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

Asp, Julia, 1973- (författare)
Göteborgs universitet, Institutionen för laboratoriemedicin, Avdelningen för klinisk kemi/transfusionsmedicin, Gothenburg University, Institute of Laboratory Medicine, Dept of Clinical Chemistry/Transfusion Medicine
Inerot, Sven, 1948- (författare)
Göteborgs universitet, Institutionen för de kirurgiska disciplinerna, Avdelningen för ortopedi, Gothenburg University, Institute of Surgical Sciences, Department of Orthopaedics
Block, J A (författare)
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Lindahl, Anders, 1954- (författare)
Göteborgs universitet, Institutionen för laboratoriemedicin, Avdelningen för klinisk kemi/transfusionsmedicin, Gothenburg University, Institute of Laboratory Medicine, Dept of Clinical Chemistry/Transfusion Medicine
visa färre...
Göteborgs universitet Sahlgrenska akademin. Institutionen för laboratoriemedicin, Avdelningen för klinisk kemi/transfusionsmedicin. 
Göteborgs universitet Sahlgrenska akademin. Institutionen för de kirurgiska disciplinerna, Avdelningen för ortopedi. 
2001
Engelska.
Ingår i: Journal of orthopaedic research : official publication of the Orthopaedic Research Society. - 0736-0266. ; 19:1, s. 149-54
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • 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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Cancer and Oncology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Klinisk laboratoriemedicin (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Clinical Laboratory Medicine (hsv//eng)

Nyckelord

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

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