## Abstract Abnormalities of the p53 gene have been identified in many malignancies, with reports of aberration in over half of colorectal, lung, breast and hepatocellular carcinoma cases. The normal gene acts as a recessive oncogene, while mutations change the apparent function to that of a domina
Cell proliferation patterns and p53 expression in gastric dysplasia
β Scribed by C. Miracco; D. Spina; C. Vindigni; M. I. Filipe; P. Tosi
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- French
- Weight
- 678 KB
- Volume
- 62
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
β¦ Synopsis
Gastric dysplasia (high-grade, HGD, and low-grade, LGD) and normal mucosa were tested for anti-pf3, anti-Ki-67 and anti-PCNA monoclonal antibodies on paraffin sections, and for relative AgNOR area and number on semithin Epon-Araldite sections. The proliferative compartment in normal mucosa was restricted to the middle layer corresponding to the neckisthmus region. In LGD and HGD there was an expansion of this compartment to the lower and upper layers of mucosa, and in HGD in particular to the upper layer. p53 was always negative in LGD as well as in normal mucosa, while it was positive in 34 out of 5 I cases of HGD. The most discriminant variables between LGD and HGD were relative AgNOR area and the percentages of MIB-I, p53 and PCNA. In p53-positive HGD the highest percentages of PCNA and MIB-I were in the middle and upper layers (PCNA) or the upper layer (MIB-I), while in p53-negative HGD cases cell proliferation was maximal in the middle layer, although also present in the upper layer. The majority of cases of LGD did not demonstrate cell proliferation in the upper layer, but 5 cases behaved similarly to the p53-negative HGD cases. No significant correlations were found among percentages of MIB-I and of PCNA and relative AgNOR area and number.
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## Abstract To clarify the significance of p150 expression, 102 gastric carcinomas were immunohistochemically investigated and 14 fresh samples of the cancer were analyzed with the immunoblot method. Tumor cell apoptosis was assessed by terminal deoxynucleotidyl transferase (TdT)βmediated dUTPβdigo
To examine the expression of p53 protein and gene alterations in oral epithelial lesions including epithelial dysplasias and primary squamous cell carcinomas, immunohistochemical and temperature gradient gel electrophoresis (TGGE) methods were applied to formalin-fixed and paraffin-embedded tissues.