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Paper 2
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
A 76 year old man presents with painless, obstructive jaundice. A liver ultrasound examination shows an echogenic soft tissue mass centred on the biliary hilum. There is focal thickening and dilatation of the right hepatic lobe bile ducts and the walls appear hyperechoic. There is dilatation up to the second order ducts in the right lobe. A subsequent MRCP demonstrates high T2 signal within the dilated right lobe bile duct walls. The hilar lesion shows delayed contrast enhancement. Cholangiocarcinoma is suspected.
Biliary Tract Cancer
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Hemant M. Kocher, Vincent S. Yip, Ajit T. Abraham
Histological and cytological confirmation is necessary for the definitive diagnosis of cholangiocarcinoma. Brush cytology is positive only in about 30% of cases, but combining cytology with endoscopic biopsy may enable correct diagnosis in 40–70% of cases of cholangiocarcinoma.45,51 Immunohistochemical markers such as CA19-9 and CA50 may distinguish cholangiocarcinoma from hepatocellular carcinoma (positive for HepPar1), and staining with anti-cytokeratin type-1 (monoclonal antibody AE1) could distinguish a biliary tract rather than hepatocyte origin. Histological diagnosis is not mandatory prior to surgical exploration.
Mid Common Bile Duct Cholangiocarcinoma Involving the Portal Vein and Right Branch of the Hepatic Artery
Published in Savio George Barreto, Shailesh V. Shrikhande, Dilemmas in Abdominal Surgery, 2020
Charles W. Kimbrough, Timothy M. Pawlik
Historically, the diagnosis of cholangiocarcinoma carries a dismal prognosis, and surgery remains the only potentially curative therapy. Long-term outcomes are largely dependent on stage at presentation and the ability to achieve a margin-negative resection. Given the anatomic location and aggressive biology, only one-third of patients are resectable at presentation. Following surgery, risk factors associated with survival include resection margin status, nodal involvement, tumor differentiation, and vascular invasion. While overall survival among patients with unresectable disease is generally less than one year, patients with margin-negative resection and no evidence of lymph node involvement can have a five-year survival rate of up to 60%. As the only risk factor potentially controlled by surgeons, the impact of margin status underscores the importance of good surgical technique. Lymph node involvement reflects aggressive systemic disease, and five-year survival drops to approximately 20% among patients with nodal disease. Ultimately, three-quarters of patients will recur following surgery, including almost all patients with metastatic disease in the lymph nodes.
Past, present, and future of FGFR inhibitors in cholangiocarcinoma: from biological mechanisms to clinical applications
Published in Expert Review of Clinical Pharmacology, 2023
Elisabeth Amadeo, Federico Rossari, Francesco Vitiello, Valentina Burgio, Mara Persano, Stefano Cascinu, Andrea Casadei-Gardini, Margherita Rimini
The last years have seen the advancement of therapeutic options in cholangiocarcinoma, starting from the introduction of immunotherapy as a first-line treatment alongside conventional chemotherapy. Nonetheless, what acted as a breakthrough in CCA therapy was the discovery of targetable pathways, one being FGFR. The application of FGFR inhibitors as a second line in clinical experimentation made it possible to hypothesize their first use in stage IV disease, if not even earlier. This systematic review gives an updated insight of ongoing clinical and laboratory studies, not to mention the most recent drug approvals by international committees. Indeed, pemigatinib resulted in one of the most promising, seeing its approval by FDA, EMA, and AIFA. Furthermore, futibatinib irreversible mechanism of action gave encouraging results with its ability to evert arising resistance in previously treated iCCA with other tyrosine kinase inhibitors, pemigatinib included. As previously stated, this might question whether specific drug application sequences might be necessary to prevent tumor resistance.
Novel biomarkers for cholangiocarcinoma: how can it enhance diagnosis, prognostication, and investigational drugs? Part-1
Published in Expert Opinion on Investigational Drugs, 2021
Ranu S Sinniah, Mark S Shapses, Mohammad Umar Ahmed, Hani Babiker, Sreenivasa R. Chandana
Pathology review is the gold standard in the diagnosis of cholangiocarcinoma. Using the IHC technique, CCA is positive for specific subtypes of cytokeratins, including CK 7 and 19, monoclonal and polyclonal CEA, and various other conventional adenocarcinoma markers, such as MOC-31, Ber-EP4, and albumin mRNA [16]. Mucins, such as MUC 4,5A, 5B may help classify CCA and predict prognosis [17]. However, these markers are not differentially expressed by normal and malignant biliary epithelium, limiting their specificity [18]. Thus, CCA is typically a histological diagnosis of exclusion. Several IHC stains, including CK20, CDX-2, TTF-1, ER, PR, BRST-2, PSA, GATA3, and synaptophysin, are useful to exclude hepatic metastases from common primary sites. Albumin mRNA FISH is a sensitive and highly specific diagnostic tool for distinguishing iCCA from metastatic adenocarcinoma, particularly pancreatic ductal adenocarcinoma [19].
Progress in research on the roles of TGR5 receptor in liver diseases
Published in Scandinavian Journal of Gastroenterology, 2021
Ke Ma, Dan Tang, Chang Yu, Lijin Zhao
Hepatic cholangiocarcinoma is a malignant tumour originating from bile duct epithelial cells. It is the second most prevalent primary liver cancer worldwide. However, limited information on its pathogenesis and the lack of early diagnostic biomarkers and treatment strategies contribute to a poor prognosis [121–123]. Previous studies have shown that TGR5 expression is higher in cholangiocarcinoma than in paracancerous tissues, specifically in extrahepatic and hilar cholangiocarcinoma [116,124]. In vitro experiments have shown that TCA and other TGR5 agonists could promote the proliferation of cholangiocarcinoma cell lines (EGI-1 and TFK-1) by EGFR activation and MAPK phosphorylation [111,116]. A recent study has shown that silencing the mortalin gene can attenuate the TGR5-induced increases in cholangiocarcinoma cell viability, colony formation, and proliferating cell nuclear antigen (PCNA) expression [121]. TGR5 positively regulates the expression of mortalin at both the protein and mRNA levels and inactivates the tumour suppressor p53, thereby promoting the proliferation of cholangiocarcinoma cells [121]. These results provide insight into the molecular mechanisms underlying cholangiocarcinoma; however, the mechanism underlying the relationship between TGR5 and mortalin remains to be elucidated.