Molecular relapse was defined as any patient with persistent and/or reappearance of pretransplant molecular genetic abnormalities ( JAK2 V617F, CALR and MPL). MF relapse was defined as any evidence of persistent or recurrent morphologic disease. Patients with double cord or haploidentical donors or with primary graft failure were excluded. We further explored the correlation between myeloid chimerism and molecular relapse of MF.Įighty-two consecutive patients with primary or secondary MF who underwent their first allo-SCT at The University of Texas MD Anderson Cancer Center from January 2005 to July 2015 were identified. Therefore, we aimed to determine the role of MMC in predicting relapse in MF patients after allo-SCT. 14-18 The influence of MMC on posttransplantation relapse of MF has not been well studied. 7, 11-13 Few studies have focused on the potential role of mixed chimerism in predicting early relapse, particularly in those with mixed myeloid chimerism (MMC). 10 Detecting the JAK2 V617F mutation after SCT in MF is a strong predictor of relapse and a potential marker for guiding adoptive immunotherapy.

1, 8 Strategies for detecting early relapse and improving outcomes in these high-risk patients represent an unmet need.Īssessing response and confirming early relapse after transplant for MF is often challenging based on the clinical criteria, 9 and it usually takes a few months for fibrosis to resolve and the bone marrow morphologic remission to be achieved.

3-7 However, relapse after transplantation remains a frequent cause of death, with relapse rates ranging from 10-43% after allo- SCT. 1, 2 The 5-year overall survival (OS) rates in MF patients after allo-SCT have improved over the past several years, ranging from 47% to 62%. Allogeneic stem cell transplantation (allo-SCT) remains the only potentially curative treatment for myelofibrosis (MF).

Myelofibrosis stem cell transplant