Abstract
The PML gene, involved in the t(15;17) chromosomal translocation of acute promyelocytic leukemia (APL), encodes a protein which localizes to the PML-nuclear body, a subnuclear macromolecular structure. PML controls apoptosis, cell proliferation, and senescence. Here, we review the current understanding of its role in tumor suppression.
MeSH Terms
Adaptor Proteins, Signal Transducing
Animals
Apoptosis/physiology
Carrier Proteins/metabolism
Cell Division
Cell Transformation, Neoplastic
Cellular Senescence
Co-Repressor Proteins
Genes, Tumor Suppressor/physiology
Humans
Intracellular Signaling Peptides and Proteins
Molecular Chaperones
Neoplasm Proteins/genetics,metabolism,physiology
Neoplasms/genetics,physiopathology
Nuclear Proteins/genetics,metabolism
Oncogene Proteins, Fusion/genetics,metabolism
Promyelocytic Leukemia Protein
Receptors, Retinoic Acid/genetics,metabolism
Retinoic Acid Receptor alpha
Transcription Factors/genetics,metabolism,physiology
Tumor Suppressor Protein p53/metabolism
Tumor Suppressor Proteins
Chemicals
Adaptor Proteins, Signal Transducing
Carrier Proteins
Co-Repressor Proteins
DAXX protein, human
Intracellular Signaling Peptides and Proteins
Molecular Chaperones
Neoplasm Proteins
Nuclear Proteins
Oncogene Proteins, Fusion
Promyelocytic Leukemia Protein
RARA protein, human
Receptors, Retinoic Acid
Retinoic Acid Receptor alpha
Transcription Factors
Tumor Suppressor Protein p53
Tumor Suppressor Proteins
PML protein, human
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Salomoni Paolo
Molecular Biology Program and Department of Pathology, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.
Pandolfi Pier Paolo