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Ashley Richards Biology 1615 11/10/15 HER2 Phosphorylation Is Maintained by a PKB Negative Feedback Loop in Response to Anti-HER2 Herceptin in Breast Cancer Breast cancer is the most common malignancy in American women. Receiving treatment for breast cancer is increases the survival rate. Roughly 1 in 8 women in America, will develop invasive breast cancer in their lifetime. Various epithelial cancers have dysregulated human epidermal growth factors. HER2 is a protein that is affiliated with the epidermal growth factor receptor. This protein is detected in about 1/5 of breast cancer diagnoses. HER2 is a very aggressive form of breast cancer. Patients that are diagnosed with HER2-positive tumors are given an antibody called Herceptin, which stops the signaling of HER2. Recent studies have shown that Herceptin does not always reduce HER2 activation. Research suggests that some patients develop resistance to Herceptin monotherapies. Researchers are investigating why Herceptin does not decrease HER2 phosphorylation and the effects of acute and long term Herceptin treatment. Researchers suggest that Herceptin should be combined with other inhibitors to help conquer the drug resistance in patients with HER2 breast cancer. Furthermore, there is evidence that suggests other therapies also have resistance to targeting HER Receptors. Scientists report that Herceptin should be combined with other inhibitors to help combat the drug resistance in patients with HER2 breast cancer. Furthermore, there is also evidence that suggests that other therapies also have resistance to targeting HER Receptors. This article reports that specific cells were collected from a cancer research facility in the UK. Antibodies were gathered from Cell Signaling Technology. Researchers injected human breast cancer cells into the inguinal portion of male mice. After 25 days, the tumor volume typically reached an approximate average. 10 mice were then randomly selected according to their tumor volume and were treated twice a day with Herceptin or other mechanisms. Tumor size and weights were measured twice a week. The mice were also tested for signs of toxicity throughout the duration of this treatment. The most common side effects included “anorexia, dehydration, death, lethargy, hypothermia, and labored breathing.” (Gijsen, el al., 2010) Scientists were able to also develop a formula for data analysis, treatment and control ratios were calculated by the final tumor volumes. The article suggests there was evidence leading researchers to believe that the anti-HER2 monoclonal antibody Herceptin, inhibits HER2 signaling. However, recent studies have suggested that Herceptin doesn’t decrease HER2 phosphorylation. Herceptin was believed to inhibit HER2 receptor activity. It is still unclear why mechanisms do not decrease HER2 phosphorylation. Mammary stem cell production increases from HER2. This study suggested that Herceptin decreased the positive mammary stem cells, after a prolonged period of time. However, it does not eliminate all of the stem cells. Furthermore, researchers were able to demonstrate that the PKB negative feedback loop is activated by receiving Herceptin. It activates all HER2 Receptors and maintenance of HER2 phosphorylation. Researchers have been able to determine that more feedback loops are involved in the Herceptin resistance. Ultimately, the goal is to improve the survival rates in patients with HER2 breast cancer. The data from this research, offers treatment opportunities for patients with HER2-positive breast cancers. With the current influx of breast cancer diagnoses, more research may benefit the outcomes for patients fighting this disease. Works Cited Gijsen, Merel. "HER2 Phosphorylation Is Maintained by a PKB Negative Feedback Loop in Response to Anti-HER2 Herceptin in Breast Cancer." HER2 Phosphorylation Is Maintained by a PKB Negative Feedback Loop in Response to Anti-HER2 Herceptin in Breast Cancer (n.d.): n. pag. HER2 Phosphorylation Is Maintained by a PKB Negative Feedback Loop in Response to Anti-HER2 Herceptin in Breast Cancer. PLOS Biology, 21 Dec. 2010. Web. 22 Oct. 2015.