ALBERT

Description: BACKGROUND: Peripheral blood progenitor cell (PBPC) mobilization strategies vary considerably. Optimization of this critical aspect of autologous hematopoietic stem cell transplantation (ASCT) requires efficient use of resources including apheresis kits, machine run time, nursing and cell processing time and consumables. Equally important is the patient experience, which is strongly influenced by collection days and caregiver time that reduces their economic productivity and raises their expenses. We developed a mobilization algorithm designed to collect the target number of cells on day 1 of collection. The algorithm utilizes pre-emptive day 4 plerixafor to maximize collection day peripheral blood (PB) CD34+ cell numbers. METHOD: We analyzed data on all patients with multiple myeloma undergoing PBPC mobilization between March 2014 and July 2016. All patients were mobilized with the intent of collecting sufficient numbers of progenitor cells to permit two ASCT procedures. Patients received filgrastim 10 mcg/kg daily x 4 days. Patients in whom the PB white blood cell (WBC) count was 〈 50K/uL on day 4 received an extra dose of filgrastim that evening and plerixafor at 0.24 mg/Kg (Figure 1) or a fixed dose of 12mg (Figure 2) if the PBCD34 was 〈 50/uL. A fixed dose was administered if a patient could be paired with another patient simultaneously undergoing PBPC mobilization. The number of days of apheresis, run time, collection efficiency (CE2) and other relevant variables were analyzed and compared between the standard and fixed dose cohorts. We defined successful mobilization as ≥ 8 million CD34+ cells/Kg (based on our institutional ideal dose of 4 million CD34+ cells/Kg for a single ASCT), optimal mobilization as ≥ 6 million CD34+ cells/Kg (based on the International Myeloma Working Group (IMWG) recommended minimum dose of 3 million CD34+ cells/Kg for an ASCT), suboptimal mobilization as ≥ 2 million but 〈 6 Million CD34+ cells/Kg, and mobilization failure as 〈 2 million CD34+ cells/Kg. RESULTS: We identified 105 patients with MM. Median age was 61 years (range, 25 - 76) and 57% were female. Disease status at mobilization included: 7 CR, 14 stringent CR, 5 unconfirmed CR, 52 very good PR (VGPR), and 27 PR. The median day 4 PBCD34+ cell number was 19.9/uL (range, 0.8 - 118.7/uL), and median day 5 PBCD34+ count was 107.8/uL (range, 15.6 - 307.8/uL). Ninety percent of patients required plerixafor of which 16% (n = 17) received the 12 mg fixed dose. The median increase in day 4 to day 5 PBCD34+ cell count for patients receiving plerixafor was 6.6 fold (range, 1.5 - 56.4 fold). In patients not receiving plerixafor, the median increase was 1.8 fold (range, 1.5 - 2.6 fold). The median collection yield was 10.95 million CD34+ cells/Kg (range, 2.9 - 22.5 million CD34+ cells/Kg) no significant difference between patients who received standard dose or fixed dose plerixafor. By the criteria outlined above 96.2% of patients had an optimal mobilization i.e. ≥ 6 million CD34+ cells/Kg sufficient for 2 ASCT procedures with 94.2% achieving this with only 1 day of collection. Per our institutional criteria, 71.4% achieved a successful collection (〉 8 million CD34+ cells/Kg) in 1 day. There was no significant difference in days of collection among patients receiving 4 or less cycles of lenalidomide versus those receiving more than 4 cycles (p value = 0.104). The median duration of collection was 399 minutes (range, 180 - 495 minutes) with a median collection efficiency (CE2) of 42.3%. The mean number of days of collection was 1.23 days (range, 1 - 2 days). The median transplanted CD34+ cell dose was 5.48 million CD34+ cells/Kg. All patients had hematopoietic recovery with median neutrophil and platelet engraftment of 11 days and 18 days, respectively. CONCLUSION: The pre-emptive use of plerixafor on day 4 is effective and results in a high percentage of optimal day 1 collections. The cost of a more liberal plerixafor algorithm is offset by the savings incurred from reduced collection day numbers with the majority of patients requiring only 1 day of collection. Cost savings include limiting days away from work and family for the patient and caregiver and decreasing expenses for travel and overnight stays. Reducing collection day numbers also reduces the impact on quality of life for patients, caregivers and family members. Collectively, these data demonstrate utility of the pre-emptive day 4 plerixafor-based mobilization algorithm described here. Disclosures Usmani: Amgen: Consultancy, Research Funding, Speakers Bureau; Sanofi: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Celgene: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Takeda: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Onyx: Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Janssen: Membership on an entity's Board of Directors or advisory committees, Research Funding; BioPharma: Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Pharmacyclics: Research Funding; Britsol-Myers Squibb: Consultancy, Research Funding; Skyline: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Array: Research Funding; Millenium: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Novartis: Speakers Bureau. Jacobs:Magellan Health: Consultancy; Pharmacyclics: Consultancy, Speakers Bureau. Bhutani:Onyx, an Amgen subsidiary: Speakers Bureau; Bristol-Myers Squibb: Speakers Bureau; Takeda Oncology: Research Funding, Speakers Bureau; Prothena: Research Funding. Avalos:Seattle Genetics: Membership on an entity's Board of Directors or advisory committees.

Description: BACKGROUND: DLBCL is the most common and a potentially curable non-Hodgkin lymphoma. Multiple previous studies have shown that minority populations have worse outcomes compared to Caucasians (Tao L, Blood 2014; Griffiths R, BMC Cancer 2010; Koroukian et al, Cancer, 2010, Shenoy PJ Cancer 2010). Moreover, it has been reported that uninsured and Medicaid insured patients with DLBCL have inferior survival compared to privately insured patients (Han X, Cancer 2014; Koroukian et al, Cancer 2010;). It has also been well established that minorities are underrepresented in clinical trials (Gerrero S, Sci Rep 2018; Kwiatkowski K, Cancer 2013). We present the baseline characteristics, treatment paradigms and outcomes of Caucasian (C) and non-Caucasian (NC) patients with de novo DLBCL treated at a single academic hybrid cancer center. METHODS: We collected demographic, disease, insurance coverage, treatment characteristics, and treatment outcomes for patients with de novo DLBCL who presented between January 2016 and January 2019 at Levine Cancer Institute, Charlotte, North Carolina. Patient race, C or NC were self-reported. Insurance was categorized as Government (Medicaid or Medicare), Private, or Uninsured. We used the Revised International Prognostic Index (R-IPI) to risk stratify patients. Double-hit lymphomas (DHL) were defined as having the MYC translocation with either BCL2 or BCL6 translocation on fluorescent in situ hybridization. Treatments included standard chemoimmunotherapies, stem cell transplantation and clinical trials including chimeric antigen receptor therapies (CART). Outcomes of overall survival (OS) and progression free survival (PFS) were calculated using the Kaplan Meier method and compared with log rank test. Demographic data was compared using Fisher's Exact tests. RESULTS: One hundred and ninety-six consecutive patients with de novo DLBCL were included in the analysis [155 (79%) = C, 41 (21%) = NC] (Table). The NC group was predominantly African American (71%) followed by Hispanic (15%). Prognostic scores (R-IPI) and the incidence of DHL were similar between C and NC. The median age at diagnosis in the NC group was lower than in C. There were significant differences in insurance coverage between the 2 groups (p=0.012). The C group did not have any uninsured patients and had more patients with private insurance (33%) compared to the NC group (7% uninsured and 27% with private insurance). The most common frontline treatment was RCHOP (C=66%, NC=70%) followed by dose adjusted REPOCH (C=12%, NC=15%). Median follow up was 31.6 months. There was no difference in OS and PFS between the 2 groups (Figure 1). OS at 2 years from date of diagnosis was 81% for C and 84% for NC, p=0.852. Two-year PFS from time of diagnosis were similar for both groups: 61% for C and 63% for NC, p=0.999. Similar numbers of patients in both groups developed relapsed or refractory (R/R) disease after frontline therapy. Median number of treatments was 2 for both groups, p=0.582. For patients who developed R/R DLBCL, the 2-year OS was 60% for C and 63% for NC, p=0.590. Similar proportions underwent stem cell transplantation: 11% for C and 20% for NC, p= 0.186. Clinical trial enrollment was comparable: 11% for C and 12% for NC, p=0.785. CONCLUSION: Unlike previous population-based studies that have shown racial disparities with superior outcomes for Caucasians and for patients with private insurance, our single center experience demonstrates similar survival outcomes between Caucasians and non-Caucasians diagnosed with de novo DLBCL, despite differences in insurance coverage favoring Caucasians. In the R/R setting, similar proportions of both groups underwent stem cell transplantation and enrolled on clinical trials. The likely explanation is that our safety net cancer center, with extensive nurse navigator support and access to standard treatments, stem cell transplants and cutting-edge clinical trials may abrogate the inferior outcomes in minority populations that have been previously reported. Disclosures Symanowski: Immatics: Consultancy; Eli Lilly: Consultancy; Carsgen Therapeutics: Consultancy; Boston Biomedical: Consultancy. Park:Rafael Pharma: Membership on an entity's Board of Directors or advisory committees; BMS: Consultancy, Research Funding; Gilead: Speakers Bureau; Teva: Consultancy, Research Funding; G1 Therapeutics: Consultancy; Seattle Genetics: Research Funding, Speakers Bureau. Avalos:Juno: Membership on an entity's Board of Directors or advisory committees; Best Practice-Br Med J: Patents & Royalties: receives royalties from a coauthored article on evaluation of neutropenia. Jacobs:Genentech: Speakers Bureau; AstraZeneca: Speakers Bureau; TG Therapeutics: Honoraria, Research Funding; AbbVie: Consultancy, Speakers Bureau; JUNO: Consultancy; Gilead: Consultancy; Pharmacyclics LLC, an AbbVie Company: Research Funding, Speakers Bureau. Ghosh:TG Therapeutics: Consultancy, Honoraria, Research Funding; SGN: Consultancy, Honoraria, Research Funding, Speakers Bureau; Bristol-Myers Squibb: Honoraria, Speakers Bureau; Gilead: Consultancy, Honoraria, Speakers Bureau; Janssen: Consultancy, Honoraria, Research Funding, Speakers Bureau; Pharmacyclics LLC, an AbbVie Company: Consultancy, Honoraria, Research Funding, Speakers Bureau; Celgene: Consultancy, Research Funding; Genentech: Research Funding; AstraZeneca: Honoraria, Speakers Bureau; Forty Seven Inc: Research Funding.

Description: In 1991, we reported the results of 127 patients with Acute Myeloid Leukemia (AML) who underwent conditioning for allogeneic transplant with busulfan, 4 mg/kg on each of 4 days and cyclophosphamide 60 mg/kg on each of 2 days. In the current abstract, we report data on 295 patients, including the initial cohort, who underwent allogenic transplantation for AML from 1984 to 1995 at 7 participating institutions. Median age of patients is 33. One hundred forty nine men and 126 women underwent transplant. All patients received marrow from related HLA-identical donors. One hundred seven patients (36%) remain alive. One hundred forty one patients were transplanted in first remission (group I), 43 in second remission (group II) and 111 patients were in 〉 2nd remission or had refractory disease (group III). The median follow-up of patients in the initial study was 3 years and is 12 years in the current study. Seventy-five percent of patients surviving 3 years after transplantation are estimated survivors 12 years after transplant. Relapse (20), chronic GVHD (5) and infection (3) were the major causes of death in patients who died more than 3 years after transplantation. The estimated relapse rate for group I at 3 and 12 years is 18%(95% CI: 2–32%) and 29% (95% CI 11–47%) for group II is 40% (95% CI: 8–72%) and 52% (95% CI: 16–84%), and group III is 59% (95% CI: 37–81%) and 69% (95% CI: 45–93%) respectively. The estimated leukemia-free survival (LFS) for group I at 3 and 12 years is 60% (95% CI: 44–76%) and 47% (95% CI: 29–65%), for group II is 47% (95% CI: 17–77%) and 34% (95% CI: 4– 64%)and group III is 22% (95% CI: 6–38%) and 15% (95% CI: 1–29%) respectively. Remission stage was predictive of long-term LFS (P

Description: BACKGROUND: The immune system plays an essential role in both promoting and inhibiting the growth of MM. Loss of anti-myeloma immunity involves altered activation and polarization of effector cells as well as immunosuppressive cytokines. Immune dysfunction associated with MM can be partially or totally reversed when patients achieve clinical remission. Detection of MRD has become an achievable goal in MM, and is a powerful predictor of progression-free survival and overall survival. We hypothesized that the immune profile of MRDpos patients is distinct from MRDneg patients. PATIENTS AND METHODS : We studied peripheral NK, NK-T and T cell distribution/activation, and measured bone marrow MRD status by flow cytometry in 30 newly diagnosed MM patients 60+ days after ASCT. Patients were divided in 2 groups based on κ/λ ratio and MM-plasma cell (MM-PC) distribution: MRDneg (n=6), with κ/λ ratio ≤1.8 and MM-PC≤15 per million or MRDpos (n=24), with MM-PC〉15 per million. Plasma was also collected from 17 of these patients (5 MRDneg and 12 MRDpos) 60+ days after ASCT to quantify inflammatory cytokines, chemokines and growth factors by multiplex protein assay. Linear regression was used to determine association between each tested variable (25 by flow cytometry and 27 by multiplex protein assay) and MRD status. Unsupervised hierarchical cluster analysis was then applied to post-ASCT samples with selected variables that were differentially expressed between MRDneg and MRDpos patients (p

Description: Recently, somatic mutations in the granulocyte colony-stimulating factor receptor (CSF3R) have been identified in the majority of patients with chronic neutrophilic leukemia (CNL). The T618I mutation is the most common of these mutations, and it has been suggested that this specific mutation be added to the current WHO criteria for the diagnosis of CNL. In vitro studies of cells transfected with the T618I mutation have demonstrated that the mutant receptor confers a hyperproliferative phenotype. We report here a case of congenital neutrophlia with an associated germline T618I CSF3R mutation. The patient, currently a 10 year old female, has had an elevated but stable leukocytosis (WBC 24,000 - 35,000) since birth, comprised of approximately 80% neutrophils. She has been healthy, with no increase in frequency of infections. Bone marrow studies performed at 5 months and 10 years of age have shown the marrow to be hypercellular, with normal karyotype/FISH (including BCR/ABL negative) and no dysplastic features. Additionally, no mutations have been detected in JAK2, MPL, CALR, PDGFA/B, and FGFR1. DNA was extracted from whole blood and buccal cells collected from the patient, and using next generation sequencing a T618I mutation in CSF3R was identified in both her buccal and blood cells, confirmed by Sanger sequencing. The T618I mutation was present at an approximately 50% allele frequency in both tissues. Using a combination of next generation and Sanger sequencing, the patient's DNA was also analyzed for the presence of mutations in ASXL1, SETBP1, and TET2; as these have been reported in combination with the T618I mutation in many cases of CNL. However, no such additional mutations were detected in our patient. Congenital neutrophilia arising from another activating mutation in CSF3R has previously been reported in a family from France (Plo et al., J Exp Med 2009). The mutation identified in that family was reported to be at amino acid position 617 (T617N) (numbering from the methionine 1, which includes the leader sequence, this correlates to a T640N mutation). Similar to the T618I mutation in our patient, none of the 12 affected family members (ages 8-80 years) progressed to an acute leukemia. Collectively, these observations suggest that activating CSF3R mutations, including the T618I mutation, may result in chronic neutrophilic leukemia but that subsequent disease progression may be due to other, cooperating mutations. Disclosures No relevant conflicts of interest to declare.

Description: BACKGROUND: Lenalidomide is an immunomodulatory drug (IMiD) with co-stimulatory effects on immune effector cells in vitro and is an approved treatment for multiple myeloma (MM), although its mode of action in patients is not well defined. We studied the impact of lenalidomide maintenance therapy, following autologous stem cell transplant (ASCT), on NK and NK-T polarization (i.e. activating or inhibitory molecules) and, T cell activation (early vs. late activation) in patients with multiple myeloma. PATIENTS AND METHODS: In this ongoing prospective study with a targeted enrollment of 28 newly diagnosed multiple myeloma patients, blood samples are being collected at 2 to 3 months post ASCT, before starting lenalidomide maintenance therapy (baseline), and serially after 1, 3 and 6 months of treatment (T+1mo, T+3mo, T+6mo). Using a 9 color flow cytometry panel, peripheral blood samples were analyzed for expression of CD3 and CD56 to define NK (CD56+ CD3-), NKT (CD56+ CD3+), and T cell (CD56- CD3+) subsets. Killer 'inhibitory' Ig-like receptors, (KiR2DS4, KiR3DL1) natural killer group 2 proteins (NKG2a, NKG2D) and natural killer p46 protein (NKp46) expression were quantified to assess polarization of NK, and NK-T cells. Programmed death receptor 1 (PD-1) and T-cell Ig and mucin receptor 3 (Tim3) expression was quantified to assess T cell activation state. Flow cytometry data were acquired on a BD FACSAria II, and analyzed using FlowJo version X software. RESULTS: Samples from 11 patients have been collected and analyzed so far (11 baseline, 6 T+1mo, 4 T+3mo). At baseline lymphoid cells represent 12-46% of white blood cells (WBC), this heterogeneity being mainly driven by a wide range of T cell relative distribution among patients (30-74 % lymphoid cells). Phenotypically, NK cells at baseline mainly express natural cytotoxicity receptors (NKp46 and NKG2D), whereas NK-T cell also express NKG2D but approximately 1/3 also express PD-1 indicating they may be functionally defective. T cells at baseline express early T cell activation markers NKG2D and approximately 1/3 also stained positive for late T cell activation marker PD-1. Lymphoid cells relative distribution among WBC tends to normalize at T+1mo of treatment (15 to 35 % of WBC) before expanding at T+3mo (35 to 43 % of WBC). Phenotypically, across the 27 immune variables analyzed, each multiple myeloma patient displayed high level of immune homeostasis after 1 or 3 months of lenalidomide treatment. Noticeably, Nkp46 expression by NK cell and PD-1 expression by NK-T cells decreased in 4/6 patients and, NKG2D expression by T cell decreased in all but one patient during lenalidomide therapy. CONCLUSION: To our knowledge, this is the first study examining the influence of lenalidomide maintenance on the comprehensive immune repertoire in the post-ASCT setting in MM patients. The wide heterogeneity of NK, NK-T and T cell distribution observed at baseline among lymphoid cells indicates the potential effect of post-ASCT immune reconstitution and immunomodulatory the impact of lenalidomide. The capacity of lenalidomide to mediate effects on several immune cells raises the question as to which, if any, of these changes correlate with clinical responses. In our study, serially collected data from each patient, when completed would determine the impact of lenalidomide immunomodulatory effect of therapeutic efficacy and PFS duration in relation to immune reconstitution stage. Disclosures Cogdill: Millennium: Speakers Bureau; Onyx: Speakers Bureau; Celgene: Speakers Bureau; Novartis: Speakers Bureau. Ghosh:Celgene: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Pharmacyclics: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau. Usmani:Sanofi: Honoraria, Research Funding; Millennium: Honoraria, Speakers Bureau; Onyx: Honoraria, Research Funding, Speakers Bureau; Pharmacyclics: Research Funding; Celgene: Honoraria, Speakers Bureau; Janssen Oncology: Honoraria, Research Funding; Array BioPharma: Honoraria, Research Funding.

Description: Background. Among patients with newly diagnosed diffuse large B cell lymphoma (DLBCL), undergoing standard immunochemotherapy R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone), overall survival is significantly worse for those with activated B cell-like (ABC) subtype compared with germinal center B cell-like (GCB) subtype. Among the key differences between DLBCL subtypes, constitutive activation of nuclear factor kappa B (NFκB) in the ABC-subtype has been associated with a rise of circulating myeloid-derived suppressor cells (MDSC). Patients and Methods. In this pilot study, blood samples were collected from 6 ABC-subtype and 5 GCB-subtype newly diagnosed DLBCL patients prior to and after R-CHOP therapy. To assess the systemic impact of constitutive NFκB activation in ABC-subtype compared with GCB-subtype DLBCL, serum concentrations of 27 immune analytes (15 NF-κB-dependent chemokines, cytokines and growth factors, 12 NFκB-independent chemokines and cytokines) were measured retrospectively using a BioPlex platform. ABC-subtype and GCB-subtype DLBCL immune profiles were further investigated using a 6-color flow cytometry panel (BD FACS Aria II), in which peripheral blood samples were prospectively analyzed for expression of CD11b, HLA-DR, CD33 and IL-4R to define MDSC (CD11b+, HLA-DR-/low, CD33+, IL-4R+), either monocytic (IL-14+) or granulocytic (CD15+). Results. Among the 11 patients enrolled in the study, 7 (5 ABC and 2 GCB) have completed R-CHOP therapy and are in complete remission. Twenty out of 27 immune analytes surveyed to establish DLBCL immune profiles were either not detected or constitutively expressed among ABC and GCB patients (pre or post therapy). At baseline, the predominant difference between DLBCL subtypes was centered around 3 NFκB-independent immune analytes. The IRF4-dependent chemokine CXCL10 was highly expressed in ABC-subtype DLBCL while elevated IL-12p70 and IL-13, (T-bet and Gata3-dependent cytokines, respectively) were mainly found in GCB-subtype DLBCL. Post R-CHOP therapy, serum concentrations of NFκB-dependent innate immune mediators, the cytokine IL-6 and the chemokine CXCL8, decreased by »50% regardless of DLBCL subtypes. While no systemic difference in NFκB-dependent immune analytes could distinguish the ABC-subtype from GCB-subtype DLBCL, circulating gMDSC and mMDSC were 8 and 3 times more prevalent among ABC patients. Following R-CHOP, their levels decreased to those observed in patients with the GCB subtype. Conclusions. Although constitutive NFκB activation is the hallmark of ABC-subtype DLBCL, no systemic NFκB-dependent immune analyte could distinguish ABC from GCB-subtype DLBCL in this pilot study. Despite the lack of a "NFκB immune signature", MDCSs (especially mMDSC) were predominantly found in ABC-subtype DLBCL. Significant differences were also observed among NFκB-independent immune analytes, predominantly adaptive cytokines, indicating GCB-subtype DLBCL have a more profound effect on T cell polarization, specifically TH2, than ABC-subtype. Disclosures Ghosh: Pharmacyclics: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Celgene: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau.

Description: Acquired mutations in the granulocyte colony-stimulating factor receptor (G-CSFR) occur in a subset of patients with severe congenital neutropenia (SCN) who develop acute myelogenous leukemia (AML). These mutations affect one allele and result in hyperproliferative responses to G-CSF, presumably through a dominant-negative mechanism. Here we show that a critical domain in the G-CSFR that mediates ligand internalization is deleted in mutant G-CSFR forms from patients with SCN/AML. Deletion of this domain results in impaired ligand internalization, defective receptor downmodulation, and enhanced growth signaling. These results explain the molecular basis for G-CSFR mutations in the pathogenesis of the dominant-negative phenotype and hypersensitivity to G-CSF in SCN/AML.

Description: In 1992, we published the results of the first multi-institutional study of BuCy2 (busulfan 4mg/kg daily for four days and cyclophosphamide 60mg/kg on each of two days) preparation for allogeneic transplantation using related HLA-identical donors in chronic myeloid leukemia (CML). Median follow-up was 3 years. This report updates outcomes to July 1, 2006 for a total of 294 patients, including the original cohort, who underwent allogeneic transplantation with the BuCy2 regimen at 7 centers between March 1984 and December 1995. The median follow-up of surviving patients is 13 years. Two hundred patients underwent transplantation in chronic phase, 58 in accelerated phase and 36 in blastic phase. One hundred thirty two patients (45%) remain alive. Seventy-nine percent of patients surviving 3 years after transplantation are estimated survivors 13 years after transplantation. The estimated survivals at 3 and 13 years are 69% (95% CI: 57–81%) and 56% (42–70%) for chronic phase patients, 38% (14–62%) and 25% (1–49%) for accelerated phase patients, and 17% (0–41%) and 4% (0–16%) for those in blastic phase. Estimated relapse rates, according to stage of disease, are 6% (0–14%), 21% (1–49%), and 55% (7–100%) respectively at 3 years and 22% (6–38%), 42% (0–84%) and 74% (20–100%) respectively at 13 years. Of 51 patients who developed hematologic or persistent cytogenetic relapse, 28 relapsed within 3 years of transplantation and 23 (45%) relapsed more than 3 years from transplantation (longest: 15 years) Twenty-five of the 28 patients who relapsed within 3 years have died. Of the 23 who relapsed beyond 3 years, 7 have died. Death occurred more frequently (P

Description: Background: Financial Toxicity (FT) is increasingly recognized as a major contributor to morbidity and mortality in a variety of cancers. Previous research has demonstrated patients with myeloproliferative neoplasms (MPNs) exhibit a substantial comorbidity burden and have an increased risk of mortality. The purpose of this study was to define rates of FT and the implications on morbidity and mortality in this population using patient reported data. Methods: All patients seen at the Levine Cancer Institute, a tertiary hospital-based specialty practice, were surveyed prior to their visit over a six-month period. All patients were aged ≥18 years and diagnosed with Philadelphia chromosome−negative classical MPNs including myelofibrosis (MF), polycythemia vera (PV), and essential thrombocythemia (ET). The survey consisted of the PROMIS Global-10 measure and two questions from the COST measure. FT was defined as scoring 4 or less (maximum: 10) in agreement with the COST questions: "I know that I have enough money in savings, retirement, or assets to cover the costs of my treatment" and "I am satisfied with my current financial situation." Patient disease and treatment characteristics were summarized with frequencies and proportions for categorical variables and medians and ranges for continuous variables. Correlation of numerical FT scores with PROMIS scores was assessed with Pearson correlation coefficients and ANOVA regression. Additionally, model selection was carried out using logistic regression to identify factors impacting the incidence of financial toxicity (where FT score 4 compared to patients with FT scores 4 (p =.287). There also appeared to be a separation of the survival curves when looking at both time from diagnosis and time from survey administration (Figures 2 and 3). Age, race, gender, insurance type, distance from the hospital, disease type, disease specific risk classification, medications utilized, and history of blood/marrow transplant were not found to be significantly different in the two groups. Conclusions: Patients with myeloproliferative neoplasms represent an extremely vulnerable population for financial toxicity with quantifiably increased distress related to this toxicity increasing morbidity and potentially mortality. These findings should be validated in a larger patient cohort and interventions devised to reduce financial distress. Disclosures Knight: Foundation for Financial Planning: Research Funding. Ai:InCyte: Speakers Bureau; Amgen: Speakers Bureau. Trivedi:Incyte: Speakers Bureau. Avalos:Best Practice-Br Med J: Patents & Royalties: receives royalties from a coauthored article on evaluation of neutropenia; Juno: Membership on an entity's Board of Directors or advisory committees. Symanowski:Boston Biomedical: Membership on an entity's Board of Directors or advisory committees; Carsgen Therapeutics: Membership on an entity's Board of Directors or advisory committees; Eli Lilly: Membership on an entity's Board of Directors or advisory committees; Immatics: Membership on an entity's Board of Directors or advisory committees. Grunwald:Amgen: Consultancy; Novartis: Research Funding; Genentech/Roche: Research Funding; Pfizer: Consultancy; Daiichi Sankyo: Consultancy; Trovagene: Consultancy; Agios: Consultancy; Incyte: Consultancy, Research Funding; Cardinal Health: Consultancy; Forma Therapeutics: Research Funding; Abbvie: Consultancy; Celgene: Consultancy; Merck: Consultancy; Medtronic: Equity Ownership; Janssen: Research Funding.