Transforming growth factor-β in breast cancer: too much, too late

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

Complexities of TGF-β targeted cancer therapy.

Many advanced tumors produce excessive amounts of Transforming Growth Factor-β (TGF-β) which, in normal epithelial cells, is a potent growth inhibitor. However, in oncogenically activated cells, the homeostatic action of TGF-β is often diverted along alte

Transforming growth factor-beta in breast cancer: too much, too late.

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