IN-VITRO SUSCEPTIBILITY OF ACUTE-LEUKEMIA CELLS TO THE CYTOTOXIC ACTIVITY OF ALLOGENEIC AND AUTOLOGOUS LYMPHOKINE-ACTIVATED KILLER (LAK) EFFECTORS - CORRELATION WITH THE RATE AND DURATION OF COMPLETE REMISSIONAND WITH SURVIVAL

Acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AM L) blasts were studied for their sensitivity to the lytic activity of normal allogeneic Interleukin 2 (IL-2) activated killer (LAK) cells, a nd of autologous LAK effecters generated at the time of complete remis sion (CR). In 12 of 23 ALL cases (52%), the blasts were susceptible to normal LAK cells (>15% lysis) and ten of them achieved a CR. Of the r emaining 11 LAK-resistant cases, seven obtained a CR. No correlation w as found between susceptibility to LAK activity, cytomorphology, immun ophenotype, CR duration and survival. Eighteen of the 26 AMLs tested ( 70%) were susceptible to normal LAK cells, and nine of the 13 cases st udied (70%) were also lysed by autologous LAK effecters generated at C R. No clearcut correlation was observed between blast sensitivity to n ormal LAK cells and morphologic cytotype, though a higher incidence of resistant cases was observed in the M4 subgroup. All AMLs susceptible to normal LAK cells but one achieved a CR, while this occurred only i n three of the eight resistant cases (p=0.004). The median survival an d event-free survival duration in the resistant patients were signific antly shorter (p=0.03 and p=0.02, respectively) compared to those of t he susceptible patients. In ten ALL and in six AML, which at presentat ion displayed less than 10% circulating blasts, the susceptibility of the leukemic population to normal and autologous LAK effecters could b e tested, both at diagnosis and at remission. All cases but one were r esistant to autologous LAK cells generated at diagnosis, while at CR, seven cases (four ALL and three AML) became susceptible to autologous LAK cells (p=0.01). The remaining nine were resistant to both allogene ic and autologous LAK effecters. Taken together, these findings sugges t that in AML, but not in ALL, the LAK cell compartment may play a rol e in the clinical course and overall outcome of the disease.