[Rich66]

http://shared.web.emory.edu/whsc/new...t-cancers.html

She says the rationale for the combination grows out of a concept called “enhanced oncogene addiction.” The idea is that mTOR inhibitors can make cells more dependent on a growth pathway that another drug can attack. Winship researchers have found this approach to be successful with breast cancers that become resistant to Herceptin.
More detail on this concept: http://jnci.oxfordjournals.org/content/101/5/288.full
EGFR (epithelial growth factor receptor) is a molecule that is hyper-activated in many cancers, such as lung, colon, and head and neck cancer. The drug lapatinib is a chemical that interferes with the function of EGFR. Lapatinib indirectly attacks an enzyme called Akt, which mTOR inhibitors force cells to depend on.
Although triple-negative breast cancers share some characteristics, they’re not all the same on the molecular level. O’Regan says researchers are trying to understand what mutations and genetic signatures distinguish patients who have a better chance of responding. To help scientists gather data on this, as part of the clinical study, patients have an initial biopsy and then optional biopsy 6-8 months after the treatment begins.
The clinical study is designed for patients with triple-negative breast cancer who have already been through first-line chemotherapy. The principal investigator of the EGFR/mTOR clinical trial is Navneet Dhillon, MD, assistant professor of hematology and medical oncology. Trial information: http://www.clinicaltrials.gov/ct2/show/NCT01272141
Winship researchers are also testing an approach against breast cancer cells that have lost the estrogen receptor and are treated with drugs that could coax the estrogen receptor into turning on again. The reappearance of the estrogen receptor could make the cancer cells vulnerable to tamoxifen. Trial info: http://www.clinicaltrials.gov/ct2/show/NCT01194908
The research was supported by the Wilbur and Hilda Glenn Foundation and the Georgia Cancer Coalition.