Materials and Methods: RCAS1 and CD68 antigens immunoreactivity was determined in 50 tissue samples of salivary gland adenocarcinomas and in 50 tissue samples of their stroma and 30 tissue samples of healthy control (palatine tonsils) by immunohistochemistry method in the Department of Pathology. Results: RCAS1 immunoreactivity was identified in both adenocarcinoma and healthy stromal samples. Significantly higher RCAS1 immunoreactivity was shown in the cancer samples than in stromal samples. RCAS1 immunoreactivity in stromal samples was significantly higher in patients with the presence of lymph node metastases in comparison to patients without metastases. We also observed Vactosertib significantly higher number of CD68

positive cells (macrophages) in adenocarcinoma samples and in stromal samples than in the control group. Moreover, the number of CD68 positive cells in adenocarcinoma and stroma were higher in patients with lymph node metastases in comparison to patients without metastases. Additionally, in our study macrophages

were identified to possess the immunoreactivity of RCAS1, RCAS1 expressing macrophages were observed in the mucous. Conclusion: In the present study we have demonstrated that RCAS1 expression Cell Cycle inhibitor by the tumor cells, tumor microenvironment and tumor associated macrophages participate in creating the immunosuppressive microenvironment in salivary adenocarcinomas. O71 Tumor Microenvironment Rapamycin in vitro Induced Drug and Radio Resistance in Invasive Breast Cancer Cells Sumanta Goswami 1,2 1 Anatomy and Structural Biology, Albert Einstein College of Medicine of Yeshiva University, Bronx, NY, USA, 2 Department of Biology, Yeshiva University, New York, NY, USA Metastasis, drug and radio resistance continue to cause significant morbidity and patient mortality. This is in spite of recent introduction of a number of different chemotherapy agents and newer radiotherapy protocols. Using unique animal models and cell separation techniques coupled with sensitive assays we have recently discovered that the invasive breast cancer cells are hypoproliferative and antiapoptotic. Since the invasive cells have shut

down their cell cycle and have become dormant they continue to resist cytotoxic drugs and ionizing radiation. We have used cells isolated from the primary tumor, invasive cells, circulating tumor cells and lung metastasis to identify the underlying molecular mechanism for drug and radio resistance. We used a combination of cytotoxic and cytostatic drugs along with molecular pathway directed drugs to target the invasive, drug and radio resistant breast cancer cells. https://www.selleckchem.com/products/oicr-9429.html Secondly using both classical gene expression studies as well as by the identification of different invasion and resistance specific splice variants we have identified a genetic signature which will predict potentially invasive, chemo and radio resistant cancers.