Presentation
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Presentation |
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6th Internet World Congress for Biomedical Sciences |
Xing Fan(1), Lourdes Gómez(2), Angel Pestaña(3), Luis Santamaría(4), Manuel Nistal(5), Javier Saez Castresana(6)
(1)Department of Genetics. University of Navarre - Pamplona. Spain
(2)Department of Genetics. University of Navarra - Pamplona . Spain
(3)Instituto de Investigaciones Biomedicas, CSIC - Madrid. Spain
(4)Department of Morphology (Histology) . Universidad Autonoma de Madrid (UAM) - Madrid. Spain
(5)Department of Morphology (Histology). Universidad Autónoma de Madrid (UAM) - Madrid . Spain
(6)Departamento de Genetica. Universidad de Navarra - Pamplona. Spain
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Contact address: |
Xing Fan Department of Genetics University of Navarre Irunlarrea, s/n Pamplona Navarre E-31008 Spain fanxing@unav.es |
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Neuroblastoma, a tumor arising from the sympathetic nervous system, is one of the most common childhood tumors. At the molecular level, a)MYCN oncogene amplification correlates with advanced disease stage, b) loss of heterozygosity studies show that chromosome arms 1p and 14q independently suffer losses of genetic material in neuroblastoma, and c) the expression of HRAS , SRC, TRK and LNGFR oncogenes correlate significantly with a better overall prognosis in neuroblastoma patients.
We have previously demonstrated that p53 does not suffer mutations in neuroblastic tumors (No TP53 mutations in neuroblastomas detected by PCR-SSCP analysis. Genes Chromosom. Cancer 10:136-138, 1994). But it is not clear whether p53 suffers inactivation through other mechanisms. In this study we present the expression profiles of p53 and PCNA in 29 neuroblastic tumors, assayed by immunohistochemistry, together with data accumulated in our laboratories on the status of the N-myc (gene amplification) and chromosomome 1p deletion, in the same group of tumors. Mouse monoclonal primary antibodies for p53 (Oncogene Research Products) and PCNA (Biomeda) were used at dilutions of 1:20 and 1:400 respectively. Sections were incubated with biotynilated goat antimouse IgG (Dako) as the secondary antibody, at a dilution of 1:400. Signal was visualized using the streptavidin-biotin-peroxidase method. The slides were counter stained with methyl green.
p53 immunostaining was detected in 22 cases (2 corresponded to nuclear staining and 20 to cytoplasmic staining) (Fig. 1-4, Table 1). PCNA expression (Fig.5,6) was related to neuroblastomas located at the adrenal gland, presenting low stroma content and genetic markers positive for N-myc amplification and/or chromosome 1p deletion (Table 2). These parameters have been documented to be related to bad prognosis.
In conclusion, p53 wild type protein seems to accumulate in the cytoplasm of neuroblastic tumors representing a non-mutational mechanism of p53 inactivation, as this molecule needs to act in the cell nucleus as a transcription factor. On the other hand, PCNA expression might predict a bad prognosis in neuroblastoma. Nevertheless, these results need to be confirmed with expression studies on a bigger number of neuroblastic tumors.
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