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Investigating the efficacy of Cetuximab Monotherapy versus Continuation after induction treatment with chemotherapy + Cetuximab in inoperable or irresectable and non-progressive metastatic colorectal cancer after first line induction treatment for 24 weeks with mFOLFOX6/FOLFIRI and Cetuximab treatment. Reinduction treatment will be done in case of progression.
Investigating the efficacy of Cetuximab Monotherapy versus Continuation after induction treatment with chemotherapy + Cetuximab in inoperable or irresectable and non-progressive metastatic colorectal cancer after first line induction treatment for 24 weeks with mFOLFOX6/FOLFIRI and Cetuximab treatment. Reinduction treatment will be done in case of progression. This treatment is continued until progression or severe toxicity.
Allocation: Randomized, Intervention Model: Parallel Assignment, Masking: Open Label, Primary Purpose: Treatment
Cetuximab, mFOLFOX6, FOLFIRI
Not yet recruiting
Published on BioPortfolio: 2016-12-01T16:08:21-0500
To compare the efficacy in terms of progression free survival (PFS) of the addition of cetuximab to FOLFIRI versus FOLFIRI alone given as first line therapy in patients with advanced color...
This randomized, multicenter, open label study will evaluate the safety and effi cacy of RO5083945 in combination with FOLFIRI as compared to FOLFIRI plus cetuxi mab or FOLFIRI alone as se...
This randomized, open-label study will evaluate the safety and efficacy of Avastin (Bevacizumab) added to standard mFOLFOX6 chemotherapy in treatment-naïve patients with Stage IV metastat...
This will be a randomized, open-label, multicenter, phase II study. The study p opulation will consist of first-line metastatic colorectal cancer patients.
- To investigate whether cetuximab alone (given until progression or cumulative toxicity) after 8 cycles of FOLFIRI + cetuximab results in a non inferior Progression Free Surviv...
Adding cetuximab to first-line FOLFIRI in the phase 3 CRYSTAL trial significantly improved progression-free survival (PFS), overall survival (OS), and objective response rate (ORR) in patients with KR...
Two germline Fc-γ receptor (FCGR) polymorphisms, rs1801274 [FCGR2A;His(H)131Arg(R)] and rs396991 [FCGR3A;Phe(F)158Val(V)] produce altered proteins through amino acid substitutions; both are reported ...
To investigate tumour biomarker status and efficacy of first-line panitumumab+FOLFIRI for metastatic colorectal carcinoma (mCRC).
This randomized phase II trial compared panitumumab plus fluorouracil, leucovorin, and irinotecan (FOLFIRI) with bevacizumab plus FOLFIRI as second-line chemotherapy for wild-type (WT) KRAS exon 2 met...
Cetuximab has activity against colorectal cancers. Recent studies demonstrated that cetuximab induces antibody-dependent cell-mediated cytotoxicity via immune cells, and a new immune-related mechanism...
Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.
Tumor suppressor genes located in the 5q21 region on the long arm of human chromosome 5. The mutation of these genes is associated with the formation of colorectal cancer (MCC stands for mutated in colorectal cancer).
Tumor suppressor genes located in the 18q21-qter region of human chromosome 18. The absence of these genes is associated with the formation of colorectal cancer (DCC stands for deleted in colorectal cancer). The products of these genes show significant homology to neural cell adhesion molecules and other related cell surface glycoproteins.
A group of autosomal-dominant inherited diseases in which COLON CANCER arises in discrete adenomas. Unlike FAMILIAL POLYPOSIS COLI with hundreds of polyps, hereditary nonpolyposis colorectal neoplasms occur much later, in the fourth and fifth decades. HNPCC has been associated with germline mutations in mismatch repair (MMR) genes. It has been subdivided into Lynch syndrome I or site-specific colonic cancer, and LYNCH SYNDROME II which includes extracolonic cancer.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
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