Tropes

futurity_medicine 00353.txt

#Common virus targets triple-negative breast cancer A virus not known to cause disease kills triple-negative breast cancer cells and killed tumors grown from these cells in mice, report researchers. Understanding how the virus kills cancer may lead to new treatments. Adeno-associated virus type 2 (AAV2) infects humans but is known not to cause sickness. In prior studies, the researchers tested the virus on a variety of breast cancers that represent degrees of aggressiveness and on human papillomavirus-positive cervical cancer cells. The virus initiated apoptosisatural cell deathn cancer cells without affecting healthy cells. TRIPLE-NEGATIVE BREAST CANCER reatment of breast cancer remains difficult because there are multiple signaling pathways that promote tumor growth and develop resistance to treatment, says Craig Meyers, professor of microbiology and immunology at the Penn State College of Medicine. Signaling pathways involve molecules in a cell that control cell functionsuch as cell divisiony cooperation. For example, the first molecule in the process receives a signal to begin. It then tells another molecule to work, and so on. Treatment of breast cancer differs by patient due to differences in tumors. Some tumors contain protein receptors that are activated by the hormones estrogen or progesterone. Others respond to another protein called human epidermal growth factor receptor 2, or HER2. Each of these is treated differently. A triple-negative breast cancer does not have any of these protein receptors and is typically aggressive. here is an urgent and ongoing need for the development of novel therapies which efficiently target triple-negative breast cancers, Meyers says. DAY BY DAY RESULTS In the current study, the researchers tested AAV2 on a cell-line representative of triple-negative breast cancer. They report their results in Cancer Biology & Therapy. The AAV2 killed 100 percent of the cells in the laboratory by activating proteins called caspases, which are essential for the cell natural death. In addition, consistent with past studies, AAV2-infected cancer cells produced more Ki-67, an immunity system activating protein and c-Myc, a protein that helps both to increase cell growth and induce apoptosis. The cancer cell growth slowed by day 17 and all cells were dead by day 21. AAV2 mediated cell killing of multiple breast cancer cell lines representing both low and high grades of cancer and targeted the cancer cells independent of hormone or growth factor classification. The researchers then injected AAV2 into human breast cancer cell line-derived tumors in mice without functioning immune systems. Mice that received AAV2 outlived the untreated mice and did not show signs of being sick, unlike the untreated mice. Tumor sizes decreased in the treated mice, areas of cell death were visible and all AAV2 treated mice survived through the study, a direct contrast to the untreated mice. hese results are significant, since tumor necrosisr deathn response to therapy is used also as the measure of an effective chemotherapeutic, Meyers says. Future studies should look at the use of AAV2 body-wide in mice, which would better model what happens in humans, according to Meyers. Other researchers on this project contributed from Penn State, PPD Vaccines and Biologics Laboratory, Feinstein Institute for Medical Research, and Central Michigan University college of Medicine r

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