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Biliary Tract Adenocarcinoma clinical trials

View clinical trials related to Biliary Tract Adenocarcinoma.

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NCT ID: NCT05350943 Enrolling by invitation - Clinical trials for Biliary Tract Adenocarcinoma

HAIC Combined With Toripalimab and Donafenib for Advanced BTC

Start date: March 1, 2022
Phase: Phase 2
Study type: Interventional

This is a single center, single arm, phase II, prospective study to evaluate the efficacy and safety of Hepatic Arterial Infusion Chemotherapy (HAIC) combined with PD-1 inhibitor immunotherapy Toripalimab and Tyrosine Kinase Inhibitor Donafenib in patients with advanced biliary tract cancer.

NCT ID: NCT04156958 Not yet recruiting - Clinical trials for Biliary Tract Adenocarcinoma

Fruquintinib as Second-line Treatment for Advanced/Metastatic Biliary Tract Adenocarcinoma

FSTAMBTA
Start date: December 2019
Phase: Phase 2
Study type: Interventional

The prospective, multicenter, single-arm design study is to evaluate the efficacy and safety of fruquintinib for patients with advanced or metastatic biliary tract adenocarcinoma who failed first-line chemotherapy with gemcitabine, platinum/S-1, and albumin paclitaxel.

NCT ID: NCT01588860 Active, not recruiting - Clinical trials for Biliary Tract Adenocarcinoma

Mutation Analysis and Copy Number Changes of KRAS and BRAF Gene in Taiwanese Cases of Biliary Tact Adenocarcinoma

Start date: January 2011
Phase: N/A
Study type: Observational

Cholangiocarcinoma is a fatal malignant neoplasm originating from biliary tracts and constitutes about 5-10% of primary liver cancers, characterized by a poor prognosis. High prevalence in southeast and eastern Asia has been observed. At present, the cellular and molecular mechanisms leading to oncogenesis of cholangiocarcinoma remain unclear. The RAS gene product has a key role in controlling cell growth and differentiation through its intrinsic GTPase activity. Point mutations that activate the RAS protein and its downstream cascade have been observed in human tumors. Both KRAS and BRAF are members of the RAS-RAF-MEK-ERK-MAP kinase pathway which mediates cellular response to growth signals. Somatic KRAS mutations are found at high rates in leukemia, colon cancer, pancreatic cancer and lung cancer. Studies from European and Japanese groups have recently described that activating KRAS/ BRAF mutations may play a role in the carcinogenesis of cholangiocarcinoma of the biliary tracts, but our preliminary data demonstrated low frequency of KRAS and BRAF mutation in the same tumor as well as the results from Thailand. In this study, the investigators hypothesize copy number changes rather than genetic mutation of either KRAS or BRAF genes may be the key findings of Taiwanese cases of the adenocarcinoma from the biliary tracts.