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1. Rose D, Haferlach T, Schnittger S, Perglerová K, Kern W, Haferlach C: Subtype-specific patterns of molecular mutations in acute myeloid leukemia. Leukemia; 2017 Jan;31(1):11-17
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  • [Title] Subtype-specific patterns of molecular mutations in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) can be grouped into morphologically or genetically defined subtypes.
  • Today, the AML phenotype-genotype associations, that is, FAB/WHO (French-American-British/World Health Organization) definitions and recurrent molecular mutations, are not fully understood.
  • Therefore, we evaluated the impact of molecular mutations on the AML differentiation stage by molecular profiling of 4373 adult de novo AML patients in 7 cytomorphological subtypes.
  • We investigated mutations in 20 genes, including myeloid transcription factors (CEBPA, RUNX1), tumor suppressors (TP53, WT1), DNA modifiers (DNMT3A, IDH1/2, TET2), chromatin modifiers (ASXL1, MLL), signal transduction genes (FLT3, KRAS, NRAS) and NPM1.
  • FLT3, NPM1 and WT1 mutations were associated with an immature phenotype in myeloblastic AML, whereas other combinations involving ASXL1, RUNX1, MLL-PTD, CEBPA or KRAS were more frequent in myeloblastic AML with maturation.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Mutation
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Genetic Association Studies. Humans. Male. Middle Aged. Monocyte-Macrophage Precursor Cells. Monocytes. Mutation Rate. Young Adult


2. Craddock C, Nagra S, Peniket A, Brookes C, Buckley L, Nikolousis E, Duncan N, Tauro S, Yin J, Liakopoulou E, Kottaridis P, Snowden J, Milligan D, Cook G, Tholouli E, Littlewood T, Peggs K, Vyas P, Clark F, Cook M, Mackinnon S, Russell N: Factors predicting long-term survival after T-cell depleted reduced intensity allogeneic stem cell transplantation for acute myeloid leukemia. Haematologica; 2010 Jun;95(6):989-95
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  • [Title] Factors predicting long-term survival after T-cell depleted reduced intensity allogeneic stem cell transplantation for acute myeloid leukemia.
  • BACKGROUND: Reduced intensity conditioning regimens permit the delivery of a potentially curative graft-versus-leukemia effect in older patients with acute myeloid leukemia.
  • Although T-cell depletion is increasingly used to reduce the risk of graft-versus-host disease its impact on the graft-versus-leukemia effect and long-term outcome post-transplant is unknown.
  • DESIGN AND METHODS: We have characterized pre- and post-transplant factors determining overall survival in 168 patients with acute myeloid leukemia transplanted using an alemtuzumab based reduced intensity conditioning regimen with a median duration of follow-up of 37 months.
  • CONCLUSIONS: Disease stage, presentation karyotype and post-transplant CsA exposure are important predictors of outcome in patients undergoing a T-cell depleted reduced intensity conditioning allograft for acute myeloid leukemia.
  • These data confirm the presence of a potent graft-versus-leukemia effect after a T-cell depleted reduced intensity conditioning allograft in acute myeloid leukemia and identify CsA exposure as a manipulable determinant of outcome in this setting.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / surgery. T-Lymphocytes. Transplantation Conditioning / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Disease-Free Survival. Female. Follow-Up Studies. Graft vs Host Disease / immunology. Graft vs Host Disease / mortality. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Predictive Value of Tests. Time Factors. Transplantation, Homologous. Treatment Outcome. Young Adult

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  • (PMID = 19951968.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ PMC2878799
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3. Prakash S, Hoffman R, Barouk S, Wang YL, Knowles DM, Orazi A: Splenic extramedullary hematopoietic proliferation in Philadelphia chromosome-negative myeloproliferative neoplasms: heterogeneous morphology and cytological composition. Mod Pathol; 2012 Jun;25(6):815-27
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  • We studied 24 spleens with extramedullary hematopoietic proliferation (EMHP), a key feature of advanced-stage Philadelphia chromosome-negative myeloproliferative neoplasms, obtained from 24 patients (14 primary myelofibrosis, 7 polycythemia vera and 3 unclassifiable).

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  • (PMID = 22388763.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA108671; United States / NCI NIH HHS / CA / 2P01CA108671-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ NIHMS452936; NLM/ PMC3632395
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4. Fangmann J, Kathrin Al-Ali H, Sack U, Kamprad M, Tautenhahn HM, Faber S, Hauss J, Niederwieser D, Lindner T, Bachmann A: Kidney transplant from the same donor without maintenance immunosuppression after previous hematopoietic stem cell transplant. Am J Transplant; 2011 Jan;11(1):156-62
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  • In January 2005, an 18-year-old male patient with acute myeloid leukemia (AML) received a haploidentical hematopoietic stem cell transplantation (HSCT) from his father.
  • He developed hemolytic uremic syndrome and end-stage renal disease (ESRD) requiring hemodialysis on day 357 after HSCT.
  • As of June 2010, 66 months after HSCT and 32 months after KT, the patient has had neither rejection episodes nor clinical manifestations of transplantation-related complications.
  • [MeSH-minor] Adolescent. Adult. Humans. Immunosuppression. Leukemia, Myeloid, Acute / therapy. Male. Transplantation Chimera

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  • [Copyright] ©2010 The Authors Journal compilation©2010 The American Society of Transplantation and the American Society of Transplant Surgeons.
  • (PMID = 21199355.001).
  • [ISSN] 1600-6143
  • [Journal-full-title] American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
  • [ISO-abbreviation] Am. J. Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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5. Li X, Romain RD, Park D, Scadden DT, Merchant JL, Arnaout MA: Stress hematopoiesis is regulated by the Krüppel-like transcription factor ZBP-89. Stem Cells; 2014 Mar;32(3):791-801
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  • Previous studies have shown that ZBP-89 (Zfp148) plays a critical role in erythroid lineage development, with its loss at the embryonic stage causing lethal anemia and thrombocytopenia.
  • Its role in adult hematopoiesis has not been described.
  • We now show that conditional deletion of ZBP-89 in adult mouse hematopoietic stem/progenitor cells (HSPC) causes anemia and thrombocytopenia that are transient in the steady state, but readily uncovered following chemically induced erythro/megakaryopoietic stress.
  • Unexpectedly, stress induced by bone marrow transplantation of ZBP89(-/-) HSPC also resulted in a myeloid-to-B lymphoid lineage switch in bone marrow recipients.
  • The erythroid and myeloid/B lymphoid lineage anomalies in ZBP89(-/-) HSPC are reproduced in vitro in the ZBP-89-silenced multipotent hematopoietic cell line FDCP-Mix A4, and are associated with the upregulation of PU.1 and downregulation of SCL/Tal1 and GATA-1 in ZBP89-deficient cells.
  • These data identify an important role for ZBP-89 in regulating stress hematopoiesis in adult mouse bone marrow.

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  • [Copyright] © 2013 AlphaMed Press.
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  • (PMID = 24549639.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / K01 AR061434; United States / NIDDK NIH HHS / DK / P30 DK043351; United States / NIDDK NIH HHS / DK / R01 DK081920; United States / NIDDK NIH HHS / DK / DK081920; United States / NIDDK NIH HHS / DK / R56 DK055732; United States / NIDDK NIH HHS / DK / R01 DK055732; United States / NIDDK NIH HHS / DK / DK55732
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / GATA1 Transcription Factor; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Zfp148 protein, mouse; 0 / proto-oncogene protein Spi-1
  • [Other-IDs] NLM/ NIHMS541178; NLM/ PMC3930080
  • [Keywords] NOTNLM ; Erythroid progenitors / Hematopoietic stem cells / Stress hematopoiesis / Transcription factors / Transplantation
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6. Mehta HM, Futami M, Glaubach T, Lee DW, Andolina JR, Yang Q, Whichard Z, Quinn M, Lu HF, Kao WM, Przychodzen B, Sarkar CA, Minella A, Maciejewski JP, Corey SJ: Alternatively spliced, truncated GCSF receptor promotes leukemogenic properties and sensitivity to JAK inhibition. Leukemia; 2014 May;28(5):1041-51
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  • Granulocyte colony-stimulating factor (GCSF) drives the production of myeloid progenitor and precursor cells toward neutrophils via the GCSF receptor (GCSFR, gene name CSF3R).
  • Children with severe congenital neutropenia chronically receive pharmacologic doses of GCSF, and ∼30% will develop myelodysplasia/acute myeloid leukemia (AML) associated with GCSFR truncation mutations.
  • We found elevated expression of the alternatively spliced isoform, class IV CSF3R in adult myelodysplastic syndrome/AML patients.
  • Aside from its association with monosomy 7 and higher rates of relapse in pediatric AML patients, little is known about the biology of the class IV isoform.
  • We found developmental regulation of CSF3R isoforms with the class IV expression more representative of a progenitor cell stage.

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  • (PMID = 24170028.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL098608; United States / NCI NIH HHS / CA / R29 CA074422; United States / NCI NIH HHS / CA / R01 CA108922; United States / NCI NIH HHS / CA / P01CA55164; United States / NCI NIH HHS / CA / T32CA079447; United States / NCI NIH HHS / CA / CA100632; United States / NHLBI NIH HHS / HL / KO2-HL03794; United States / NCI NIH HHS / CA / R21 CA159203; United States / NHLBI NIH HHS / HL / K02 HL003794; United States / NCI NIH HHS / CA / R01-CA108992
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Granulocyte Colony-Stimulating Factor; EC 2.7.10.2 / Janus Kinases
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7. Tang W, Fan X, Wang L, Hu J: Busulfan and fludarabine conditioning regimen given at hematological nadir of cytoreduction fludarabine, cytarabine, and idarubicin chemotherapy in patients with refractory acute myeloid leukemia undergoing allogeneic stem cell transplantation: a single arm pilot consort study. Medicine (Baltimore); 2015 Apr;94(15):e706
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  • [Title] Busulfan and fludarabine conditioning regimen given at hematological nadir of cytoreduction fludarabine, cytarabine, and idarubicin chemotherapy in patients with refractory acute myeloid leukemia undergoing allogeneic stem cell transplantation: a single arm pilot consort study.
  • To improve the outcome of allogeneic stem cell transplantation in refractory acute myeloid leukemia (AML), we conducted a single-arm phase II clinical trial to evaluate the efficacy and feasibility of conditioning regimen following cytoreduction chemotherapy with 7-day interval.
  • Adult patients with refractory AML were enrolled in the study and received fludarabine, cytarabine, and idarubicin (FLAG-IDA) as cytoreductive chemotherapy followed by busulfan and fludarabine (Flu-BU) conditioning regimen and transfusion of mobilized peripheral stem cells from human leukocyte antigen-matched sibling or unrelated donor.
  • The primary endpoint of the study was 2-year leukemia-free survival (LFS) and secondary endpoints included complete-remission rate, 2-year overall survival (OS), nonrelapse mortality (NRM), and relapse rate.
  • Based on the Simon 2-stage design, 5 out of first eligible 14 patients remained leukemia-free for more than 2 years after allogeneic hematopoietic stem cell transplantation; thus, the null hypothesis of the study will be rejected and the study protocol is accepted as being warranted for further study.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods. Transplantation Conditioning / methods
  • [MeSH-minor] Adolescent. Adult. Busulfan / administration & dosage. Cytarabine / administration & dosage. Disease-Free Survival. Female. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Recurrence. Remission Induction. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Young Adult

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  • (PMID = 25881847.001).
  • [ISSN] 1536-5964
  • [Journal-full-title] Medicine
  • [ISO-abbreviation] Medicine (Baltimore)
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT01496547
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
  • [Other-IDs] NLM/ PMC4602511
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8. Walter MJ, Shen D, Ding L, Shao J, Koboldt DC, Chen K, Larson DE, McLellan MD, Dooling D, Abbott R, Fulton R, Magrini V, Schmidt H, Kalicki-Veizer J, O'Laughlin M, Fan X, Grillot M, Witowski S, Heath S, Frater JL, Eades W, Tomasson M, Westervelt P, DiPersio JF, Link DC, Mardis ER, Ley TJ, Wilson RK, Graubert TA: Clonal architecture of secondary acute myeloid leukemia. N Engl J Med; 2012 Mar 22;366(12):1090-8
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  • [Title] Clonal architecture of secondary acute myeloid leukemia.
  • BACKGROUND: The myelodysplastic syndromes are a group of hematologic disorders that often evolve into secondary acute myeloid leukemia (AML).
  • The genetic changes that underlie progression from the myelodysplastic syndromes to secondary AML are not well understood.
  • METHODS: We performed whole-genome sequencing of seven paired samples of skin and bone marrow in seven subjects with secondary AML to identify somatic mutations specific to secondary AML.
  • We then genotyped a bone marrow sample obtained during the antecedent myelodysplastic-syndrome stage from each subject to determine the presence or absence of the specific somatic mutations.
  • We identified recurrent mutations in coding genes and defined the clonal architecture of each pair of samples from the myelodysplastic-syndrome stage and the secondary-AML stage, using the allele burden of hundreds of mutations.
  • RESULTS: Approximately 85% of bone marrow cells were clonal in the myelodysplastic-syndrome and secondary-AML samples, regardless of the myeloblast count.
  • The secondary-AML samples contained mutations in 11 recurrently mutated genes, including 4 genes that have not been previously implicated in the myelodysplastic syndromes or AML.
  • In every case, progression to acute leukemia was defined by the persistence of an antecedent founding clone containing 182 to 660 somatic mutations and the outgrowth or emergence of at least one subclone, harboring dozens to hundreds of new mutations.
  • CONCLUSIONS: Nearly all the bone marrow cells in patients with myelodysplastic syndromes and secondary AML are clonally derived.
  • Genetic evolution of secondary AML is a dynamic process shaped by multiple cycles of mutation acquisition and clonal selection.

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  • (PMID = 22417201.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101937-09; United States / NCI NIH HHS / CA / P01CA101937; United States / NHLBI NIH HHS / HL / R01 HL082973; United States / NCI NIH HHS / CA / P01 CA101937-09; United States / NHLBI NIH HHS / HL / RC2 HL102927; United States / NHLBI NIH HHS / HL / R01HL082973; United States / NHGRI NIH HHS / HG / U54 HG003079-06; United States / NCRR NIH HHS / RR / UL1RR024992; United States / NCRR NIH HHS / RR / UL1 RR024992; United States / NHGRI NIH HHS / HG / U54HG003079; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / P01 CA101937; United States / NHGRI NIH HHS / HG / U54 HG003079; United States / NHLBI NIH HHS / HL / RC2 HL102927-02; United States / NHLBI NIH HHS / HL / R01 HL082973-04; United States / NHLBI NIH HHS / HL / RC2HL102927
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS366063; NLM/ PMC3320218
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9. Grace C, Nacheva EP: Significance Analysis of Microarrays (SAM) Offers Clues to Differences Between the Genomes of Adult Philadelphia Positive ALL and the Lymphoid Blast Transformation of CML. Cancer Inform; 2012;11:173-83
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  • [Title] Significance Analysis of Microarrays (SAM) Offers Clues to Differences Between the Genomes of Adult Philadelphia Positive ALL and the Lymphoid Blast Transformation of CML.
  • These include chronic myeloid leukemia (CML) and de novo acute Philadelphia positive (Ph(+)) leukemia of both myeloid, and lymphoid origin.
  • We used Significance Analysis of Microarrays (SAM) to analyze comparative genomic hybridization (aCGH) data from 30 CML (10 each of chronic phase, myeloid and lymphoid blast stage), 10 Ph(+)ALL adult patients and 10 disease free controls and were able to: (a) discriminate between the genomes of lymphoid and myeloid blast cells and (b) identify differences in the genome profile of de novo Ph(+)ALL and lymphoid blast transformation of CML (BC/L).

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  • [Journal-full-title] Cancer informatics
  • [ISO-abbreviation] Cancer Inform
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3448499
  • [Keywords] NOTNLM ; arraycgh / chr 9p / chr7p / cml / igh rearrangements / lymphoid blast crisis / ph+all / sam / significance analysis / tarp
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10. Flörcken A, van Lessen A, Terwey TH, Dörken B, Arnold R, Pezzutto A, Westermann J: Anti-leukemia T cells in AML: TNF-α⁺ CD8⁺ T cells may escape detection and possibly reflect a stage of functional impairment. Hum Vaccin Immunother; 2013 Jun;9(6):1200-4
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  • [Title] Anti-leukemia T cells in AML: TNF-α⁺ CD8⁺ T cells may escape detection and possibly reflect a stage of functional impairment.
  • Leukemia-associated antigens such as proteinase-3 (PR3) and Wilms' tumor protein-1 (WT-1) are potential targets of T-cell responses, which can be monitored by T-cell assays within vaccination trials and after allogeneic stem cell transplantation (SCT).
  • In chronic myeloid leukemia (CML) an aberrant cytokine profile of antigen-specific T-cells with predominant TNF-α secretion has previously been described.
  • The aim of this study was to investigate whether these TNF-α(+)/IFN-γ(-) CD8(+) T-cells can also be observed in AML patients after SCT.
  • Eight HLA-A2(+) AML patients at different time points after SCT were evaluated for HLA-A2-restricted CD8(+) T-cell responses against PR3, WT-1 and influenza-A using pentamer staining and different cytokine-based T-cell assays.
  • TNF-α(+)/IFN-γ(-) CD8(+) T-cells are an interesting biological phenomenon which can obviously be observed also in AML patients.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Leukemia, Myeloid, Acute / therapy. Myeloblastin / immunology. Stem Cell Transplantation. Transplantation, Homologous. Tumor Necrosis Factor-alpha / secretion. WT1 Proteins / immunology
  • [MeSH-minor] Adult. Female. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 23571180.001).
  • [ISSN] 2164-554X
  • [Journal-full-title] Human vaccines & immunotherapeutics
  • [ISO-abbreviation] Hum Vaccin Immunother
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 0 / WT1 Proteins; 0 / WT1 protein, human; EC 3.4.21.76 / Myeloblastin
  • [Other-IDs] NLM/ PMC3901807
  • [Keywords] NOTNLM ; AML / IFN-γ / T cell response / TNF-α / cytokine profile
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