Estimation of glycogen levels in human colorectal cancer tissue: relationship with cell cycle and tumor outgrowth

Citation
S. Takahashi et al., Estimation of glycogen levels in human colorectal cancer tissue: relationship with cell cycle and tumor outgrowth, J GASTRO, 34(4), 1999, pp. 474-480
Citations number
29
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
JOURNAL OF GASTROENTEROLOGY
ISSN journal
09441174 → ACNP
Volume
34
Issue
4
Year of publication
1999
Pages
474 - 480
Database
ISI
SICI code
0944-1174(199908)34:4<474:EOGLIH>2.0.ZU;2-W
Abstract
In this study, we quantitatively measured glycogen levels in tissue samples obtained from tumors, regions adjacent to tumor, and regions of normal col orectum to determine whether the levels were related to cell cycle and canc er growth. Glycogen levels were analyzed in relation to histopathological f actors, (tumor size and stage of disease) and cell cycle progression. The g lycogen level was found to be highest in the cancer tissue, lower in normal tissue, and lowest in the adjacent tissue. The difference in glycogen leve l between the cancer tissue and the other two regions was significant (P < 0.05). There was a negative correlation between glycogen level and tumor si ze, but it was not significant. The level of glycogen in cancer tissues dec reased as the stage of the disease progressed, but a significant difference was not found between stages. There was a negative correlation between the glycogen level and the proliferation index. There was a positive correlati on between the glycogen level and the proportion of cancer cells in G(1) ph ase, while there was a negative correlation with S and G(2)M phases. Glycog en levels were highest in cancers with a high proportion of cells in G(1), and decreased with progression to S phase. It may be that glycogen is utili zed in the progression to S phase, and the cancer tissues are supplied with glycogen from the tumors themselves as well as their adjacent tissues. Can cer growth may be inhibited by artificial control of the glycogen level in the G(1) phase of cancer cells.