title: Therapeutically targeting SELF-reinforcing leukemic niches in acute myeloid leukemia: A worthy endeavor?
abstract: A tight relationship between the acute myeloid leukemia (AML) population and the bone marrow (BM) microenvironment has been convincingly established. The AML clone contains leukemic stem cells (LSCs) that compete with normal hematopoietic stem cells (HSCs) for niche occupancy and remodel the niche; whereas, the BM microenvironment might promote AML development and progression not only through hypoxia and homing/adhesion molecules, but also through genetic defects. Although it is still unknown whether the niche influences treatment results or contains any potential target for treatment, this dynamic AML-niche interaction might be a promising therapeutic objective to significantly improve the AML cure rate.
authors.affiliation: Division of Hematology, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy.
authors.forename: Paolo
authors.initials: P
authors.lastname: Bernasconi
authors.affiliation: Division of Hematology, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy.
authors.forename: Mirko
authors.initials: M
authors.lastname: Farina
authors.affiliation: Division of Hematology, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy.
authors.forename: Marina
authors.initials: M
authors.lastname: Boni
authors.affiliation: Division of Hematology, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy.
authors.forename: Irene
authors.initials: I
authors.lastname: Dambruoso
authors.affiliation: Division of Hematology, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy.
authors.forename: Celeste
authors.initials: C
authors.lastname: Calvello
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001596:Benzylamines; D001853:Bone Marrow / Q000473:pathology; D015687:Cell Hypoxia / Q000187:drug effects; D019070:Cell Lineage; D054377:Chemokine CXCL12 / Q000037:antagonists & inhibitors / Q000276:immunology / Q000502:physiology; D002986:Clinical Trials as Topic; D003131:Combined Modality Therapy; D036101:Cord Blood Stem Cell Transplantation; D000080027:Cyclams; D004164:Diphosphonates / Q000627:therapeutic use; D004195:Disease Models, Animal; D006571:Heterocyclic Compounds / Q000627:therapeutic use; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology; D015470:Leukemia, Myeloid, Acute / Q000188:drug therapy / Q000473:pathology / Q000628:therapy*; D051379:Mice; D058990:Molecular Targeted Therapy; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors / Q000502:physiology; D014411:Neoplastic Stem Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D019718:Receptors, CXCR4 / Q000037:antagonists & inhibitors / Q000276:immunology / Q000502:physiology; D055153:Stem Cell Niche / Q000187:drug effects*; D017154:Stromal Cells / Q000145:classification / Q000187:drug effects / Q000473:pathology; D014183:Transplantation, Heterologous; D059016:Tumor Microenvironment / Q000187:drug effects
chemical_list: D000911:Antibodies, Monoclonal; D000970:Antineoplastic Agents; D001596:Benzylamines; C515255:CXCL12 protein, human; C527276:CXCR4 protein, human; D054377:Chemokine CXCL12; D000080027:Cyclams; D004164:Diphosphonates; D006571:Heterocyclic Compounds; D036341:Intercellular Signaling Peptides and Proteins; D009363:Neoplasm Proteins; D047428:Protein Kinase Inhibitors; D019718:Receptors, CXCR4; C088327:plerixafor