View clinical trials related to Breast Cancer.
Filter by:Background: - The p53 gene normally helps to stop cancer cells from growing. However, when the p53 gene is mutated or damaged, cancer cells may grow unchecked. Researchers have been working on a vaccine that will help the immune system recognize and destroy cells that have the p53 mutation and may be cancerous. - CT-011 is another drug that may help the body's immune system to fight cancer. This drug blocks a chemical found on tumor cells that prevents the immune system from recognizing and destroying them. Research studies have shown that CT-011 slows the growth of tumors. By combining the p53 vaccine and CT-011, researchers hope to slow or stop tumor growth in people whose cancer that has not responded to standard treatments. Objectives: - To test the safety and effectiveness of CT-011 and the p53 genetic vaccine to treat adults with solid tumors that have not responded to standard treatments. Eligibility: - People at least 18 years of age who have solid tumors that have not responded to standard treatments. Design: - Participants will be screened with a medical history and physical exam. They will also have blood tests and tumor imaging studies. - Participants will receive the p53 vaccine as an injection in the arm or thigh. - Two days after receiving the p53 vaccine, those in the study will receive CT-011 as an infusion over about 2 hours. Participants will be monitored during the infusion for any side effects. - The combination of p53 vaccine and CT-011 will be repeated every 3 weeks (one cycle). Treatment will continue as long as the side effects are not severe and the tumor does not grow. - Three weeks after the second dose of p53 vaccine and CT-011, participants will have a full physical exam. They will also have blood tests, and tumor imaging studies. This exam set will be repeated after every two cycles of p53 vaccine and CT-011. - Participants will have regular follow-up visits for up to a year after stopping treatment.
The purpose of this study is to find out what effects, administering infusions of AUY922 with hormonal therapy (letrozole) and oral targeted drug (lapatinib) will have on the patients with advanced breast cancer known as ER+ HER2 +.
This is a treatment protocol designed to accompany the ongoing institutional 124I PET/CT pilot imaging study for patients with invasive breast cancer. Women whose tumors express NIS [Na+I- symporter, sodium iodide symporter] and demonstrate radioiodide uptake on 124I PET/CT scans will be eligible for 131I treatment if, (1) tumor dosimetry calculations yield a cumulative radiation dose of at least 30Gy in target tumor, (2) estimated cumulative thyroid irradiation is less than 500 cGy and, (3) the therapeutic dose of 131I is in the range of 25 to 100 mCi.
In 2008 there were more than 40,000 deaths caused by metastatic breast cancer in the United States. The development of new treatment strategies is essential to improve outcome for patients with metastatic breast cancer There is significant preclinical and clinical evidence indicating that creating new blood vessels (neoangiogenesis) to provide nutrients to solid tumors, including breast cancer, provides the necessary conditions to allow tumor growth. Vascular endothelial growth factor (VEGF) is one of the important molecules regulating new blood vessel formations and subsequent invasion and metastases. As a result, agents that inhibit VEGF are of substantial interest for the treatment of advanced diseases. This study will further the body of research of motesanib which has been shown in preclinical pharmacology and clinical pharmacology studies to be a potent, orally bioavailable multi-kinase inhibitor with anti-angiogenic and anti-tumor activity achieved by selectively targeting all known VEGF, platelet-derived growth factor (PDGF), and Kit receptors.
The goal of this clinical research study is to find the highest tolerable dose of seliciclib that can be given in combination with liposomal doxorubicin to patients with metastatic breast cancer.
The goal of this clinical research study is to find out the highest tolerable dose of an imaging solution called 18-F-fluoroacetate sodium that can be given before a positron emission tomography (PET) scan. The safety of this solution will also be studied.
The purpose of this research project is to create images of where and how the amino acid (the building blocks of proteins)Tryptophan is processed in normal and abnormal tissue in the patient's body. Tryptophan is a normal building block of proteins in the body. Sometimes in the case of cancer and other diseases, Tryptophan is processed abnormally, and possible treatments for this abnormality are of great interest because of the potential to improve cancer care.
The study will test metformin in patients with early breast cancer. Blood and tissue will be collected before and after the use of metformin.
Tamoxifen is a hormonal treatment for breast cancer. It prevents recurrent disease and decreases death. Tamoxifen is given to women with and at high risk for breast cancer. These women also commonly have breast MRI to monitor for breast cancer. Some features of normal breast tissue visible on breast MRI change depending on patient hormonal status. It has been questioned if hormonal changes due to tamoxifen are seen on breast MRI. Pilot data suggests this is true. If tamoxifen causes changes in normal breast tissue on MRI, more study could be done looking at whether breast MRI could tell us anything about whether tamoxifen is working. This study is being done to see if tamoxifen changes normal breast tissue on MRI. It will also look at if other factors like taking anti-depressants or gene type have any effect.
Women with Breast Cancer who do not respond to chemotherapy may undergo months of treatment with little or no change in tumor size or overall outcome. The Researchers have demonstrated a previously undescribed "metabolic flare" response observed very early in neoadjuvant treatment in breast cancer patients. The research can determine that this flare is predictive of overall therapy response and is due to both an inflammatory reaction and cell death induced by cytotoxic therapy.