p18 was first identified as a factor associated with a macromolecular tRNA synthetase complex. Here we describe the mouse p18 loss-of-function phenotype and a role for p18 in the DNA damage response. Inactivation of both p18 alleles caused embryonic lethality, while heterozygous mice showed high susceptibility to spontaneous tumors. p18 was induced and translocated to the nucleus in response to...

p18 is a cyclin-dependent kinase inhibitor that interferes with the Rb-kinase activity of CDK6/CDK4. Disruption of p18 in mice impairs B-cell terminal differentiation and confers increased susceptibility to tumor development; however, alterations of p18 in human tumors have rarely been described. We used a tissue-microarray approach to analyze p18 expression in 316 Hodgkin Lymphomas (HL). Nearl...

Activating mutations in the RET proto-oncogene are associated with both familial and sporadic medullary thyroid carcinoma (MTC) development; however, the genetic mechanisms underlying MTC tumorigenesis remain largely unknown. Recently, we have identified somatic inactivating mutations in the cell cycle inhibitor gene P18 in human MTC, which coincided with activating RET mutations, suggesting a ...

The most recent study, conducted by Politecnico of Milan, on food surplus management in Italy shows that in the Italian food supply chain the food surplus is around 5.5 million tons/year, and the amount of food wasted is around 5.1 million tons/year. During 2015, the charitable organizations (COs) belonging to the Italian Food Bank Network, active in recovering and distributing food for social ...

Terminal differentiation of many cell types involves permanent withdrawal from the cell division cycle. The p18INK4c protein, a member of the p16/INK4 cyclin-dependent kinase (CDK) inhibitor family, is induced more than 50-fold during myogenic differentiation of mouse C2C12 myoblasts to become the predominant CDK inhibitor complexed with CDK4 and CDK6 in terminally differentiated myotubes. We h...

Phosphoprotein p18 was identified originally on the basis of its very high level of expression in leukemic cells of different lineages. Changes in the level of p18 accumulation and phosphorylation associated with induction of differentiation of leukemic cells suggested a potential role for this phosphoprotein in cellular proliferation and differentiation and possibly in malignant transformation...

Genomic alterations leading to aberrant activation of cyclin/ cyclin-dependent kinase (cdk) complexes drive the pathogenesis of many common human tumor types. In the case of glioblastoma multiforme (GBM), these alterations are most commonly due to homozygous deletion of p16 and less commonly due to genomic amplifications of individual genes encoding cyclins or cdks. Here, we describe deletion o...