
Given the clinical utility of myeloid growth factors and erythropoietin (Epogen, Procrit) in the management of many cancer patients, it is understandable that the cloning and introduction into clinical trials of thrombopoietin was greeted with great expectations for the future utilization of this molecule in oncology. Drs. Prow and Vadhan-Raj have written a well-referenced review that summarizes the preclinical biology of thrombopoietin and the evidence that it is the physiologic regulator of thrombopoiesis in animals and humans. The authors also synopsize some of the data from early clinical trials. My own interpretation of the clinical data obtained to date with both the full-length clone (recombinant human thrombopoietin [rhTPO]) and the pegylated, truncated molecule (pegylated recombinant human megakaryocyte growth and development factor [PEG-rHuMGDF]) differs somewhat from both our initial expectations and the perspective provided by the authors.
