Aggressive chemotherapy combined with G-CSF and maintenance therapy with interleukin-2 for patients with advanced myelodysplastic syndrome, subacute or secondary acute myeloid leukemia — initial results

Abstract

Aggressive chemotherapy of advanced myelodysplastic syndrome (MDS), acute myeloid leukemia (AML) evolving from MDS, subacute AML and secondary AML has usually been associated with low complete remission (CR) rates, a high incidence of early death, and low disease-free survival. We therefore have initiated a phase-III trial of aggressive chemotherapy consisting of idarubicin, cytosine arabinoside, and VP-16 to improve the CR rate. Each chemotherapy cycle is followed by G-CSF to accelerate neutrophil recovery and to reduce the incidence of infections. Until now, 19 patients with high-risk AML have been entered. The CR rate is 47%, with only one death during induction. Patients achieving CR are randomized to receive either high-dose or low-dose interleukin-2 to eliminate residual leukemic cells and to prolong the duration of remission.

Phase-II trial of idarubicin, fludarabine, cytosine arabinoside, and filgrastim (Ida-FLAG) for treatment of refractory, relapsed, and secondary AML

“…For patients who are not able to undergo ABMT, a maintenance therapy should be discussed [10]. Further, activation of autologous cytotoxic cells by interleukin-2 may be a promising tool for elimination of minimal residual blast populations in patients with AML to prolong disease-free survival [5,25].…”

Intensive chemotherapy with idarubicin, cytosine arabinoside, and granulocyte colony-stimulating factor (G-CSF) in patients with secondary and therapy-related acute myelogenous leukemia

“…The beneficial role of G-CSF administration after the compatients (four of the 21 post-RAEB sAML patients, one of the four post-CMML sAML patients, and one of the nine tAML pletion of intensive chemotherapy in our patients remains to be proven. As discussed above, even if comparisons from one patients) remain alive with a median follow-up of 15 months (range [13][14][15][16][17][18][19].…”

Etoposide prevents apoptosis in mouse liver with ?-galactosamine/lipopolysaccharide-induced fulminant hepatic failure resulting in reduction of lethality

“…[8][9][10][11] Etoposide, a topoisomerase II inhibitor, is used for the treatment of a wide variety of neoplasms, including nonHodgkin's lymphoma and leukemia. 12,13 Generally, topoisomerase II inhibitors stabilize the covalently bound complexes formed between topoisomerase II and the 5Ј cleaved ends of DNA molecules, and interfere with DNA religation. 13,14 In addition, etoposide induces apoptosis of several malignant cell lines, such as the original human leukemia cell line, HL-60, resulting in DNA fragmentation.…”