CD34+CD38− leukemic stem cell frequency to predict outcome in acute myeloid leukemia
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V. V. D. van der Velden | M. Jongen‐Lavrencic | T. Pabst | G. Schuurhuis | G. Ossenkoppele | M. Manz | B. Löwenberg | J. Cloos | P. Valk | A. A. van de Loosdrecht | W. Zeijlemaker | A. Kelder | F. Preijers | J. Maertens | T. Grob | D. Hanekamp | Rosa Meijer | D. Breems | J. Carbaat-Ham | Y. J. Oussoren-Brockhoff | A. N. Snel | D. Veldhuizen | W. J. Scholten | J. Slomp | Diana Hanekamp | Alexander N. Snel | R. Meijer | W. Scholten | Y. Oussoren-Brockhoff
[1] Markus G. Manz,et al. Molecular Minimal Residual Disease in Acute Myeloid Leukemia , 2018, The New England journal of medicine.
[2] G. Schuurhuis,et al. Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia , 2018, Journal of visualized experiments : JoVE.
[3] C. Bloomfield,et al. Prognostic impact of the CD34+/CD38− cell burden in patients with acute myeloid leukemia receiving allogeneic stem cell transplantation , 2017, American journal of hematology.
[4] E. Vellenga,et al. Therapeutic value of clofarabine in younger and middle-aged (18-65 years) adults with newly diagnosed AML. , 2017, Blood.
[5] Claude Preudhomme,et al. A 17-gene stemness score for rapid determination of risk in acute leukaemia , 2016, Nature.
[6] P. Vyas,et al. Genetically distinct leukemic stem cells in human CD34− acute myeloid leukemia are arrested at a hemopoietic precursor-like stage , 2016, The Journal of experimental medicine.
[7] Yashma Patel,et al. Assessment of Minimal Residual Disease in Standard-Risk AML. , 2016, The New England journal of medicine.
[8] G. Schuurhuis,et al. A simple one-tube assay for immunophenotypical quantification of leukemic stem cells in acute myeloid leukemia , 2016, Leukemia.
[9] C. Hourigan,et al. Advancing the Minimal Residual Disease Concept in Acute Myeloid Leukemia. , 2015, Seminars in hematology.
[10] P. Vyas,et al. An immunophenotypic pre‐treatment predictor for poor response to induction chemotherapy in older acute myeloid leukaemia patients: blood frequency of CD34+ CD38low blasts , 2015, British journal of haematology.
[11] G. Schuurhuis,et al. Absence of leukaemic CD34+ cells in acute myeloid leukaemia is of high prognostic value: a longstanding controversy deciphered , 2015, British journal of haematology.
[12] E. Estey,et al. Relation of clinical response and minimal residual disease and their prognostic impact on outcome in acute myeloid leukemia. , 2015, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[13] P. Vyas,et al. Prognostic value of monitoring a candidate immunophenotypic leukemic stem/progenitor cell population in patients allografted for acute myeloid leukemia , 2014, Leukemia.
[14] T. Pabst,et al. Leukemic Stem Cell Frequency: A Strong Biomarker for Clinical Outcome in Acute Myeloid Leukemia , 2014, PloS one.
[15] G. Schuurhuis,et al. Tumor heterogeneity makes AML a “moving target” for detection of residual disease , 2013, Cytometry. Part B, Clinical cytometry.
[16] Robert K Hills,et al. Prognostic relevance of treatment response measured by flow cytometric residual disease detection in older patients with acute myeloid leukemia. , 2013, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[17] Bob Löwenberg,et al. High prognostic impact of flow cytometric minimal residual disease detection in acute myeloid leukemia: data from the HOVON/SAKK AML 42A study. , 2013, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[18] E. Estey,et al. Significance of minimal residual disease before myeloablative allogeneic hematopoietic cell transplantation for AML in first and second complete remission. , 2013, Blood.
[19] Yu Wang,et al. MRD-directed risk stratification treatment may improve outcomes of t(8;21) AML in the first complete remission: results from the AML05 multicenter trial. , 2013, Blood.
[20] F. Lo‐Coco,et al. Identification of emerging FLT3 ITD‐positive clones during clinical remission and kinetics of disease relapse in acute myeloid leukaemia with mutated nucleophosmin , 2013, British journal of haematology.
[21] J. Gratama,et al. Tumor heterogeneity makes AML a "moving target" for detection of residual disease. , 2013, Cytometry. Part B, Clinical cytometry.
[22] Todd A Alonzo,et al. Residual disease detected by multidimensional flow cytometry signifies high relapse risk in patients with de novo acute myeloid leukemia: a report from Children's Oncology Group. , 2012, Blood.
[23] S. Jang,et al. Flow cytometric quantification and immunophenotyping of leukemic stem cells in acute myeloid leukemia , 2012, Annals of Hematology.
[24] Ø. Bruserud,et al. The surface molecule signature of primary human acute myeloid leukemia (AML) cells is highly associated with NPM1 mutation status , 2012, Leukemia.
[25] Y. Assaraf,et al. The role of minor subpopulations within the leukemic blast compartment of AML patients at initial diagnosis in the development of relapse , 2012, Leukemia.
[26] Joshua F. McMichael,et al. Clonal evolution in relapsed acute myeloid leukemia revealed by whole genome sequencing , 2011, Nature.
[27] C. Jordan,et al. Leukemia stem cells in 2010: current understanding and future directions. , 2011, Blood reviews.
[28] M. Ebinger,et al. High Proportion of Leukemic Stem Cells at Diagnosis Is Correlated with Unfavorable Prognosis in Childhood Acute Myeloid Leukemia , 2011, Pediatric hematology and oncology.
[29] P. Vyas,et al. Coexistence of LMPP-like and GMP-like leukemia stem cells in acute myeloid leukemia. , 2011, Cancer cell.
[30] M. Carroll,et al. Human acute myelogenous leukemia stem cells are rare and heterogeneous when assayed in NOD/SCID/IL2Rγc-deficient mice. , 2011, The Journal of clinical investigation.
[31] D. Gold,et al. Genomic, immunophenotypic, and NPM1/FLT3 mutational studies on 17 patients with normal karyotype acute myeloid leukemia (AML) followed by aberrant karyotype AML at relapse. , 2010, Cancer genetics and cytogenetics.
[32] Y. Assaraf,et al. High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine. , 2010, Blood.
[33] J. Gribben,et al. Leukemia-initiating cells from some acute myeloid leukemia patients with mutated nucleophosmin reside in the CD34(-) fraction. , 2010, Blood.
[34] G. Schuurhuis,et al. Minimal residual disease in acute myeloid leukemia: already predicting a safe haven? , 2010, Expert review of hematology.
[35] Satoshi Tanaka,et al. Chemotherapy-resistant human AML stem cells home to and engraft within the bone-marrow endosteal region , 2007, Nature Biotechnology.
[36] Q. Waisfisz,et al. High Stem Cell Frequency in Acute Myeloid Leukemia at Diagnosis Predicts High Minimal Residual Disease and Poor Survival , 2005, Clinical Cancer Research.
[37] Paola Fazi,et al. Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype. , 2005, The New England journal of medicine.
[38] G. Schuurhuis,et al. MRD parameters using immunophenotypic detection methods are highly reliable in predicting survival in acute myeloid leukaemia , 2004, Leukemia.
[39] D. Olive,et al. Human acute myeloid leukemia CD34+/CD38- progenitor cells have decreased sensitivity to chemotherapy and Fas-induced apoptosis, reduced immunogenicity, and impaired dendritic cell transformation capacities. , 2000, Cancer research.
[40] Robert Gray,et al. A Proportional Hazards Model for the Subdistribution of a Competing Risk , 1999 .
[41] J. Dick,et al. Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell , 1997, Nature Medicine.
[42] E. Kelemen. Specific thrombopoietin cloned and sequenced--with personal retrospect and clinical prospects. , 1995, Leukemia.