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Failure to detect colonic mucosal hyperproliferation in mutation positive members of a family with hereditary non‐polyposis colorectal cancer
Author(s) -
JASS J.R.,
AJIOKA Y.,
RADOJKOVIC M.,
ALLISON L.J.,
LANE M.R.
Publication year - 1997
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1046/j.1365-2559.1997.d01-589.x
Subject(s) - colorectal cancer , proliferating cell nuclear antigen , immunohistochemistry , pathology , pathological , cancer , labelling , staining , biology , medicine , biochemistry
Mucosal proliferation was studied in biopsies obtained from the ascending colon from four mutation positive members of a hereditary non‐polyposis colorectal cancer family (group I) and compared to subjects with some positive family history of colorectal cancer but lacking the clinical and pathological features of hereditary non‐polyposis colorectal cancer (group II). Labelling indices were derived through immunohistochemical staining of the cell cycle associated nuclear proteins proliferating cell nuclear antigen (PCNA) and Ki–67. Only perfectly longitudinally sectioned crypts were assessed and good intra‐ and interobserver reproducibility was demonstrated. The labelling indices and proliferative compartment locations were similar in both groups. The mean Ki‐67 derived labelling indices (group I 18.0% and group II 17.5%) were similar to values obtained for normal subjects in other studies. PCNA derived labelling indices (group I 58.5% and group II 57.0%) were high, but probably reflect optimization of staining through methacarn fixation. The negative findings do not fit with most published data but critical appraisal of the literature indicates that they are likely to be correct.