UNLABELLED: It has been reported that poorly-differentiated clusters of cancer cells at the invasive front, namely "tumour budding", may reflect malignancy of colorectal cancer. The aim of the present study was to evaluate the activity of cathepsin D and B in tumours and in normal mucosa from pT3 and G2 colorectal cancers, and to analyse their association with tumour budding at the invasion front of colorectal cancer. PATIENTS AND METHODS: A total of 40 patients classified as pT3, G2 underwent curative resection of colon cancer between 1997 and 2001. The fragments of tumours and normal colorectal tissue were obtained for biochemical examinations. We also categorized tumour budding (TB) at the front of invasion. Two groups were used for classification of the TB phenomenon: the first where no bud was observed- TB(-), and the second where at least one bud was found -TB(+) at the front of invasion in the examined slice. RESULTS: The activity of cathepsins D and B was found to be statistically significantly higher both in the neoplastic tissue cytosol and homogenate, compared to the cytosol and homogenate of adjacent healthy tissue (p<0.05). There was, however, no significant difference between tumour budding and the activity of cathepsin D in tumour tissue, but we found a statistically significant difference between the activity of cathepsin B in the homogenate and cytosol of tumour tissue and budding-positive tumours (p=0.027, p=0.004, respectively). CONCLUSION: These results suggest that the activity of cathepsin D is not involved in tumour budding. In our opinion, much more attention should be paid to cathepsin B, as a potentially responsible factor in tumour progression, since it strongly increased with the presence of tumour budding.
UNLABELLED: It has been reported that poorly-differentiated clusters of cancer cells at the invasive front, namely "tumour budding", may reflect malignancy of colorectal cancer. The aim of the present study was to evaluate the activity of cathepsin D and B in tumours and in normal mucosa from pT3 and G2 colorectal cancers, and to analyse their association with tumour budding at the invasion front of colorectal cancer. PATIENTS AND METHODS: A total of 40 patients classified as pT3, G2 underwent curative resection of colon cancer between 1997 and 2001. The fragments of tumours and normal colorectal tissue were obtained for biochemical examinations. We also categorized tumour budding (TB) at the front of invasion. Two groups were used for classification of the TB phenomenon: the first where no bud was observed- TB(-), and the second where at least one bud was found -TB(+) at the front of invasion in the examined slice. RESULTS: The activity of cathepsins D and B was found to be statistically significantly higher both in the neoplastic tissue cytosol and homogenate, compared to the cytosol and homogenate of adjacent healthy tissue (p<0.05). There was, however, no significant difference between tumour budding and the activity of cathepsin D in tumour tissue, but we found a statistically significant difference between the activity of cathepsin B in the homogenate and cytosol of tumour tissue and budding-positive tumours (p=0.027, p=0.004, respectively). CONCLUSION: These results suggest that the activity of cathepsin D is not involved in tumour budding. In our opinion, much more attention should be paid to cathepsin B, as a potentially responsible factor in tumour progression, since it strongly increased with the presence of tumour budding.
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