Therefore, p53 mutation may precede invasion in esophageal carcinogenesis, and multifocal esophageal neoplasms may arise from independent clones of transformed cells.
Eighty-nine percent of the neoplasms were moderately or poorly differentiated, 89% expressed either an intermediate or high proliferative activity, 39% showed p53 aberrations, 71% exhibited induction of angiogenesis, and 39% had tumors that were positive for blood vessel invasion.
We demonstrate that antigen retrieval techniques increase p53 immunoreactivity in paraffin embedded melanocytic tissues. p53 protein expression in melanomas increases with depth of tumour invasion.
The presence of p53 antibodies correlated with the following prognostic factors: histological differentiation grade, shape of the tumour, and tumour invasion into blood vessels.
There was no significant association of the presence of p53 gene mutations with histologic types, extent of tumor invasion, the presence of lymph node metastasis, or tumor stage.
The LOH of p53 gene and D17S5 locus was not significantly associated with abnormal p53 expression, depth of invasion, histologic type of the tumor (Lauren's classification), or the status of lymph node metastasis.
Specific p53 nuclear staining was detected in primary tumor from 50 patients (46.7%). p53 nuclear overexpression was not significantly correlated with patients' sex, age, tumor location, differentiation, T stage, N stage, and lymphatic and/or vascular vessel invasion.
We conclude that nuclear p53 accumulation is more closely related to proliferation than to invasion and metastasis, and that it identifies some but not all breast carcinomas with high proliferative indices.
No significant association was found between p53 mutation and other histopathological parameters such as macroscopic classification, lymph-node involvement and depth of tumour invasion.
In adenocarcinomas, no correlation was found between p53 protein overexpression and histological subtype, grade of differentiation, or level of invasion.
Nuclear staining of more than 5% of neoplastic cells was observed in 124 (60.8%) adenocarcinomas, which were classified as p53 positive. p53 immunoreactivity was found to he unrelated to several clinical and pathologic variables, including age and sex of patient, tumor site, tumor stage, grade of differentiation, pattern of growth, degree of peritumoral lymphocytic infiltration, and venous invasion.
Statistically, no significant correlation between p53 overexpression and depth of invasion, lymph node involvement, or grade of tumor differentiation was detected.
Loss of heterozygosity of the p53 gene showed a significant relation to prognosis that was independent of tumor stage, histologic grade, and muscular invasion.
Positive immunostaining of p53 was observed to be significantly correlated with the degree of dysplasia and the depth of invasion, as was the expression of ras p21.
Overexpression of the p53 gene was detected in 105 of 164 (64%) de novo carcinomas regardless of size and depth of invasion, but not in 16 tumors of carcinoma-in-pyloric-gland-type adenoma, or in 51 adenomas (47 pyloric gland-type and 4 intestinal-type).
Exons 5 through 8 of the p53 gene were amplified in DNAs and the mutations detected in 28 cases (34%) did not correlate with tumor location, histopathologic classification, histologic depth of tumor invasion, lymph node involvement or clinical stage.
Among the 101 specimens examined, 37(36.6%) showed positivity in staining for p53 protein and 64(63.4%) showed no detectable p53 protein in tumor cells. p53 overexpression was correlated with depth of invasion, lymphatic invasion, lymph node metastasis and distant metastasis.
Using these 2 genetic markers, we found genetic progression to be uncommon in groups 1 and 3, whereas in group 2 an initially negative p53 staining became positive at invasion into the muscle in 5 of 12 patients (42%).