View clinical trials related to Metastatic Colorectal Cancer.
Filter by:The purpose of this study is to determine the treatment effect of panitumumab in combination with FOLFOX compared to FOLFOX alone as first line therapy for metastatic colorectal cancer
The purpose of this study is to determinate progression free survival after 9 months of treatment.
The purpose of this study is to evaluate the treatment effect of panitumumab plus FOLFIRI compared to FOLFIRI alone as second line therapy for metastatic colorectal cancer.
A comparison of prophylactic treatment with reactive treatment for skin toxicity observed in patients with metastatic colorectal cancer (mCRC) who are receiving second-line irinotecan-based chemotherapy concomitantly with panitumumab.
The primary objective of this study is to assess the effect of treatment with ABX-EGF on best overall objective response rate by modified RECIST (confirmed complete or partial response) in Japanese subjects with metastatic colorectal cancer.
Background: - Colorectal cancer (CRC) is a major public health problem in the U.S. and worldwide, and 5-year survival with widespread metastatic disease is less than 5%. - Expression of epidermal growth factor receptor (EGFR) or up-regulation of the gene occurs in the majority of CRC cases (60-80%). - Therapies targeting EGFR, like cetuximab, have shown activity in the treatment of solid tumors like CRC. - Cetuximab is FDA (Food and Drug Administration) approved for the treatment of EGFR-expressing CRC, but clinical responses to cetuximab are seen in only 10% of EGFR-expressing CRC. - One possible mechanism of resistance to cetuximab could be KRAS (Kirsten rat sarcoma) mutations. - Another major pathway implicated in colon carcinogenesis is the vascular endothelial growth factor (VEGF) pathway, which is involved in angiogenesis and is a validated target for therapy in CRC. - BAY 43-9006 is both a Raf kinase inhibitor and an inhibitor of VEGF receptor (VEGFR2) tyrosine kinase. - We hypothesize that the combined inhibition of EGFR, VEGFR2, and the Ras-(rapidly accelerated fibrosarcoma) Raf pathway will demonstrate promising clinical activity in CRC. Furthermore, in patients with mutant KRAS, combination of cetuximab with a drug that inhibits Raf kinase and acts downstream of Ras mutations, could restore tumor sensitivity to cetuximab. Objectives: - To determine the rate of response (complete response (CR) + partial response (PR) + stable disease (SD) for 4 months) and toxicity profile of combination of BAY 43-9006 and cetuximab in previously treated EGFR-expressing metastatic CRC in patients with mutant KRAS. - To evaluate BAY 43-9006 pharmacokinetics & pharmacogenomics (CYP3A4/5 (cytochrome P450 3A4/5)). - To evaluate for this combination treatment pharmacodynamics, effect on tumor vascularity and effect on angiogenic cytokines. Eligibility: - Adults with histologically or cytologically documented, measurable, EGFR-expressing metastatic CRC, which has recurred or progressed following at least one prior 5FU (Fluorouracil)-based combination chemotherapy regimen administered for the treatment of metastatic disease. - Patients must be KRAS mutation-positive. Design: - BAY 43-9006 will be administered 400 mg by mouth twice daily - Cetuximab will be administered as 400 mg/m^2 loading dose (week 1) followed by 250 mg/m^2 IV (intravenous) weekly. - If procedure may be performed safely, tumor biopsy will be obtained prior to treatment and after 4 weeks of treatment. - Optional positron emission tomography (PET)/computerized tomography (CT) imaging with 89Zr-labeled, EGFR-targeting antibody panitumumab may be performed to evaluate radiation dosimetry, safety, and tumor distribution prior to and following treatment with study agents. - Patients will be evaluated for response every 8 weeks using the RECIST (Response Evaluation Criteria in Solid Tumors) criteria. - This trial uses a phase II optimal design targeting a response rate as defined above of 20% in patients with mutant KRAS. Up to 49 patients may be treated.
Although it is possible to cure bowel cancer when it is detected at an early stage, in many cases it may spread to involve other organs and in these cases is generally incurable. Chemotherapy prolongs survival and improves quality of life in such patients, but standard chemotherapy for this disease has not been defined. There are several possible chemotherapy treatments for patients with bowel cancer, which has spread to other organs. However, these treatments are only partly effective and only work for a limited period of time. Most treatments are associated with a number of possible side effects which may have a detrimental effect on quality of life. Thus, it is imperative that more effective treatments with the lowest possible risk of side effects are developed. Previous studies have shown that the addition of a new type of antibody treatment (bevacizumab) to an intensive combination chemotherapy regimen improved survival in patients with advanced bowel cancer and extended the time before tumours began to grow. However, intensive chemotherapy is likely to only be a suitable treatment for a proportion of patients with bowel cancer, because intensive chemotherapy causes a high rate of side effects. This study compares a gentle chemotherapy treatment (capecitabine chemotherapy tablets given by mouth) with the combination of capecitabine and bevacizumab and the combination of capecitabine, bevacizumab and intravenous mitomycin C. It is expected that a gentle chemotherapy treatment or a gentle chemotherapy treatment combined with bevacizumab would be an appropriate treatment for both young and fit patients as well as older and less fit patients who would not easily tolerate intensive chemotherapy.
In Patients with metastatic colorectal cancer the following treatments first-line Folfiri+Cetuximab first-line Folfox6 + Cetuximab will be concerning efficacy and safety. The trial compares Folfiri + Cetuximab and Folfox6 + Cetuximab concerning efficacy and safety as first
Irinotecan (7-ethyl-10- {4(-1-piperidino)-1-piperidino} carbonyloxy camptothecin) is a semisynthetic camptothecin derivative introduced in the 1980's. Irinotecan is a prodrug metabolized by carboxylesterases to an active metabolite 7-ethyl-10-hydroxy-camptothecin (SN38). SN38 exerts its cytotoxic effect by forming stable complexes with topoisomerase I and DNA. These complexes collide with replication forks and cause breaks in DNA. Studies substantiated irinotecan's activity in 5FU resistant colorectal cancer and led to its approval for treatment of 5FU resistant colorectal cancer in the United States, Canada and Europe.Colorectal cancer studies demonstrated that single agent irinotecan's dose limiting toxicity was diarrhea occurring 5 to 6 days after its administration. High dose loperamide at first occurrence of diarrhea has decreased the incidence of diarrhea but the incidence of grade 3/4 diarrhea remains high at 28 to 40%.
A randomized phase II-study to evaluate the safety and efficacy of capecitabine plus irinotecan plus cetuximab compared to capecitabine plus oxaliplatin plus cetuximab in first-line treatment of patients with metastatic colorectal cancer.