Evaluation of Proliferation and Apoptotic Cell Death Indices in Human Prostate
Carcinoma and Benign Prostatic Hyperplasia
R.D. Snyder, H.W. Carter, J.H. Carter, J.L. Pullman, J.O. Johnston. Wood
Hudson Cancer Research Laboratory, 931 Isabella St., Newport, KY 41071
ABSTRACT
Recent evidence suggests that the neoplastic process is accompanied by changes
both in the fraction of tumor cells proliferating and those cells dying
via genetically programmed apoptosis. Increased proliferation in tumors,
if not balanced by equivalent cell death rates will result in net tumor
growth. However, in established neoplasms the amount of apoptosis is usually
seen to increase with histological grade. Prostate tumors with a high apoptotic
index (AI), i.e., a high percentage of cells undergoing apoptotic death,
have previously been associated with poor prognosis. This most likely reflects
a relationship between the underlying level of genetic instability and tumor
progression. We have examined the epithelial component of 25 human prostate
carcinomas of similar Gleason grades for both apoptosis, as measured by
in-situ end-labeling of DNA double strand breaks by terminal deoxynucleotidyl
transferase (TUNEL) assay, and proliferative index (PI), as measured via
immunohistochemical techniques using MIB-1 antibody against Ki-67. These
paraffin-embedded prostate carcinoma tissues which were obtained at surgery
exhibited a wide range of AI and PI values. We have also found a similar
wide range of AI and PI values in "normal" glandular epithelial
cells in a study of prostatic tissues from 80 men with benign prostatic
hyperplasia. AI values of prostatic tissues from men without prostate cancer
may reflect inherently high or low levels of genetic instability. Determination
of age-adjusted AI and PI values for noncancerous prostatic tissues may
establish critical biomarker levels that will help identify men at increased
risk of developing prostate cancer.
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