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  • 1
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 4047-4047
    Abstract: Abstract 4047 Poster Board III-982 Hepcidin (hep), a 25-amino-acid peptide, is the central regulator of iron homeostasis. Its transcription is upregulated by inflammatory cytokines and iron and is downregulated by iron deficiency, ineffective erythropoiesis, and hypoxia. Also HFE gene mutations are associated with less liver hepcidin messenger RNA. Both inherited (HFE genotype) and treatment-related factors influencing hep expression in patients (pts) with AML prior to and after allogeneic hematopoietic cell transplantation (HCT) as blood transfusions (BT), body iron and anemia were studied. The impact of chemotherapy, conditioning regimen, and Graft versus Host Disease (GvHD) on serum hep was analysed. Patients and methods 42 consecutive pts (23 male/19 female, median age 57 [range:18-70] years) with AML who underwent allogeneic HCT from February, 2008 - February, 2009 at the University of Leipzig were included. Each patient was assessed 10 days prior to and at a median of 3 (range: 3-5) months after HCT. Donors were matched related in 8 (19%) and matched unrelated (MUD) in 34 (81%) pts. Preparative regimen consisted of 12 Gy TBI/cyclophosphamid 120 mg/kg (ATG was included for unrelated HCT) in 13 (31%) and fludarabin 30 mg/m2/day for 3 days/2 Gy TBI) in 29 (69%) pts. Acute GvHD 〉 grade II was present in 13 (31%) and chronic GvHD in 17 (40%) pts. HFE genotype prior to and after HCT was assessed by PCR technique. Body iron was assessed by serum ferritin (sf) (normal values 〈 400ng/mL). Serum hep was measured by hepcidin C-ELISA at Intrinsic LifeSciences LLC, La Jolla, CA.(normal values: male 29-254 ng/mL, female: 17-286 ng/mL). Hep levels of 21 age-and gender-matched healthy volunteers (6 m/15 f, median age 57 years) were used as a control. Results Median serum hep was much higher in pts both prior to [median 358 (range:56-1096) ng/ml] and after HCT [median 398 (range:172-941) ng/ml] compared with the control group [median 52 (range:8.3-131) ng/ml] (p 〈 0.0001). Age and gender had no influence on hep values. Similarly, liver function, interval between diagnosis and HCT, number of chemotherapies, conditioning regimen, antibiotic- or antifungal-treatments had no impact on hep level. Iron overload was already seen in all pts prior to HCT with a median sf of 1945 (range: 617-6981) ng/mL after a median number of 22 units BT. Although after HCT the number of BT mounted to a median of 30 units (p 〈 0.0001), sf with a median of 2260 ng/mL remained elevated comparable to the level prior to HCT. Lower hep levels significantly correlated with fewer BT (p=0.001), but surprisingly not with sf values. Hep correlated inversely with the degree of anemia (p=0.002). Mutations in the HFE gene were found in 19 (46%) pts prior to HCT (heterozygosity (het) for H63D, n=11, het C282Y, n=3, het S65C, n=1, and homozygosity (homo) for H63D, n=4) and in 15 (37.5%) pts after HCT reflecting donor genotype (het for H63D,n=12, het C282Y, n=1, compound-het, n=1). Mutations in the HFE gene were not associated with lower hep levels. After HCT, 19 (45%) pts showed a decline in hep level of 155 (range: 394.8-9.5) ng/ml and 23 (55%) pts had an increase in hep levels of 138 (range: 43.3- 620.9) ng/ml compared with pre-transplantaion levels. None of the above mentioned parameters could predict or correlate with these changes in serum hep. Iron overload prior to HCT strongly correlated with later extensive chronic GvHD (p=0.003) and tended to correlate with limited GvHD (p=0.06). On the other hand, hep levels at any time point did not correlate with acute or later chronic GvHD. Conclusions Serum hepcidin is highly elevated in pts with AML prior to as well as after allogeneic HCT compared with healthy controls mainly because of frequent blood transfusions leading to elevated iron stores. This suggests that hepcidin synthesis and upregulation remain intact despite intensive chemotherapy and HCT. Hepcidin normally binds to ferroportin, leading to intracellular retention of iron in macrophages and to a reduction of extracellular serum iron. This may explain why serum hepcidin correlates with blood transfusions but not with serum ferritin values. Actually, overexpression of hepcidin may play an important protective role in this setting as it may prevent an increased ferroportin-mediated iron export from macrophages thereby reducing the severity of parenchymal iron loading and damage. Disclosures: Westerman: INTRINSIC LIFESCIENCES LLC: Consultancy, Employment, Equity Ownership. Hehme:Novartis: Employment. Niederwieser:Novartis: Speakers Bureau. Al-Ali:Novartis: Research Funding.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 2
    In: Blood, American Society of Hematology, Vol. 140, No. Supplement 1 ( 2022-11-15), p. 6224-6225
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2022
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 3
    In: Advances in Hematology, Hindawi Limited, Vol. 2011 ( 2011), p. 1-8
    Abstract: Hepcidin is upregulated by inflammation and iron. Inherited (HFE genotype) and treatment-related factors (blood units (BU), Iron overload) affecting hepcidin (measured by C-ELISA) were studied in 42 consecutive patients with AML prior to and after allogeneic hematopoietic cell transplantation (HCT). Results . Elevated serum ferritin pre- and post-HCT was present in all patients. Median hepcidin pre- and post-HCT of 358 and 398 ng/mL, respectively, were elevated compared to controls (median 52 ng/mL) ( P 〈 .0001 ). Liver and renal function, prior chemotherapies, and conditioning had no impact on hepcidin. Despite higher total BU after HCT compared to pretransplantation ( P 〈 .0005 ), pre- and posttransplant ferritin and hepcidin were similar. BU influenced ferritin ( P = .001 ) and hepcidin ( P = .001 ). No correlation of pre- or posttransplant hepcidin with pretransplant ferritin was found. HFE genotype did not influence hepcidin. Conclusions . Hepcidin is elevated in AML patients pre- and post-HCT due to transfusional iron-loading suggesting that hepcidin synthesis remains intact despite chemotherapy and HCT.
    Type of Medium: Online Resource
    ISSN: 1687-9104 , 1687-9112
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2011
    detail.hit.zdb_id: 2494501-8
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  • 4
    In: HemaSphere, Ovid Technologies (Wolters Kluwer Health), Vol. 7, No. S3 ( 2023-08), p. e43178c6-
    Type of Medium: Online Resource
    ISSN: 2572-9241
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2922183-3
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  • 5
    In: Science Signaling, American Association for the Advancement of Science (AAAS), Vol. 7, No. 321 ( 2014-04-15)
    Abstract: The BAALC / miR-3151 locus on chromosome 8q22 contains both the BAALC gene (for brain and acute leukemia, cytoplasmic) and miR-3151 , which is located in intron 1 of BAALC . Older acute myeloid leukemia (AML) patients with high expression of both miR-3151 and the BAALC mRNA transcript have a low survival prognosis, and miR-3151 and BAALC expression is associated with poor survival independently of each other. We found that miR-3151 functioned as the oncogenic driver of the BAALC / miR-3151 locus. Increased production of miR-3151 reduced the apoptosis and chemosensitivity of AML cell lines and increased leukemogenesis in mice. Disruption of the TP53-mediated apoptosis pathway occurred in leukemia cells overexpressing miR-3151 and the miR-3151 bound to the 3′ untranslated region of TP53 . In contrast, BAALC alone had only limited oncogenic activity. We found that miR-3151 contains its own regulatory element, thus partly uncoupling miR-3151 expression from that of the BAALC transcript. Both genes were bound and stimulated by a complex of the transcription factors SP1 and nuclear factor κB (SP1/NF-κB). Disruption of SP1/NF-κB binding reduced both miR-3151 and BAALC expression. However, expression of only BAALC , but not miR-3151 , was stimulated by the transcription factor RUNX1, suggesting a mechanism for the partly discordant expression of miR-3151 and BAALC observed in AML patients. Similar to the AML cells, in melanoma cell lines, overexpression of miR-3151 reduced the abundance of TP53, and knockdown of miR-3151 increased caspase activity, whereas miR-3151 overexpression reduced caspase activity. Thus, this oncogenic miR-3151 may also have a role in solid tumors.
    Type of Medium: Online Resource
    ISSN: 1945-0877 , 1937-9145
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2014
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  • 6
    In: Leukemia, Springer Science and Business Media LLC, Vol. 33, No. 7 ( 2019-7), p. 1620-1634
    Type of Medium: Online Resource
    ISSN: 0887-6924 , 1476-5551
    RVK:
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2008023-2
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  • 7
    In: Leukemia, Springer Science and Business Media LLC, Vol. 34, No. 2 ( 2020-02), p. 358-368
    Type of Medium: Online Resource
    ISSN: 0887-6924 , 1476-5551
    RVK:
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2008023-2
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  • 8
    In: Leukemia, Springer Science and Business Media LLC, Vol. 33, No. 3 ( 2019-3), p. 809-810
    Type of Medium: Online Resource
    ISSN: 0887-6924 , 1476-5551
    RVK:
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2008023-2
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  • 9
    In: Blood, American Society of Hematology, Vol. 138, No. Supplement 1 ( 2021-11-05), p. 221-221
    Abstract: Background: AML is a highly aggressive hematologic malignancy. Patient (pt) outcomes are affected by disease-related factors including cytogenetic findings and gene mutations, as well as pt-related factors, such as age and race. Younger pts have superior survival: ~50% of pts diagnosed as AYAs (18-39 years) may be cured of their disease. However, the impact of race on the outcome and associated disease profiles in this pt population are unknown. Methods: We compared survival and molecular profiles of 655 Non-Hispanic Black and Non-Hispanic White (hereafter referred to as Black, n=89 and White, n=566) AYA AML pts treated on frontline Cancer and Leukemia Group B/Alliance for Clinical Trials in Oncology protocols based on standard intensity cytarabine/anthracycline induction therapy between 1986 and 2016. Three hundred ten pts were analyzed molecularly via targeted sequencing of 81 genes. Additionally, we performed integrated genomic profiling (whole-exome sequencing and transcriptome sequencing) and measured residual disease (MRD) in serial samples of 4 Black pts who relapsed with their disease. Results: A comparison of clinical characteristics of AYA AML pts by race revealed almost identical age and sex distribution, and we found no significant differences between clinical features at diagnosis. With regard to genetic profiles, 42% of White pts were cytogenetically normal, whereas only 18% of Black pts had cytogenetically normal AML (CN-AML; p & lt;0.001). The abnormal karyotypes in Black pts more often contained abnormalities associated with core-binding factor (CBF) AML (39% v 25%, p=0.01; Fig. 1A). White pts had more known pathogenic NPM1 variants (29% v 9%, p=0.01), whereas Black pts had a higher incidence of ZRSR2 pathogenic variants (9% v 0.4%, p=0.004) and tended to have pathogenic KRAS variants more often (12% v 5%, p=0.11; Fig. 1B). Black AYA AML pts had worse outcomes including a higher early death rate (ED, defined as death within 30 days of diagnosis; 11% v 2%, p & lt;0.001), a trend towards lower complete remission (CR) rate (73% v 82%, p=0.06) and a shorter overall survival (OS; median, 1.5 v 3.1 years [y], p=0.002). Notably, this survival disparity was almost exclusively driven by pts aged 18-29 y: Black pts had a higher ED rate (16% v 3%, p=0.002), a lower CR rate (66% v 83%, p=0.01) and shorter OS (median, 1.3 v 10.2 y, p & lt;0.001) but not disease-free survival (DFS; p=0.16) than White pts aged 18-29 y. In contrast, there were no significant differences in these outcome metrics between Black and White pts aged 30-39 y (Fig. 2). Among all pts consolidated with intensive chemotherapy (n=566), multivariable analysis revealed Black race as an independent prognosticator of shorter DFS (p=0.04) and OS (p & lt;0.001). These differences in OS were also significant when we included pts who received allogeneic transplantation in 1st CR (n=655; p & lt;0.001). 18-29 y old Black pts with any non-CBF AML had very poor OS compared to White pts (5-y rates, 12% v 45%, p & lt;0.001). CBF-AML pts aged 18-29 y tended to have an inferior OS compared with White pts (5-y rates, 41% v 44%, p=0.10). To gain insights into the genetic features of Black AYA AML pts at different stages of the disease, we performed integrated genomic profiling on paired leukemic samples from diagnosis and relapse of 4 Black AYA pts. In all pts, the original dominant leukemic clone persisted and was dominant at relapse (Fig. 3). This suggests that the leukemic clone persists during treatment with conventional cytotoxic chemotherapy. This observation was further supported by MRD detection of NPM1 mutations in NPM1-mutated pts at time of morphologic CR. Conclusion: Black AYA AML pts present with distinct molecular features, including very high frequencies of CBF AML, and low frequency of NPM1. Pts aged 18-29y account for the race-associated survival disparity, especially non-CBF pts who have dramatically poor survival. On the one hand, the lower CR rates combined with persistence of dominant clones at relapse suggest reduced response to induction chemotherapy, and suggests the need for different treatment intensities and/or modalities in this pt cohort. On the other hand, high early death rates are indicative of delay in diagnosis and care, including health inequities, calling for systematic changes particularly for this population. Figure 1 Figure 1. Disclosures Blachly: KITE: Consultancy, Honoraria; INNATE: Consultancy, Honoraria; AbbVie: Consultancy, Honoraria; AstraZeneca: Consultancy, Honoraria. Mims: Leukemia and Lymphoma Society's Beat AML clinical study: Consultancy, Research Funding; Aptevo: Research Funding; Daiichi Sankyo: Consultancy, Research Funding; Glycomemetics: Research Funding; Kartos Pharmaceuticals: Research Funding; Xencor: Research Funding; Genentech: Consultancy; Abbvie: Consultancy; BMS: Consultancy; Kura Oncology: Consultancy; Syndax Pharmaceuticals: Consultancy; BMS: Consultancy; Jazz Pharmaceuticals: Consultancy; Aptevo: Research Funding. Walker: Karyopharm Therapeutics: Current Employment, Current holder of individual stocks in a privately-held company, Current holder of stock options in a privately-held company. Blum: Leukemia and Lymphoma Society: Research Funding; Syndax: Honoraria; AmerisourceBergen: Honoraria; Abbvie: Honoraria; Celyad Oncology: Research Funding; Nkarta: Research Funding; Forma Therapeutics: Research Funding; Xencor: Research Funding. Larson: Rafael Pharmaceuticals: Research Funding; Epizyme: Consultancy; Astellas: Consultancy, Research Funding; Gilead: Research Funding; CVS/Caremark: Consultancy; Takeda: Research Funding; Novartis: Research Funding; Cellectis: Research Funding. Stone: Onconova: Consultancy; Boston Pharmaceuticals: Consultancy; Innate: Consultancy; Jazz: Consultancy; Novartis: Consultancy, Research Funding; AbbVie: Consultancy; GlaxoSmithKline: Consultancy; Gemoab: Membership on an entity's Board of Directors or advisory committees; Foghorn Therapeutics: Consultancy; Janssen: Consultancy; Arog: Consultancy, Research Funding; Aprea: Consultancy; Elevate Bio: Membership on an entity's Board of Directors or advisory committees; Bristol Myers Squibb: Consultancy; BerGen Bio: Membership on an entity's Board of Directors or advisory committees; Astellas: Membership on an entity's Board of Directors or advisory committees; Amgen: Membership on an entity's Board of Directors or advisory committees; Actinium: Membership on an entity's Board of Directors or advisory committees; Syndax: Membership on an entity's Board of Directors or advisory committees; Celgene: Consultancy; Syntrix/ACI: Membership on an entity's Board of Directors or advisory committees; Syros: Membership on an entity's Board of Directors or advisory committees; Takeda: Consultancy; Agios: Consultancy, Research Funding; Macrogenics: Consultancy. Paskett: Pfizer: Research Funding; Merck: Research Funding. Byrd: Vincerx Pharmaceuticals: Current equity holder in publicly-traded company, Membership on an entity's Board of Directors or advisory committees; Newave: Membership on an entity's Board of Directors or advisory committees; Novartis, Trillium, Astellas, AstraZeneca, Pharmacyclics, Syndax: Consultancy, Honoraria. Eisfeld: Karyopharm (spouse): Current Employment.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2021
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 10
    In: Blood, American Society of Hematology, Vol. 138, No. Supplement 1 ( 2021-11-05), p. 3369-3369
    Abstract: Background: WBC levels vary widely in AML pts at diagnosis. Together with various cytogenetic and molecular abnormalities, WBC is a main prognostic factor for AML pts. Treatment decisions like need for intrathecal chemotherapy, trial enrollment eligibility, and stem cell transplant (SCT) considerations are often influenced by degree of WBC elevation. Despite such high clinical relevance, there are no standardized WBC-associated groups that improve prognostication and treatment guidance for AML pts. Aims: (1) define clinically relevant WBC level groups associated with outcome, (2) determine if WBC level has an independent prognostic impact in addition to established prognostic features [i.e., 2017 European LeukemiaNet (ELN) genetic-risk classification] and (3) characterize WBC level-associated gene-expression profiles to provide biologic insights into factors influencing WBC levels. Methods: We analyzed clinical and molecular features of 1,121 younger de novo AML pts similarly treated on frontline Cancer and Leukemia Group B/Alliance for Clinical Trials in Oncology protocols. No pt received an allogeneic SCT in 1 st complete remission (CR). Targeted next generation sequencing of 81 cancer- and leukemia-associated genes was done using MiSeq platform. We defined 3 WBC groups: low ( & lt;10,000/µL, n=298 pts), intermediate (10,000-49,999/µL, n=488 pts) and high (≥50,000/µL, n=335 pts) that were tested for associations with prognosis. Analysis of differentially expressed genes within each WBC group was done on blood samples via total transcriptome RNAseq with subsequent gene set enrichment analyses (GSEA) via Hallmark/Kegg pathways. Results: Pts in the high WBC group had higher extramedullary disease burden at diagnosis than pts in the intermediate and low groups (38% vs 29% and 12%, respectively; P & lt;.001). Pts in the intermediate WBC group more often had core-binding factor (CBF) AML (P & lt;.001), and the low WBC group pts had complex karyotype more often (P & lt;.001). Concerning clinical outcome, there was no steady decrease in any outcome endpoint with WBC increasing above 50,000/µL by 10,000/µL increments, or any linear changes in endpoints associated with WBC decreasing below 10,000/µL in 1,000/µL increments in the entire cohort. Pts in the intermediate WBC group had a higher CR rate (P & lt;.001), longer overall (OS; P & lt;.001; Fig. 1A), event-free (EFS; P & lt;.001), and disease-free survival (DFS; P=.002) than pts in the other 2 WBC groups. Intermediate WBC group pts also had a longer DFS in multivariable modeling (P=.01) after adjusting for DNMT3A, RUNX1, TP53 and WT1 mutation status. Among pts categorized according to ELN classification, those in the Favorable group who had an intermediate WBC had longer OS (P=.03; Fig. 1B), DFS (P=.04) and EFS (P & lt;.001) than pts with high and low WBC. WBC group did not affect pt outcome in the ELN Intermediate or Adverse groups. Within the ELN Favorable group, intermediate WBC was associated with longer OS (P=.001), DFS (P=.02) and EFS (P & lt;.001) in pts with CEBPA double mutations or NPM1 mutations with no FLT3-ITD or FLT3-ITD with low allelic ratio, but not in pts with CBF-AML. WBC group-associated gene expression profiles differed among WBC groups. Pts in the high WBC group had upregulation of CXCL10 and HILPDA and downregulation of FN1 and MSLN compared to the intermediate group. MMP7 and GZMA were upregulated in the low WBC group compared with the intermediate WBC group (Fig. 1C, D). There were also significant differences in GSEA in blood among the WBC groups. Compared with the intermediate WBC group, genes associated with inflammatory signaling (i.e., interferon α/γ) were upregulated in the low WBC group (Fig. 1E) and genes associated with glycolysis and fatty acid metabolism were upregulated in the high WBC group (Fig. 1F). Conclusion: The 3 WBC groups we propose offer additional prognostic information for younger AML pts. An intermediate WBC group was associated with better outcome among all pts and in pts included in the ELN Favorable group, especially those with non-CBF-AML. We also showed differences in the metabolic pathways among WBC groups. Our results suggest that the paradigm that all pts who present with a high WBC have a poor prognosis should be re-evaluated, and can help guide therapy decisions for younger AML pts. U10CA180821, U10CA180882, U24CA196171, https://acknowledgments.alliancefound.org; Clinicaltrials.gov Ids: NCT00048958, NCT00899223, NCT00900224 Figure 1 Figure 1. Disclosures Walker: Karyopharm Therapeutics: Current Employment, Current holder of individual stocks in a privately-held company, Current holder of stock options in a privately-held company. Blachly: AstraZeneca: Consultancy, Honoraria; INNATE: Consultancy, Honoraria; KITE: Consultancy, Honoraria; AbbVie: Consultancy, Honoraria. Larson: Takeda: Research Funding; CVS/Caremark: Consultancy; Gilead: Research Funding; Astellas: Consultancy, Research Funding; Epizyme: Consultancy; Rafael Pharmaceuticals: Research Funding; Cellectis: Research Funding; Novartis: Research Funding. Stone: Amgen: Membership on an entity's Board of Directors or advisory committees; Syntrix/ACI: Membership on an entity's Board of Directors or advisory committees; Foghorn Therapeutics: Consultancy; Bristol Myers Squibb: Consultancy; Gemoab: Membership on an entity's Board of Directors or advisory committees; Elevate Bio: Membership on an entity's Board of Directors or advisory committees; Aprea: Consultancy; Arog: Consultancy, Research Funding; Actinium: Membership on an entity's Board of Directors or advisory committees; Boston Pharmaceuticals: Consultancy; AbbVie: Consultancy; BerGen Bio: Membership on an entity's Board of Directors or advisory committees; Astellas: Membership on an entity's Board of Directors or advisory committees; Syros: Membership on an entity's Board of Directors or advisory committees; Syndax: Membership on an entity's Board of Directors or advisory committees; GlaxoSmithKline: Consultancy; Innate: Consultancy; Janssen: Consultancy; Jazz: Consultancy; Novartis: Consultancy, Research Funding; Onconova: Consultancy; Takeda: Consultancy; Agios: Consultancy, Research Funding; Celgene: Consultancy; Macrogenics: Consultancy. Byrd: Newave: Membership on an entity's Board of Directors or advisory committees; Vincerx Pharmaceuticals: Current equity holder in publicly-traded company, Membership on an entity's Board of Directors or advisory committees; Novartis, Trillium, Astellas, AstraZeneca, Pharmacyclics, Syndax: Consultancy, Honoraria. Eisfeld: Karyopharm (spouse): Current Employment. Mims: Kura Oncology: Consultancy; BMS: Consultancy; Abbvie: Consultancy; Genentech: Consultancy; Xencor: Research Funding; Leukemia and Lymphoma Society's Beat AML clinical study: Consultancy, Research Funding; Syndax Pharmaceuticals: Consultancy; Aptevo: Research Funding; Daiichi Sankyo: Consultancy, Research Funding; Glycomemetics: Research Funding; Kartos Pharmaceuticals: Research Funding; BMS: Consultancy; Jazz Pharmaceuticals: Consultancy; Aptevo: Research Funding.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2021
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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