p53 immunostaining positive cells correlated positively with S phase cells as measured by BrdU in the esophageal precancerous lesions from the subjects at high incidence area for esophageal cancer in northern China

Abstract

AIM: To characterize the S phase cell distribution as measure d by BrdU in esophageal precancerous lesions and to correlate the changes of p53 protein accumulation with S phase cell proliferation for further undrstanding the mechanism of p53 protein accumulation in esophageal carcinogenesis .

METHODS: One hundred and nine symptom free subjects from Henan were examined with endoscopy and histopathologically. The biopsies from the esophagi were incubated with BrdU for 1 h and then fixed with 85% ethanol, embedded in paraffin and cut at 5 μm for H&E staining and immunohistochemistry (ABC). Quantitative analysis was performed by recording the positive immunostaining cells for p53 and BrdU per mm² of the tissue section.

RESULTS: Histopathologically, 53 subjects were found with normal esophageal epithelia, 46 with basal cell hyperplasia and 10 with dysplasia. In tense nuclear immunostaining for p53 and BrdU was observed in the normal and different severity of esophageal lesions. Quantitative analysis showed that the positive immunostaining cells for p53 was low in normal (70 ± 31, mean ±s ), and increased in basal cell hyperplasia (91 ± 82, mean ±s), and dramatic ally increased in dysplasia (402 ± 48, mean ±s) (P < 0.05). On the other hand, BrdU positive cell number increased with disease progressing and was a little lower than that of p53 in normal and basal cell hyperplasia, but much lo wer in dysplasia (402 vs 98). p53 immunostaining positive cells correlated positively with S phase cells as measured by BrdU with the epithelia progressing from norm al to basal cell hyperplasia and to dysplasia (P < 0.05).

CONCLUSION: BrdU is an valuable biomarker to measure cell proliferation of esophageal biopsy. p53 immunostaining positive cells correlated positively with S phase cells as measured by BrdU during the disease progressing, which can be explained by the loss of normal p53 function due to mutation.

Key Words: Esophageal neoplasms, p53 protein, Preca ncerous condition, BrdU