Cell-cycle inhibitor p27/Kip-1 expression in non-astrocytic and non-oligodendrocytic human nervous system tumors

• Published in: Neuroscience letters 1999-04, Vol.264 (1), p.29-32
• Main Authors: Schiffer, D, Bortolotto, S, Bosone, I, Cancelli, I, Cavalla, P, Schiffer, P, Piva, R
• Format: Article
• Language: English
• Subjects: Apoptosis - physiology; Biological and medical sciences; Cell Cycle - physiology; Cell Cycle Proteins; Cell Differentiation - physiology; Cyclin-Dependent Kinase Inhibitor p27; Ependymoma - metabolism; Ependymoma - pathology; Humans; Immunohistochemistry; Medical sciences; Medulloblastoma - metabolism; Medulloblastoma - pathology; Meningioma - metabolism; Meningioma - pathology; Microtubule-Associated Proteins - metabolism; Nervous System Neoplasms - metabolism; Nervous System Neoplasms - pathology; Nervous system tumors; Neuroblastoma - metabolism; Neuroblastoma - pathology; Neurology; p27/kip-1; Tumor Suppressor Proteins; Tumors of the nervous system. Phacomatoses
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(99)00171-8

p27/kip-1 is a `universal inhibitor' which inhibits cyclin complexes with cyclin-dependent kinases (CDKs), preventing cell cycle from the G1-S progression. It is expressed in normal oligodendrocytes and in differentiated glial tumors, decreasing with anaplasia and malignancy. In non-astrocytic and non-oligodendrocytic tumors of the nervous system, such as meningiomas, schwannomas, medulloblastomas, neuroblastomas and malignant lymphomas, p27/kip-1 is inconstantly and sometimes poorly expressed. This can be due to the lacking of p27 expression in the normal counterpart of tumor cells. In some tumors, p27/kip-1 expression can be attributed to a differentiation process, as in the pale islands of desmoplastic medulloblastoma and in neuroblastomas. A correlation of p27/kip-1 expression with histology was not found, with the exception of apoptosis in medulloblastomas. p27/kip-1 is in feed-back with cyclins and CDKs for the control of cell proliferation and its expression may occur where requested by the interplay with cyclins and other inhibitors.