A message from Ginny Mason, RN, BSN

Executive Director

Inflammatory Breast Cancer Research Foundation

 

July 13, 2009

 

 

We have received a number of questions regarding the recent article that appeared in our July 2009 Newsletter titled "Essential Role for eIF4G1 Overexpression in Inflammatory Breast Cancer Pathogenesis"  such as the following from an IBC survivor, followed by my response to her.  As she suggested, we are sharing this publicly to aid in understanding.

 

We appreciate your questions and know that this new research data has raised many questions for patients/survivors.  A link to the EurekaAlert press release about Dr. Schneider's findings went out to our two email discussion lists and our next e-newsletter will also carry an article.  Dr. Schneider, and colleagues, have been working on this research for a couple of years, moving from cell lines to mouse models, and then studying tissue samples from IBC patients.  Our organization has been serving as collaborators on the study providing patient/advocate input.  We are looking forward to further collaboration as Dr. Schneider and colleagues move forward in the development of a therapeutic that will target this substance associated with IBC.
 
One of the challenges in dealing with medical terms, especially in the field of cancer, is the word "gene."   For most of us that word is associated with something that is passed along from parent to child and thought of as hereditary.  Most breast cancer is not associated with any known genetic mutation (ie: hereditary.)  Rather, most breast cancer is the result of mutations in the body's DNA that cannot be repaired and go awry. 
 
In Dr. Schneider's paper (Essential role for eIF4GI overexpression in the pathogenesis of inflammatory breast cancer: Nature Cell Biology July 2009) he doesn't use the term "gene" at all, he uses the term "translation initiation factor" for eIF4GI.  This translational initiation factor is over-expressed in cases of IBC, as opposed to non-IBC cases.  eIF4GI plays a significant role along with E-cadherin, the surface component that causes IBC tumor cells to stick so tightly together forming tumor emboli.  We've known for a long time that E-cadherin is over-expressed in IBC.  Over-expression of eIF4GI promotes formation of IBC tumor emboli by enhancing translation of IRES-containing p120 mRNAs, which promote IBC tumor cell survival and formation of tumor emboli.  These tumor emboli help to make IBC difficult to treat and move to other sites in the body.
 
I realize the above is rather technical, but I hope it will give more explanation into what eIF4GI is and isn't.  Regarding the question, "If I have the gene, do I have a higher chance of recurrence?"  Chances are eIF4GI would be found in the tumor tissue.  However, measuring that would not tell us anything about the chance of recurrence.  It would just let someone know that the IBC tumor tissue was like 80% of other IBC tumor tissue.  Testing your tissue (that's the only place this substance would be found) would not give you information to aid in your survival.  However, studying this substance in tissue from the Inflammatory Breast Cancer Research Foundation BioBank, is the kind of thing that moves research forward.  By studying human IBC tissue, researchers learn the things that set IBC apart from other breast cancers and help identify targets for treatment.
 
This new research is exciting as it may provide a new drugable target.  Compounds will need to be developed then tried in cell lines and animal models, prove to be effective in those settings and, if worthy, move on to human clinical trials.  It is a long process, but exciting to think that we might have a treatment option coming designed specifically to target one of the key components of IBC.