A polymorphism, that affected LTA expression, was found in the first intron of the gene at nucleotide position +252A®G [8]. This polymorphism was located within a phorbol-ester-responsive DNA element with a high affinity to the activator proteins (AP-1, JUN) and c-fos hetero­dimer transcription factor family. The presence of the LTA*GG genotype was shown to result in a significantly higher production of LTA by phytohemagglutinin-stimu­lated peripheral blood mononuclear cells due to an in­crease of LTA gene transcription [8].

Several studies have demonstrated the linkage dis­equilibrium between both –308TNF and +252LTA poly­morphic sites, and with other allelic markers within the cluster of HLA genes [6]. In the present study, we assumed that these polymorphisms were in association with differ­ent forms of hematological malignancies in children.

We have not found any statistically reliable associa­tion between –308TNF and +252LTA polymorphisms and ALL. Our results did not contradict those of Stanulla et al. [16] who did not find any association between –308TNF and +252LTA gene polymorphisms and children with ALL. Takeuchi et al. [17] also proved that genetic poly­morphisms in the TNF locus had a limited effect on the outcome of childhood ALL.

TNF*GA and LTA*AG genotypes in our study were associated with AML in children. Probably, higher consti­tutive and inducible transcription level of the TNF and LTA genes had an impact on the poor outcome of the most aggressive form of hematological malignancies in chil­dren.