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Protein linked to therapy resistance in breast cancer
Date:9/11/2012

development of many types of cancer.

"We hypothesized that resistance to EGFR-TKIs originated, at least in part, from molecular alterations that activated phosphorylation signaling downstream of EGFRs," Furuta says.

Using a unique three-dimensional cell culture assay based on phenotypic reversion that was originally developed by Bissell and her research group, the co-authors of the JCI paper screened for genes involved in EGFR-TKI resistance in both normal and cancerous human breast cell lines. They found that, while normal human breast tissue doesn't produce FAM38A, the protein is highly expressed in cancerous tissue. This was true for every breast cancer cell line they examined, and was particularly pronounced in those cell lines that have been the most resistant to treatment with EGFR-TKIs. Further studies showed that FAM83A interacts with and causes phosphorylation of critical signaling proteins downstream of EGFRs, as the researchers hypothesized. This downstream phosphorylation would act to blunt or negate any therapeutic effects of EGFR-TKIs that took place further upstream.

The results of this research are consistent with clinical data showing that breast cancer patients with high levels of FAM83A have a significantly lower survival rate than patients with low levels of FAM83A. However, while Bissell, Furuta and their colleagues note that a number of questions about FAM83A and other members of the FAM83 protein family remain to be addressed, the importance of these proteins as potential drug targets for therapy seems clear.

"The beauty of this study is that it not only helps explain why some breast cancer patients are resistant to EGFR-TKIs, but it also reveals a whole new family of potential oncogenes that could be a target for all types of cancer, including breast cancer," Bissell says.

Bissell says the results of this study also demonstrate the potential of using 3D phenotypic reversion assays as a new path
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Contact: Lynn Yarris
lcyarris@lbl.gov
510-486-5375
DOE/Lawrence Berkeley National Laboratory
Source:Eurekalert  

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