Fractionated TBI and methotrexate-cyclosporin do not seem to increase relapses in BMT for first chronic phase CML patients: results of a single centre study.

Fractionated total body irradiation (FTBI) and methotrexate-cyclosporin A(MTX-CSA) have been found useful in reducing interstitial pneumonia (IP) and acute graft-versus-host-disease (GVHD) in bone marrow transplantation patients, but an increase in relapse rate has been observed by some authors when these strategies are used. To evaluate this relapse risk, we performed a retrospective analysis in 24 consecutive first chronic phase chronic myeloid leukemia patients who received an HLA-identical non-T cell-depleted graft in a single institution. All were conditioned with cyclophosphamide plus FTBI (12 Gy in six fractions delivered twice daily for 3 days) (CY-FTBI) and received MTX-CSA as GVHD prophylaxis. Serial hematologic and cytogenetic bone marrow analysis were performed at least three times (days +30, +100, +360) and at variable intervals thereafter in long-term survivors. Actuarial probabilities of developing IP and acute GVHD greater than or equal to II were respectively 5.9% and 44.2%, with a GVHD-associated mortality of 33%. Four-year actuarial relapse and disease-free survival rates were 7.7% and 48.2% respectively. No exclusively cytogenetic relapses were observed. Our results suggest that CY-FTBI and MTX-CSA are not associated with an increase in relapse rate in 1CP-CML patients.

[Cytogenetic study of 22 adults and 3 children with acute lymphoblastic leukemia]. / Estudio citogenético en 22 adultos y tres niños con leucemia linfoblástica aguda.

Between 1987 and 1990 cytogenetic studies of bone marrow and lymphocytes from peripheral blood from 25 patients with de novo ALL were performed. All cases had chromosomal aberrations; however in 23 patients a normal cell line was also present. The most important structural aberrations found were: t(17;19)(q11;p13), t(2;9;22)(q34;q34;11), t(1;7)(p13;q33), t(6;11)(q26;p16), t(3;4)(q24-25;q26), t(1;12)(q23;q34), t(2;18)(q15;p12), t(2;4)(q23;q35) and t(4;11)(q21;q23). These chromosome abnormalities correlate with the response to treatment and survival and improve the identification of high-risk patients. Our study shows the presence of some chromosomal abnormalities different to those reported in the literature; however the breakpoints involved seem to be the same which suggests that these critical regions may be directly involved in the pathogenesis of these disorders.