Tumorgenesis has been recognized for years as a multistep process. accompanied
by accumulation of mutations and changes in oncogenes and tumor suppressor
genes leading to changes in behaviour of the affected cell and transformation into
malignant cell (Shpltz et al., 1995).
One cf the mechanisms that contributes to malignant transformation is increased
cell proliferation (Hall & Coates, 1995), Gastrointestinal tract epithelium is
characterized by active and rapid cell turnover. During their growth, proliferating
cells divide by the cell cycle which is controlled by numerous regulatory proteins
such as oncoproteins and cyclins including the proliferating cell nuclear antigen
(PCNA) (Murakami et al., 1995).
Despite the most recent technologic advances. cancer of the large bowel is still
a major cause of neoplastic morbidity and mortality. The first step in multistage colonic
carcinogenesis is increased cell proliferation and an upward shift of the proliferating
zone in colonic crypts (Shpitz et al., 1997).
Aspirin (acetylsalicylic acid) has been well known for its anti-pyretic and antiinflammatory
action over the past century. However, in recent years there has been
an evidence suggesting that aspirin could reduce the risk of colorecral cancer but the
exact mechanism by which aspirin exerts this chemopreventive effect is unclear and
complex (Law et al., 2000).
Therefore, this work was designed to assess the effect of aspirin intake on epithelial
cell proliferation in the colonic crypts of adult rats aiming at clarifying how
aspirin protects against development of cancer colon.