We measured HPRT Mfs from 130 peripheral blood samples from 45 children with ALL (13, low risk; 22, standard risk; and 10, high risk) from the time of diagnosis, as well as during and after the completion of therapy.
We investigated the in vivo clonality and mutational spectra of hypoxanthine-guanine phosphoribosyltransferase (HPRT) mutations in T cells from children with acute lymphocytic leukemia (ALL) to gain insight into the mutagenic mechanisms associated with leukemogenesis.
Structural hypoxanthine-guanine phosphoribosyl transferase (hprt) gene alterations, as determined by Southern blot analysis, were seen in 23% (12/52) of mutant clones derived from ALL patients, but not in those from the controls.