Lauric Acid inhibited the viability of both cancer cell types without altering the growth of MCF - 10A
normal breast epithelial cells, thus suggesting its specific potential to trigger antiproliferative effects in malignant cells.
In subsequent experiments, the Einstein team deciphered other parts of the Rac1 signaling cascade during invasion and showed that this signaling mechanism is regulated differently in
normal breast epithelial cells.
Not exact matches
By manipulating it in vitro, a team of researchers led by Prof. David Mooney at Harvard SEAS have identified a possible mechanism by which
normal cells turn malignant in mammary
epithelial tissues, the tissues frequently involved in
breast cancer.
They found that the protein seems to help maintain several traits in
normal breast cells, including the ability to adhere to other
epithelial cells, and the presence of molecules marking the cells as differentiated and not capable of self - renewal like
breast stem cells.
Using cutting - edge techniques enabled by next - generation sequencing, the authors generated complete methylome maps at single nucleotide resolution in a low - passage
breast cancer cell line and
normal breast tissue (primary human mammary
epithelial cells).
Normal breast tissue showed acini lined by
epithelial cells resting on an intact myoepithelial cell layer (Figure 1A).
Cambridge, Mass. — June 16, 2014 — A team of researchers led by David J. Mooney, Robert P. Pinkas Family Professor of Bioengineering at the Harvard School of Engineering and Applied Sciences (SEAS), have identified a possible mechanism by which
normal cells turn malignant in mammary
epithelial tissues, the tissues frequently involved in
breast cancer.