Clinical Lymphoma, Myeloma & Leukemia, Vol.20, Suppl.1 - September 2020

Abstracts Clinical Lymphoma, Myeloma & Leukemia September 2020 S202 found that PTCy was significantly associated with a 90% reduced risk of aGVHD (HR= 0.1; 95% CI: 0.02–0.6; P=.01). No chronic GVHD or grade  2 immune-related adverse events were reported. The PTCy group had a significantly longer median PFS (22.4 vs. 5.2 months, P=.02) and a trend toward longer median OS (22.4 vs. 5.2 months, P=.08). Fourteen patients (67%) died, and no deaths were attributed to aGVHD. Conclusions: The use of ICI for AML/ MDS relapse after allo-SCT may be a safe and feasible option. PTCy appears to decrease the incidence of aGVHD in this cohort of patients. Keywords: stem cell transplant, cyclophosphamide, AML, MDS, nivolumab, ipilimumab AML-317 O u t c o mes o f Sec o nd All o geneic Hema to p o ie t ic Cell Transplan t a t i o n f o r Pa t ien t s wi t h Acu t e Myel o id Leukemia Fevzi Yalniz*, Rima Saliba, Uri Greenbaum, Jeremy Ramdial, Amin Alousi, Jacinth Joseph, Amanda Olson, Gheath Alatrash, David Marin, Katayoun Rezvani, Chitra Hosing, Jin Im, Elizabeth Shpall, Rohtesh Mehta, Muzaffar Qazilbash, Uday Popat, Betul Oran, Richard Champlin, Partow Kebriaei The University of Texas MD Anderson Cancer Center, Stem Cell Transplantation Department, Houston, TX Context: Relapse after allogeneic hematopoietic cell transplantation (allo-HCT1) leads to poor survival in patients with acute myeloid leukemia (AML). A second allo-HCT can achieve durable remission in a subset of patients. Objective: To assess outcomes of patients who underwent allo-HCT2 for relapsed AML and identify risk factors associated with survival. Design: We reviewed consecutive medical records of 91 adult patients (age >18 years) with AML who underwent allo-HCT2 for relapsed disease at our institution from January 2000 until August 2019. Results: At allo-HCT2, median age was 43 (range, 18–67), donor types were HLA-identical sibling 41%, HLA-matched-unrelated 35%, haploidentical 21%, and cord-blood 1%. Donors were different at allo-HCT2 in 53% patients. The majority of patients received reduced intensity conditioning (78%) and were in remission (58%) at allo-HCT2. The median remission duration after allo-HCT1 was 8.4 months (range, 1–70); median time between transplants 13.6 months (range, 2.6–73). The median follow-up of surviving patients after allo-HCT2 was 25 months (range, 4–70), with 32% alive at time of analysis; the most common cause of death was disease recurrence (87%). At 2-years, progression-free-survival, overall survival, and cumulative incidence of relapse were 30% (95% CI, 18–37%), 36% (95% CI, 26–47%) and 42% (95% CI, 32–54%), respectively. The cumulative incidence of grades II–IV acute and chronic GVHD were 35% and 18%, respectively. In multivariate analysis, persistent disease at time of allo-HCT1 and allo-HCT2, along with high leukemia burden at allo-HCT2 (defined as BM blast >10%) [HR,2.4; p=0.006], development of cGVHD after allo- HCT1 [HR,3.1; p<0.001)], and poor performance status (HCT- CI >2) [HR, 2.1; p=0.01] were associated with inferior PFS after allo-HCT2. These factors also predicted for OS. A total of 19, 55, and 17 patients had neither, one, or more than one adverse factors, respectively. Two-year OS was 60%, 40%, and 0%, and PFS was 47%, 28%, and 0% in these 3 respective groups. Conclusions: Long-term survival benefit is possible after allo-HCT2 in patients with AML who relapsed after allo-HCT1. This can be achieved in patients without cGVHD after allo-HCT1 who are fit and in remission at time of allo-HCT1, along with <10% blasts at the time of allo-HCT2. Outcomes of allo-HCT2 are extremely poor in patients with a history of cGVHD. Keywords: acute myeloid leukemia, AML, relapse after allogeneic cell transplant, second allogeneic cell transplant, survival AML-318 Predic to rs o f O u t c o mes in AML wi t h MLL Rearrangemen t Ghayas Issa*, Jabra Zarka, Koji Sasaki, Nicholas Short, Elias Jabbour, Tapan Kadia, Gautam Borthakur, Guillermo Garcia-Manero, Hagop Kantarjian, Farhad Ravandi Department of Leukemia, The University of Texas MD Anderson Cancer Center Context: Outcomes and determinants of response in AML with rearrangements of the Mixed Lineage Leukemia (MLL) gene are unknown. Objectives: To determine the mutational, phenotypic, and clinical characteristics of MLLr AML. Design: A retrospective analysis including adult patients with newly diagnosed MLLr AML at MD Anderson from 1990–2019. Setting: Tertiary care center. Patients: One hundred seventy-four patients with newly diagnosed MLLr AML were analyzed and compared to 522 age-matched patients with a diploid karyotype (Dp). Main Outcomes Measures: Mutational and immunophenotypic profiles, in addition to responses and survival outcomes. Results: MLLr patients were younger (median age: 51 vs 61 years for Dp, P<0.0001) and had higher LDH (median: 1783 vs 1358 U/L for Dp), higher bone marrow blast % (median: 66% vs 53%), and lower platelet counts (median: 57 vs 71x10 9 /L) (P<0.02 for all). Sixty-five (37%) MLLr patients had therapy-related (t-AML) (vs 9% of Dp, P<0.0001). MLLr had fewer mutations vs Dp (median 0.5 vs 1.2 mutation/patient, P<0.0001), most commonly affecting the RAS and TP53 genes. Blasts in MLLr had lower expression of CD7 (median: 6% vs 14%), CD13 (median: 58% vs 74%), and CD34 (median: 16% vs 38%), and higher CD33 (median: 94% vs 82%) (P<0.001). MLLr had similar response rate to age matched Dp (CR/CRi: 82 vs 80%, P=0.7) but worse OS (median: 0.9 vs 2 years, P<0.0001). In a landmark analysis, hematopoietic stem cell transplant (HSCT) was associated with markedly improved outcomes in MLLr (median OS of 10.7 vs 1.1 years, P<0.0001). In a multivariate analysis of factors predicting overall survival in MLLr AML, HSCT was associated with a lower risk of death with a HR of 0.38 (95% CI 0.24–0.58, P<0.0001). The only other adverse predictors identified in this model included an elevated creatinine (HR of 1.43, 95% CI 1.12–1.83, P=0.004) and an elevated WBC (HR of 1.00, 95% CI 1.00–1.01, P<0.0002). Conclusions: MLLr AML has unique molecular and phenotypic