Before the advent of diagnostic imaging, palpation was one of the main methods of clinical investigation for the evaluation of tumours. Malignant tumours feel harder that benign ones and this physical property is related to their coefficient of elasticity. Direct comparison of tissue images before and after application of a force is too crude a measure of elasticity except at extremes of differences in elasticity. Analysis of the raw imaging data, which contains very much more information than can be displayed for visual perception, can detect very much smaller differences in elasticity.

The radio frequency data of returning ultrasound echoes contain much more data than appears in an ultrasound image. Comparison, of the datasets of uncompressed tissue with compressed tissue, of a region of interest allows production of a strain (elasticity) image of that same region of interest. Change in tissue which is not visible on B-mode (greyscale) imaging can now be detected with real time strain imaging which is beginning to be developed on commercial ultrasound equipment. The information obtained with strain/elasticity imaging is now showing potential in influencing management of patients with breast problems.

Citation of original article:

K. B. Ewan, H. A. Oketch-Rabah, S. A. Ravani, G. Shyamala, H. L. Moses, M. H. Barcellos-Hoff. Proliferation of estrogen receptor-alpha-positive mammary epithelial cells is restrained by transforming growth factor-beta1 in adult mice. American Journal of Pathology 2005; 167(2): 409–17.

Abstract of the original article:

Transforming growth factor (TGF)-beta1 is a potent inhibitor of mammary epithelial proliferation. In human breast, estrogen receptor (ER)-alpha cells rarely co-localize with markers of proliferation, but their increased frequency correlates with breast cancer risk. To determine whether TGF-beta1 is necessary for the quiescence of ER-alpha-positive populations, we examined mouse mammary epithelial glands at estrus. Approximately, 35% of epithelial cells showed TGF-beta1 activation, which co-localized with nuclear receptor-phosphorylated Smad 2/3, indicating that TGF-beta signaling is autocrine. Nuclear Smad co-localized with nuclear ER-alpha. To test whether TGF-beta inhibits proliferation, we examined genetically engineered mice with different levels of TGF-beta1. ER-alpha co-localization with markers of proliferation (i.e., Ki-67 or bromodeoxyuridine) at estrus was significantly increased in the mammary glands of TGF-beta1 C57/bl/129SV heterozygote mice. This relationship was maintained after pregnancy but was absent at puberty. Conversely, mammary epithelial expression of constitutively active TGF-beta1 via the MMTV promoter suppressed proliferation of ER-alpha-positive cells. Thus, TGF-beta1 activation functionally restrains ER-alpha-positive cells from proliferating in adult mammary gland. Accordingly, we propose that TGF-beta1 dysregulation may promote proliferation of ER-alpha-positive cells associated with breast cancer risk in humans.