Conspirators in a capital crime: co-deletion of p18INK4c and p16INK4a/p14ARF/p15INK4b in glioblastoma multiforme.
Glioblastoma multiforme (GBM) is one of the most dreaded cancer diagnoses due to its poor prognosis and the limited treatment options. Homozygous deletion of the p16(INK4a)/p14(ARF)/p15(INK4b) locus is among the most common genetic alterations in GBM. Two recent studies have shown that deletion and mutation of another INK4 family member, p18(INK4c), also drives the pathogenesis of GBM. This minireview will discuss the known roles for p18(INK4c) in the initiation and progression of cancer and suggest opportunities for future studies.
Solomon
David A
DA
Department of Oncology, Tumor Biology Training Program, Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, District of Columbia 20057, USA.
Kim
Jung-Sik
JS
Jean
Walter
W
Waldman
Todd
T
D001932:Brain Neoplasms / Q000235:genetics*; D050762:Cyclin-Dependent Kinase Inhibitor p15 / Q000235:genetics*; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics*; D050763:Cyclin-Dependent Kinase Inhibitor p18 / Q000235:genetics*; D017353:Gene Deletion; D016147:Genes, Tumor Suppressor; D005909:Glioblastoma / Q000235:genetics*; D006801:Humans; D025803:Tumor Suppressor Protein p14ARF / Q000235:genetics*
D050762:Cyclin-Dependent Kinase Inhibitor p15; D019941:Cyclin-Dependent Kinase Inhibitor p16; D050763:Cyclin-Dependent Kinase Inhibitor p18; D025803:Tumor Suppressor Protein p14ARF