Holbrook Kohrt

Publication Details

  • Reduced intensity conditioning is superior to nonmyeloablative conditioning for older chronic myelogenous leukemia patients undergoing hematopoietic cell transplant during the tyrosine kinase inhibitor era BLOOD Warlick, E., Ahn, K. W., Pedersen, T. L., Artz, A., de Lima, M., Pulsipher, M., Akpek, G., Aljurf, M., Cahn, J., Cairo, M., Chen, Y., Cooper, B., Deol, A., Giralt, S., Gupta, V., Khoury, H. J., Kohrt, H., Lazarus, H. M., Lewis, I., Olsson, R., Pidala, J., Savani, B. N., Seftel, M., Socie, G., Tallman, M., Ustun, C., Vij, R., Vindelov, L., Weisdorf, D. 2012; 119 (17): 4083-4090


    Tyrosine kinase inhibitors (TKIs) and reduced intensity conditioning (RIC)/nonmyeloablative (NMA) conditioning hematopoietic cell transplants (HCTs) have changed the therapeutic strategy for chronic myelogenous leukemia (CML) patients. We analyzed post-HCT outcomes of 306 CML patients reported to the Center for International Blood and Marrow Transplant Research aged 40 years and older undergoing RIC/NMA HCT from 2001 to 2007: 117 (38%) aged 40 to 49 years, 119 (39%) 50 to 59 years, and 70 (23%) 60 years or older. The majority (74%) had treatment with imatinib before HCT. At HCT, most patients aged 40 to 49 years were in chronic phase (CP) 1 (74%), compared with 31% aged 60 years or older. Siblings were donors for 56% aged 40 to 49 years; older cohorts had more unrelated donors. The majority received peripheral blood grafts and RIC across all age groups. 3 year overall survival (54%, 52%, and 41%), day + 100 grade II-IV acute GVHD (26%, 32%, and 32%), chronic GVHD (58%, 51%, and 43%), and 1-year treatment-related mortality (18%, 20%, and 13%) were similar across ages. The 3-year relapse incidence (36%, 43%, and 66%) and disease-free survival (35%, 32%, and 16%) were inferior in the oldest cohort. Importantly, for CP1 patients, relapse and disease-free survival were similar across age cohorts. Allogeneic RIC HCT for older patients with CML can control relapse with acceptable toxicity and survival in TKI-exposed CML, especially if still in CP1.

    View details for DOI 10.1182/blood-2012-02-409763

    View details for Web of Science ID 000305282900031

    View details for PubMedID 22408257

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