Combined Biological Treatment and Chemotherapy for Patients With Inoperable Cholangiocarcinoma
|Cholangiocarcinoma||Drug: Gemcitabine, Oxaliplatin, Capecitabine, Drug: Panitumumab, Gemcitabine, Oxaliplatin, Capecitabine||Phase 2|
|Study Design:||Allocation: Non-Randomized
Intervention Model: Factorial Assignment
Masking: None (Open Label)
Primary Purpose: Treatment
|Official Title:||Combined Biological Treatment and Chemotherapy for Patients With Inoperable Cholangiocarcinoma|
- Progression free survival [ Time Frame: Up to 6 months ]
- Response rate [ Time Frame: 6 months ]
- Overall survival [ Time Frame: 6 months. ]
|Study Start Date:||September 2008|
|Study Completion Date:||March 2016|
|Primary Completion Date:||March 2016 (Final data collection date for primary outcome measure)|
Drug: Panitumumab, Gemcitabine, Oxaliplatin, Capecitabine
Gemcitabine: 1,000 mg/m2 day 1 Oxaliplatin: 60 mg/m2 day 1 Capecitabine: 1,000 mg/m2 x 2 daily days 1-7 Panitumumab: 6 mg/kg day 1
Inclusion has been completed in the KRAS mutation arm.
Drug: Gemcitabine, Oxaliplatin, Capecitabine,
Gemcitabin: 1,000 mg/m2 day 1 Oxaliplatin: 60 mg/m2 day 1 Capecitabine: 1,000 mg/m2 x 2 daily days 1-7
Cholangiocarcinoma is a relatively rare disease. In Denmark approximately 150 patients are diagnosed each year. A small part of the patients can be offered surgery, but the operation will rarely be radical, and most patients with cholangiocarcinoma are therefore candidates for chemotherapy.
In Denmark the combination therapy of Gemcitabine, Oxaliplatin and Capecitabine has been used in recent years. Based on experience with gastrointestinal tumors, however, there seems to be an effect of new biological substances, including EGFR antibodies. There are casuistic reports on the specific effect of a monoclonal antibody against EGFR in cholangiocarcinoma.
The effect of EGF is mediated through an intracellular pathway involving the KRAS protein. It has been shown that a mutation of KRAS causes the EGF system to be constantly activated. Effect in patients with a KRAS mutation is therefore not to be expected. Approximately 50% of the patients present this mutation.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00779454
|Vejle Hospital, Dept. of Oncology|
|Vejle, Denmark, DK-7100|
|Study Chair:||Anders Jakobsen, DMSc||Vejle Hospital, Vejle, Denmark|