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Discovery of a cell mechanism that reduces effectiveness of breast cancer treatment
Date:10/19/2011

mage response," by activating ATM kinase. In this way, the cell cycle is stopped and the DNA is repaired in order to maintain chromosome stability.

HOXB9 expression causes an increase in survival of cells that have been exposed to radiation. This higher resistance occurs because of the acceleration of response to radiation and its higher recovery capacity after DNA damage. On the other hand, reduction of the levels of this protein, leads to increased cell sensitivity to radiation. Furthermore, the growth factor TGFbeta (a HOXB9 target) is also involved. Therefore, HOXB9 facilitates DNA repair by activation of the TGFbeta signalling pathway, which elevates ATM phosphorylation, accelerates DNA damage response and radiation resistance.

The published research is the continuation of another study carried out last year by CIC bioGUNE, Massachusetts General Hospital and Harvard Medical School, which showed that this same protein (HOXB9) is overexpressed in breast cancer and that its expression levels are associated with high tumour grade.


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