Abstract：
:Disruption of the homeostatic balance between proliferation and apoptosis is widely believed to contribute to human oral carcinogenesis. Using the Syrian hamster oral cancer model, we examined normal, hyperplastic, dysplastic and malignant oral epithelium for the fraction of apoptotic, proliferating and p12(doc-1) expressing keratinocytes using the TUNEL assay, as well as PCNA and p12(doc-1) immunostaining, respectively. The percentage of TUNEL positive cells progressively increased from normal to dysplastic epithelium (P<0.0019), but returned to normal keratinocyte levels in the malignant epithelium (P<0.20). However, PCNA positive cells increased progressively through hamster oral malignant progression (P<0.0012). The overall ratio of apoptotic to proliferating keratinocytes remains similar until the transition between dysplastic and malignant epithelium, where the ratio is markedly reduced (P<0.05). p12(doc-1) labeling demonstrated a similar expression pattern (P<0.008). This study demonstrates that apoptosis, proliferation and the expression of p12(doc-1) reflects alterations reported during human oral carcinogenesis and supports the use of the Syrian hamster model for the further examination of these pathways.
journal_name
Oral Oncoljournal_title
Oral oncologyauthors
Kohno Y,Patel V,Kim Y,Tsuji T,Chin BR,Sun M,Bruce Donoff R,Kent R,Wong D,Todd Rdoi
10.1016/s1368-8375(01)00055-0subject
Has Abstractpub_date
2002-04-01 00:00:00pages
274-80issue
3eissn
1368-8375issn
1879-0593pii
S1368837501000550journal_volume
38pub_type
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