Georgios D Ayiomamitis1, George Notas2, Apostolos Zaravinos3, Adamantia Zizi-Sermpetzoglou4, Maria Georgiadou5, Ourania Sfakianaki5, Elias Kouroumallis6. 1. The Gastroenterology Research Laboratory, University of Crete, School of Medicine, Heraklion, and the Department of Surgery, Tzanion General Hospital, Zanni & Afentouli str, Piraeus, Greece. 2. The Gastroenterology Research Laboratory, and the Laboratory of Experimental Endocrinology, University of Crete, School of Medicine, Heraklion, Greece. 3. The Laboratory of Clinical Virology, University of Crete, School of Medicine, Heraklion, Greece. 4. The Department of Pathology, Tzanion General Hospital, Zanni & Afentouli str, Piraeus, Greece. 5. The Gastroenterology Research Laboratory, University of Crete, School of Medicine, Heraklion, Greece. 6. The Gastroenterology Research Laboratory, and the Department of Gastroenterology & Hepatology, University Hospital of Heraklion, Heraklion, Crete, Greece.
Abstract
BACKGROUND: Colorectal cancer is one of the most common cancers and the third leading cause of cancer death in both sexes. The disease progresses as a multistep process and is associated with genetic alterations. One of the characteristic features of cancer is telomerase activation. We sought to evaluate the differences in telomerase activity between colon cancer and adjacent normal tissue and to correlate the differences in telomerase activity between different locations with clinicopathological factors and survival. METHODS: Matched colon tumour samples and adjacent normal mucosa samples 10 cm away from the tumour were collected during colectomy. We assessed telomerase activity using real time polymerase chain reaction. Several pathological characteristics of tumours, including p53, Ki-67, p21, bcl2 and MLH1 expression were also studied. RESULTS: We collected samples from 49 patients. There was a significantly higher telomerase activity in colon cancer tissue than normal tissue. Adenocarcinomas of the right colon express significantly higher telomerase than left-side cancers. Colon cancers and their adjacent normal tissue had significantly more telomerase and were more positive to MLH1 than rectal cancers. The expression of p53 negatively correlated to telomerase activity and was linked to better patient survival. CONCLUSION: Colon and rectal cancers seem to have different telomerase and MLH1 profiles, and this could be another factor for their different biologic and clinical behaviour and progression. These results support the idea that the large bowel cannot be considered a uniform organ, at least in the biology of cancer.
BACKGROUND:Colorectal cancer is one of the most common cancers and the third leading cause of cancer death in both sexes. The disease progresses as a multistep process and is associated with genetic alterations. One of the characteristic features of cancer is telomerase activation. We sought to evaluate the differences in telomerase activity between colon cancer and adjacent normal tissue and to correlate the differences in telomerase activity between different locations with clinicopathological factors and survival. METHODS: Matched colon tumour samples and adjacent normal mucosa samples 10 cm away from the tumour were collected during colectomy. We assessed telomerase activity using real time polymerase chain reaction. Several pathological characteristics of tumours, including p53, Ki-67, p21, bcl2 and MLH1 expression were also studied. RESULTS: We collected samples from 49 patients. There was a significantly higher telomerase activity in colon cancer tissue than normal tissue. Adenocarcinomas of the right colon express significantly higher telomerase than left-side cancers. Colon cancers and their adjacent normal tissue had significantly more telomerase and were more positive to MLH1 than rectal cancers. The expression of p53 negatively correlated to telomerase activity and was linked to better patient survival. CONCLUSION: Colon and rectal cancers seem to have different telomerase and MLH1 profiles, and this could be another factor for their different biologic and clinical behaviour and progression. These results support the idea that the large bowel cannot be considered a uniform organ, at least in the biology of cancer.
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