次のページ:この薬で他の癌も予防できるのか? Next up: Does the medication offer protection against other forms of cancer?
2022-06-09 カリフォルニア大学校アーバイン校(UCI)
研究チームは、アスピリンが、大腸がん細胞の出生率と死亡率を変化させることを発見しました。具体的には、アスピリンは、腫瘍細胞の分裂率を低下させ、細胞死率を上昇させるのです。
<関連情報>
- https://news.uci.edu/2022/06/09/uci-researchers-find-that-aspirin-alters-colorectal-cancer-evolution/
- https://elifesciences.org/articles/71953
アスピリンの細胞運動パラメータに対する効果が、進行性大腸腺腫の発症抑制に寄与していることをマルチスケール計算機シミュレーションにより明らかにした Aspirin’s effect on kinetic parameters of cells contributes to its role in reducing incidence of advanced colorectal adenomas, shown by a multiscale computational study
Yifan Wang,C Richard Boland,Ajay Goel,Dominik Wodarz,Natalia L Komarova
eLife Published Apr 13, 2022
DOI:https://doi.org/10.7554/eLife.71953
Abstract
Aspirin intake has been shown to lead to significant protection against colorectal cancer, for example with an up to twofold reduction in colorectal adenoma incidence rates at higher doses. The mechanisms contributing to protection are not yet fully understood. While aspirin is an anti-inflammatory drug and can thus influence the tumor microenvironment, in vitro and in vivo experiments have recently shown that aspirin can also have a direct effect on cellular kinetics and fitness. It reduces the rate of tumor cell division and increases the rate of cell death. The question arises whether such changes in cellular fitness are sufficient to significantly contribute to the epidemiologically observed protection. To investigate this, we constructed a class of mathematical models of in vivo evolution of advanced adenomas, parameterized it with available estimates, and calculated population level incidence. Fitting the predictions to age incidence data revealed that only a model that included colonic crypt competition can account for the observed age-incidence curve. This model was then used to predict modified incidence patterns if cellular kinetics were altered as a result of aspirin treatment. We found that changes in cellular fitness that were within the experimentally observed ranges could reduce advanced adenoma incidence by a sufficient amount to account for age incidence data in aspirin-treated patient cohorts. While the mechanisms that contribute to the protective effect of aspirin are likely complex and multi-factorial, our study demonstrates that direct aspirin-induced changes of tumor cell fitness can significantly contribute to epidemiologically observed reduced incidence patterns.
