The contribution of transforming growth factor (TGF)beta to breast cancer has been studied from a myriad perspectives since seminal studies more than two decades ago. Although the action of TGFbeta as a canonical tumor suppressor in breast is without a doubt, there is compelling evidence that TGFbeta is frequently subverted in a malignant plexus that drives breast cancer. New knowledge that TGFbeta regulates the DNA damage response, which underlies cancer therapy, reveals another facet of TGFbeta biology that impedes cancer control. Too much TGFbeta, too late in cancer progression is the fundamental motivation for pharmaceutical inhibition.
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Barcellos‐Hoff et al. (2009) studied this question.
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