Kurzfassung: The March 2020 onset of the coronavirus pandemic and the surge of cases that followed it has fundamentally changed the American healthcare landscape. Of course, the health sector is better acquainted with sweeping structural changes than most others, but it has never undergone so multifaceted a transition. Fear of contagion continues to motivate patients to seek care remotely, postpone elective treatments, and grapple with questions of how to pay steep out-of-pocket costs in the face of job instability and financial hardship. The offshoring of medical equipment manufacturing has yielded supply shortages (King, 2020), making providers less agile in their responses to the sudden increase in demand for treatment (OECD, 2020). Payers rushed to streamline access to care by extending coverage to COVID-related hospitalizations, waiving cost-sharing requirements, and cutting back on administrative red tape (Liss, 2020). The evolution of care delivery combined with the formation of unlikely partnerships under the duress of the pandemic may have forged a healthcare sector with fewer administrative barriers, more flexible delivery of care, and a superior pricing model. 

Kurzfassung: Randomized trials have demonstrated superior progression free (PFS)and overall survival (OS) with autologous stem cell transplant (ASCT) for patients with relapsed chemosensitive non-Hodgkin lymphoma (NHL) compared with conventional dose salvage chemotherapy. More recent trials have proven that ASCT is also feasible in pts with AIDS associated NHL (ARL). However, the impact of the HIV infection on long term outcome is unknown. We therefore, undertook a retrospective case control analysis of ASCT for high risk B cell NHL in HIV positive (HIV Pos) and HIV negative (HIV Neg) pts. Twenty-nine pts with ARL who underwent ASCT between 1998 and 2007 were matched with HIV Neg controls. Pts were matched for gender, time from NHL dx to ASCT, age at ASCT, dz status at ASCT, number of prior regimens, conditioning regimen (chemo vs. FTBI). Histology was matched as closely as possible with the exception that there were more high-grade NHL pts in the HIV Pos group. Patient HIV Pos HIV Neg P value* (* P value by Fishers exact test or Wilson signed rank sum test) Age at ASCT 42 (11–68) 48(21–65) .06 HISTOLOGY Large cell 19 25 Burkitts 10 0 Follicular gr 3 0 3 Marginal zone 0 1 Disease status 1CR/PR 16 16 IF 2 2 1.0 Relapse 11 11 Prior regimens 2(1–4) 2(1–4) .33 Conditioning - - FTBI 4 4 1.0 Non TBI 25 25 Median followup for HIV Pos pts is 46.7 months and 43.3 months for HIV neg controls (NS). Pts engrafted WBC at a median of 10 days (HIV Pos) and 11 days (HIV Neg) (NS) respectively. Non-relapse mortality (NRM) was 8% (95% CI 2–26) in HIV Pos pts and 4% (95%CI 0.7–25)in HIV Neg controls (NS). Two year PFS for the HIV Pos cohort was 76% (95% CI 62–85) and 56% (95% CI 45–66) for the controls (NS). OS was also similar at 75% (95% CI 61–85) versus 75% (95% CI 60–85)respectively{ see figure }. In conclusion, despite the inclusion of more poor risk pts by histology in the HIV Pos cohort, our series demonstrated matching OS for HIV Pos and HIV Neg pts undergoing ASCT for NHL The equivalent NRM also provides further evidence that HIV status does not affect the outcome of ASCT for NHL and therefore, should be considered a standard approach for select pts with ARL. Figure Figure

Kurzfassung: Current CGVHD prognostic and staging systems are still undergoing development and have identified plt count; CGVHD types progressive(P), quiescent(Q), de novo(DN); KPS, and GI involvement as significant risk factors affecting outcome. A simple reproducible staging system such as used for AGVHD to apply in clinical trials is still lacking. We evaluated whether the PSE dose required to control CGVHD at 3 months from diagnosis would have a prognostic effect on survival and in and of itself serve as a criteria for secondary intervention or investigational therapy. We hypothesized that by 3 months from start of treatment patients would be on the lowest dose dictated by medical necessity rather than by physician driven dose preference. A retrospective analysis of charts from 109 patients diagnosed with CGVHD between 6/2000 and 6/2003 was done. Data collected included age, donor type(mud/sib), plt count, CGVHD type(P/Q/DN), KPS, GI involvement. Outcome analysis included survival and cause of death. PSE dose was calculated in mg/kg at 3 months from first diagnosis of CGVHD. With a median follow up of 47.2 months(range 6.6–67.2) relapse censored survival of patients on a 3 month PSE dose of more than .3 mg/kg was 53% compared to all lower doses 86%(P.03). In a univariate analysis only PSE dose (P .05) and KPS (P & lt;.01) were significant with plt count approaching significance (P .11). In a multivariate analysis again only PSE dose and KPS were significant (Table 1). Table Univariate Multivariate Variable Value N # of deaths Hazard Rate Ratio (95% CI) p value Hazard Rate Ratio (95% CI) p value Prednisone at 3 month 0 20 1 Baseline 0.05 Baseline 0.1–0.14 18 2 3.0 (0.3–32.7) 3.7 (0.3–43.4) 0.33 0.15–0.29 22 3 2.9 (0.3–28.2) 3.4 (0.3–34.5) 0.32 0.3–0.59 16 7 9.8 (1.2–79.4) 9.3 (1.1–76.0) 0.04 0.6–0.99 0 0 n/a n/a n/a ≥1.0 0 0 n/a n/a n/a cGVHD class Denovo 29 5 Baseline 0.54 Progressive 23 7 1.9 (0.6–6.0) Quiescent 57 13 1.3 (0.5–3.8) Donor type Sibling 48 9 Baseline 0.40 Unrelated 61 16 1.4 (0.6–3.2) Platelet count at 3 month & lt;100 28 9 Baseline 0.11 Baseline ≥100 81 16 0.5 (0.2–1.1) 0.7 (0.2–2.3) 0.59 KPS at 3 month & lt;80 14 7 Baseline & lt;0.01 Baseline ≥80 95 18 0.2 (0.1–0.5) 0.3 (0.0–1.3) 0.03 Lower GI at 3 month No 98 22 Baseline 0.78 Yes 9 2 1.2 (0.3–5.2) Overall survival by Prednisone dose Overall survival by Prednisone dose The analysis of this data to date suggests the PSE dose at 3 months may be an important independent clinical marker for subsequent CGVHD prognosis which could be used to decide which patients to include in 2nd line and experimental therapy trials.

Kurzfassung: Background: Despite recent advances in treatment that have improved the prognosis for patients with multiple myeloma (MM), the disease remains incurable. There is a need for MM treatments with new mechanisms of action. Leflunomide, a commercially available oral immunosuppressive agent that has been FDA-approved since 1998 for the treatment of rheumatoid arthritis (RA) was evaluated as a potential MM therapy. The primary mechanism of action is de novo inhibition of pyrimidine synthesis by targeting dihydroorotate dehydrogenase (DHODH), and thus achieving an anti-proliferative effect in B- and T-lymphocytes. A secondary mechanism of action is inhibition of cytokine and growth factor receptor-associated tyrosine kinase activity. Methods and Results: Pre-clinical studies of teriflunomide, the active metabolite of leflunomide, showed that it inhibited cell growth and induced apoptosis in MM cell lines (MM.1S, MM.1R, U266, H929, RPMI-8226) and primary MM patients' (CD138+) plasma cells at clinically achievable concentrations (50-200 uM) in a time- and dose-dependent manner. We also found that teriflunomide induces cell-cycle arrest in both, glucocorticoid-sensitive (MM.1S) and resistant (MM.1R) MM cell lines at 〈 200 uM. In addition, teriflunomide and dexamethasone synergized in the in vitro growth inhibition of MM cell line MM.1S. To identify MM-associated mRNAs and miRNAs whose expression levels are frequently altered upon teriflunomide exposure, MM cell lines (RPMI-8226, U266, MM.1S, NCI-H929) and CD138-enriched primary plasma cells from two MM patient samples were treated with 200 µM teriflunomide or DMSO control for 24 h before extraction and purification of mRNA and microRNA. mRNA-seq and miRNA-seq analysis from teriflunomide-treated MM samples revealed that similar changes were present between patient samples and cell lines. A total of 382 genes were found to be differentially expressed (225 upregulated, 157 downregulated). Upregulated genes included those that participate in defense response and negative regulation of cell growth. Genes involved in mitosis, rRNA biogenesis/processing, and immune response were generally downregulated. Analysis of microRNA-seq data from these samples revealed five differentially expressed, mostly newly discovered miRNAs that have unknown function. Conclusions: Leflunomide and its analogues demonstrated anti MM effects in vitro as well as synergy with dexamethasone. Based on our promising pre-clinical results we have initiated a single-agent phase I/II clinical trial in patients with relapsed/refractory MM. Disclosures No relevant conflicts of interest to declare.

Kurzfassung: Background: Clinical outcomes for patients with HIV-related lymphomas who have undergone autologous hematopoietic cell transplantation (AHCT) are similar to HIV-negative patients (Alvarnas et al., Blood 2016). Here we report a detailed, longitudinal immunophenotypic and functional evaluation of immune recovery of patients enrolled on the BMT CTN 0803/AMC 071 multicenter phase II study (clinicaltrials.gov NCT01141712). Methods: Comprehensive analysis of cellular immunome was performed using 5 color flow cytometry. Acquisition and analysis was performed via FC500 cytometry analyzers with CXP software and prism plot. Comparisons were made between HIV+ and HIV- cohorts of peripheral blood mononuclear cell (PBMC) subsets at 56, 180, and 360 days post AHCT. The HIV- cohort was collected from 30 multiple myeloma patients enrolled in a longitudinal immune recovery study after AHCT (median age 52.5 years (18-71); 57% male, no post AHCT exposure to IMID or other treatment). Control samples were collected from 72 healthy volunteers (median age of 49 (21-68); 53%, M). A Wilcoxon rank sum test was utilized to compare the HIV+ and HIV- groups to controls and to each other at each time point for 18 immune cell subsets common to all three panels. An unsupervised analysis was performed utilizing a principal component analysis (PCA) to look for overall differences in the cohorts. Similar methodologies were used to compare HIV+ to controls that analyzed 100 PBMC subsets. Functional immune recovery was evaluated by IFNg Elispot assay where 2x105 PBMC collected at each time point were pulsed with control, EBV (BZLF1) or HIV (GAG) pepmix preparations. As a control for TCR responsiveness, anti CD3/CD28 antibody-beads were used to immobilize TCR in ELISPOT assay. T cell responses from PBMCs of each of the three time points of HIV+ patients on trial were compared to PBMCs from HIV- donors (n=6). Results: Wilcoxon Rank sum tests show significant differences between transplant patients and controls and between HIV+ and HIV- patients at all visits. There are fewer cell subsets significantly different at day 365 compared to day 56 or 120 in all comparisons. The PCA showed group differences between HIV+, HIV- and control subjects. CD3+/HLA-DR+ (late activation), CD8+/CD25- (cytotoxic T cells) and CD3+/CD314+ (T cells with activating NKG2D) were found to be more prevalent in HIV+ transplant patients. These findings may be consistent with expanded populations of chronically activated cytotoxic T lymphocytes in HIV+ transplant patients. Subsets of NK, Th1 and Th2 cells showed statistically significant differences between HIV+ (low), HIV- (higher) and controls (higher). When the principal components are plotted by visit there is a pattern of both HIV+ and HIV- transplant patients clustering closer to controls as patients recover from AHCT. The PCA was also utilized to compare the HIV+ cohort to controls which had the same panel of cell subsets tested and allowed for the use of 100 cell subsets in the analysis. This analysis showed a similar group separation and pattern of clustering closer to controls in later visits. These findings demonstrate complex interactions between T and NK cell subsets. Functional assessment of antigen-specific T cell responsiveness was evaluated in Elispot assays with EBV (BZLF1) and HIV (GAG) recall antigens and anti-CD3/CD28 controls. Of 30 evaluable patients, 28 HIV+ patients demonstrated measurable IFNg production in response to GAG (spots/2x105 PBMC, range: 8-615), 21 showed measurable response to BZLF1 pepmix (range 12-450); and all patients demonstrated responsiveness to anti CD3/CD28 stimulation. Magnitude of IFNg production from HIV+ samples was generally higher than that observed healthy, HIV- controls. Assessment of NK cell responsiveness is currently underway. Conclusions: While clinical outcomes following AHCT between HIV+ and HIV- patients is comparable, clear distinctions were observed with immune recovery of specific PBMC subsets during the first year following AHCT with differences diminishing as patients recover post transplant. Longitudinal immune responsiveness of PBMC from HIV+ patients to EBV and HIV recall antigens and TCR stimulation generally showed more robust IFNg production compared to PBMCs from HIV- volunteer controls. These data provide further justification supporting AHCT as an option for HIV+ patients provided they meet standard transplant criteria. Disclosures Little: This study was coordinated by the ECOG-ACRIN Cancer Research Group (Robert L. Comis, MD and Mitchell D. Schnall, MD, PhD, Group Co-Chairs) and supported by the National Cancer Institute of the National Institutes of Health under the following award number: Employment. Noy:Pharmacyclics, LLC, an AbbVie Company: Other: travel, accommodations, expenses, Research Funding. Krishnan:celgene: Consultancy, Speakers Bureau; takeda: Consultancy, Speakers Bureau; janssen: Consultancy, Speakers Bureau; onyx: Speakers Bureau. Hofmeister:Signal Genetics, Inc.: Membership on an entity's Board of Directors or advisory committees; Celgene: Research Funding; Arno Therapeutics, Inc.: Research Funding; Incyte, Corp: Membership on an entity's Board of Directors or advisory committees; Janssen: Pharmaceutical Companies of Johnson & Johnson: Research Funding; Karyopharm Therapeutics: Research Funding; Takeda Pharmaceutical Company: Research Funding; Teva: Membership on an entity's Board of Directors or advisory committees. Forman:Mustang Therpapeutics: Other: Construct licensed by City of Hope. Lozanski:Boehringer Ingelheim: Research Funding; Beckman Coulter: Research Funding; Stemline Therapeutics Inc.: Research Funding; Genentech: Research Funding. Baiocchi:Essanex: Research Funding.

Kurzfassung: Background: Radiation therapy has been used primarily for palliation in pts with MM. Ablative dose total body irradiation (TBI) of 800 cGy in combination with high-dose melphalan (MEL) as part of single cycle AT was found to be too toxic, and therefore inferior, in comparison to MEL. TMI, a form of image-guided targeted TBI using intensity modulated helical tomotherapy, when given as the sole ablative regimen during the second cycle of TAT, may improve the efficacy of MEL without unacceptable toxicities. Patients and Methods: We designed a phase I-II TAT study in pts with Durie-Salmon stages I–III MM in response or with stable disease (SD), who were ≤ 70 years old. Pts received MEL 200 mg/m2 and AT (cycle 1), and, following recovery, TMI and AT was administered (cycle 2). The dose of TMI started at 1000 cGy, and was to be escalated by an increment of 200 cGy per cohort, up to 200 cGy twice daily x 5 days. Following cycle 2 of TAT, maintenance therapy consisted of dexamethasone 40 mg/day x 4 days and thalidomide (Thal) 50–200 mg daily on a 28-day cycle, administered for 6 cycles for pts in complete response (CR), or for a minimum of 12 cycles for pts not in CR. Results: The median age was 53.5 years (35–66). Twenty three pts (13 female, 10 male) with stages I (1), II (6), III (16) MM received MEL at a median time of 10 mos (7–18) from diagnosis; 22 pts received TMI (1000 cGy through 1800 cGy); 1 pt did not receive TMI due to post-MEL toxicities. The median time between MEL and TMI was 63.5 days (range, 44–119). Granulocyte recovery to 〉 1000/microliter following Mel was 14 days (13–15) versus 15 days after TMI (range; 13–19). Platelet recovery to 〉 20,000/microliter was identical: 13 days (range: 0–16 versus 0–17). Reversible grade 3 non-hematologic toxicities by TMI dose levels included febrile neutropenia (levels 1 and 2: 1 pt each); none (level 3); fatigue (level 4: 1 pt). Dose limiting toxicities (DLT) at level 5 (1800 cGy) were reversible, and included grade 3 radiation pneumonitis/congestive heart failure necessitating administration of oxygen, steroids, and oral cardiac medications, and abdominal pain/enteritis requiring parenteral feeding (n: 1), and grade 3 hypotension requiring pressor support (n: 1), defining the maximum tolerated dose (MTD) at 1600 cGy (200 cGy twice daily x 4 days). The estimated median radiation dose to normal organs was 14–64% of the targeted bone marrow dose in the 6 pts each treated at doses 1600 and 1800 cGy. Late toxicities included reversible enteritis in the pt previously experiencing the same symptom as DLT after receiving 1800 cGy of TMI, and lower extremity deep venous thrombosis (DVT) during maintenance therapy in 2 pts. We observed neither primary nor secondary engraftment failure. Best responses included CR (n: 12), very good partial response (VGPR, n: 4) PR or stable disease (n: 6). At a median follow-up of 22 months (range, 10–39+ months) 5 pts progressed (at 7.5, 8, 16, 21, and 22 months) and 8 pts continue on maintenance. Conclusion: We defined the MTD of TMI as 1600 cGy. Delayed toxicities are limited so far, but underline the need for careful long-term monitoring and DVT prophylaxis during Thal-based maintenance. Phase II of this trial at the MTD of 1600 cGy of TMI is ongoing.

Kurzfassung: Background: Double-hit lymphomas (DHL) are a subset of diffuse large B-cell lymphoma (DLBCL) with concurrent chromosomal rearrangements involving the MYC and BCL2 or BCL6 genes, and are associated with dismal outcomes with standard upfront therapy. Double expressing lymphomas (DEL) are a subset of DLBCL with co-expression of MYC and BCL2 by immunohistochemistry (IHC), and also have a poor prognosis with standard therapy. While DHL status may be associated with inferior outcomes in patients with relapsed or refractory (rel/ref) disease (Cuccuini, Blood, 2012), little is known about the outcome of DHL patients with rel/ref disease who proceed to autologous stem cell transplantation (ASCT), and no study to date has examined the outcome of patients with DEL following ASCT. We evaluated the prognostic impact of DHL and DEL status in patients with rel/ref DLBCL who underwent ASCT at 2 centers. Methods: We retrospectively studied patients with rel/ref DLBCL, including transformed indolent lymphoma (TIL), who underwent ASCT at Brigham and Women's Hospital/Dana-Farber Cancer Institute (DFCI) and City of Hope (COH) between 1/2000 and 7/2013. The most recent biopsy prior to ASCT was used for testing when possible. IHC for MYC and BCL2 were performed using the Ventana (MYC: DFCI) and Leica BOND III (MYC: COH; BCL2: DFCI, COH) platforms according to standard protocols. For DEL, IHC cutoffs of ≥ 40% MYC-positive and ≥ 50% BCL2-positive cells were used (Johnson, JCO, 2012). Fluorescence in situ hybridization (FISH) for MYC was performed using LSI MYC dual-color break-apart probes (Abbott Molecular, Des Plaines, IL). MYC -rearranged cases had FISH for BCL2 and BCL6 performed using LSI BCL2 and BCL6 dual-color break-apart probes. DHL was defined as 〉 20% nuclei with break-apart signals for MYC and BCL-2 and/or BCL-6. Results: 201 patients with available archival tissue and clinical data were included. The median age was 60 (range 30-77) years; 60% were male; 26% had TIL; the median number of prior lines of therapy was 2 (range 2-5); 99% had prior rituximab; 53% had primary refractory disease or early ( 〈 6 mo) relapse; 60% were in CR by PET at ASCT; and conditioning regimens were: 66% CBV v 16% BEAM v 10% rituximab and/or ibritumomab tiuxetan-BEAM v 8% other. Overall, the 4y progression-free survival (PFS) and overall survival (OS) were 44% and 61%, respectively. Among 185 patients with complete IHC data, 38% were DEL. The 4y PFS and OS in patients with DEL compared to non-DEL patients were 37% v 52% (p =0.001), and 51% v 69% (p =0.005), respectively [Figure 1]. Results were similar using other reported IHC cutoffs for DEL (e.g. MYC ≥ 40%/BCL2 ≥ 70%, Green, JCO, 2012). Among 93 patients with complete FISH and IHC data available, 13% had MYC rearrangement: 4% were MYC/BCL2 DHL, 3% were MYC/BCL6 DHL, and 2% had rearrangements of all 3 loci. The 4y PFS and OS in DHL v non-DHL were 30% v 42% (p =0.042), and 40% v 57% (p =0.026), respectively. Patients with DEL (excluding DHL) and patients with DHL had similar PFS, which was inferior to non-DEL/non-DHL patients (4y PFS 35% v 30% v 45%, respectively, p =0.026) [Figure 2] . In multivariable models testing pre-ASCT variables, including PET response to salvage, DEL (HR 2.1, p=0.0002), TIL histology (HR 1.8, p=0.009), and SD/PD at ASCT (HR 2.9, p=0.025) were associated with poorer PFS, while DEL (HR 2.0, p=0.004) and SD/PD (HR 3.1, p=0.021) were associated with poorer OS. Neither MYC (≥ 40%) nor BCL2 (≥ 50%) expression alone was independently associated with PFS or OS. When analysis was restricted to the subset of patients with complete IHC and FISH data, DEL (HR 1.9, p=0.023), DHL (HR 2.4, p =0.048), and SD/PD at ASCT (HR 7.6, p =0.009) were associated with inferior PFS. No center effect was observed. Conclusions: DEL and DHL status are both associated with inferior PFS in patients with rel/ref DLBCL who undergo ASCT, regardless of remission status. Although ASCT remains a potentially curative approach, these patients should be targeted for study of pre- or post-ASCT relapse risk reduction strategies. Figure 1. (A) Overall survival and (B) Progression-Free Survival after ASCT in DEL vs non-DEL Patients Figure 1. (A) Overall survival and (B) Progression-Free Survival after ASCT in DEL vs non-DEL Patients Figure 2. Progression-Free Survival after ASCT in Patients with DEL vs DHL vs non-DEL/DHL Figure 2. Progression-Free Survival after ASCT in Patients with DEL vs DHL vs non-DEL/DHL Disclosures Herrera: Genentech: Research Funding; Pharmacyclics: Research Funding; Sequenta, Inc.: Research Funding. Budde:Atara Biotherapeutics: Consultancy; Seattle Genetics, Inc.: Research Funding; Merck: Research Funding; Ikara Inc: Patents & Royalties. Chen:Seattle Genetics, Inc.: Consultancy, Other: Travel expenses, Research Funding, Speakers Bureau; Genentech: Consultancy, Speakers Bureau; Millennium: Consultancy, Research Funding, Speakers Bureau. Davids:Pharmacyclics: Consultancy; Janssen: Consultancy; Genentech: Other: ad board. Nademanee:Seattle Genetics Inc.: Research Funding; Celgene: Consultancy; Gilead: Consultancy; Spectrum: Research Funding. Siddiqi:Pharmacyclics: Research Funding, Speakers Bureau; Janssen: Speakers Bureau. Forman:Mustang: Research Funding; Amgen: Consultancy. Rodig:Perkin Elmer: Membership on an entity's Board of Directors or advisory committees; Bristol Myers Squibb: Research Funding. Krishnan:Onyx: Speakers Bureau; Janssen: Consultancy; Millenium: Speakers Bureau; BMS: Consultancy; Jazz: Consultancy; Celgene: Consultancy, Speakers Bureau. Armand:Merck: Consultancy, Research Funding; Infinity: Consultancy, Research Funding; BMS: Research Funding; Sequenta, Inc.: Research Funding.

Kurzfassung: Abstract 3403 Poster Board III-291 Autologous PSCT remains standard treatment in younger patients (pts) with multiple myeloma. However, relapse is the major cause of treatment failure. Several studies have reported improved progression-free survival (PFS) and possibly overall survival with thalidomide alone or in combination with steroid and chemotherapy as maintenance/consolidation therapy post autologous PSCT. We performed a phase II study investigating the role of sequential velcade/thalidomide/dexamethasone (VTD) as maintenance therapy post single PSCT. The objectives were to examine the toxicities of prolonged course of sequential VTD, CR rate, PFS and overall survival following single autologous PSCT. Within 4-8 weeks of autologous PSCT using melphalan 200mg/m2, pts received weekly velcade (vel) at 1.3mg/m2 /wk x 3 weeks with 1 week rest and dexamethasone (dex) at 40mg/d x 4 d for 6 months, followed by thalidomide (thal) at 50 -200mg/d and dexamethasone (dex) at 40mg/dx4 d for 6 more months. Single agent thalidomide was then continued until disease progression. Twenty-eight pts have been enrolled. Median age is 54 years (29-66). Median time from diagnosis is 7.9 mo. (4.2 – 145). Disease stage at diagnosis; by Salmon-Durie (II/III 6/22) and by ISS (I/II/III 11/9/7/missing data in 1 pt). Pts received induction treatment with thal/dex (14), velcade based (15) and revlimid based regimens (7). Median B2M at enrollment is 1.75 mg/L (1.14 -5.3). Disease status at enrollment; CR (7) VGPR (9), PR (11), SD (1). Three pts have chromosome 13 abnormalities (1 pt by karyotype and 2 pts by FISH). Results: All pts have undergone transplant. Four pts were unable to start planned maintenance therapy due to development of grade II or more neuro toxicities (3), and persistent thrombocytopenia (1) after PSCT. Twenty-four pts started maintenance vel/dex within 4-8 weeks of PSCT. Nine pts have completed 6 months of vel/dex. Two pts stopped vel/dex because of low WBC (1) or PN (1). With a median F/U of 5.2 mo. (1.2 -17.3) nine of 28 pts (33%) have achieved CR post PSCT and six out of 11 evaluable pts (55%) have achieved CR after vel/dex. Six out of 9 pts (66%) who have completed 6 mo. of vel/dex achieved CR. Two out of 9 pts (22%) have upgraded their response with vel/dex. Four pts have completed 6 month of thal/dex and are beyond 1 year post PSCT. Two out of 4 pts remain in CR at one year post PSCT. One pt is in PR and 1 pt has progressed. Two pts could not complete thal/dex phase of therapy because of relapse (1) and grade III GI toxicity (1). Three pts have relapsed of whom 1 pt died of relapsed myeloma (leptomeningeal disease). No grade IV toxicity has been noted. Grade III toxicities have occurred in 4 pts; low platelet (1), fatigue (1), mood alteration (1), GI (severe constipation) (1). Thirteen pts have peripheral neuropathy (PN). Ten pts had PN grade I at enrollment. Only 3 pts have developed PN on the study and all are grade I - II. Median velcade dose is 1.3 mg /m2/wk and thalidomide dose is 100mg /d. Conclusion: Prolonged sequential velcade/thalidomide/dexamethasone maintenance therapy post single autologous PSCT is well tolerated with no severe peripheral neuropathy. Fifty-five percent of pts have achieved CR and 22% have upgraded their response after six months of velcade/dexamethasone therapy suggesting this is an active and well tolerated maintenance strategy post PSCT. Disclosures: Sahebi: Celgene: Honoraria; Millennium Pharmaceutical: Research Funding. Off Label Use: The use of bortezomib(Velcade)in combination with thalidomide and dexamethasone is investigated as maintenance therapy post autologuous stem cell transplant in patients with multiple myeloma.