View clinical trials related to Metastatic Breast Cancer.
Filter by:We hypothesize that changes in tumor gene expression profiles vary in response to different sequences and types of chemotherapy, and that gene expression changes will correlate with tumor response. We are also looking to correlate drug pharmacokinetics and treatment toxicity with genotype of drug metabolizing enzymes and tranporters.Patients with metastatic breast cancer and who have measurable primary breast tumor will be randomized to one of two alternating sequences of adriamycin and docetaxel. Serial tumor biopsies and plasma samples will be obtained for gene expression and proteomic studies to identify biomarkers that will predict for chemotherapy response.
Tumors are heterogeneous with varying response to chemotherapeutic agents. We hypothesize that tumors that are sensitive to a particular chemotherapeutic agent have a distinctive tumor protein profile compared to those that are resistant. We further hypothesize that since tumor is continuously perfused by serum, serum protein profile can be used as a surrogate marker of tumor protein profile. The primary objective of this study is to identify a serum protein profile that predicts gemcitabine/carboplatin sensitivity or resistance in breast cancer patients with prior exposure to anthracyclines and taxanes. Secondary objectives are to establish the serum protein profile of breast cancer patients who have had prior exposure to anthracyclines and taxanes, and to study the pharmacogenetics of gemcitabine toxicity by correlating germline genotype of transporters and drug metabolizing enzymes with plasma and intracellular gemcitabine pharmacokinetics.
Both capecitabine and oxaliplatin have single agent activity in breast cancer. The combination has improved activity in other solid tumors. This study seeks to assess the activity of the combination in breast cancer.
The study aim to show if vaccination with autologous dendritic cells pulsed with onco-peptides in combination with adjuvant cytokine can induce a measurable immune response in patients with metastatic breast cancer, and to evaluate the clinical effect (objective response rate) of the vaccination regime.
This is an open label, two arms, randomized, unblinded phase 2 study in patients with locally advanced or metastatic breast cancer who have been previously treated with anthracycline with/without taxane based regimen in the adjuvant/neoadjuvant or 1st line metastatic setting. Gemcitabine will be administered via intravenous infusion over approximately 30 minutes at a dose of 1250mg/m2 on days 1 and 8 of each 21-day cycle. In arm A:Cisplatin will be given via intravenous infusion over approximately 60-120 minutes at a dose of 70 mg/m2 on Day 1 of each 21-day cycle. The investigator may attempt to give Cisplatin with at least one liter of fluids for hydration and on an outpatient basis. Patients will remain in the study until disease progression or when a maximum of six cycles have been administered. Study therapy may continue until: - There is evidence of progressive disease - The patient experiences unacceptable toxicity. - The investigator decides that the patient should be discontinued. - The patient requests discontinuation - The patient has received 6 cycles of the regimen (if the physician decides to continue after 6 cycles-this will be done after consultation with the sponsor) - Discontinuation from study therapy is indicated according to the additional guidelines described in the protocol After patients discontinue from study therapy, they proceed to the post-study follow up phase of the study.
To investigate efficacy, safety and PK of GEM monotherapy after prior chemotherapy with anthracycline and taxane regimen for patients with metastatic breast cancer
The purpose of this feasibility study is to identify appropriate surrogate parameters for a randomized study to examine the efficacy of a complementary therapy with an extract of viscum album (Iscador P) in patients with breast cancer.
Phase IV trial to investigate the effect of the combination of Letrozole with trastuzumab in metastatic breast cancer patients
Trastuzumab or Herceptin is an antibody directed against Her-2. Her-2 is a growth factor receptor which is present on the tumors of 25% of patients with breast cancer. The addition of trastuzumab to chemotherapy has been shown in a randomized clinical trial to increase the response rate to chemotherapy, the duration of response to chemotherapy, and to improve the duration of survival of patients with metastatic breast cancer. The anticancer mechanism of action of trastuzumab is unknown, but it is possible that trastuzumab acts by promoting antibody-dependent cell mediated cytotoxicity (ADCC), or direct killing of cancer cells by immune cells, triggered by antibodies bound to the surface of the cancer cell. G-CSF is a drug which is a growth factor for certain types of immune cells. G-CSF has two favorable effects on ADCC. G-CSF increases the pool of circulating cancer-killing immune cells, and G-CSF increases the strength of binding of cancer-killing immune cells to a specific part of the antibody. Therefore, priming with G-CSF significantly increases the efficiency of ADCC, and four days of treatment with G-CSF has been shown to optimize ADCC in some studies. Recent data from the investigators' laboratory indicates that chemotherapy can augment ADCC directed against tumor cells. The investigators' hypothesis is that pre-treatment with the drug G-CSF would increase the effectiveness of chemotherapy given with trastuzumab.
The combination of capecitabine and docetaxel is given to treat several different types of cancer. Capecitabine is usually given by mouth for 14 days, and docetaxel is given IV on the first day of capecitabine. The effects of changes in the schedule of the combination of docetaxel and capecitabine has been examined in human breast cancer cells. A capecitabine by-product was given orally to breast cancer-bearing animals for 14 consecutive days. Docetaxel was given IV at a variety of times between days 1 and 15. The greatest reductions in the volume of the cancer were seen when animals were treated with docetaxel between days 6 and 10. In two other breast cancer models, the maximal degree of delay in growth of the tumors was achieved when the animals were treated with docetaxel on day 8 of a 14 day course of capecitabine. The extent of tumor response was not explained by changes in tumor levels of the enzyme thymidine phosphorylase, which is thought to be the mechanism behind the interaction of capecitabine and docetaxel. In the breast cancer cells, capecitabine increases the level of proteins which promote death of cancer cells, and it inhibits the levels of proteins which block death of cancer cells. Our hypothesis is that capecitabine and docetaxel interact with each other, because capecitabine primes the pro-death machinery of the cell by increasing the ratio of death-promoting proteins to death-inhibiting proteins. Cells are more susceptible to killing by docetaxel when the pro-death machinery is activated by capecitabine. This is a safety study to find the highest dose of capecitabine that can be given safely for 14 days, in combination with docetaxel given at a fixed dose on day 8. Once this dose of capecitabine has been determined, an additional nine patients with tumors that can be biopsied will be treated at this dose, and levels of capecitabine, its byproducts, and docetaxel will be measured in the bloodstream. Biopsies of tumors will also be taken before and after the docetaxel is given, and the levels of pro-death and anti-death proteins will be measured.