This trial is active, not recruiting.

Condition cholangiocarcinoma
Treatments gemcitabine, oxaliplatin, capecitabine,, panitumumab, gemcitabine, oxaliplatin, capecitabine
Phase phase 2
Sponsor Vejle Hospital
Start date September 2008
End date March 2016
Trial size 70 participants
Trial identifier NCT00779454, 2612-3769, GOX-P, S-20080081


The purpose of this study is partly to continue the good experience the investigators have with chemotherapy and partly to optimize treatment of inoperable cholangiocarcinoma by adding a biological antibody to the treatment of patients with wild-type Kirsten rat sarcoma viral oncogene homolog (KRAS).

United States No locations recruiting
Other Countries No locations recruiting

Study Design

Allocation non-randomized
Endpoint classification safety/efficacy study
Intervention model factorial assignment
Masking open label
Primary purpose treatment
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.
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

Primary Outcomes

Progression free survival
time frame: Up to 6 months

Secondary Outcomes

Response rate
time frame: 6 months
Overall survival
time frame: 6 months.

Eligibility Criteria

Male or female participants from 18 years up to 80 years old.

Inclusion Criteria: - Histologically verified adenocarcinoma arisen from gallbladder, extra or intrahepatic bile ducts or malignant cells consistent with the above and concomitant radiologic findings consistent with cholangiocarcinoma. - Curative treatment presently discounted (surgery, stereotactic radiotherapy, etc.) - KRAS analyzed and found wild-type (wt) or mutated - PS 0-2 - Evaluable disease according to RECIST criteria, i.e., the disease does not need to be measurable - Haematology: - ANC ≥ 1.5 x 10^9/l - Thrombocytes ≥ 100x10^9/l - Biochemistry: - Bilirubinaemia ≤ 3 x upper normal value - ALAT ≤ 5 x upper normal value - Creatinin ≤ upper normal value. If raised creatinin, the measured or calculated GFR must be at least 50% of the lower normal value. - Fertile women must present a negative pregnancy test and use birth control during and 3 months after treatment. The following methods are considered safe birth control: Birth control pills, coil, gestagen deposit injection, subdermal implantation, hormonal vagina ring, and transdermal deposit band-aid) - Oral and written informed consent Exclusion Criteria: - Chemotherapy within 4 weeks - Radiotherapy within 4 weeks - Immunotherapy within 4 weeks - Other concomitant experimental treatment - Known neuropathy ≥ grade 2 - Serious congruous medical disease - Other previous malignant disease within 5 years, excl. non-melanoma skin cancer and carcinoma in situ cervicis uteri - Previous serious and unexpected reactions to fluoropyrimidine treatment - Hypersensitivity to one or more of the active substances, auxiliary substances or fluoruracil - Patients with interstitial pneumonitis or pulmonary fibrosis

Additional Information

Official title Combined Biological Treatment and Chemotherapy for Patients With Inoperable Cholangiocarcinoma
Description 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.
Trial information was received from ClinicalTrials.gov and was last updated in June 2016.
Information provided to ClinicalTrials.gov by Vejle Hospital.