Current acute myeloid leukemia (AML) therapy fails to eliminate quiescent leukemic blasts in the bone marrow, leading to about 50% of patient relapse by increasing AML burden in the bone marrow, blood, and extramedullar sites. We developed a protein-based nanoparticle conjugated to the potent antimitotic agent Auristatin E that selectively targets AML blasts because of their CXCR4 receptor overexpression (CXCR4+) as compared to normal cells. The therapeutic rationale is based on the involvement of CXCR4 overexpression in leukemic blast homing and quiescence in the bone marrow, and the association of these leukemic stem cells with minimal residual disease, dissemination, chemotherapy resistance, and lower patient survival.
Sitges M, Boluda B, Garrido A, Morgades M, Granada I, Barragan E, Arnan M, Serrano J, Tormo M, Miguel Bergua J, Colorado M, Salamero O, Esteve J, Benavente C, Pérez-Encinas M, Coll R, Martí-Tutusaus JM, Brunet S, Sierra J, Ángel Sanz M, Montesinos P, Ribera JM, Vives S
Scute myeloid leukemia with inv(3)(q21q26.2)/t(3;3)(q21;q26.2). study of 61 patients treated with intensive protocols.
Eur. J. Haematol.3 Apr 2020, . Epub 3 Apr 2020
Inv(3)(q21q26.2)/t(3;3)(q21;q26.2) is a rare poor prognosis cytogenetic abnormality present in acute myeloid leukemia (AML) and other myeloid neoplasms.