The Multiple Tumor Suppressor 1/Cyclin-dependent Kinase Inhibitor 2 Gene in Human Central Nervous System Primitive Neuroectodermal Tumor

Neurosurgery ◽  
1995 ◽  
Vol 36 (5) ◽  
pp. 971-975 ◽  
Author(s):  
Corey Raffel ◽  
Keisuke Ueki ◽  
Griffith R. Harsh ◽  
David N. Louis
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tumor Suppressor ◽  
Primitive Neuroectodermal Tumor ◽  
Kinase Inhibitor ◽  
Neuroectodermal Tumor ◽  
Cyclin Dependent Kinase ◽  
Human Central Nervous System ◽  
Multiple Tumor ◽  
Cyclin Dependent Kinase Inhibitor

scholarly journals Frequency of polymorphisms and protein expression of cyclin-dependent kinase inhibitor 1A (CDKN1A) in central nervous system tumors

2009 ◽  
Vol 127 (5) ◽  
pp. 288-294 ◽  
Author(s):  
Mev Dominguez Valentin ◽  
Renata Canalle ◽  
Rosane de Paula Queiroz ◽  
Luiz Gonzaga Tone
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Protein Expression ◽  
Kinase Inhibitor ◽  
Expression Patterns ◽  
Cns Tumors ◽  
Control Group ◽  
Cyclin Dependent Kinase ◽  
Cross Sectional ◽  
Cyclin Dependent Kinase Inhibitor

CONTEXT AND OBJECTIVE: Genetic investigation of central nervous system (CNS) tumors provides valuable information about the genes regulating proliferation, differentiation, angiogenesis, migration and apoptosis in the CNS. The aim of our study was to determine the prevalence of genetic polymorphisms (codon 31 and 3' untranslated region, 3'UTR) and protein expression of the cyclin-dependent kinase inhibitor 1A (CDKN1A) gene in patients with and without CNS tumors. DESIGN AND SETTING: Analytical cross-sectional study with a control group, at the Molecular Biology Laboratory, Pediatric Oncology Department, Hospital das Clínicas de Ribeirão Preto. METHODS: 41 patients with CNS tumors and a control group of 161 subjects without cancer and paires for sex, age and ethnicity were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Protein analysis was performed on 36 patients with CNS tumors, using the Western Blotting technique. RESULTS: The frequencies of the heterozygote (Ser/Arg) and polymorphic homozygote (Arg/Arg) genotypes of codon 31 in the control subjects were 28.0% and 1.2%, respectively. However, the 3'UTR site presented frequencies of 24.2% (C/T) and 0.6% (T/T). These frequencies were not statistically different (P > 0.05) from those seen in the patients with CNS tumors (19.4% and 0.0%, codon 31; 15.8% and 2.6%, 3'UTR site). Regarding the protein expression in ependymomas, 66.67% did not express the protein CDKN1A. The results for medulloblastomas and astrocytomas were similar: neither of them expressed the protein (57.14% and 61.54%, respectively). CONCLUSION: No significant differences in protein expression patterns or polymorphisms of CDKN1A in relation to the three types of CNS tumors were observed among Brazilian subjects.

Expression ofOl-KIP, a cyclin-dependent kinase inhibitor, in embryonic and adult medaka (Oryzias latipes) central nervous system

2001 ◽  
Vol 222 (3) ◽  
pp. 439-449 ◽  
Author(s):  
Vân Nguyên ◽  
Eva María Candal Suárez ◽  
Ariane Sharif ◽  
Jean-Stéphane Joly ◽  
Franck Bourrat
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Kinase Inhibitor ◽  
Oryzias Latipes ◽  
Cyclin Dependent Kinase ◽  
Cyclin Dependent Kinase Inhibitor

Functional Loss of p21/Waf-1 in a Case of Benign Canine Multicentric Melanoma

1998 ◽  
Vol 35 (2) ◽  
pp. 94-101 ◽  
Author(s):  
M. G. Ritt ◽  
J. Wojcieszyn ◽  
J. F. Modiano
Keyword(s):  
Tumor Suppressor ◽  
Cell Cycle Progression ◽  
Kinase Inhibitor ◽  
P53 Gene ◽  
Tumor Formation ◽  
Cyclin Dependent Kinase ◽  
P53 Expression ◽  
Functional Loss ◽  
Normal Tissues ◽  
Cyclin Dependent Kinase Inhibitor

Mutations of tumor suppressor genes remove mechanisms that normally arrest proliferation of transformed cells, resulting in tumor formation. The p53 gene product functions as a tumor suppressor that induces p21/Waf-1, the 21-kDa product of the waf-1/cip-1/mda-6 gene. p21/Waf-1 is a pan-cyclin-dependent kinase inhibitor that arrests cell cycle progression under a variety of circumstances. We examined tissues from a dog with multiple primary pigmented proliferative lesions (benign, multicentric melanoma consisting of three distinct dermal lesions and a matrical cyst) for p21/Waf-1 and p53 expression by immunohistochemistry and immunoblotting. p21/Waf-1 and p-53 proteins were undetectable in the tumor cells and in the cyst but were present in adjacent normal tissues. Abundant cyclin-dependent kinase 4 (Cdk4), a protein related functionally to p21/Waf-1, also was present in the cyst. A somatic mutation of the waf-1 gene or of the p53 gene may have resulted in the loss of p21/Waf-1 expression in a common precursor of pigment-producing cells from the affected dog. Furthermore, this functional loss of p21/Waf-1 may play an important role in the genesis of canine benign melanoma.

scholarly journals Roles of the Tumor Suppressor p53 and the Cyclin-dependent Kinase Inhibitor p21WAF1/CIP1 in Receptor-mediated Apoptosis of WEHI 231 B Lymphoma Cells

1998 ◽  
Vol 187 (10) ◽  
pp. 1671-1679 ◽  
Author(s):  
Min Wu ◽  
Robert E. Bellas ◽  
Jian Shen ◽  
Gail E. Sonenshein
Keyword(s):  
Tumor Suppressor ◽  
B Cell ◽  
Kinase Inhibitor ◽  
Ectopic Expression ◽  
Cyclin Dependent Kinase ◽  
Lymphoma Cells ◽  
B Lymphoma ◽  
Cyclin Dependent Kinase Inhibitor ◽  
B Lymphoma Cells ◽  
Wehi 231

Treatment of WEHI 231 immature B lymphoma cells with an antibody against their surface immunoglobulin M (anti-IgM) induces apoptosis and has been studied extensively as a model of self-induced B cell tolerance. Since the tumor suppressor protein p53 has been implicated in apoptosis in a large number of cell types and has been found to be mutated in a variety of B cell tumors, here we sought to determine whether p53 and the p53 target gene cyclin-dependent kinase inhibitor p21WAF1/CIP1 were involved in anti-IgM–induced cell death. Anti-IgM treatment of WEHI 231 cells increased expression of p53 and p21 protein levels. Ectopic expression of wild-type p53 in WEHI 231 cells induced both p21 expression and apoptosis. Ectopic expression of p21 similarly induced apoptosis. Rescue of WEHI 231 cells from apoptosis by costimulation with CD40 ligand ablated the increase in p21 expression. Lastly, a significant decrease in anti-IgM–mediated apoptosis was seen upon downregulation of endogenous p53 activity by expression of a dominant-negative p53 protein or upon microinjection of an antisense p21 expression vector or antibody. Taken together, the above data demonstrate important roles for p53 and p21 proteins in receptor-mediated apoptosis of WEHI 231 B cells.

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