AcSDKP serum concentrations vary during chemotherapy in patients with acute myeloid leukaemia.
AcSDKP is a physiological negative regulator of cell proliferation in mammals. In Ara-C-treated mice its plasmatic concentrations decrease while the CFU-S start cycling. Infusion of AcSDKP protects these animals from death by blocking the proliferation of primitive haemopoietic cells. We measured AcSDKP serum concentrations in 20 AML patients during the course of high-dose cytoreductive treatment. We observed an early and sharp increase of AcSDKP during the induction treatment in 12 patients, reaching a peak during the initial 3 d of treatment in nine of them. These results are contrary to those observed in mice treated with high doses of Ara-C. They encourage further clinical investigation, and suggest that treatments with synthetic AcSDKP (Seraspenide) will perhaps have to be adjusted to the type of disease and the schedule of chemotherapy in order to optimize its myeloprotective effect.
Liozon
E
E
Service de Médecine Interne et d'Hématologie, CHRU de Limoges, France.
Volkov
L
L
Comte
L
L
Trimoreau
F
F
Pradelles
P
P
Bordessoule
D
D
Frindel
E
E
Praloran
V
V
D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002455:Cell Division; D005260:Female; D006412:Hematopoietic Stem Cells / Q000187:drug effects*; D006801:Humans; D007951:Leukemia, Myeloid / Q000097:blood* / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D009842:Oligopeptides / Q000097:blood* / Q000493:pharmacokinetics
D009842:Oligopeptides; C058504:goralatide