Ineffective platelet production has been proven to play a role in the etiology of Immune
Thrombocytopenia (ITP) in addition to increased platelet destruction. The second-generation
thrombopoietin (TPO) mimetics have shown good efficacy in boosting platelet counts in the
great majority of patients with chronic ITP in several clinical trials.1, 2 Nevertheless,
about 20% of patients with ITP fail to respond to the TPO mimetic treatment. Those
treatment-resistant patients are un-characterized and the reasons for the lack of response
have not been studied. The identification of predictive blood biomarkers of patients'
response to treatment will be useful in reducing both cost and potential side effects; and it
will be of equal importance and interest to investigate the molecular mechanisms underlying
the patients' heterogeneous responses to TPO mimetic treatment.
1. To identify blood classifier genes which correlate with patients' response to TPO
2. To compare the blood gene expression changes in responders and non-responders after TPO
mimetic treatment and explore the possible molecular mechanisms accounting for the
non-responsiveness to the treatment.