[2][3][4][5][6][7][8] These initial molecular changes may subsequently progress to cytologically recognizable premalignant foci of dysplasia, and eventually to carcinoma in situ (CIS) or cancer.
[3][4][8][11][14][16] Despite adequate resection and being histologically normal, the remaining locoregional tissue has an increased risk for developing multiple independent cancers, either synchronously or metachronously.
Field defects associated with gastrointestinal tract cancers also commonly displayed reduced apoptosis competence, aberrant proliferation and genomic instability.
[28] Field defects of the gastrointestinal tract that show those common faults occurred in the oropharynx, esophagus, stomach, bile duct, pancreas, small intestine and colon/rectum.
The diagram shows results obtained by Facista et al.[21] A particular colon resection from a colon cancer patient was evaluated for expression of 3 different DNA repair enzymes: Ku86 (active in the non-homologous end joining pathway), ERCC1 (active in the nucleotide excision DNA repair pathway) and PMS2 (active in the mismatch DNA repair pathway).
The percent of crypts in 6 tissue samples taken within the field defect were evaluated for frequency of high levels of expression of each of the repair proteins.
However, the majority of crypts in all 6 tissue samples were reduced or absent in protein expression of ERCC1 and PMS2.
"Field cancerization in oral stratified squamous epithelium; clinical implications of multicentric origin".