Breast cancer continued to be the second leading cause of cancer-related deaths, behind only lung cancer, with approximately 40,000 deaths caused by breast cancer annually. Breast cancer is also a global health problem, with more than 1 million cases of breast cancer diagnosed each year worldwide. The current treatment of breast cancer is guided by pathology, staging, and recent insights into breast cancer biology. There is an increased emphasis on defining disease biology and status in individual patients, with subsequent individual therapies. There are numerous pathways and molecular markers that have been reported to affect breast cancer outcomes, including steroid hormone receptor pathways (ER and PR), human epidermal growth factor receptor pathway (HER family), angiogenesis, cell cycle (e.g., cyclin-dependent kinases [CDKs]), apoptosis modulators, the proteasome, and p53. Pathological assessment of ER is performed on all primary tumors and predicts which patients should receive therapy directed at ER with endocrine therapy. Other molecular markers are used to select patients for systemic treatment (e.g., chemotherapy, endocrine therapy) and to predict the response of patients to these pharmacologic treatments. A multigene assay provides a recurrence score for ER-positive breast cancer that is used clinically to determine whether women with high-risk ER-positive breast cancer should receive adjuvant chemotherapy in addition to endocrine therapy (the Oncotype DX or MammaPrint assays). It is likely that tests based on critical combinations of genes will increasingly be used to assist clinical decision making when treating breast cancer; it is possible that more molecular markers are needed for further diagnosis and treatments. Cancer is the first leading cause of death in Taiwan. The elevation of the thrombomodulin (TM) protein level has been observed in many types of cancers. TM is a single-chain transmembrane glycoprotein. TM on vascular endothelial cells is an important molecule in the natural human anticoagulation system. Silencing TM expression increased cell proliferation and metastasis on breast cancer, indicating that TM may be the prognostic or therapeutic target for breast cancer. In this study, we plan to dissect the role of TM in the progression and therapeutic responses on breast cancer. Further dissection of the regulated mechanism of TM will be helpful to develop the more efficacy therapeutic strategy for breast cancer patients in clinical.
|Effective start/end date||8/1/16 → 7/31/17|