Factors that cause a particularly aggressive form of breast cancer are reported online in Nature Cell Biology. An over-abundance of a regulator of protein expression in patients with inflammatory breast cancer induces factors that make cells adhesive. These factors then transform cells into metastatic tumours. This finding could aid in the development of a targeted therapy that can stop the spread of this type of cancer.
Inflammatory breast cancer (IBC) is the most lethal form of breast cancer due to its rapid spread. Robert Schneider and colleagues show that IBC is characterized by the overexpression of a protein called eIF4GI. They found that, while this factor did not affect overall protein production, it did lead to increased levels of the cell adhesion regulators E-cadherin and p120 catenin, which allow cancers cells to clump together, rather than attaching to the surrounding tissue. These clumps of cancer cells can enter the circulation and spread throughout the body in a process called passive metastasis, which accounts for the lethality of IBC. Silencing eIF4GI, E-cadherin or p120 catenin all impair tumour growth and invasion in a mouse model for the cancer and the authors show that the role of eIF4GI in breast cancer depends on the de-regulation of p120 catenin.
Pinpointing the molecular causes of IBC metastization raises the hope that targeted therapeutic intervention can stop the spread of this particularly aggressive form of breast cancer.
Robert Schneider (New York University, School of Medicine, NY, USA)
Abstract available online.
(C) Nature Cell Biology press release.
Message posted by: Trevor M. D'Souza
Bookmark and Share this page (what is this?)
Social bookmarking allows users to save and categorise a personal collection of bookmarks and share them with others. This is different to using your own browser bookmarks which are available using the menus within your web browser.
Use the links below to share this article on the social bookmarking site of your choice.
Read more about social bookmarking at Wikipedia - Social Bookmarking