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New Theoretical Model Of Tumor Growth And Metastasis Based On Differences In Tissue Pressure

Mar. 25, 2009 — The progression of cancer is a multi-step process. Over 80% of malignant tumors are carcinomas that originate in epithelial tissues from where they invade the connective tissue. At some point, subpopulations of cells may detach from the primary tumor and spread via the bloodstream and the lymphatic system. Some of them give rise to metastases in distant organs.


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The metastatic cascade is a very inefficient process, as only one in about a thousand cells that leave the primary tumor goes on to form a macroscopic secondary tumor. The main contribution to metastatic inefficiency arises from the failure of cancerous cells to grow inside invaded organs. Metastatic tumors also show preferential growth in different organs. Hence, the efficiency of the metastatic process depends on specific interactions between the invading cancer cells and the local organ tissues.

In an Article published on the HFSP Journal website, Risler, Prost and Joanny from Institut Curie in Paris suggest that this is due to a difference of pressure between tumor cells and the host tissue. Combining the laws of mechanics and the biological state of homeostasis, the authors propose that every biological tissue regulates to a preferred pressure called homeostatic pressure, and that an increased homeostatic pressure is a generic trait of neoplastic tissues. This property can drive tumour growth at the expense of the host tissue. Metastases account for the majority of patients' deaths due to cancer, and thus understanding the metastatic process is of critical importance.

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The above story is reprinted from materials provided by HFSP Publishing, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Basan et al. Homeostatic competition drives tumor growth and metastasis nucleation. Advanced Online Publication Articles for HFSP Journal, 2009; 1 (1): 98 DOI: 10.2976/1.3086732
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