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Alterations in the regulatory pathway involving p16, pRb and cdk4 in human chondrosarcoma.

Artikel i vetenskaplig tidskrift
Författare Julia Asp
Sven Inerot
J A Block
Anders Lindahl
Publicerad i Journal of orthopaedic research : official publication of the Orthopaedic Research Society
Volym 19
Nummer/häfte 1
Sidor 149-54
ISSN 0736-0266
Publiceringsår 2001
Publicerad vid Institutionen för de kirurgiska disciplinerna, Avdelningen för ortopedi
Institutionen för laboratoriemedicin, Avdelningen för klinisk kemi/transfusionsmedicin
Sidor 149-54
Språk en
Länkar dx.doi.org/10.1016/S0736-0266(00)00...
Ämnesord Bone Neoplasms, chemistry, genetics, Chondrosarcoma, chemistry, genetics, Chromosome Aberrations, Cyclin-Dependent Kinase 4, Cyclin-Dependent Kinase Inhibitor p16, analysis, Cyclin-Dependent Kinases, analysis, Genes, p16, Humans, Proto-Oncogene Proteins, Retinoblastoma Protein, analysis, Tumor Cells, Cultured
Ämneskategorier Cancer och onkologi, Klinisk laboratoriemedicin, Cell- och molekylärbiologi

Sammanfattning

The G1 regulatory pathway involving p16, pRb and cdk4 in the cell cycle has been investigated in human chondrosarcoma. The protein expression of p16, pRb and cdk4 was analyzed by Western blot in cultured cells from eight chondrosarcomas and in two chondrosarcoma cell lines. Both cell lines and one other sample were negative for p16. Moreover, one of the cell lines was pRb-negative and showed a high expression of cdk4 as well. In the other cell line and in three other samples pRb of expected size were detected in addition to a shorter form of the protein. To further investigate the reasons for down-regulation of the p16 protein, the p16-coding gene CDKN2 was analyzed by polymerase chain reaction (PCR), methyl-specific PCR (MSP) and sequencing in all tumor samples as well as in corresponding tumor tissues from three of the samples. The p16-negative samples were all found to have homozygous deletion of CDKN2. Another sample showed partial gene methylation and a heterozygous position in codon 148 was detected in one sample. The same base substitution was also found in two of the tissue samples. Finally, cytogenetic analysis of the samples with homozygously deleted CDKN2 revealed multiple structural abnormalities in all three cases. In conclusion, the p16/pRb/cdk4 pathway may play an important role in the pathogenesis of some chondrosarcomas.

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