breast cancer cells

(University of Illinois at Urbana-Champaign) Researchers have discovered a new family of agents that inhibit the growth of estrogen-dependent breast cancer cells.

The finding, described today at a meeting of the Endocrine Society, has opened an avenue of research into new drugs to combat estrogen-dependent breast cancers.

A tiny modification called methylation on estrogen receptors prolongs the life of these growth-driving molecules in breast cancer cells.

Most breast cancers contain estrogen receptors, which enable them to grow in the presence of the hormone estrogen.

Their presence can determine whether tumors will respond to the estrogen-blocking drug tamoxifen. The finding will help researchers sort out how mutations change the estrogen receptor's function and allow some breast cancers to resist tamoxifen.

The environment surrounding breast cancer cells plays a crucial role in determining whether tumor cells grow and migrate or whether they fade away.

A new study is the first to identify the genes behind this environmental control and correlate them with patient outcome.

Bisphenol A, a chemical that leaches into food and beverages from many consumer products, causes normal, non-cancerous human breast cells to express genes characteristic of aggressive breast cancer cells.

The concentration of BPA that the researchers tested was very low (less than one tenth of a millionth of a gram per milliliter), but this concentration of BPA has been found in blood from pregnant women in both the United States and Germany.

Epigenetic regulation -- modifications to the structure of chromatin that influence which genes are expressed in a cell -- is a key player in embryonic development and cancer formation.

Researchers at the European Molecular Biology Laboratory in Heidelberg now gained new insight into one crucial epigenetic mechanism and reveal that it acts much faster than assumed.

In this week's issue of Nature they report that estrogen causes rapid epigenetic changes in breast cancer cells.