The articles in this section focus on a variety of biologic findings in the acute leukemias and their potential application to improvements in clinical care. Judith Karp (pp 3–9) describes the multiple examples of molecular mischief found in patients with myelodysplasia which produce perturbations in differentiation and cell cycle kinetics. Importantly, there is potential that some of the signal transduction and cell cycle kinetic changes might eventually be targets for pharmacologie intervention. There is enormous overlap between myelodysplasia and apparentde novoleukemia in adults, particularly in older patients, as evidenced by similarity in the karyotypes, expression of drug resistance genes (particularly P-glycoprotein), and a similar poor prognosis when treated with conventional chemotherapeutic approaches. Some patients with myelodysplasia by French-American-British morphologic criteria respond reasonably well to chemotherapy; clinical hints include a short antecedent hematologic disorder and the presence of cytogenetic findings—particularly t(8;21)—typical of acute myelogenous leukemia with better prognoses. Although there are recent provocative observations with the use of 5-azacytidine and amofostine in well established myelodysplasia, complete responses are virtually nonexistent and overall outcome remains very poor.