Serum albumin (SA) has been shown to be a prognostic marker in many hematological malignancies and in diffuse large B-cell lymphoma (DLBCL) prior to chemo-immunotherapy. SA may be a surrogate for age, comorbid status, and disease severity. Here, we aimed to assess whether SA can be an independent prognostic marker in patients with newly diagnosed DLBCL treated with rituximab, cyclophosphamide, vincristine, doxorubicin, and prednisone (R-CHOP). Patients who presented at the Moffitt Cancer Center from 2007 to 2010 for DLBCL diagnosis or treatment were identified using our institutional database. Clinical and treatment data were recorded, including SA levels at diagnosis. Survival time was estimated using the Kaplan-Meier method, with Cox proportional hazard model used to identify potential risk factors for time-to-event data. From 295 identified patients, 171 were excluded for not having primary treatment at our institution or not having R-CHOP treatment. In 124 included patients (mean age at diagnosis of 58 years, 91 % Caucasian), 25 % were categorized as poor by the revised International Prognostic Index. Overall and progression-free survival at 4 years were 65 % (95 % CI 57-75) and 58 % (95 % CI 0.49-0.69), respectively. Using multivariate analysis, we found that the hazard index of death of patients with SA ≥3.7 g/dL was 26 % (95 % CI 13-53) of the hazard for those patients who had SA <3.7 g/dL when controlling for the revised International Prognostic Index risk and initial lymphocyte count. Our study shows that SA ≥3.7 g/dL is an independent prognostic marker in DLBCL patients treated with R-CHOP.
Introduction Low serum albumin (SA) has been identified as a prognostic marker in multiple hematological malignancies including diffuse large B-cell lymphoma (DLBCL). Low SA may be an indicator of worsening disease biology, increased inflammation, or increased co-morbidities. Changing demographics and improved care of the elderly may abrogate some of the risk attributable to age. SA, however, may not be influenced by such changes. Currently the Revised International Prognostic Index (R-IPI), the currently best accepted model for prognosis in DLBCL, does not account for albumin. We therefore explored the use of albumin as a prognostic variable in conjunction with the covariates included in the R-IPI. Methods Patients with DLBCL treated between 2007-2010 with RCHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) were retrospectively identified using the Moffitt Total Cancer Care platform. Age, ECOG performance status, LDH, extrandoal sites of disease, stage, and albumin were collected and analyzed using Random Forest Modeling. Both age and extranodal involvement failed to retain statistical significance and were dropped from the model, leading to the generation of a new algorithm, the Albumin Adjusted IPI (A-IPI). This score assigned a point for SA<3.7g/dL, LDH >the upper limit of normal, ECOG performance status >=2, and Ann Arbor stage III-IV. Progression free and overall survival was compared by the risk groups using Kaplan-Meier curves along with the log rank test. Statistical analysis was done using R statistical software. Results A total of 124 patients were identified. Median age was 58 years with 62% male. 46% were over the age of 60 at diagnosis and 63% were Ann Arbor stage 3 or 4. The A-IPI score identified three groups of patients (Very good: A-IPI=0, Good: A-IPI=1-2, Poor: A-IPI=3-4), similar to the R-IPI. PFS and OS at 4 years were compared using the A-IPI and R-IPI (Table 1). Conclusions In comparison to the R-IPI, the A-IPI appears to better define poor risk patients while retaining the ability to discriminate well between low (“Very Good”) and intermediate (“Good”) risk groups. Confirmation in a larger and prospective cohort is indicated, however, these preliminary data suggest SA may be a better surrogate for co-morbid status, pro-inflammatory states, and worse disease biology than age in patients with DLBCL. Disclosures: No relevant conflicts of interest to declare.
2816 Background: The International Prognostic Scoring System (IPSS) was recently revised under the auspices of MDS foundation as a collaborative international effort. The proposed R-IPSS is suggested to refine the prognostic value of the IPSS. Instead of the 4 original IPSS categories, 5 categories are proposed by R-IPSS. To validate this prognostic model and examine its utility for therapy decisions, we tested the new risk model in a large external single institution patient cohort. Methods: Data were collected retrospectively from the Moffitt Cancer Center (MCC) MDS database and chart review. The primary objective was to validate the new risk model. The R-IPSS score was calculated as reported. Patients were divided into 5 prognostic categories (very low, low, intermediate, high and very high risk). The Kaplan–Meier method was used to estimate median overall survival. Log rank test was used to compare Kaplan–Meier survival estimates between the groups. Results: The MCC MDS database captured 1157 patients. Complete data was available for 1029 patients to calculate the R-IPSS score. Median age was 68 years, and the most common WHO subtype was RCMD (29%). Two thirds of patients were low/int-1 IPSS risk, and 44% were int-2 or high risk MDAS. (Table-1). Among those, 729 patients (77%) were RBC transfusion dependent (TD), and 264 (26%) had serum ferritin >1000 ng/l. Six hundred eighteen patients (60%) received hypomethylating agent (HMA). The median duration of follow up was 68 months (mo). Median OS according to IPSS risk score was 90 mo (95%CI 75–105), 44 mo (95%CI 39–46), 18 mo (95%CI 15–21), and 14 mo (95%CI 11–17), for low, int-1, int-2, and high risk categories, respectively (p < 0.005). According to MD Anderson risk Score, the median OS was 108 mo (95%CI 91–126), 55 mo (95%CI 50–60), 25 mo (95%CI 22–28), and 14 mo (95%CI 12–16), for low, int-1, int-2, and high risk respectively (p < 0.005). Using the R-IPSS, 106 (10%), 311 (30%), 247 (24%), 201 (20%), and 164 (16%) were classified as very low, low, int, high, and very high risk. The median OS was 82 mo (95% CI 64–100), 57 mo (95% CI 46–68), 41 mo (95% CI 33–49), 24 mo (95% CI 20–28), and 14 mo (95% CI12–16) for each of the corresponding R-IPSS groups (p <0.005). Table-2 summarizes reclassification of each IPSS risk group by R-IPSS and expected OS accordingly. Among those patients who received HMA, the median OS from time of diagnosis was 76 mo, 55 mo, 42 mo, 25 mo, and 16 mo for very low, low, int, high, and very high risk respectively (p < 0.005). A survival benefit for HMA therapy was only statistically significant in patients with very high risk R-IPSS, with a corresponding median OS of 16 mo with HMA versus 7 mo with no HMA (p< 0.005). OS in patients with very high or high R-IPSS who underwent Allogeneic Stem cell transplant (ASCT) was improved compared to corresponding patients who received non-ASCT management. Patients who had very low, low, and int risk R-IPSS had no apparent OS benefit with ASCT. (Table-3). Conclusion: Our data validates the prognostic value of the proposed R-IPSS, but refines prognostic discrimination only for intermediate risk group of IPSS. Both the R-IPSS and IPSS were valid prognostic models for patients treated with HMA. The benefit of ASCT was restricted to patients with high and very high R-IPSS groups. The utility of the R-IPSS as a tool for therapeutic decisions should be further examined before wide adaptation. Disclosures: No relevant conflicts of interest to declare.
3852 Background: Azanucleosides (AZN) and allogeneic stem cell transplantation (ASCT) are the only disease altering treatment modalities for patients with myelodysplastic syndrome (MDS). Azacitidine (AZA) demonstrated an overall survival (OS) advantage in higher risk MDS. The goal of treatment in patients with lower risk MDS is alleviation of symptomatic cytopenias. A key question remains the ability to identify the subset of lower risk MDS patients with poor risk features who may experience an OS benefit from AZN treatment. We hypothesized that recently proposed prognostic models such as the Global MD Anderson risk model (MDAS), revised International Prognostic Score (R-IPSS), and the Lower risk MD Anderson model (LR-MDAS), may identify patient subsets originally classified as lower risk by IPSS who have higher disease risk features and will benefit from AZA treatment. Methods: Patients classified as lower risk MDS by IPSS were identified retrospectively from the Moffitt Cancer Center (MCC) MDS database. The primary objective was to examine the utility of risk models identifying patients who benefit from AZA. The primary end point was OS. Patients were treated with AZA based on clinical judgment and primarily for management of cytopenias. The MDAS, R-IPSS, and LR-MDAS scores were recorded and calculated as previously described. The Kaplan–Meier method was used to estimate median OS. Log rank test was used to compare Kaplan–Meier survival estimates between the groups. Results: The MCC MDS database captured 608 MDS patients classified as low/int-1 risk by IPSS. The median age was 69 years, 2/3 were males, RCMD was the most common WHO subtype (38%), and 3 % had a poor risk karyotype. Among the 608 patients, 252 were treated with AZA. Based on IPSS, 162 patients were low risk and 56 received AZA, with a median OS of 86 mo (95%CI 64–107) vs. 94 mo (95%CI 66–121, p=0.9) for those 106 patients who did not. Among the 444 patients classified as int-1 risk, 192 were treated with AZA with a median OS of 45 mo (95%CI 37–53) vs. 33 mo (95%CI 32–54) for AZA-untreated (p=0.6). Based on MDAS, only 478 patients were lower risk, among whom 177 received AZA treatment with a median OS of 59 mo (95% CI 48–70), vs. 72 mo (95%CI 55–88) (p=0.24) in the 301 patients who did not receive AZA. The MDAS upstaged 162 patients (27%) into int-2/high risk categories, 71 of whom received AZA with a median OS of 27 mo (95%CI 21–34) compared to 17 mo (95% CI 14–21) (p=0.003) in the 55 patients did not receive AZA treatment. Characterization of LR-MDAS was available for 322 patients, 38 of whom stratified as category 1. Twelve of these patients were treated with AZA and 26 patients were not with a median OS that was not reached for both groups (p=0.25). Category 2 included 134 patients, 41 of whom received AZA with a median OS of 69 mo (95%CI 53–85) compared to 77 mo (95% CI 48–106) (p=0.22) in the 93 patients who did not receive AZA treatment. Finally, 150 patients were characterized as category 3, 87 of whom received AZA with a median OS of 46 mo (95% CI 39–53) vs. 34 mo (95%CI 8–61) (p=.85) for the 63 who did not. By R-IPSS, 539 patients were included in the very low/low/intermediate risk prognostic categories, including 212 patients treated with AZA and 327 who were not with corresponding median OS of 53 mo (95%CI 46–60) and 58 mo (95%CI 45–71) (p=0.16), respectively. The R-IPSS upstaged 67 patients (11%) to high or very high risk among whom 36 received AZA with a median OS of 56 mo (95%CI 18–93) vs. 23 mo (95% CI 17–29) (p=0.16) in the 31 patients who did not. Conclusion: The new proposed risk models identify a subset of patients with higher risk features originally stratified as lower risk by IPSS. AZA treatment yielded an OS advantage in patients upstaged to int-2 or high risk by MDAS, suggesting that disease modifying treatments effectively extend OS in such patients. A larger sample size is needed to determine the utility of LR-MDAS or R-IPSS. Disclosures: Komrokji: Celgene: Speakers Bureau. List:Celgene: Consultancy.
4542 Introduction: Consolidation with autologous transplantation (AutoSCT) may extend progression free survival when administered following initial induction. There are limited data to support the role of AutoSCT in the relapsed or refractory setting. Methods: We retrospectively evaluated all patients with MCL transplanted at our institution before 2010. We identified 57 patients, among whom 42 were transplanted in first remission (CR1, n=32; PR1 n=10), 11 in second remission (CR2, n=4, PR2, n=7), and 4 with relapsed/refractory disease beyond first remission. Results: The median PFS are: CR1 37mo, PR1 24mo, CR2 not reached, and PR2 23mo. No statistically significant difference was observed between patients transplanted CR1 vs PR1 (p one-sided =0.08), CR2 vs PR2 (p one-sided =0.10), or in CR/PR1 vs CR/PR2 (p one-sided =0.39). The median PFS for those with refractory disease, and/or those transplanted beyond second remission was 6mo which is significantly inferior to the cohort of those transplanted in first or second remission (p one-sided =.01). The median OS calculated from transplant are: CR1 63mo, PR1 50mo, CR2 not reached, PR2 45mo. No statistically significant difference was observed between patients transplanted CR1 vs PR1 (p one-sided =0.47), CR2 vs PR2 (p one-sided =0.46), or in CR/PR1 vs CR/PR2 (p one-sided =0.29). The median OS for those with refractory disease, and/or those transplanted beyond second remission was 16mo which is not statistically significantly inferior to the cohort of those transplanted in first or second remission (p one-sided =.067). MIPI data collected at diagnosis were available for 30 patients, all transplanted in first or second remission with chemosensitive disease. These data were not predictive of survival or progression from transplantation. Simplified MIPI obtained at the time of transplant were available for 44 patients, all transplanted in first or second remission with chemosensitive disease. These data were similarly uninformative for prediction of progression or survival from transplantation. Conclusions: Consolidation with AutoSCT may be similarly effective for patients in first relapse with chemosensitive disease. MIPI at diagnosis and the simplified MIPI at transplant may failed to account for survival among highly selected patients considered eligible for transplantation. Disclosures: Sokol: Celgene: Honoraria, Speakers Bureau.
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