature of this drug is more uniform release of interferon from copolymer combinations that results in a more effective action of the basic substance, reduced maximum weekly dose of the drug, reduce the severity of side effects, better tolerability, as well as better control of the disease progression. At the moment, even the proportion of patients receiving conventional interferon-а is very small. Therapy with pegylated interferon insufficiently developed. There are only a number of retrospective studies in recent years, indicating the usefulness of pegylated interferon to control the disease and improve the prognosis. According to the work pegylated interferon therapy is the most modern and effective approach to the treatment of chronic myeloproliferative neoplasms. We have studied the possibility of using of various forms of interferon-а for the treatment of myeloproliferative neoplasms.

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About the authors

A. S Polyakov

S.M. Kirov Military Medical Academy

Saint Petersburg, Russia

V. V Tyrenko

S.M. Kirov Military Medical Academy

Saint Petersburg, Russia

Ya. A Noskov

S.M. Kirov Military Medical Academy

Saint Petersburg, Russia

D. K Zhogolev

S.M. Kirov Military Medical Academy

Saint Petersburg, Russia

A. V Kovalev

S.M. Kirov Military Medical Academy

Saint Petersburg, Russia

References

  1. Aaronson N.K., Ahmedzai S., Bergman B. et al. The European Organization for Research and Treatment of Cancer QLQ-C30: A quality-of-life instrument for use in international clinical trials in oncology. J. Nation. Canc. Instit. 1993; 85: 365-76.
  2. Bacigalupo A., Soraru M., Dominietto A. et al. Allogeneic hemopoietic SCT for patients with primary myelofibrosis: a predictive transplant score based on transfusion requirement, spleen size and donor type. Bone Marrow Transplant 2010; 45: 458-63.
  3. Barbui T., Barosi G., Grossi A. et al. Practice guidelines for the therapy of essential thrombocythemia. A statement from the Italian Society of Hematology, the Italian Society of Experimental Hematology and the Italian Group for Bone Marrow Transplantation. Haematologica 2004; 89: 215-32.
  4. Barosi G., Liberato L.N., Costa A. et al. Cytoreductive effect of recombinant a interferon in patients with myelofibrosis with myeloid metaplasia. Blut. 1989;58(6): 271-4.
  5. Bellucci S., Harousseau J.L., Brice P. et al. Treatment of essential thrombocythaemia by a 2a interferon. Lancet 1988; 2(8617): 960-1.
  6. Bleeker J., Hogan W.J. Thrombocytosis: diagnostic evaluation, thrombotic risk stratification, and risk-based management strategies. Thrombosis 2011; ID536062.
  7. Bumm T.G., Elsea C., Corbin A.S. et al. Characterization of murine JAK2V617F-positive myeloproliferative disease. Cancer Res. 2006; 66: 11156-65.
  8. Campregher P.V., de Souza F.P., Guilherme S. et al. Molecular biology of Philadelphia-negative myeloproliferative neoplasms. Rev. Bras. Hematol. Hemoter. 2012;34(2): 150-5.
  9. Cervantes F., Arellano-Rodrigo E., Alvarez-Larran A. Blood cell activation in myeloproliferative neoplasms. Haematologica 2009; 94: 1484-8.
  10. Di Nisio M., Barbui T., Di Gennaro L. et al. The haematocrit and platelet target in polycythemia vera. Br. J. Haematol. 2007; 36: 249-59.
  11. Gale R.P., Barosi G., Barbui T. et al. What are RBC-transfusion-dependence and -independence? Leukemia Research 2010; 35: 8-11.
  12. Gowin K., Thapaliya P., Samuelson J. et al. Experience with pegylated interferon a-2a in advanced myeloproliferative neoplasms in an international cohort of 118 patients. Haematologica 2012; 97(10): 1570-3.
  13. Harrison C.N., Campbell P.J., Buck G. et al. Hydroxyurea compared with anagrelide in high-risk essential thrombocythemia. N. Engl. J. Med. 2005; 353: 33-45.
  14. Ianotto J.C., Boyer-Perrard F., Gyan E. et al. Efficacy and safety of pegylated-interferon a-2a in myelofibrosis: a study by the FIM and GEM French cooperative groups. Br. J. Haematol. 2013; 162(6): 783-91.
  15. Ianotto J.C., Kiladjian J.J., Demory J.L. et al. PEG-IFN-a-2a therapy in patients with myelofibrosis: a study of the French Groupe
  16. Kiladjian J.J., Masse A., Cassinat B. et al. Clonal analysis of erythroid progenitors suggests that pegylated interferon a-2a treatment targets JAK2(V617F) clones without affecting TET2 mutant cells. Leukemia 2010; 24: 1519-23.
  17. Kiladjian J.J., Cassinat B., Chevret S. et al. Pegylated interferon-alfa-2a induces complete hematologic and molecular responses with low toxicity in polycythemia vera. Blood 2008; 112: 3065-72.
  18. Lippert E., Girodon F., Hammond E. et al. Concordance of assays designed for the quantification of JAK2V617F: a multicenter study. Haematologica 2009; 94(1): 38-45.
  19. Nagata H., Worobec A.S., Oh C.K. et al. Identification of a point mutation in the catalytic domain of the protooncogene c-kit in peripheral blood mononuclear cells of patients who have mastocytosis with an associated hematologic disorder. PNAS USA 1995; 92: 10560-4.
  20. Najean Y., Rain J.D. Treatment of polycythemia vera: the use of hydroxyurea and pipobroman in 292 patients under the age of 65 years. Blood 1997; 90: 3370-7.
  21. Quintas-Cardama A., Levine R., Manshouri T. et al. High rates of molecular response after long-term follow-up of patients with advanced essential thrombocythemia (ET) or polycythemia vera (PV) treated with pegylated interferon-ALFA-2A (PEG-IFNa-2A; PEGASYS). ASH Annu. Meet. Abstr. 2010;116: 461.
  22. Sanchez-Aguilera A., Arranz L., Martin-Perez D. et al. Estrogen signaling selectively induces apoptosis of hematopoietic progenitors and myeloid neoplasms without harming steady-state hematopoiesis. Cell Stem Cell. 2014; 15: 791-804.
  23. Silver R.T. Long-term effects of the treatment of polycythemia vera with recombinant interferon-a. Cancer 2006; 107(3): 451-8.
  24. Squizzato A., Romualdi E., Middeldorp S. Antiplatelet drugs for polycythaemia vera and essential thrombocythaemia. Cochrane Database Syst. Rev. 2008; 16: 1-15.
  25. Stewart W.A., Pearce R., Kirkland K.E. et al. The role of allogeneic SCT in primary myelofibrosis: a British Society for Blood and Marrow Transplantation study. Bone Marrow Transplant 2010; 45(11): 1587-93.
  26. Tefferi A. The history of myeloproliferative disorders: before and after Dameshek. Leukemia 2008; 22: 3-13.
  27. Wilson A., Laurenti E., Oser G. et al. Hematopoietic stem cells reversibly switch from dormancy to selfrenewal during homeostasis and repair. Cell 2008; 135: 1118-29.
  28. Zhan H. The diagnosis and management of polycythemia vera, essential thrombocythemia, and primary myelofibrosis in the JAK2 V617F era. Spivak. Clin. Adv. Hematol. Oncol. 2009: 7: 33-42.

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