Expression of p53 in oesophageal squamous epithelium from surgical specimens resected for squamous cell carcinoma of the oesophagus, with special reference to uninvolved mucosa

P53 and Ki-67 overexpression in gastroesophageal reflux disease - Barrett's esophagus and adenocarcinoma sequence

“…Under normal conditions, the Tp53 gene generates a short‐lived protein (wild p53) that cannot be detected by immunohistochemistry. In cases with mutations, the altered Tp53 gene produces a more stable protein that extends the protein's half life by 6 h, and the intra‐nuclear accumulation makes it possible to detect p53 by immunohistochemistry 20,25,44,51 . However, the use of immunohistochemistry should be carefully considered, as the absence of staining does not necessarily exclude the existence of mutations 22,26 …”

“…Gastroesophageal reflux causes inflammation and may explain the positive reactivity of p53 in these patients. However, inflammatory alterations are closely related to the process of esophageal carcinogenesis, and are capable of modifying the function of many proteins that regulate the cell cycle, such as p53 51,55 …”

“…Immunohistochemistry has been used in the investigation of various genes, including the study of the Tp53 tumor suppressor gene and the Ki-67 nuclear antigen in gastrointestinal carcinogenesis. 21,[51][52][53] Under normal conditions, the Tp53 gene generates a short-lived protein (wild p53) that cannot be detected by immunohistochemistry. In cases with mutations, the altered Tp53 gene produces a more stable protein…”

“…P53 and Ki-67 in Barrett's esophagus 591 that extends the protein's half life by 6 h, and the intra-nuclear accumulation makes it possible to detect p53 by immunohistochemistry. 20,25,44,51 However, the use of immunohistochemistry should be carefully considered, as the absence of staining does not necessarily exclude the existence of mutations. 22,26 We identified p53 protein expression associated to the severity of the histological findings, that is, the immunoexpression of p53 occur in ascendant fashion Ki-67 activity in the normal epithelium-esophagitiscolumnar epithelium without and with IM -adenocarcinoma sequence: « P < 0.001 G1 between G2, G3, G4 and G5; ® P < 0.05 G2 between G4 and G5; ¥ P < 0.05 between G3 and G5.…”

Field cancerization, clonality, and epithelial stem cells: the spread of mutated clones in epithelial sheets

“…Extremely relevant to this is the growing recognition that mutations in important genes such as p53 are found in metaplastic tracheobronchial squamous epithelium preceding any dysplastic change, and even in normal aerodigestive tract mucosa. [164][165][166][167][168][169][170][171] Similarly, clones of keratinocytes are seen with immunoreactive p53 and p53 mutations (exons 5-8) in sun-exposed but otherwise normal skin, 7,172-175 present as tiny clones 60-3000 cells in size. There are, on average, about 30 clones/cm 2 .…”