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NCAM1 supports therapy resistance and LSC function in AML
Stephen M. Sykes
Division of Hematology & Oncology
DBBS - Molecular Cell Biology
Siteman Cancer Center
Roy and Diana Vagelos Division of Biology & Biomedical Sciences (DBBS)
DBBS - Biochemistry, Biophysics, and Structural Biology
DBBS - Cancer Biology
Research output
:
Contribution to journal
›
Review article
›
peer-review
3
Scopus citations
Overview
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Keyphrases
Acute Myeloid Leukemia
100%
Stem Cell Activation
100%
Supportive Therapy
100%
Leukemia Stem Cells
100%
Therapy Resistance
100%
NCAM1
100%
Mitogen-activated Protein Kinase
50%
Chemotherapy Resistance
25%
Cell Function
25%
Vulnerability
25%
Cytarabine
25%
Pharmacological Inhibitors
25%
Treatment Decisions
25%
Acute Myeloid Leukemia Cells
25%
Cell Surface Markers
25%
Ara-C
25%
CD56
25%
L1 Cell Adhesion Molecule (L1CAM)
25%
Leukemia-initiating Cells
25%
Medicine and Dentistry
Acute Myeloid Leukemia
100%
Cell Function
100%
Leukemia
100%
Stem Cell
100%
Therapy Resistance
100%
Cytarabine
50%
Biological Marker
25%
Leukemia Cell
25%
Mitogen-Activated Protein Kinase
25%
Nerve Cell Adhesion Molecule
25%
MAPK Signaling
25%
Cell Surface Marker
25%
Cell Adhesion Molecule 1
25%
Biochemistry, Genetics and Molecular Biology
Stem Cell
100%
Cell Function
100%
Myeloid
100%
Cytarabine
50%
Mitogen-Activated Protein Kinase
25%
Cell Surface Marker
25%
Neural Cell Adhesion Molecule
25%
Cell Adhesion Molecule 1
25%
MAPK Signaling
25%
Pharmacology, Toxicology and Pharmaceutical Science
Leukemia
100%
Acute Myeloid Leukemia
100%
Therapy Resistance
100%
Cytarabine
50%
Biological Marker
25%
Chemotherapy
25%
Nerve Cell Adhesion Molecule
25%
Cell Surface Marker
25%
Cell Adhesion Molecule 1
25%