A cyclin-dependent kinases Cdk4 and Cdk6 are attributed a crucial role in the initiation of cell cycle in response to mitogenic stimuli. They are, therefore, be targets toward which the biomedical sciences and pharmaceutical industry directed its efforts to intervene in the trigger mechanisms of cancer (some ant tumor drugs in Phase II clinical research, which has placed considerable trust, act inhibiting its activity).

However, a group warns CNIO, following the results recently published in Cell, although these kinases are triggers of tumors are not a good target. Previous studies had shown that Cdk4 was not essential for cell proliferation, and it was thought that the Cdk6 could have a compensatory effect.

However, the work of this group of Molecular Oncology Program in animal models (mice) that have caused them suppressor mutations of these kinases, or both, show that for Cdk6 null mice are also viable and develop normally, except for some changes in hematopoiesis. When they are both kinases which are missing, defective embryos die at the end of embryogenesis from severe anemia, while these same embryos show normal organogenesis, and are able to proliferate in vitro, like the majority of cell types. These observations are not surprising to the authors, as the Cdk involved in the development of the hematopoietic system.

However, these and other data relating to the viability of the cells in the absence of these kinases question its suitability as enzymes essential for cell division and therefore, as therapeutic targets of choice in the fight against cancer.

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