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Venetoclax, a small-molecule B-cell lymphoma 2 (BCL-2) inhibitor, selectively eradicates leukemic stem cells (LSCs). While venetoclax has revolutionized the treatment of acute myeloid leukemia (AML), treatment failure and disease relapse are common. Mechanisms underlying venetoclax resistance are surprisingly heterogeneous. Venetoclax resistance encompasses a spectrum of genetic and epigenetic changes, with numerous pathways contributing to the upregulation of additional anti-apoptotic proteins. In this review, we address the mechanisms of venetoclax resistance in the context of signal transduction. We emphasize how aberrant cell signaling impairs apoptosis and predisposes to venetoclax failure. Commonly activated pathways, such as FLT3, PI3K/AKT/mTOR, and RAS, contribute to upregulated anti-apoptotic mediators and are frequently responsible for refractory disease or disease relapse. We highlight novel combination strategies aimed at disabling constitutively active signal transduction to augment response and overcome venetoclax resistance.

e19033 Background: The use of venetoclax, a BCL-2 antagonist, in combination with decitabine or azacitidine has become routine for the upfront treatment of patients with acute myeloid leukemia (AML) not eligible for intensive induction. The impact of the addition of venetoclax to hypomethylating agents (HMAs) on outcomes with respect to various gene mutations is currently unclear. The aim of this study was to investigate response and survival of patients with AML receiving venetoclax-based induction with respect to specific molecular aberrations. Methods: We retrospectively analyzed 41 patients with AML treated with upfront venetoclax + HMAs from July 2017 to December 2020 at VCU Massey Cancer Center. Baseline patient demographics were obtained, including molecular profiling either through PCR or NGS at the time of induction, alongside cytogenetic risk, doses of induction regimens, response including MRD analysis, and survival. The event for calculating the overall survival (OS) was the date of death. Patients were otherwise censored at the date of last contact. Results: Nine patients were identified with NPM1mut and 66.6% were ELN adverse risk. The composite response rate (CRR = CR + CRi) was 44.4% and the OS was 8.2 months. Seven patients had either DNMT3Amut or DNMT3Bmut and 57.1% were classified as adverse risk. The CRR was 28.6% and the mOS was not reached after a median follow-up time of 15.1 months. Eleven patients had FLT3-ITDmut or FLT3-TKDmut and 81.8% were classified as adverse risk. The CRR was 45.6% and the OS was 6.3 months. Six patients had either NRASmut or KRASmut. The CRR was 16.7% and the OS was 8.9 months. Seven patients had ASXL1mut, the CRR was 28.5% with the OS not reached at a median follow-up time of 8.9 months. Six patients with RUNX1mut demonstrated a CRR of 50.0% and the OS was not reached at a follow-up time of 12.8 months. Nine patients had TP53mut with a CRR of 33.3% and OS 12.6 months. Conclusions: Survival with venetoclax + HMA appears to numerically favor TP53mut AML when compared to more intensive strategies, consistent with prior literature reporting favorable responses to HMA monotherapy in this subset of disease. FLT3mut appeared to have a relatively lower OS, though not significantly different from either NPM1mut or TP53mut at the time of this analysis. DNMT3mut AML may preferentially respond to venetoclax + HMAs given the 15.1 month duration of follow-up, though longer follow-up with larger cohorts are needed to further identify subsets of molecularly stratified preferential responders to venetoclax-based strategies.[Table: see text]

e19035 Background: Prior work investigating the optimal dose of daunorubicin in combination with cytarabine for upfront treatment of AML has resulted in several studies suggesting differential responses following daunorubicin dose optimization when analyzed by molecular cohort (such as NPM1, FLT3-ITD, or DNMT3A). While some studies advocated for a dose of 90 mg/m2 in younger patients with NPM1mut (following induction with either daunorubicin 45 mg/m2 versus 90 mg/m2), little is known regarding outcomes stratified by molecular lesion between daunorubicin 60 mg/m2 and daunorubicin 90 mg/m2. Methods: We retrospectively analyzed 92 patients with AML treated with upfront daunorubicin 60 mg/m2 or 90 mg/m2 from July 2017 to December 2020 at VCU Massey Cancer Center. Baseline patient demographics were obtained, including cytogenetic risk, molecular profiling either through PCR or NGS at the time of induction, doses of induction regimens, response including MRD analysis (when available), and survival. Results: In the 60 mg/m2 cohort, 10 patients had NPM1mut, the CRR (CR+CRi) was 60.0% and the OS was 1.7 y. Four patients with DNMT3mut had a CRR of 25.0% and a 4.1 m. OS. Nine patients with FLT3-ITD or FLT3-TKD all treated with FLT3 inhibitors achieved a CRR of 22.2% with a 4.9 m. OS. Ten patients with NRASmut or KRASmut had a CRR of 50.0% and a 20.7 m. OS. In the adverse category, five with ASXL1mut had a 20.0% CRR and a 6.4 m. OS; 7 with RUNX1mut had a CRR of 42.9% and a 14.5 m. OS; and 6 with TP53mut demonstrated a CRR of 0% and an 13.1 m. OS. In the 90 mg/m2 cohort, 8 patients had NPM1mut with a CRR of 75.0% and an 18.8 m. OS. Two patients with DNMT3mut both achieved CR and the OS was not reached. Three of 5 patients with FLT3mut treated with midostaurin achieved CR or CRi and a 16.2 m. OS. Four of 5 patients with RASmut achieved CR and the OS was not reached at a 15.8 m. follow-up time. In the adverse category, there were no patients treated with a dose of 90 mg/m2 with ASXL1mut and one with RUNX1mut with non-evaluable response. Two out of 4 patients achieved CR or CRi with TP53mut and the OS was not reached. Conclusions: Response rates appear numerically higher across molecular subtypes favoring daunorubicin 90 mg/m2, although no significant differences in survival were appreciated, likely due to limited sample size. This may argue for intensification of anthracycline doses in carefully selected patients regardless of molecular profiling. Toxicity with high-dose daunorubicin must be weighed against any potential response or survival benefit, particularly for TP53mut and ASXL1mut – especially in the setting of alternative induction strategies such as CPX-351 and venetoclax with a hypomethylating agent. Larger prospective studies analyzing outcomes with regards to molecular profiling and treatment strategies are warranted.

e19032 Background: Presence of the Philadelphia chromosome (Ph+) or IKZFmut is associated with a poor prognosis in B-cell ALL. The clinical impact of both mutations occurring together in adult patients is currently unknown. We sought to analyze outcomes of patients with Ph+ B-ALL and IKZFmut treated with induction with TKI-based regimens outside of the context of clinical trials. Methods: We identified 10 patients with Ph+ B-ALL treated at our institution during January 2015 to January 2021 that had IKFZmut identified through NGS. Seven had IKFZmut at the time of diagnosis and three acquired IKFZmut at the time of relapse. Baseline patient demographics were obtained, including age, performance status and comorbidities at diagnosis, cytogenetic and molecular profiling through NGS, doses of induction, toxicity, response, measurable residual disease (MRD) analysis, and survival, and incidence of relapse. The event for calculating the overall survival (OS) was the date of death and patients were otherwise censored at the date of last contact. Results: The median age of the 7 patients IKFZmut with at diagnosis was 58 years (range: 44 - 72), 57.1% were male, the median ECOG score was 1 (range: 1 - 3), and the median Charlson Comorbidity Index score was 4. Other commonly occurring mutations were ABL1 (42.9%), with CDKN2A, ETV6, and PTPN11 occurring at 14.3% each. Dasatinib was the most common TKI given in 85.7% of patients in combination with hyperCVAD (42.9%), EWALL-Ph-01 (28.6%), ECOG 1910 (14.3%), and ECOG 2993 (14.3%). In total, 71.4% achieved CR, with 50.0% in CR by MRD. Two patients received allogeneic stem cell transplant (HSCT) and 28.6% had relapsed or refractory disease by 1.2 years. At a median follow-up time of 1.7 years, the median survival was not reached. Three additional patients were found to have IKZFmut at the time of relapse or refractory disease. The median age was 38 years, 2 (66.6%) had a co-occurring mutation in ABL1, and all were treated with dasatinib at time of salvage, two in combination with hyperCVAD and one with EWALL-Ph-01. There were no deaths during induction and two patients had evaluable responses and both achieved CR, and one by MRD. Conclusions: To the best of our knowledge, these are among the first of limited reports regarding outcomes of adult patients with Ph+ B-ALL and IKZFmut. Although the cohort is limited by sample size due to the rarity of the co-occurring mutations, the response rates appear to be numerically similar in upfront treatment of Ph+ and IKZFmut compared to historical data for Ph+ B-ALL alone in the era of TKIs. Gain of IKZFmut may be a sign of clonal evolution of disease, and further work to elucidate prognostic implications in the relapsed and refractory group is warranted. Larger prospective, randomized studies investigating differential responses to modern combinatorial chemoimmunotherapy + TKI approaches are warranted in this population.

12067 Background: Philadelphia chromosome-positive (Ph+) ALL is an aggressive hematological neoplasm with a dismal prognosis. Hematopoietic stem cell transplant (HSCT) remains the standard of care for those reaching complete remission due to high relapse rates with conventional therapy alone. We have previously demonstrated findings concerning for imbalanced outcomes among racial groups in AML. In the era of TKIs targeting BCR-ABL1 in combination with conventional therapy, it is unclear whether trends noted in AML are also seen in Ph+ ALL. Thus, the purpose of this study was to investigate the impact of healthcare disparities on outcomes in Ph+ ALL with regards to access to care, response rates, toxicities, and overall outcomes. Methods: We retrospectively analyzed 59 patients with Ph+ B-ALL treated at our institution with TKIs +/- chemoimmunotherapy during January 2015 to January 2021. Baseline patient demographics were obtained, including insurance type, performance status at diagnosis, cytogenetic and molecular profiling, dates and doses of induction, toxicity, response, MRD analysis, and HSCT access and outcomes. Race was determined by patient self-report as recorded in the electronic medical record. Results: We divided 58 patients (one excluded as race was unknown) into two cohorts: 23 (39.7%) patients that identified as minorities, including African American, Hispanic/Latino, and Asian, and 35 (60.3%) identifying as White. There were no differences in baseline characteristics including age (p =.367), sex (p =.788), ECOG at diagnosis (p =.438), Charlson Comorbidity Index scores (p =.551), or presence of additional poor-prognostic mutations (p >.999). Despite this, minorities were significantly more likely to be treated with lower-intensity regimens compared to non-minorities (p =.022). Achievement of CR by MRD was approaching statistical significance favoring the non-minority cohort (60.0% versus 27.3%, p =.055). Receipt of HSCT numerically favored the non-minority cohort, approaching statistical significance (54.3% versus 26.1%, p =.056). At a median follow-up time of 3.3 y., the median OS was not reached between the two groups and there was no difference in survival between the two groups (p =.662). Conclusions: Despite similar patient-related characteristics, minority populations are more likely to be treated with lower-intensity strategies, concerning for bias in regimen selection. Achievement of CR by MRD and receipt of HSCT appeared to be numerically lower in the minority cohort. While there appeared to be no difference between the two cohorts with regards to survival during the follow-up period, it is unclear if this would be maintained with longer follow-up. These findings highlight the need for ongoing vigilance regarding physician biases and increasing the need for improving access to curative treatment for all patients.

e19052 Background: Presence of the Philadelphia chromosome (Ph+) in newly diagnosed B-cell acute lymphoblastic leukemia (ALL) conveys high-risk disease and a poor prognosis. Hematopoietic stem cell transplant (HSCT) following induction and achievement of remission remains the standard of care. In the era of TKIs targeting BCR-ABL1 in addition to newer combination strategies, the impact of HSCT in the first complete remission (CR) remains unclear, particularly in the context of measurable residual disease (MRD) negativity. We present the outcomes of Ph+ B-ALL patients with and without HSCT, stratified with respect to MRD negativity. Methods: We identified 32 patients with Ph+ B-cell ALL from January 2015 to January 2021 at our institution who were treated with TKIs and received HSCT with evaluable MRD prior to transplant. Baseline patient demographics were obtained, including labs, performance status at diagnosis, comorbidities, molecular profiling by NGS, doses of induction, toxicities, response, MRD analysis by PCR, HCT-CI scores, and HSCT outcomes. The event for calculating the overall survival (OS) was the date of death. Patients were otherwise censored at the date of last contact. Results: Of the 25 patients who underwent HSCT, the median age was 46 years and 48.0% were male. TKIs in combination with high-intensity regimens were given in 88.0% of patients at induction. There were no deaths within 60 days following induction. Twenty (80.0%) patients achieved CR or CRi, and of those, 56% were MRD-negative by the time of HSCT. At a median follow-up time of 4.74 years, the OS of patients that achieved CR following induction and HSCT was not reached, and there were no significant differences between the two groups (p = .1326). We then compared the 14 MRD-negative patients undergoing HSCT to 7 MRD-negative patients who did not undergo transplant aged ≤65 years with ECOG ≤2. There was no difference in age (p = .5353), ECOG score (p = .6364), or Charlson Comorbidity Index score (p = .7018) between the two groups. The median OS in the MRD-negative HSCT group was not reached and the median OS in the MRD-negative non-HSCT was 5.45 years (p = .0210). Conclusions: In the era of combination chemotherapy with TKIs, MRD positivity at the time of allogenic HSCT does not appear to impact survival at 5 years in this small retrospective cohort. Post-transplant TKI maintenance may abrogate MRD implications at the time of HSCT. Our findings demonstrate that Ph+ ALL patients benefit from HSCT when candidates, regardless of MRD status, as those undergoing HSCT demonstrated a statistically superior survival. HSCT appears to remain the standard of care despite newer combination strategies and MRD-driven treatment.

e19030 Background: The optimal selection and sequence of salvage regimens during treatment of acute myeloid leukemia (AML) remains unclear. While venetoclax augmentation of a hypomethylating agent backbone is now routinely used as salvage following impressive performance in the front-line setting, little is known about outcomes in relapsed or refractory AML, especially when compared to re-inductions with anthracycline-based regimens. Thus, the aim of this study was to compare outcomes of venetoclax-based regimens versus FLAG-IDA in patients under 70 years. Methods: We retrospectively analyzed 47 patients with AML that were younger than 70 years in the relapsed and refractory setting treated with either FLAG-IDA (fludarabine, cytarabine, G-CSF, and idarubicin) or venetoclax in combination with decitabine or azacitidine from July 2017 to December 2020. Two cohorts were created: a FLAG-IDA cohort and a matched venetoclax cohort for age, ECOG score, and comorbidities. Cytogenetic risk and molecular profiling (through next-generation sequencing [NGS]) at diagnosis and throughout treatment, dates and doses of induction, toxicity, responses, and measurable residual disease (MRD) analysis were recorded and analyzed. Results: In the venetoclax cohort of 32 patients, the median age was 60 years, the median ECOG score was 1, and the median Charlson Comorbidity Index (CCI) score was 4. Six out of 22 evaluable patients achieved either a CR or CRi for a composite response rate (CRR) of 27.3%. Out of three evaluable patients that responded, none were MRD-negative by NGS. The overall survival (OS) of the venetoclax cohort was 8.2 months. In the FLAG-IDA cohort of 15 patients, there were no statistical differences between age (p = .114), ECOG score (p = .249), or CCI score (p = .137) compared to the venetoclax cohort. The CRR of the FLAG-IDA cohort was 85.7%, a significant difference from the venetoclax cohort (p = .011), and 50% were negative for MRD by either NGS or PCR. The overall survival was not reached at a median follow-up time of 15.5 months, significantly different compared to the venetoclax cohort by the log-rank test (p = .001). A Cox proportional hazards model was used to investigate the effects of commonly mutated genes ( NPM1, ASXL1, FLT3, IDH1/2, RAS, TP53, TET2) on OS in venetoclax-based re-induction, and identified IDH1/2 mutations as having a favorable impact in the relapsed/refractory setting (HR 0.01, 95% CI 0.0001-0.7214). Conclusions: Our results highlight the efficacy of FLAG-IDA compared to venetoclax-based regimens with respect to CRR and survival, significantly favoring FLAG-IDA at the time of relapsed or refractory disease. Although limited by sample size, IDH1/2 mutations may convey a better prognosis in the relapsed/refractory setting when treated with venetoclax + HMAs. Larger studies are needed to confirm these findings.

e19040 Background: The optimal treatment of adults with Philadelphia chromosome-positive (Ph+) B-ALL remains unclear. Use of pediatric-inspired regimens (PIRs) featuring asparagine depletion is associated with high responses, although at the expense of increased toxicity. Moreover, PIRs have not directly been compared with regimens that do not contain asparagine depletion (e.g., hyperCVAD). Thus, the aim of this study was to compare toxicity and efficacy of asparagine-depleting PIRs versus hyperCVAD in a matched retrospective population of adults with Ph+ B-ALL. Methods: We identified 30 patients ≥21 years with Ph+ B-ALL treated at our institution during January 2015 to January 2021. In the upfront setting, 9 were treated with PIRs. A comorbidity-matched cohort of 21 patients ≤60 years treated with hyperCVAD was selected as a comparison. Baseline patient demographics were obtained, including age, ECOG score, and comorbidities at diagnosis, cytogenetic and molecular profiling, toxicity, response, MRD analysis, survival, and receipt of hematopoietic stem cell transplant (HSCT). Results: In the PIR cohort, the median age was 37, 55.6% were male, median ECOG score was 1, and median Charlson Comorbidity Index (CCI) score was 2. CALGB 10403 was used in 88.9% of patients and 11.1% received ECOG 1910; all patients received a TKI. All patients experienced at least one grade ≥3 toxicity, and there was a total of 31 unique grade ≥3 toxicities and no deaths during induction. The composite response rate (CRR) was 77.8% and 50.0% of responders were MRD-negative. In the cohort treated with hyperCVAD and TKIs, there was no difference in age (p = .125), sex (p = .694), ECOG (p = .538), or CCI score (p = .851). There were 18 unique grade ≥3 or higher toxicities, which was significantly fewer than the PIR cohort (p = .021), though the rate of neutropenic fever was higher in hyperCVAD (p = 0.016). There were no deaths during induction and the CRR was 94.4% – not significantly different from the PIR cohort (p = .250) with 60.0% MRD-negative. HSCT was performed for 61.9% of patients in the hyperCVAD group versus 44.4% in the PIR cohort (p = .443). Despite this, the median survival was not reached in either cohort after a median follow-up time of 3.3 years. The cumulative probability of survival at 5.4 years was 100% in the PIR cohort and 76.9% in the hyperCVAD cohort. Conclusions: Our findings suggest that PIRs feature significantly increased grade ≥3 toxicity with evidence of a higher probability of survival at 5.4 years compared to hyperCVAD, although the median survival was not reached and there was no difference between the two arms at the time of follow-up. Patients must be carefully selected for receipt of PIRs given the expected increased burden of toxicity with these regimens. Although long-term survival appears to favor PIRs, larger studies and longer follow-up are needed to confirm these findings.

7060 Background: Myelofibrosis (MF) is a myeloproliferative neoplasm characterized by unregulated, clonal proliferation of a hematopoietic stem cells in the bone marrow and is commonly associated with gene mutations in JAK2, CALR, or MPL. Front-line therapy may include the JAK1/2 inhibitor ruxolitinib (RUX), resulting in spleen volume reductions and improvement in MF-related symptoms. Despite the therapeutic effect of RUX, most patients (pts) eventually progress and thus novel combinations are required to increase responses and delay progression. Selinexor (SEL) is an oral selective inhibitor of nuclear export (SINE) compound, specifically inhibiting exportin-1 (XPO1), and currently approved for treatment of multiple myeloma and diffuse large B-cell lymphoma. Significant activity of SEL in combination with RUX has been shown in preclinical studies, and SEL monotherapy in MF refractory to JAK inhibitors demonstrated robust clinical activity and a tolerable safety profile (NCT03627403). Here, we present the initial results of a phase 1 dose escalation study of the combination SEL and RUX in treatment-naïve MF. Methods: The ongoing multicenter, open-label, Phase 1/2 study (NCT04562389) is evaluating the efficacy and safety of SEL plus RUX in JAKi-naïve MF pts. Two dose levels of SEL were evaluated, 40mg and 60mg once-weekly (QW) plus RUX twice daily (BID) as per label in 28-day cycles, using a 3+3 design. All pts received 5-HT3 antagonist for nausea prophylaxis. Primary objectives include safety, maximum tolerated dose (MTD), recommended Phase 2 dose (RP2D), and preliminary efficacy. Secondary objectives include spleen, symptom, and anemia response, and OS. Results: As of 31 Jan 2022, 10 pts have been dosed in 2 dose levels (40mg (n = 3), and 60mg (n = 7) SEL QW plus RUX). RUX starting dose was 20 mg in 8 pts, 15 mg in one patient and 10 mg in one patient. The median age was 64 (range 45-76). Seven pts had primary MF and 3 had post-ET MF. DIPSS risk category was int-1 (n = 4), int-2 (n = 4) and high risk (n = 2). No dose limiting toxicities have been reported at either dose levels of SEL. One patient required dose interruption due to dizziness and later discontinued treatment due to new onset of atrial fibrillation and pulmonary hypertension (unrelated to SEL and RUX) after 5 months of therapy. All other pts remain on study. There was no grade 3 neutropenia or thrombocytopenia observed. Hemoglobin level was maintained without any significant worsening. The most common treatment-emergent adverse event was low grade nausea (30%). All pts experienced improvement in their white blood cell count. Four of the first 5 evaluable pts demonstrated ≥35% spleen volume reduction at week 12. Conclusions: The combination of SEL and RUX has been well-tolerated and with a manageable side effect profile. No dose limiting toxicities were observed in pts with treatment-naïve MF in cohort 1 of once weekly oral SEL 40 and 60 mg with RUX. Clinical trial information: NCT04562389.

e19039 Background: The rapid adoption of BCR-ABL1 TKIs in Ph+ B-ALL occurred despite a lack of comparative trials, leading to an absence of data regarding the additive toxicities of BCR-ABL1 TKIs with many standard chemotherapy regimens. BCR-ABL1 TKIs have been associated with severe adverse events and may significantly impact treatment-related morbidity and mortality. The objective of this study is to describe the cumulative toxicity imposed by BCR-ABL1 TKIs and chemotherapy regimens. Methods: A total of 48 patients with Ph+ B-ALL treated with a BCR-ABL1 TKI plus chemotherapy between January 2015 and October 2021 were eligible to assess treatment-related toxicity. High-intensity chemotherapy regimens included HyperCVAD, CALGB 10403, ECOG1910, and ECOG2993; low to moderate intensity regimens included EWALL-Ph-01, TKI + POMP, TKI + corticosteroids, and TKI monotherapy. Regimens containing blinatumomab and inotuzumab ozogamicin in combination with a TKI were assessed separately. The primary outcome was the occurrence of grade 3/4 toxicities, as defined by the Common Terminology Criteria for Adverse Events (CTCAE) version 5.0. The first occurrence of CTCAE toxicities was collected for each line of therapy patients received. Results: Among the 48 patients analyzed, 71 total lines of therapy were identified. Of these, 54.9% (n = 39) were classified as high-intensity, 29.6% (n = 21) were low-moderate intensity, 9.9% (n = 7) were blinatumomab, and 5.6% (n = 4) were inotuzumab ozogamicin. In high- and low-moderate intensity regimens, a mean of 10.1 and 6.9 grade 3/4 toxicities occurred with dasatinib and imatinib, respectively (p = 0.076). Among low-moderate intensity regimens with dasatinib (n = 11), 63.6% (n = 7) discontinued dasatinib, 9.1% (n = 1) decreased the dasatinib dose, and 36.4% (n = 4) decreased or discontinued dasatinib due to toxicity. High-intensity chemotherapy regimens with dasatinib demonstrated 51.6% (n = 16) discontinuation, 38.7% (n = 12) dasatinib dose reduction, and 62.1% (n = 18) decreased or discontinued dasatinib due to toxicity. Conversely, among low-moderate (n = 4) and high-intensity (n = 5) regimens in combination with imatinib, no discontinuations or dose reductions occurred. These data demonstrate a greater dose reduction and discontinuation rate with dasatinib compared to imatinib in high-intensity regimens (p = 0.011); differences in low-moderate intensity regimens were not observed (p = 0.174). A secondary analysis did not reveal an association with dasatinib discontinuation rate and CR rate (p = 0.829) or overall survival (p = 0.941). Conclusions: A greater incidence of grade 3/4 toxicity leading to dose changes or discontinuation occurred with dasatinib compared to imatinib. While differences in CR or OS due to TKI-related toxicity were not identified, their occurrence likely contributes to treatment-related morbidity.

e19031 Background: Treatment options for Philadelphia chromosome-positive (Ph+) ALL are increasing. When combined with TKIs, it is unclear if high-intensity regimens lead to a survival benefit compared to reduced-intensity regimens in patients that are not candidates for allogenic hematopoietic stem cell transplant (HSCT). In this study, we sought to examine outcomes of high-intensity and reduced-intensity induction regimens and concurrent TKI administration with respect to toxicity, response, and survival in non-transplant candidates. Methods: We retrospectively analyzed 31 patients with Ph+ B-ALL treated at our institution during January 2015 to January 2021 that were not candidates for HSCT. Baseline patient demographics were obtained, including age, performance status at diagnosis, cytogenetic and molecular profiling through NGS, doses of induction, toxicity, response, MRD analysis, and survival. The event for calculating the overall survival (OS) was the date of death and patients were otherwise censored at the date of last contact. Results: We divided the cohort of 31 patients into two sub-cohorts: a high-intensity cohort of 22 patients treated with TKIs and hyperCVAD, CALGB 10403, or ECOG 1910 and a low-intensity cohort of 9 patients treated with TKI + steroids + vincristine, TKI + steroids, or TKI alone. There was expectedly a significant difference in age between the two groups (p = .002) with more advanced age in the reduced-intensity cohort, though no difference in sex (p≥.999), ECOG score at diagnosis (p = .886), or Charlson Comorbidity Index score (p = .180). Grade 3 or higher toxicity was approaching statistical significance with more toxicity in the higher-intensity group (p = .075). With fewer deaths during induction, achievement of CR or CRi was higher in the reduced-intensity cohort (100% versus 73.7%), though was not significantly different between the groups (p = .288) and the median OS was not reached in either cohort (p = .935) after a median follow-up time of 3.29 years. Conclusions: Acknowledging the limits of a small sample size and retrospective nature of the study, there was no observed difference in survival between high-intensity and reduced-intensity induction with TKIs for patients ineligible for HSCT. Reduced-intensity inductions were associated with a trend toward less severe toxicity. These findings are suggestive that reduced-intensity induction with TKIs in Ph+ ALL may represent a reasonable option for those ineligible for HSCT. Prospective randomized controlled trials in this population are warranted.

We have initiated a single center phase I study in patients with hematologic malignancies progressively substituting day +4 posttransplant cyclophosphamide (PT-CY) with bendamustine (PT-BEN) following myeloablative conditioning (MAC) and T-cell replete haploidentical bone marrow transplantation (haplo-BMT). We report herein our interim analysis of our first three cohorts PT-CY (mg/kg)/PT-BEN (mg/m

Myeloid sarcoma is a rare variant of acute myeloid leukemia (AML) which presents as an extramedullary soft tissue mass. Due to the rarity of this disease, along with nonspecific presenting symptoms, diagnosis can be delayed or missed without a high index of suspicion. In this case, we discuss a patient diagnosed with AML relapse in the form of myeloid sarcoma two years after allogeneic hematopoietic stem cell transplant (alloHSCT) for myelodysplastic syndrome (MDS) with the initial presentation for back pain misdiagnosed as spinal stenosis. This case report aims to help healthcare providers in recognizing the early signs and symptoms of this disorder as well as provide information in regards to treatment options and risk assessment.

Background Myelofibrosis (MF) is a chronic hematologic malignancy with poor prognosis for which the only curative therapy is allogeneic stem cell transplant (alloHSCT). It is suggested that eligible patients with Intermediate-2 and high-risk disease proceed to transplant. Frequency of transplant for MF is increasing, given the advent of reduced intensity conditioning regimens and earlier identification of high-risk disease with mutation testing. Patients with MF are at high risk of regimen related toxicities and poor transplant outcomes due to increased risk of prolonged engraftment and graft failure. These concerns may contribute to a greater reluctance to embrace alternative donor source allografts such as haploidentical (haplo) donors. Herein, we report a case series of patients with MF undergoing alloHSCT. Methods A retrospective analysis was performed on all patients having received a haploidentical HSCT at our institution. Results Three patients were identified as having received haplo HSCT for MF. All received a bone marrow graft. Median age was 57 (range 46-61). One patient had primary MF, one post-PV MF, and one post-ET MF. Risk category at time of transplant by DIPSS was Intermediate -2 in two patients, and high in one. Two of the three patients had a major ABO mismatch. All patients and donors were positive for CMV IgG. Mean cell dose was 2.07 × 10^6 CD34+/kg recipient body weight (range 1.65 × 10^6 to 3.19 × 10^6). All patients received busulfan/fludarabine/melphalan conditioning (one myeloablative dosing, two reduced intensity). Post-transplant cyclophosphamide on days +3 and +4, tacrolimus, and mycophenolate mofetil were used for GvHD prophylaxis in all cases. Median time to neutrophil engraftment was Day +22 (range 20-24), median time to platelet engraftment was 67 days (range 37 - > 70). All patients had complete donor chimerisms at Day +30. Recovery of marrow cellularity was delayed in all patients. All patients had CMV reactivation by PCR, one patient had CMV esophagitis. Infectious complications were common, including BK virus, C. difficile colitis, invasive pulmonary aspergillosis, and klebsiella bacteremia Two patients developed chronic GvHD; one with cGVH of eyes & mouth not requiring systemic therapy, one with cGVH of upper GI tract/mouth. All patients are currently off immunosuppression. All patients are alive at a median follow up of 1.5 years post-transplant (range 456-656 days). Discussion Our case series using a haploidentical donor source and busulfan/fludarabine/melphalan conditioning along with post-transplant cyclophosphamide for patients with MF demonstrates outcomes at least comparable to conventional donor source transplants for MF. While infectious complications and slightly prolonged engraftment were noted in the early transplant period, these can be overcome with aggressive supportive care.

Globoid cell leukodystrophy (GLD) is a progressive neurodegenerative disorder caused by the deficiency of galactocerebrosidase (GALC), resulting in accumulation of toxic metabolites in neural tissues. Clinically variable based on age of onset, infantile GLD is generally a rapidly fatal syndrome of progressive neurologic and cognitive decline, whereas later-onset GLD has a more indolent, protracted clinical course. Animal models, particularly the twitcher mouse, have allowed investigation of both the pathophysiology of and the potential treatment modalities for GLD. Cellular therapy for GLD, notably hematopoietic cell transplantation (HCT; transplantation of bone marrow, peripheral blood stem cells, or umbilical cord blood cells) from a normal related or unrelated allogeneic donor provides a self-renewing source of GALC in donor-derived cells. The only currently available treatment option in human GLD, allogeneic HCT, can slow the progression of the disease and improve survival, especially when performed in presymptomatic infants. Because persistent neurologic dysfunction still occurs after HCT in GLD, preclinical studies are evaluating combinations of HCT with other treatment modalities. © 2016 Wiley Periodicals, Inc.

Background Transplant-associated thrombotic microangiopathy (TA-TMA) is a rare, potentially lethal complication of allogeneic stem cell transplant. It is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal dysfunction. Endothelial injury and terminal complement activation contribute to the pathogenesis of TA-TMA. Several risk factors have been identified including certain conditioning regimens, acute graft versus host disease (GvHD) and/or calcineurin inhibitors (CNI), and viral infections. Eculizumab, a monoclonal antibody directed against C5 which prevents the formation of the C5b-9 membrane attack complex, is effective in treatment of TA-TMA, but with significant infection risk. Here, we review our institution's experience with TA-TMA treated with eculizumab. Methods A retrospective review was performed on all adult and pediatric patients with TA-TMA treated at our institution with eculizumab since 2015. Results Five patients with TA-TMA ages 4.5, 8.5, 11.4, 33, and 37 years (2 female) were treated with eculizumab. All patients received myeloablative conditioning, three TBI-based. Donor source was haploidentical (n=2), matched-unrelated (n=2), and cord (n=1). All patients were on a CNI at diagnosis. TA-TMA therapy required cessation of CNI in 3 of 5 patients. Median day of diagnosis from transplant was 73 days (range 17-251). All patients had renal impairment, three requiring dialysis. Median days from TMA diagnosis to treatment with eculizumab was 3 (range 1-5). Median doses received was 6 (range 4 - >25). Resolution of hemolysis with eculizumab was brisk, ranging from 25-59 days. Figure 1 illustrates a representative trend with regards to LDH, Haptoglobin, CH50, and eculizumab dosing. Four of five patients were alive with a median follow-up of 10.3 months (range 1 - 45 months). The one death was due to Stage IV GvHD and candidemia, present before diagnosis of TMA. Infections were common, including viral and fungal. There were no deaths due to TMA. Two patients continue on dialysis 2.5 and 34.5 months after diagnosis. Discussion Our experience confirms variable clinical presentations, as our patients differed in presence and severity of acute GvHD, confounding role of CNI or triggering of TA-TMA by viral infections. All patients were started on eculizumab promptly following diagnosis, with a high awareness for and prophylaxis of potential infectious complications, which has mitigated the reported high mortality risk of TA-TMA.

Background: Patients with acute myeloid leukemia (AML) who achieve complete remission with induction therapy require consolidation therapy. The standard of care consolidation is HiDAC based on age and risk stratification. Consolidation therapy has historically been administered in the inpatient setting. The rising cost of inpatient care, alternative payment model implementation and patient preference has prompted institutions to consider shifting therapy to the outpatient setting. However, the safety and feasibility of outpatient high dose Cytarabine (HiDAC) consolidation therapy is not well established. The University of Arizona Cancer Center developed an Outpatient Program (OP) to facilitate administration of hematologic chemotherapy regimens in the outpatient setting. We hypothesized that OP administration of HiDAC consolidation therapy would be safe and efficacious and have large cost-savings implications under alternative payment model pilots, such as the oncology care model. Methods: We conducted a retrospective chart review on high-risk MDS/AML patients who were 18 years or older and received HiDAC consolidation therapy at UACC following induction therapy from November 1st 2013 to June 1st 2019. Interim data collection included age, risk stratification, treatment history, clinic visits, number of cycles received in the OP versus inpatient setting, supportive care, hospitalizations, and chemotherapy related adverse events. Our Outpatient HiDAC protocol consisted of a one-hour infusion for all cytarabine doses administered at 7:30am and 4:00pm, with neurologic checks prior to each dose. Growth factor support, if required was administered on the same day as the last dose of cytarabine Results: We evaluated 19 patients at our cancer center who received 52 total cycles of HiDAC consolidation therapy. The median patient age was 49.6 yrs with 21.1 % being over the age of 60. Thirty-three cycles were administered in the outpatient setting, with 19 cycles being administered inpatient. None of the patients who were administered HiDAC in either the IP or OP setting had reported clinically significant neurotoxicity (≥ grade III). Nine patients receive all of their cycles in the outpatient setting. 57.9% of our patients developed febrile neutropenia, with 47.4% of the patients requiring hospitalization for neutropenic fever. The average inpatient HiDAC length of stay was 6 days. Transitioning HiDAC to the outpatient setting led to a savings of 198 hospital days, with a corresponding cost reduction to our healthcare system of $529,650. Transitioning HiDAC to the outpatient setting also improved patient satisfaction. Conclusion: Outpatient administration of HiDAC consolidation therapy for AML patients is a safe and effective treatment option. In addition, transitioning HiDAC to the outpatient setting led to a reduced overall cost of care for AML treatment , under an OCM based practice model. Utilization of outpatient HiDAC for the outpatient setting provides a unique opportunity for select patients. Disclosures Maher: Agios: Consultancy. Anwer:Seattle Genetics: Membership on an entity's Board of Directors or advisory committees; In-Cyte: Speakers Bureau. Campen:Coherus: Speakers Bureau; Teva: Speakers Bureau; Amgen: Consultancy. McBride:teva: Consultancy; Sandoz: Consultancy; Sanofi Genzyme: Consultancy.

Background The nearly universal donor accessibility afforded by haploidentical bone marrow transplantation (haplo-BMT) is salient for our program, as half of the patients undergoing hematopoietic cell transplantation (HCT) are ethnic or racial minorities. This highlights the need for effective haplo-BMT regimens and improvements in graft-versus-host disease (GvHD) prophylaxis. Balancing GvHD prevention with the maintenance of graft-versus-leukemia (GvL) is an ongoing challenge in the field of HCT. We have previously shown in mice that bendamustine (BEN) can safely replace cyclophosphamide (CY) as post-transplant (PT) GvHD prophylaxis following haplo-BMT, with comparable protection from GvHD and superior GvL effects. Based on our preclinical data, we have initiated a Phase I/II study to replace PT-CY (given on days +3 and +4) with PT-BEN following haplo-BMT. Methods Phase I is a standard 3 + 3 dose escalation design with six dose level cohorts. The first three cohorts (1-3) consist of a combination of sequentially reduced doses of CY and increased doses of BEN on day +4 post-BMT with the dose of CY on day +3 remaining unchanged. The next three cohorts (4-6) will involve progressive substitution of CY with BEN on day +3. We are enrolling patients ages 8-60 years with a diagnosis of acute leukemia, chronic myeloid leukemia, myelodysplastic syndrome, Hodgkin's or non-Hodgkin's lymphoma who do not have a readily available HLA-matched (10/10) donor. Myeloablative busulfan, fludarabine, and melphalan or TBI and fludarabine are used as conditioning regimens. Engraftment, immune reconstitution, T-cell receptor β (TRB) diversity, GvHD, infections, relapse, non-relapse mortality (NRM), event-free survival (EFS) and overall survival (OS) are monitored. Patients undergoing haplo-BMT (using the same conditioning regimens) who do not wish to receive PT-BEN are consented as PT-CY controls for the clinical endpoints and immune reconstitution studies. Results We have enrolled through Cohort 2 with no dose-limiting toxicities. Cohort 2 of PT-BEN had significantly earlier neutrophil engraftment than PT-CY controls (median day +13 compared to +17), with >5-fold higher neutrophil to lymphocyte ratios through day +100. PT-BEN patients displayed higher CD4 to CD8 ratio and demonstrated significantly greater TRB diversity than PT-CY only patients through 1 year following transplant. Patients receiving PT-BEN had a trend toward a lower incidence of CMV reactivation, 33% compared to 100% in PT-CY controls. No PT-BEN patient has developed grade III-IV acute GvHD or chronic GvHD. Conclusions PT-BEN has been well-tolerated, with patients demonstrating early engraftment. Preliminary data with PT-BEN indicate potential differences in immune reconstitution and TRB diversity. This may be advantageous in viral control, as well as in GvHD and GvL responses.

Background: Acute Myeloid Leukemia (AML) is a disease of the elderly with a median age of diagnosis of 70 years. Prognosis in this age group is poor, with median overall survival of those undergoing treatment ranging from seven to twelve months. Treatment is difficult for a variety of reasons, including - higher incidence of co-morbid conditions (including frailty and decline in functional status), decreased ability to tolerate infections, socioeconomic considerations, and more aggressive disease phenotype. We present a single-institution retrospective review of acute myeloid leukemia outcomes with respect to these and other variables. Methods: A retrospective chart review was performed on all patients with a new diagnosis of AML from November 2013 through October 2017. Descriptive statistics were performed using excel, inferential statistics including Kaplan-Meier with comparison of survival curves by Logrank test and Cox-proportional hazard regression analysis, and correlation coefficients were performed using MEDCALC statistical software package. Results: Eighty-four AML patients in total were diagnosed with acute myeloid leukemia within the specified time frame, of these, 45 patients were age 65 or older (elderly) and were included in further analysis. Median age of elderly AML patients in this study was 70 years. Six of these patients were diagnosed with secondary AML (having arisen from MDS (N = 4), or other hematologic malignancy (N=2), and two had therapy-related AML. Eight patients had favorable risk disease, 13 intermediate risk, and 24 adverse risk according to ELN 2017 criteria. The median survival of all elderly patients was 322 days. Median survival of elderly AML according to ELN 2017 risk category criteria (Favorable, Intermediate, or Poor) was not reached (mean 880 days), 390 days, and 117 days, respectively (p = 0.0368 by cox hazard regression). Survival was not affected by type of treatment (induction vs hypomethylating agent (HMA); median 579 and 166 days (p = 0.1378) and mean 1552 and 364 days, respectively. This is likely due to small sample size, although survival does appear to favor intensive induction. Survival was not affected by number of medical co-morbidities (p = 0.66), presence of infectious complications (p=0.152), or unplanned hospitalization (p = 0.144). Overall use of clinical trials (N=3) and transplant (N=2) were low, precluding meaningful statistical analysis. However, both patients undergoing transplant exceeded the median OS (579 and 4745 days). Median OS of patients identified as White/Caucasian was greater than those identified as Hispanic/Latino (166 days vs 66 days, respectively), this did not reach statistical significance. Conclusion: Given the limitations of a retrospective review and relatively small sample size, our data shows that the 2017 ELN risk category is the strongest predictor of overall survival. Statistically, those undergoing intensive induction did not have a longer overall survival than those treated with HMAs, highlighting the need for careful selection of induction therapy candidates, and the need for clinical trials investigating other less intense treatment options for patients in this category. Interestingly, number of medical co-morbidities did not influence overall survival, nor did unplanned hospitalizations, presence/absence of significant infections during therapy, or race/ethnicity. Our data suggest an under-utilization of clinical trials and allogeneic hematopoietic stem cell transplant, both of which may serve to improve prognosis. Disclosures No relevant conflicts of interest to declare.

Background - Acute myeloid leukemia (AML) in elderly patients (>65 years) is associated with poor prognosis with median overall survival (mOS) of 6 months. Hypomethylating agents (Azacytidine (Aza) and Decitabine) are used in elderly patients who are not candidates for intensive chemotherapy. Aza has resulted in complete remission/complete remission with incomplete hematologic recovery (CR/CRi) of 18-27.8% and mOS of 10.4-24.5 months. Decitabine resulted in CR/CRi of 18-47% and mOS of 7.7-8 months. We conducted a systemic review to assess survival benefit of novel combination drug regimens (CDR) involving hypomethylating agent (HMA) in elderly patients with newly diagnosed AML. Methods - Comprehensive literature search was conducted in Medline, Embase and Cochrane database. We included phase I/II studies only that used CDR involving HMA. Results - Initial database search (since inception) lead to 975 studies. After exclusion (duplicates, case reports, relapsed/refractory AML) final analysis included 17 studies(n=540) Ten phase I/II CDR studies involving Aza (n=334) were included. The various drugs used in combination included valproic acid/all trans retinoic acid (n= 42 ,CR/CRi=26.2% mOS= 18.1 m), thalidomide (n= 14,CR/CRi= 29%, mOS= 13.2 m ), gemtuzumab ozogamicin (GO) (n= 142,CR/CRi = 35-44%, mOS= 11 m), lenalidomide (n= 45,CR/CRi=28-44% , mOS= 3-8.2 m), panobinostat (n=38,CR/CRi=10-22.4%, mOS= 8 m), midostaurin (n=12,CR/CRi=25%, mOS=6 m) , entinostat (n=18 ,CR/CRi=0% ,mOS= 6 m ), Seven phase I/II CDR studies(n=206) involving decitabine were included. Drugs used in combination included low dose cytarabine and aclarubicin (n= 85 ,CR/CRi = 64.7% , mOS= 10-12 m ), tosedostat (n=17 ,CR/CRi= 59% mOS= 11.5 m ), bexarotene(n= 4 ,CR/CRi= 0% mOS= 9.2 m), valproic acid(n= 62 ,CR/CRi= 9% mOS= 7.4m) , GO (n= 40,CR/CRi= 45% , mOS= 7m ),bortezomib (n= 10,CR/CRi= 50% ), vorinostat(n = 31,CR/CRi= 30%). Seven studies reported outcomes for patients with adverse cytogenetics separately. Of these, Aza with lenalidomide (n= 11) had a mOS of 9.5 months and with panobinostat (n=12) the overall response rate was 25% and mOS of 7 months. Similarly, decitabine with vorinostat (n = 8) and tosedostat(n =12) resulted in CR/CRi of 25% and 43% respectively. Long term outcomes for these CDR with decitabine were not reported. In two additional studies, valproic acid/all trans retinoic acid given with AZA and low dose cytarabine & aclarubicin with decitabine(p=0.023) showed poor outcome through multivariable cox model analysis. Five studies reported response rates for subgroup of patients with secondary AML using HMA. Of these, Aza with lenalidomide (n= 16) had a CR/CRi = 27% with median response duration of 21.3 weeks, a CR/CRi of 0% with entinostat (n= 18) and CR/CRi of 22% with thalidomide(n=9). Decitabine given with tosadostat (n= 10) had CR/CRi of 60% and with bortezomib(n=3) the CR/CRi was 66%. The long term outcomes were not reported for these patients. Conclusion - Novel combinations involving Aza with valproic acid/all trans retinoic acid, thalidomide, or GO showed similar CR/CRi and mOS compared to Aza alone. Tosedostat, low dose cytarabine, and aclarubicin given in combination with decitabine showed best results with superior CR/CRi and mOS compared to decitabine alone. Bexarotene with decitabine also improved mOS over decitabine alone despite lower CR/CRi. In patients with adverse cytogenetics, Aza with lenalidomide or panobinostat showed superior CR/CRi and mOS. Decitabine given with vorinostat and tosedostat also showed superior CR/CRi. In patients with secondary AML, Aza in combination with lenalidomide or thalidomide and decitabine with tosedostat or bortezomib showed superior CR/CRi. These CDR for patients with adverse cytogenetics and secondary AML need further testing in studies designed with this specific patient population in which long term outcomes are also measured. These CDR need to be evaluated in large, randomized, prospective studies to assess definitive benefit. Disclosures No relevant conflicts of interest to declare.

7050Background: Relapse after allogeneic hematopoietic stem cell transplantation (AlloHSCT) for Ph+ve acute lymphoblastic leukemia (Ph+ ALL) remains the major cause of treatment failure. Use of tyr...

Introduction: The relative incidence of adenocarcinoma of the lung is increasing, and it is now the most common primary lung malignancy. This study examines certain clinical and pathological factors which may affect patient survival in lung adenocarcinoma in the developing country of Pakistan. Methods: This is a descriptive study involving 56 patients with biopsy-proven primary adenocarcinoma of lung. Biopsy tissues were reviewed along with medical record case histories. Formalin-fixed, paraffin-embedded tissue specimens were used for mucin histochemistry with mucicarmine, periodic acid Schiff (PAS) and alcian blue stains. Immunohistochemistry (IHC) with monoclonal antibodies against CD34 was used for assessment of microvascular density. Mast cell density was measured on Toluidine blue stained sections. Results: Mean age of patients was 55.96 ± 1.67 years. Male to female ratio was 3:2. 51.8% of patients were smokers, and weight-loss was seen in 46.4% of the patients. A majority (66.1%) had stage III/IV tumors with positive lymph nodes, and 26.8% tumors were mucinous. High mast cell density was found in 32.1% and high microvessel density in 44.6% tumor specimens. Weight-loss, stage, nodal status, mucin production and microvessel density showed significant deleterious effect on patient survival. Conclusions: The current study illustrates that for this population, weight loss, advanced stage of tumor, nodal status, mucin production by the tumor, and increased angiogenesis are predictors of poor survival in patients with primary pulmonary adenocarcinoma. Further prospective work will need to be performed to determine if these factors can assist in prognostication or formulation of treatment plan in newly diagnosed individuals in the general population.

Background Plerixafor and granulocyte-colony stimulating factor (G-CSF) are commonly used in combination to mobilize CD34+ cells for collection for autologous hematopoietic stem cell transplantation (HSCT). Standard protocol involves four consecutive days of G-CSF followed by plerixafor, administered 11 hours before apheresis (for 8 am harvest next day, 9 pm administration the night before harvest). However, this timing is often logistically impractical for both patients and staff members. To examine whether plerixafor could be given on a less stringent timeline without compromising efficacy, we conducted a retrospective review of multiple myeloma patients who underwent mobilization and collection at our institution from 2010 to 2013. A further subset analysis was also performed on patients based on patient comorbidities such as age, BMI, and prior treatment with Lenalidomide to assess whether or not the earlier administration of plerixafor would affect cell collections in patients with differing characteristics. Methods 52 consecutive patients with multiple myeloma at the University of Arizona Cancer Center were studied to analyze the effectiveness of G-CSF/Plerixafor mobilization with plerixafor given at approximately 14 to 17 hours before apheresis instead of 11 hours as instructed by plerixafor package insert. G-CSF was given according to standard protocol, with patients receiving a rounded dose of 10mcg/kg, to either 300 or 480mcg daily, at 0800 for four consecutive days. Plerixafor was given on the 4th day at 14 to 17 hours (2-5 PM instead of 9PM) before apheresis, which commenced at 0800 the following morning. Patients were given additional doses of plerixafor if inadequate numbers of cells were collected in the initial apheresis session. Results The patient population consisted of 52 consecutive patients, aged 36 to 77 years old, with BMIs ranged 18.7 to 46.6, of which 28 had previously been treated with Lenalidomide. The median number of apheresis sessions to reach goal CD34+ count of 2 X 10^6 was 1 (range 1-4). 11 patients required 2 or more collections (6 patients required 2 collections, 4 required 3, and one individual required 4 collections). Mean CD34+ count collected after all required apheresis sessions per patient was 9.74 x 10^6 (range 2.07 x 10^6 - 24.99 x 10^6). All patients collected sufficient stem cells to proceed with autologous HSCT. Patient were then divided into further groups for further analysis: age (62 or less vs greater than 62), BMI (less than 28 vs 28 or greater), and lenalidomide treatment in the past. None of those three characteristics showed any statistical difference in the number of CD34+ stem cells collected (See graph 1, 2, and 3). Conclusion Based on these data, plerixafor mobilization remains an effective method of stem cell mobilization despite lengthening of the interval from medication administration to apheresis. Moreover, this alleviates the major logistical disadvantage of using plerixafor for stem cell mobilization. Figure 1 Figure 1. Figure 2 Figure 2. Figure 3 Figure 3. Disclosures McBride: Sanofi: Research Funding.