Kooperativer Bibliotheksverbund

In: British Journal of Haematology, Wiley, Vol. 72, No. 3 ( 1989-07), p. 350-356

Type of Medium: Online Resource

ISSN: 0007-1048 , 1365-2141

URL: Article

DOI: 10.1111/j.1365-2141.1989.tb07715.x

Language: English

Publisher: Wiley

Publication Date: 1989

detail.hit.zdb_id: 1475751-5

In: Annals of Hematology, Springer Science and Business Media LLC, Vol. 102, No. 9 ( 2023-09), p. 2529-2542

Abstract: Therapeutic donor lymphocyte infusions (tDLI) are used to reinforce the graft-versus-leukemia (GvL) effect in relapse after allogeneic stem cell transplantation (alloSCT). In contrast, the role of prophylactic DLI (proDLI) in preventing leukemia relapse has been less clearly established, although supported by retrospective, case-control, and registry analyses. We report a prospective, monocentric, ten year cohort of patients with high risk acute leukemias (AL) or myelodysplasia (MDS) in whom proDLI were applied beyond day +120 post alloSCT to compensate for lack of GvL. 272 consecutive allotransplanted AL or MDS patients in complete remission and off immunosuppression at day +120 were stratified according to the prior appearance of relevant GvHD (acute GvHD °II-IV or extensive chronic GvHD) as a clinical indicator for GvL. Escalating doses of unmodified proDLI were applied to 72/272 patients without prior relevant GvHD. Conversely, 157/272 patients with prior spontaneous GvHD did not receive proDLI, nor did 43/272 patients with contraindications (uncontrolled infections, patient refusal, DLI unavailability). By day 160-landmark analysis (median day of first DLI application), proDLI recipients had significantly higher five-year overall (OS) and disease free survival (DFS) (77% and 67%) than patients with spontaneous GvHD (54% and 53%) or with contraindications (46% and 45%) (p=0.003). Relapse incidence for patients with proDLI (30%) or spontaneous GvHD (29%) was significantly lower than in patients with contraindications (39%; p=0.021). With similar GvHD incidence beyond day +160, non-relapse mortality (NRM) was less with proDLI (5%) than without proDLI (18%; p=0.036). In conclusion, proDLI may be able to compensate for lack of GvL in alloSCT recipients with high risk AL or MDS.

Type of Medium: Online Resource

ISSN: 0939-5555 , 1432-0584

URL: Article

DOI: 10.1007/s00277-023-05276-5

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 2023

detail.hit.zdb_id: 1458429-3

In: Journal of Chromatography B, Elsevier BV, Vol. 787, No. 2 ( 2003-4), p. 357-368

Type of Medium: Online Resource

ISSN: 1570-0232

URL: Article

DOI: 10.1016/S1570-0232(02)00966-2

Language: English

Publisher: Elsevier BV

Publication Date: 2003

detail.hit.zdb_id: 1491259-4

SSG: 11

In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 32, No. 36 ( 2014-12-20), p. 4134-4140

Abstract: Patients with relapsed or refractory acute lymphoblastic leukemia (ALL) have a dismal prognosis. CD19 is homogenously expressed in B-precursor ALL and can be targeted by the investigational bispecific T cell–engager antibody blinatumomab. A phase II trial was performed to determine clinical activity in this patient cohort. Patients and Methods Thirty-six patients with relapsed or refractory B-precursor ALL were treated with blinatumomab in cycles of 4-week continuous infusion followed by a 2-week treatment-free interval in a single-arm study with a dose-finding stage and an extension stage. The primary end point was complete remission (CR) or CR with partial hematologic recovery (CRh). Major secondary end points included minimal residual disease (MRD) response, rate of allogeneic hematopoietic stem-cell transplantation (HSCT) realization, relapse-free survival (RFS), overall survival (OS), and incidence of adverse events (AEs). Results Median age was 32 years (range, 18 to 77 years). Twenty-five patients (69%) achieved a CR or CRh, with 88% of the responders achieving an MRD response. Median OS was 9.8 months (95% CI, 8.5 to 14.9), and median RFS was 7.6 months (95% CI, 4.5 to 9.5). Thirteen responders (52%) underwent HSCT after achieving a CR or CRh. The most frequent AE during treatment was pyrexia (grade 1 or 2, 75%; grade 3, 6%). In six patients with nervous system or psychiatric disorder AEs and in two patients with cytokine release syndrome, treatment had to be interrupted or discontinued. These medical events were resolved clinically. Conclusion The data support further investigation of blinatumomab for the treatment of adult patients with relapsed or refractory ALL in a larger confirmatory study.

Type of Medium: Online Resource

ISSN: 0732-183X , 1527-7755

URL: Article

DOI: 10.1200/JCO.2014.56.3247

Language: English

Publisher: American Society of Clinical Oncology (ASCO)

Publication Date: 2014

detail.hit.zdb_id: 2005181-5

In: Blood, American Society of Hematology, Vol. 113, No. 9 ( 2009-02-26), p. 2028-2037

Abstract: Neurotrophins (NTs) and their receptors play a key role in neurogenesis and survival. The TRK (tropomyosin-related kinase) receptor protein tyrosine kinases (TRKA, TRKB, TRKC) are high-affinity NT receptors that are expressed in a variety of human tissues. Their role in normal and malignant hematopoiesis is poorly understood. In a prospective study involving 94 adult patients we demonstrate for the first time cell-surface expression of the 3 TRKs and constitutive activation in blasts from patients with de novo or secondary acute leukemia. At least one TRK was expressed in 55% of the analyzed cases. We establish a clear correlation between the TRK expression pattern and FAB classification. Although only few point mutations were found in TRK sequences by reverse-transcriptase–polymerase chain reaction (RT-PCR), we observed coexpression of BDNF (ligand for TRKB) in more than 50% of TRKB+ cases (16/30). Activation of TRKA or TRKB by NGF and BDNF, respectively, efficiently rescued murine myeloid cells from irradiation-induced apoptosis. Coexpression of TRKB/BDNF or TRKA/NGF in murine hematopoietic cells induced leukemia. Moreover, activation of TRKs was important for survival of both human and murine leukemic cells. Our findings suggest that TRKs play an important role in leukemogenesis and may serve as a new drug target.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood-2008-05-155200

Language: English

Publisher: American Society of Hematology

Publication Date: 2009

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 120, No. 21 ( 2012-11-16), p. 3049-3049

Abstract: Abstract 3049 Introduction Graft-versus-host-disease (GvHD) remains one of the major complications post allogeneic hematopoietic stem cell transplantation (HSCT) which is still the only curative treatment for hematologic malignancies and non-malignant hematopoietic disorders. Early detection of developing GvHD prior to clinical manifestation is in the focus of research in order to optimize therapeutic approaches and possibly lower transplant related morbidity and mortality. We previously published proteomic patterns in urine generated by capillary electrophoresis coupled on-line to mass spectrometry (CE-MS) allowing early detection of acute GvHD onset (Weissinger et al., 2007; Weissinger et al., 2009). In an effort to compare our CE-MS results to other proteomic approaches and to contribute to harmonization of results generated by different laboratories, we analyze biomarkers detected in urine as well as those described by others using proteomic approaches such as ELISA and Bio-Luminex in plasma collected from the same patients analyzed by CE-MS. We aim to (1) compare the predictive value of the proteomic pattern with other methods and (2) evaluate these methods for early diagnosis of GvHD. Methods We established an urine/plasma sample bank from patients transplanted since 2006 at MHH; of this four patient groups were chosen to set up the methods for monitoring emerging GvHD on the basis of plasma-biomarkers: patients at onset of aGvHD (aGvHD, n=20), patients at similar time-points early post HSCT without aGvHD (con_aGvHD, n=14), patients at diagnosis of cGvHD (cGvHD, n=13) and patients without GvHD ( 〉 day +100; con_cGvHD, n=33). For Bio-Luminex analysis, the angiogenesis marker panel was used (Luft et al., 2011), including: G-CSF, PECAM-1, HGF, VEGF, Leptin, PDGF-BB, Angiopoetin, Follistatin and IL-8. ELISAs were performed for the following previously identified markers: IL-2Rα, sTNFR1, ST2/IL-1R4, Reg3α, Semaphorin 5a, Elafin (Levine et al., 2012), CD99 and β2-microglobulin (CE-MS-analysis, Weissinger et al., submitted). Results & Discussion Within the training set analysis by Bio-Luminex no significant differences between aGvHD, cGvHD and respective controls was found for G-CSF, VEGF and PDGF, implying vascular processes due to immunosuppressive antibodies or toxicities early post-HSCT. Changes observed in the aGvHD group were more prominent when compared to the con_cGvHD group. However, this might reflect the completion of immunosuppression in most patients in the con_cGvHD-group. Interestingly, Leptin was significantly higher in patients w/o aGvHD shortly after HSCT compared to patients with aGvHD, but was also low in the cGvHD and con_cGvHD groups. For angiopoetin significantly different levels were found comparing aGvHD vs. con_aGvHD, as well as for cGvHD vs. con_cGvHD. Analysis of the training set showed a trend for angiopoetin distinguishing between patients with aGvHD and tolerant patients. Within the investigated markers of the ELISA analysis, CD99, TNFR1, IL-2Rα, and ST2/IL-1R4 yielded significant differences between the aGvHD and the control groups. First results for patients in the training set are shown in Figure 1. As the detected plasma concentration for these markers did not differ significantly in con_aGvHD and con_cGvHD, the control groups were merged. Preliminary analyses suggest that these markers might be suitable to distinguish patients with aGvHD from tolerant patients, as confirmed by receiver operated characteristics (ROC)-curves. Conclusions and future perspectives According to our preliminary results, the most promising markers to detect aGvHD in plasma samples are Leptin, Angiopoetin, TNFR1, β2-microglobulin, and IL-2Rα. In order to improve the predictive power of the ELISA and Bio-Luminex testing, a multiparametric model (support vector machines) will be applied to the training set data. Based on the training set, prospective screening of a validation set of patients will take place soon. Furthermore, by sequencing further relevant peptides from the urine proteomic pattern, we aim to identify additional biomarkers for GvHD. Disclosures: No relevant conflicts of interest to declare.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V120.21.3049.3049

Language: English

Publisher: American Society of Hematology

Publication Date: 2012

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 1164-1164

Abstract: Abstract 1164 Poster Board I-186 Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a curative treatment for many hematologic malignancies or hematopoietic dysfunction syndromes, but the application is still limited due to major complications, such as severe graft versus host disease (GvHD) and infectious complications. Diagnosis chronic GvHD is based on clinical features and biopsies, a non invasive, unbiased laboratory test does not exist. We used the urine collected from 20 patients (10 with limited cGvHD, 10 with extensive cGvHD) to establish a proteomic pattern that allowed the diagnosis of cGvHD development and tested the resulting set of polypeptide markers (27 differentially excreted peptides) on more than 200 patients prospectively and blinded for the correct classification of cGvHD samples. The majority of the patients included were transplanted for hematological malignancies (n=209), 6 for hematopoietic failure syndromes. Conditioning regimens included dose reduced conditioning regimens (FLAMSA and ClaraC for the majority of the patients of MHH), as well as standard conditioning regimens (TBI+Cy or Busulfan+Cy) for about 35% of the patients, with GvHD-prophylaxis including cyclosporine A and mycophenolate (MMF) or metothrexate (MTX) as appropriate. Eighty percent of the patients received ATG (antithymocyte globulin) prior to HSCT. A peptide pattern of 27 peptides, differentiating chronic from acute GvHD was developed. Controls were patients at least 100 days post HSCT, with no GvHD in the history, no infections and without relapse at the time of sampling. Prospective and blinded evaluation of the patients revealed the correct classification of patients developing cGvHD with a sensitivity of 85% and specificity of 95%.Further evaluation of the cGvHD patterns specific for particular organ manifestations of cGvHD are currently ongoing. Interestingly, the cGvHD pattern seems to be predictive for GvHD developing post DLI, while the aGvHD-specific proteomic pattern only predicts GvHD of the intestine, which may be more similar to “late acute GvHD”. Disclosures Krons: mosaiques-diagnostics GmbH: Employment. Metzger:mosaiques-diagnostics GmbH: Employment.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V114.22.1164.1164

Language: English

Publisher: American Society of Hematology

Publication Date: 2009

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 114, No. 17 ( 2009-10-22), p. 3718-3719

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood-2009-07-231159

Language: English

Publisher: American Society of Hematology

Publication Date: 2009

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 126, No. 23 ( 2015-12-03), p. 680-680

Abstract: Introduction. MRD in ALL is defined as detection of leukemic cells in bone marrow by polymerase chain reaction (PCR) or flow cytometry with hematologic complete remission (CR). Pts with persistent/recurrent MRD after first-line induction therapy have a higher risk of relapse than those with complete MRD response (no detectable MRD with minimum sensitivity 0.01%). Interventions, including hematopoietic stem cell transplantation (HSCT), are used to improve the outcome of these pts. Blinatumomab, a bispecific T cell engager (BiTE®) antibody construct, redirects CD3+ T cells to CD19+ target cells, resulting in serial lysis of CD19+ B cells. In a multicenter, international phase 2 study in MRD+ ALL (Goekbuget N et al. Blood 2014;124:379), blinatumomab resulted in complete MRD response in cycle 1 in 78% of pts including multiple subgroups such as pts in second-line treatment, those with high MRD burden, and older pts. No subgroups with higher MRD complete response rates were identified. This analysis evaluated long-term outcomes, including overall survival (OS), relapse-free survival (RFS), and duration of remission (DOR). Methods. Adults (≥18 years) with B-cell precursor ALL with hematologic CR ( 〈 5% blasts in bone marrow) and MRD ≥10-3 after ≥3 intensive chemotherapy treatments were eligible. Pts with CNS pathology or extramedullary disease, previous allogeneic HSCT, or Philadelphia-chromosome positive (Ph+) ALL eligible for tyrosine kinase inhibitors were excluded. Blinatumomab 15 µg/m²/day was given by continuous IV infusion for 4 weeks, followed by a 2-week break (1 cycle). MRD was measured by a central laboratory using PCR per EuroMRD guidelines. MRD responders in cycle 1 received up to 3 additional cycles or underwent HSCT. Pts with hematologic relapse discontinued treatment. We report here preliminary follow-up data as of 1 July 2015. Final data from the preplanned 18-mo follow-up analysis will be available for the meeting. Results. 116 pts enrolled and received blinatumomab. Median age was 45 years (range 18-76); 15 (13%) pts were age ≥65 years. 90 (78%) pts received HSCT after blinatumomab. 62 (53%) pts were still being followed. 35 pts relapsed and 26 pts died in CR (23 of them after subsequent HSCT). Median OS, with median follow-up of 29.5 mo, was 36.5 mo (95% CI, 19.1 mo to not reached [n.r.]): 40.4 vs 12.0 (P =.001) in pts with (n=88) or without (n=24) MRD complete response in cycle 1. 110 pts were evaluable (CR at study entry, Ph-) for RFS and DOR. Median RFS was 18.9 mo (95% CI, 12.3 to 35.2 mo): 24.6 vs 11.0 (P =0.005) in pts treated in first (n=75) vs later (n=35) remission; and 35.2 vs 7.1 (P =0.002) in pts alive and relapse-free after 45 days with (n=85) or without (n=15) MRD complete response in cycle 1 (Figure). Median DOR was n.r. (95% CI, 24.6 mo to n.r.): n.r. vs 15.0 mo (P =0.002) in pts treated in first vs later remission; and n.r. vs 15.0 mo (P =0.015) in pts with DOR ≥ 45 days with (n=85) or without (n=13) MRD complete response in cycle 1. In time-dependent Cox model analyses, HSCT vs no HSCT were not different for OS (hazard ratio [HR] , 1.39; 95% CI, 0.68 to 2.82; P =0.368) or RFS (HR, 0.89; 95% CI, 0.47 to 1.69; P =0.730); DOR (treating death as a competing risk) was longer for HSCT vs no HSCT (HR, 0.36; 95% CI, 0.17 to 0.77; P =0.008). All pts experienced at least one AE. The most clinically relevant were neurologic events, including tremor (30%), aphasia (13%) dizziness (8%), ataxia and paraesthesia (6% each), and encephalopathy (5%). Rates decreased over time (cycles 1, 2, 3, and 4) for any neurologic event (47%, 24%, 15%, and 15%) and any grade ≥3 neurologic event (10%, 4%, 0%, and 0%). 12 (10%) pts interrupted treatment due to grade ≥3 neurologic events: 5 resumed without another interruption and 2 resumed then stopped treatment for another neurologic event. Investigators reported 4 deaths as fatal AEs during follow-up (brain injury, disease progression, gastrointestinal hemorrhage, and multiorgan failure); all 4 pts received HSCT after blinatumomab. Conclusion. In this long-term follow-up analysis of the first large prospective trial with an experimental compound in MRD+ ALL, MRD complete response induced by single-agent blinatumomab treatment was associated with longer OS, RFS, and DOR compared with not achieving an MRD complete response after blinatumomab treatment. This strengthens the current strategy of MRD-based treatment in ALL before occurrence of clinical relapse. Disclosures Gökbuget: Sanofi: Equity Ownership; Pfizer: Consultancy, Honoraria, Research Funding; GlaxoSmithKline: Honoraria, Research Funding; Erytech: Consultancy; Eusapharma/Jazz: Consultancy, Honoraria, Research Funding; Gilead Sciences: Consultancy; Kite: Consultancy; Medac: Consultancy, Honoraria, Research Funding; Mundipharma: Consultancy, Honoraria, Research Funding; Bayer: Equity Ownership; SigmaTau: Consultancy, Honoraria, Research Funding; Novartis: Consultancy, Honoraria, Research Funding; Amgen: Consultancy, Honoraria, Research Funding; Bristol-Myers Squibb: Honoraria. Off Label Use: Blinatumomab (BLINCYTO®) is approved for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). It has not been approved for use in patients in hematologic remission, but with presence of minimal residual disease (MRD), from ALL.. Dombret:Amgen: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding. Bonifacio:Amgen: Consultancy; Ariad Pharmaceuticals: Consultancy; Pfizer: Consultancy; Novartis Farma: Research Funding. Reichle:University Hospital Regensburg: Employment. Graux:Novartis: Honoraria, Membership on an entity's Board of Directors or advisory committees; Amgen: Honoraria, Membership on an entity's Board of Directors or advisory committees; Celgene: Honoraria, Membership on an entity's Board of Directors or advisory committees. Faul:Amgen: Honoraria. Topp:Astra: Consultancy; Regeneron: Consultancy; Affimed: Consultancy, Research Funding; Roche: Consultancy, Other: Travel Support; Jazz: Consultancy; Pfizer: Consultancy; Amgen: Consultancy, Honoraria, Other: Travel Support. Brüggemann:Amgen: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Roche: Honoraria. Horst:Pfizer: Research Funding; MSD: Research Funding; Gilead: Honoraria, Research Funding; Amgen: Honoraria, Research Funding; Boehringer Ingleheim: Research Funding. Stieglmaier:Amgen Research (Munich) GmbH: Employment; Amgen Inc: Equity Ownership. Wessels:Amgen: Employment. Haddad:Amgen Ltd.: Employment; Amgen Inc.: Equity Ownership. Zugmaier:Amgen Res. Munich: Employment. Nagorsen:Amgen: Employment, Equity Ownership, Patents & Royalties: Inventor on blinatumomab-related patent. Bargou:University of Wuerzburg, Germany: Employment; Novartis: Consultancy, Honoraria; GEMoaB GmbH: Consultancy, Honoraria; Pfizer: Consultancy, Honoraria; Amgen: Consultancy, Honoraria, Patents & Royalties: Patent for blinatumomab.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V126.23.680.680

Language: English

Publisher: American Society of Hematology

Publication Date: 2015

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 3262-3262

Abstract: BACKGROUND: Extramedullary acute leukemias (EM AL) following allogeneic hematopoietic stem cell transplantation (allo-SCT) are rare, but devastating events. Little is known about their incidence (0.05% to 30% according to registry data and small series, respectively), biology (sanctuary sites? uneven graft-versus-leukemia efficacy?), risk factors (acute myeloid leukemia, AML, with FAB M4 or M5? Philadelphia chromosome positive acute lymphoblastic leukemia, ALL? conditioning with busulfan?), treatment, and outcome. Our purpose was to compare clinical features and outcome of EM AL occurring prior to and after allo-SCT in a large cohort of patients. PATIENTS AND METHODS: In this single center, retrospective analysis, we report on 350 consecutive patients who received an allo-SCT for acute leukemias at our institution in the decade between January 1998 to December 2007, allowing for at least six months of follow-up until July 2008. 160 were females and 190 males, with a median age of 48 years (range: 17 to 71). 191 had been diagnosed with de novo AML, 78 with AML secondary after myelodysplasia or myeloproliferative disease (sAML), and 81 with ALL. According to molecular, cytogenetic and response criteria, 47 were considered standard and 303 high risk patients. 118 of 350 patients (34%) suffered a relapse after allo-SCT. RESULTS: Of the 350 patients, 42 (12%) had extramedullary manifestations prior to allo- SCT: 20 within the central nervous system (CNS), 16 cutaneous or lymphonodular, 2 musculoskeletal, and 4 urogenital manifestations. 21 of 350 patients (6%; 13 AML, 6 ALL, 2 sAML) had EM AL relapses after allo-SCT: 8 CNS, 6 cutaneous or lymphonodular, 5 musculoskeletal, and 2 urogenital; EM relapses were associated with marrow recurrences in 11 of 21 patients. However, there was little overlap between the EM AL groups prior to and after allo-SCT: only 6 patients belonged to both groups, and only 3 patients actually relapsed in the same EM compartment as before allo-SCT. After a median follow-up of 16 months (range: 0 to 122), survival probabilities at 5 years were 42% for patients without EM AL compared to 34% for EM AL patients prior to allo-SCT (not significant), and 12% for all acute leukaemia relapses versus 13% for EM AL patients after allo-SCT (not significant). For the latter, factors associated with adverse outcome included: no complete remission at allo-SCT (p = 0.081), reduced intensity conditioning (p = 0.034), prior donor lymphocyte infusions (DLI) (p = 0.034), and relapse within the first year after allo- SCT (p = 0.0017). Conversely, gender, age, diagnosis, AML FAB subtype, Philadelphia chromosome positive ALL, EM AL before allo-SCT, busulfan as part of the conditioning regimen, donor status, human leukocyte antigen (HLA) match, and graft-versus-hostdisease (GvHD) before EM relapse did not play a significant role for survival of patients with EM AL after allo-SCT. CONCLUSION: In this largest single-center study to date, extramedullary acute leukemias occured quite frequently both prior to and after allo HSCT. Patients with or without EM AL had comparable outcomes, both in continuous remission or relapse. Since EM AL occurred at identical sites in different patients prior to or after allo-SCT, and since some patients with EM AL after allo-SCT are cured due to a graft-versus-leukemia effect, the concept of “disease sanctuaries” seems unlikely. We speculate that temporo-spatial changes in immune surveillance might be mechanisms involved. Local blast control, e.g. through radiation, and systemic chemotherapeutic as well as immunomodulatory approaches may help to improve the prognosis of patients with EM AL both prior to and after allo-SCT. Figure: Kaplan-Meier-curves for overall survival:
 (prior to Tx): 308 patients without EM AL (dotted line) versus 42 patients with EM AL (solid line)
 (post Tx): 97 patients without EM AL relapse (dotted line) versus 21 patients with EM AL relapse (solid line) Figure:. Kaplan-Meier-curves for overall survival:
 (prior to Tx): 308 patients without EM AL (dotted line) versus 42 patients with EM AL (solid line)
 (post Tx): 97 patients without EM AL relapse (dotted line) versus 21 patients with EM AL relapse (solid line)

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V112.11.3262.3262

Language: English

Publisher: American Society of Hematology

Publication Date: 2008

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7