May 05, 2008
(Helsinki, May 5th) – In the vast majority of colon cancer cases, the tumors arise from benign polyps that become malignant. The mechanisms behind this change to tumor formation, however, are not known. In a study published today in Cancer Cell, a group from the Finnish Academy Center of Excellence on Cancer Biology at the University of Helsinki, Finland, have identified the PROX1 protein as a key driver of tumorigenesis.
The PROX1 protein controls formation of normal organs, such as liver or eye, during embryogenesis. However, the Finnish team found that PROX1 is overproduced at early stages of carcinoma development and likely confers the ability of the benign cells to grow uncontrollably. When PROX1 was removed from the cancer cells, the malignant behavior was reversed. These findings indicate that PROX1 might be a target for the development of future therapies.
The senior author of the study was Professor Kari Alitalo, an Affiliate of the international Ludwig Institute for Cancer Research, at the Biomedicum Helsinki, University of Helsinki.
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