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{userid:"gaetano.finocchiaro", "articletype":"article","pages":"709-11","author":"R Albarosa, S DiDonato, G Finocchiaro","year":"1995","title":"Redefinition of the coding sequence of the MXI1 gene and identification of a polymorphic repeat in the 3' non-coding region that allows the detection of loss of heterozygosity of chromosome 10q25 in glioblastomas","month":"","journal":"Hum Genet","publisher":"","volume":"95","number":"6","note":"0340-6717 (Print) xD;Journal Article xD;Research Support, Non-U.S. Gov't","tags":"Base Sequence,Basic Helix-Loop-Helix Transcription Factors,Brain Neoplasms\/*genetics,Chromosomes, Human, Pair 10\/*genetics,DNA-Binding Proteins\/*genetics,Genes, Tumor Suppressor\/genetics,Glioblastoma\/*genetics,Heterozygote,Humans,Molecular Sequence Data,Open Reading Frames\/*genetics,Polymorphism, Genetic,Regulatory Sequences, Nucleic Acid\/genetics,Repetitive Sequences, Nucleic Acid\/genetics,*Transcription Factors,Tumor Suppressor Proteins","booktitle":"","editor":"","abstract":"The MXI1 gene encodes a protein interacting with Max, a regulatory factor of the Myc oncogene, and is located on chromosome 10q25, a region showing frequent loss of heterozygosity in malignant gliomas. We have reassessed the coding sequence of MXI1 and found that, at the 3' end, the open reading frame is 28 codons shorter than previously described. We have also found an AAAAC polymorphic repeat (two alleles, 45% heterozygosity) in the 3' non-coding region of the gene. Six anaplastic astrocytomas and nine glioblastomas, the most malignant form of glioma, were informative for this polymorphism. Loss of heterozygosity was demonstrated in all glioblastomas, but not in the remaining tumors.","address":"","school":"","issn":"","doi":"","pubmed":"","key":"Albarosa1995","howpublished":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7789959 ","urllink":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7789959 ","refid":58}
,

{userid:"gaetano.finocchiaro", "articletype":"article","pages":"1-4","author":"E Chiariello, L Roz, R Albarosa, I Magnani, G Finocchiaro","year":"1999","title":"Identification of PTEN-related sequences in glioma cells and in non-neoplastic cell lines","month":"","journal":"Cancer Lett","publisher":"","volume":"138","number":"1-2","note":"0304-3835 (Print) xD;Journal Article xD;Research Support, Non-U.S. Gov't","tags":"Fibroblasts\/metabolism,*Genes, Tumor Suppressor,Glioma\/*genetics,Humans,Mutation,PTEN Phosphohydrolase,Phosphoric Monoester Hydrolases\/*genetics,Reverse Transcriptase Polymerase Chain Reaction,Tumor Cells, Cultured,*Tumor Suppressor Proteins","booktitle":"","editor":"","abstract":"The PTEN gene, which encodes a tumor suppressor with phosphatase activity, is located on chromosome 10q23 and is mutated in different tumors, including glioblastomas (GBM). We found evidence for a PTEN-related sequence (PTEN-rs) on genomic DNA of GBM and non-neoplastic cells. PTEN-rs does not contain introns and presents several conserved missense mutations, including a T to G transversion at the initiation codon. Rsa I digestion may help to identify this putative PTEN pseudogene which, according to RT-PCR analysis on glioma, fibroblast, brain and lung cells, does not appear to be transcribed.","address":"","school":"","issn":"","doi":"","pubmed":"","key":"Chiariello1999","howpublished":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10378766 ","urllink":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10378766 ","refid":44}
,

{userid:"gaetano.finocchiaro", "articletype":"article","pages":"541-5","author":"E Chiariello, L Roz, R Albarosa, I Magnani, G Finocchiaro","year":"1998","title":"PTEN\/MMAC1 mutations in primary glioblastomas and short-term cultures of malignant gliomas","month":"","journal":"Oncogene","publisher":"","volume":"16","number":"4","note":"0950-9232 (Print) xD;Journal Article xD;Research Support, Non-U.S. Gov't","tags":"Astrocytoma\/genetics,Chromosomes, Human, Pair 10\/*genetics,Genes, Tumor Suppressor\/*genetics,Glioblastoma\/genetics,Glioma\/*genetics,Humans,Loss of Heterozygosity,Neoplasm Proteins\/*genetics,PTEN Phosphohydrolase,*Phosphoric Monoester Hydrolases,Polymorphism, Single-Stranded Conformational,Protein Tyrosine Phosphatases\/*genetics,Tumor Cells, Cultured,*Tumor Suppressor Proteins","booktitle":"","editor":"","abstract":"A novel tumor suppressor, PTEN\/MMAC1, was recently found on chromosome 10q23 and mutations of this gene were described in about 20% of primary glioblastomas (GBM) and 60% of GBM cell lines. To define further the relevance of PTEN\/MMAC1 mutations in GBM we investigated by SSCP analysis its coding sequence in 44 gliomas, including 41 GBM, and in 21 short-term cultures (15 GBM and six malignant astrocytomas). Loss of heterozygosity (LOH) at 10q23 was present in at least one marker in the vicinity of the PTEN\/MMAC1 locus in 59% of the informative GBM (primary tumors and cell cultures). SSCP variant bands were found in seven primary GBM (17%) and in one short-term GBM culture and sequence analysis confirmed the presence of somatic mutations in all these cases (five missense, one splicing mutation and two small deletions). These data indicate that PTEN\/MMAC1 is inactivated in a subset of GBM and suggest that the high mutation frequency previously found in GBM established cell lines reflects culture condition artifacts rather than the true mutation frequency in vivo. Other suppressors, located on chromosome 10q, may also have a critical role in glioma tumorigenesis.","address":"","school":"","issn":"","doi":"","pubmed":"","key":"Chiariello1998","howpublished":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9484844 ","urllink":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9484844 ","refid":46}
,

{userid:"gaetano.finocchiaro", "articletype":"article","pages":"345-9","author":"R Albarosa, G Finocchiaro, E Chiariello, G Russo, L Susani, P Vezzoni, I Zucchi","year":"1997","title":"Construction of a 5-Mb YAC contig from the putative 10q25 tumor-suppressor region for glioblastomas","month":"","journal":"Genomics","publisher":"","volume":"41","number":"3","note":"0888-7543 (Print) xD;Journal Article xD;Research Support, Non-U.S. Gov't","tags":"Base Sequence,Brain Neoplasms\/*genetics,Chromosome Mapping,Chromosomes, Artificial, Yeast\/*genetics,Chromosomes, Human, Pair 10\/*genetics,DNA Primers\/genetics,DNA, Complementary\/genetics,DNA, Neoplasm\/genetics,*Genes, Tumor Suppressor,Genetic Markers,Glioblastoma\/*genetics,Humans,Molecular Sequence Data,Sequence Tagged Sites","booktitle":"","editor":"","abstract":"During the final step of the malignant progression to glioblastoma multiforme (GBM), the most frequent and malignant of primary brain tumors, more than 90% of the cases exhibit loss of genetic material on chromosome 10. We previously identified a 4-cM deletion interval in the 10q24-qter region that is common to all the GBM we have examined. A contig of 20 YACs spanning the 5 Mb of chromosomal DNA in the region has been assembled. Overlaps between YACs have been verified by STS content, fingerprinting analysis, and\/or Alu-Alu PCR. The contig contains 17 known microsatellite markers, 15 new STSs derived from the insert ends of YACs, 9 ESTs, and 11 others STSs, for a total of 52 STSs (average marker density 1\/100 kb). The physical map of this region will facilitate the search for a candidate tumor-suppressor gene(s) that is inactivated during the information of GBM.","address":"","school":"","issn":"","doi":"","pubmed":"","key":"Albarosa1997","howpublished":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9169131 ","urllink":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=9169131 ","refid":51}
,

{userid:"gaetano.finocchiaro", "articletype":"article","pages":"477-84","author":"I Manni, P Tunici, N Cirenei, R Albarosa, B M Colombo, L Roz, A Sacchi, G Piaggio, G Finocchiaro","year":"2002","title":"Mxi1 inhibits the proliferation of U87 glioma cells through down-regulation of cyclin B1 gene expression","month":"","journal":"Br J Cancer","publisher":"","volume":"86","number":"3","note":"0007-0920 (Print) xD;Journal Article xD;Research Support, Non-U.S. Gov't","tags":"Basic Helix-Loop-Helix Transcription Factors,Cell Cycle\/physiology,Cell Differentiation\/*physiology,Cell Division\/*drug effects\/*physiology,Cyclin B\/*genetics,DNA-Binding Proteins\/genetics\/*metabolism,G2 Phase,*Gene Expression Regulation, Neoplastic,Genes, Reporter,Glioma,Humans,Kinetics,Mitosis,Recombinant Proteins\/pharmacology,Time Factors,Transcription Factors\/genetics\/*metabolism,Transcription, Genetic,Transfection,Tumor Cells, Cultured,Tumor Suppressor Proteins","booktitle":"","editor":"","abstract":"Mxi1 is a Mad family member that plays a role in cell proliferation and differentiation. To test the role of Mxi1 on tumorigenesis of glioma cells we transfected a CMV-driven MXI1 cDNA in U87 human glioblastoma cells. Two clones were isolated expressing MXI1 levels 18- and 3.5-fold higher than wild-type U87 cells (clone U87.Mxi1.14 and U87.Mxi1.22, respectively). In vivo, U87.Mxi1.14 cells were not tumorigenic in nude mice and delayed development of tumours was observed with U87.Mxi1.22 cells. In vitro, the proliferation rate was partially and strongly inhibited in U87.Mxi1.22 and U87.Mxi1.14 cells respectively. The cell cycle analysis revealed a relevant accumulation of U87.Mxi1.14 cells in the G(2)\/M phase. Interestingly, the expression of cyclin B1 was inhibited to about 60% in U87.Mxi1.14 cells. This inhibition occurs at the transcriptional level and depends, at least in part, on the E-box present on the cyclin B1 promoter. Consistent with this, the endogenous Mxi1 binds this E-box in vitro. Thus, our findings indicate that Mxi1 can act as a tumour suppressor in human glioblastomas through a molecular mechanism involving the transcriptional down-regulation of cyclin B1 gene expression.","address":"","school":"","issn":"","doi":"","pubmed":"","key":"Manni2002","howpublished":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11875718 ","urllink":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11875718 ","refid":31}
,

{userid:"gaetano.finocchiaro", "articletype":"article","pages":"87-9","author":"L Montanini, C Regna-Gladin, M Eoli, R Albarosa, F Carrara, M Zeviani, M G Bruzzone, G Broggi, A Boiardi, G Finocchiaro","year":"2005","title":"Instability of mitochondrial DNA and MRI and clinical correlations in malignant gliomas","month":"","journal":"J Neurooncol","publisher":"","volume":"74","number":"1","note":"0167-594X (Print) xD;Comparative Study xD;Journal Article","tags":"Base Sequence,Brain Neoplasms\/*genetics\/mortality\/pathology,DNA, Mitochondrial\/*genetics,Genomic Instability,Glioma\/*genetics\/mortality\/pathology,Humans,Molecular Sequence Data,Polymerase Chain Reaction,Polymorphism, Genetic,Prognosis,Survival Analysis,Tumor Markers, Biological\/*genetics","booktitle":"","editor":"","abstract":"Mutations and instability of mitochondrial DNA (mtDNA) are frequent in tumors but their pathogenic relevance is not established. To assess their role in the clinical management of malignant gliomas we have studied the D loop of mtDNA in 42 such tumors. Alterations were found in 36% of the cases. The MRI and the clinical follow-up of these patients suggest that these mutations are not associated with increased aggressiveness. mtDNA could be amplified from post-surgical tumor cavities in patients undergoing a loco-regional treatment. These results imply that mtDNA mutations are unlikely to play a role in diagnostic or prognostic evaluations of gliomas: their detection, however, could be of use for the clinical follow-up of malignant gliomas.","address":"","school":"","issn":"","doi":"","pubmed":"","key":"Montanini2005","howpublished":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16078113 ","urllink":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16078113 ","refid":19}
,

{userid:"gaetano.finocchiaro", "articletype":"article","pages":"1260-7","author":"R Albarosa, B M Colombo, L Roz, I Magnani, B Pollo, N Cirenei, C Giani, A M Conti, S DiDonato, G Finocchiaro","year":"1996","title":"Deletion mapping of gliomas suggest the presence of two small regions for candidate tumor-suppressor genes in a 17-cM interval on chromosome 10q","month":"","journal":"Am J Hum Genet","publisher":"","volume":"58","number":"6","note":"0002-9297 (Print) xD;Journal Article xD;Research Support, Non-U.S. Gov't","tags":"Brain Neoplasms\/*genetics\/pathology,Centromere,Child,Chromosome Mapping,*Chromosomes, Human, Pair 10,DNA, Neoplasm\/analysis,*Gene Deletion,*Genes, Tumor Suppressor,Genetic Markers,Genomic Library,Glioma\/*genetics\/pathology,Humans,In Situ Hybridization, Fluorescence,Karyotyping,Magnetic Resonance Imaging,Telomere","booktitle":"","editor":"","abstract":"The loss of genetic material on chromosome 10q is frequent in different tumors and particularly in malignant gliomas. We analyzed 90 of these tumors and found loss of heterozygosity (LOH) in >90% of the informative loci in glioblastoma multiforme (GBM). Initial studies restricted the common LOH region to 10q24-qter. Subsequently, the study of a pediatric GBM suggested D10S221 and D10S209, respectively, as centromeric and telomeric markers of a 4-cM LOH region. It is interesting to note that, in one subset of cells from this tumor, locus D10S209 seems involved in the allelic imbalance of a larger region, with D10S214 as telomeric marker. This 17-cM region contains the D10S587-D10S216 interval of common deletion recently defined on another set of gliomas.","address":"","school":"","issn":"","doi":"","pubmed":"","key":"Albarosa1996","howpublished":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8651304 ","urllink":"http:\/\/www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8651304 ","refid":54}
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