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2012, Number 3

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Rev Cubana Hematol Inmunol Hemoter 2012; 28 (3)

Interferon: phoenix in the treatment of chronic myeloid leukemia

Hernández-Ramírez P

Language: Spanish
References: 32
Page: 226-234
PDF size: 79.31 Kb.


ABSTRACT

According to the universal myth, as its end approaches the phoenix built a nest where it cremated itself and then rose from its ashes. This legend can be metaphorically applied to what happened in recent years with interferon (IFN) in the treatment of chronic myeloid leukemia (CML), which was replaced by tyrosine kinase activity inhibitors. Before the introduction of imatinib, the gold standard for the treatment of CML chronic phase was based on INF-? protocols, but the results obtained with the drug favored tyrosine kinase inhibitors to be accepted as the best initial treatment for newly diagnosed CML. However, the experience with the tyrosine kinase inhibitors has shown that this treatment is usually not completely effective in a number of patients. Given this fact plus deepening the understanding of IFN-? action mechanisms, its reinstating in CML treatment was considered, since it might be a complement and contribute to inhibitors of tyrosine kinase activity. This idea promoted the interest of associating INF-?, which had been virtually eliminated from CML therapy, with inhibitors of tyrosine kinase activity. The results achieved with its association with imatinib are unquestionable and very promising, which made INF-? a phoenix arising from its ashes with renewed spirit. Although the results are significant, the extension of studies of that combination therapy is considered necessary to better clarify its effects, mainly in long terms.


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