Cholangiocarcinoma is the second most common primary liver malignancy after hepatocellular carcinoma (HCC). It is classified by anatomical site into intrahepatic (iCCA), perihilar (pCCA) and distal (dCCA) tumours. Mass-forming cholangiocarcinoma is the dominant growth pattern of iCCA and the one radiologists meet most often: a hypodense, irregularly marginated hepatic mass showing rim arterial enhancement with progressive centripetal fill-in, capsular retraction, peripheral biliary dilatation and vascular encasement without gross tumour thrombus. This page covers the CT and MRI findings, the WHO 5th edition small-duct versus large-duct subtypes, LI-RADS LR-M categorisation, AJCC staging and what the report must contain to drive current management.
Cholangiocarcinoma radiology at a glance
| Feature | Mass-forming iCCA | Why it happens |
|---|---|---|
| Non-contrast CT | Homogeneously hypoattenuating, irregular lobulated margin | Fibrous stroma with low cellularity |
| Arterial phase | Rim (peripheral) hyperenhancement | Viable tumour cells concentrated at the periphery |
| Portal venous / delayed phase | Progressive centripetal fill-in; peripheral washout | Slow contrast accumulation in central desmoplastic stroma |
| T2-weighted MRI | Moderately hyperintense, often targetoid (hypointense centre) | Central fibrosis darker than cellular rim |
| DWI | Targetoid diffusion restriction (peripheral rim bright) | Hypercellular periphery, hypocellular fibrotic core |
| Hepatobiliary phase (gadoxetate) | Hypointense with targetoid or cloud-like central retention | No functioning hepatocytes; interstitial trapping centrally |
| Capsular retraction | Present in a large proportion of tumours | Desmoplastic fibrosis pulling the liver surface inward |
| Bile ducts | Peripheral ductal dilatation distal to the mass | Duct obstruction or encasement |
| Vessels | Encasement and narrowing; gross tumour thrombus uncommon | Infiltration along vessel wall rather than luminal growth |
| Segmental change | Lobar or segmental atrophy with crowded ducts | Chronic portal venous occlusion plus biliary obstruction |
Classification: anatomical site and growth pattern
Two classifications run in parallel and both belong in the report. The anatomical classification determines surgical approach and staging system; the growth-pattern classification determines what the tumour looks like on imaging.
| Anatomical type | Location | Approximate share of cholangiocarcinoma | Typical imaging problem |
|---|---|---|---|
| Intrahepatic (iCCA) | Proximal to the second-order bile ducts | 10 to 20 percent | Characterising a liver mass; separating it from HCC and metastases |
| Perihilar (pCCA, Klatskin tumour) | Right and left hepatic ducts to the cystic duct insertion | 50 to 60 percent | Mapping longitudinal ductal extent and vascular involvement |
| Distal (dCCA) | Cystic duct insertion to the ampulla | 20 to 30 percent | Separating it from pancreatic head and ampullary carcinoma |
| Growth pattern | Imaging appearance | Comment |
|---|---|---|
| Mass-forming | Round or lobulated parenchymal mass with targetoid enhancement and capsular retraction | Most common intrahepatic pattern; the subject of this page |
| Periductal-infiltrating | Longitudinal soft tissue cuffing along a duct with duct wall thickening and upstream dilatation, no discrete mass | Typical of perihilar disease; easily missed on portal venous phase alone |
| Intraductal-growing | Polypoid or papillary intraluminal lesion, duct dilated out of proportion to the lesion, sometimes mucin-related | Best prognosis of the three; overlaps with intraductal papillary neoplasm of the bile duct |
| Mixed (mass-forming plus periductal-infiltrating) | Mass with contiguous ductal cuffing | Behaves aggressively; grouped with mass-forming for reporting |
Small-duct versus large-duct iCCA (WHO 5th edition)
The 2019 WHO classification split intrahepatic cholangiocarcinoma into small-duct and large-duct types. This is not academic. The two subtypes differ in risk factor, prognosis and — critically — in which druggable mutations they carry. Small-duct tumours are the ones enriched for FGFR2 fusions and IDH1 mutations, the two alterations with approved targeted drugs. Large-duct tumours carry KRAS mutations and do worse.
| Feature | Small-duct iCCA | Large-duct iCCA |
|---|---|---|
| Site of origin | Small bile ducts, ductules, canals of Hering | Large intrahepatic ducts, peribiliary glands |
| Location in liver | Peripheral | Near the hilum |
| Background liver | Chronic hepatitis, cirrhosis, metabolic disease | Hepatolithiasis, primary sclerosing cholangitis, liver fluke |
| Precursor lesion | None recognised | Biliary intraepithelial neoplasia, intraductal papillary neoplasm |
| Gross morphology | Almost always mass-forming | Periductal-infiltrating, intraductal or mixed |
| Arterial enhancement | Rim hyperenhancement common | Frequently hypoenhancing |
| Biliary dilatation | Often absent | Characteristic and often diffuse |
| Targetoid T2 and DWI | Common | Frequently absent |
| Perineural and lymphovascular invasion | Less frequent | Frequent |
| Immunohistochemistry | NCAM positive, N-cadherin positive, mucin negative | S100P positive, mucin positive |
| Actionable mutations | IDH1 or IDH2 mutation, FGFR2 fusion | KRAS mutation |
| Prognosis | Better | Worse |
MRI can predict the subtype preoperatively. In a surgical series of 140 gadoxetate-enhanced studies, four features independently favoured the large-duct type: infiltrative contour (odds ratio 14.2), absence of arterial phase hyperenhancement (odds ratio 17.8), diffuse biliary dilatation (odds ratio 9.7) and vascular invasion (odds ratio 4.5). Two or more of these features gave 95.7 percent specificity for large-duct type, and patients with two or more features had significantly shorter recurrence-free and overall survival.
CT protocol and findings
A non-contrast series plus a triphasic (late arterial, portal venous and 3 to 5 minute delayed) acquisition is mandatory. Omitting the delayed phase is the single commonest protocol error: on portal venous images alone, a mass-forming cholangiocarcinoma looks like a non-specific hypodense lesion, and the diagnostic centripetal fill-in is invisible.
- Non-contrast: homogeneously hypoattenuating mass, irregular but reasonably well-defined margin. Peripheral satellite nodules in up to a third of cases.
- Late arterial: irregular peripheral rim enhancement. Degree of enhancement is inversely related to the amount of central fibrosis.
- Portal venous and delayed: progressive concentric fill-in toward the centre, with the periphery becoming relatively hypodense (peripheral washout).
- Capsular retraction: flattening or inward puckering of the adjacent liver surface. Highly suggestive when combined with delayed enhancement.
- Biliary dilatation: peripheral to the mass, in the affected segment. Look specifically for crowded ducts in an atrophic segment.
- Vascular involvement: portal vein encasement and obliteration causing segmental atrophy. Tumour extending as a discrete intraluminal plug is unusual and should redirect you toward HCC.
- Nodes: assess the hepatoduodenal ligament, retropancreatic and coeliac stations. Nodal disease is the strongest prognostic factor after resection.
MRI, MRCP and the target sign
| Sequence | Finding |
|---|---|
| T1-weighted | Hypointense to liver |
| T2-weighted | Moderately hyperintense; central hypointensity from fibrosis produces the targetoid appearance. Marked, near-fluid T2 signal favours abscess or a mucinous tumour. |
| DWI and ADC | Targetoid restriction: hyperintense peripheral rim on high b-value images with a less restricted centre. One of the most reproducible discriminators from a simple cyst or haemangioma. |
| Dynamic (extracellular agent) | Rim arterial hyperenhancement, peripheral washout, delayed central enhancement |
| Hepatobiliary phase (gadoxetate) | Hypointense mass, often with a cloud-like or targetoid central area of retained contrast. Note that transitional phase hypointensity is not equivalent to washout with gadoxetate — cholangiocarcinomas routinely look hypointense in that phase. |
| MRCP | Maps the biliary tree above and below the obstruction, defines longitudinal ductal extent and detects a second, unsuspected stricture. Non-invasive and does not carry the cholangitis risk of ERCP. |
Ultrasound remains the first test in most patients: a homogeneously intermediate to slightly hyperechoic mass with an irregular margin, a hypoechoic rim of compressed parenchyma, peripheral duct dilatation and, on contrast-enhanced ultrasound, rim arterial enhancement with early (under 60 seconds) and marked washout — a pattern that is itself an LR-M feature.
FDG PET/CT does not make the primary diagnosis but changes management in roughly one in five patients by finding unsuspected nodal or distant metastases; a meta-analysis of preoperative staging reported a pooled diagnostic odds ratio of 9.34 and an area under the summary ROC curve of 0.86 for detecting primary cholangiocarcinoma, with better performance for intrahepatic than extrahepatic tumours.
LI-RADS: why iCCA is LR-M, not LR-5
Cirrhosis is a risk factor for intrahepatic cholangiocarcinoma as well as HCC, so in a LI-RADS population the two compete for the same observation. CT/MRI LI-RADS v2018 handles this with the LR-M category — probably or definitely malignant, but not specific for HCC. Any single LR-M feature is sufficient to assign LR-M, and doing so protects LR-5 from being contaminated by tumours that must never be treated as HCC without tissue.
| LR-M feature type | Feature |
|---|---|
| Targetoid | Rim arterial phase hyperenhancement |
| Peripheral washout | |
| Delayed central enhancement | |
| Targetoid diffusion restriction | |
| Targetoid transitional or hepatobiliary phase appearance | |
| Non-targetoid | Infiltrative appearance |
| Marked diffusion restriction | |
| Necrosis or severe ischaemia | |
| Other feature the radiologist judges to suggest non-HCC malignancy |
LR-M is not a synonym for cholangiocarcinoma. A meta-analysis of 3,812 observations across 18 studies found that LR-M lesions were malignant in 96 percent of cases — but 29 percent of them were HCC and 67 percent were non-HCC malignancies. Rim arterial phase hyperenhancement was the most frequent LR-M feature in non-HCC malignancy, present in 68 percent. The practical consequence: an LR-M observation needs biopsy, not ablation or transplant listing on imaging grounds alone.
For the full category set, see our LI-RADS calculator, and for the background liver findings that put a patient in the LI-RADS population, our guide to cirrhosis and portal hypertension on imaging.
Differential diagnosis
| Diagnosis | Features favouring it | Features favouring mass-forming iCCA |
|---|---|---|
| Hepatocellular carcinoma | Non-rim arterial hyperenhancement, non-peripheral washout, enhancing capsule, gross tumour thrombus, elevated AFP | Rim arterial enhancement, delayed central fill-in, capsular retraction, biliary dilatation, elevated CA 19-9 |
| Combined hepatocellular-cholangiocarcinoma | Mixed features of both; frequently categorised LR-M | Cannot be reliably separated on imaging — biopsy decides |
| Hepatic abscess | Thick enhancing wall, central near-fluid T2 signal, restricted diffusion of the centre not the rim, perilesional oedema, fever and leucocytosis, cluster sign | Solid centre, delayed central enhancement, capsular retraction, no clinical sepsis |
| Hypovascular metastasis | Multiple similar lesions, known primary, central necrosis with T2 hyperintensity | Solitary, capsular retraction, segmental biliary dilatation and atrophy |
| Confluent hepatic fibrosis | Wedge-shaped, radiates from the hilum, involves segments IV, VIII and medial left lobe, no mass effect, associated atrophy, stable over time | Rounded, mass effect on vessels, restricted diffusion, growth on follow-up |
| Epithelioid haemangioendothelioma | Multiple peripheral subcapsular nodules, capsular retraction, lollipop sign, coalescence | Solitary dominant mass, biliary obstruction |
| Sclerosed haemangioma | Very high T2 signal, prior imaging showing typical peripheral nodular discontinuous enhancement | Moderate T2 signal, targetoid diffusion restriction |
Staging: AJCC 8th edition (intrahepatic)
Intrahepatic, perihilar and distal cholangiocarcinoma each have their own AJCC staging system. For iCCA, the T category turns on size, number and vascular invasion — all radiological determinations.
| Category | Definition |
|---|---|
| T1a | Solitary tumour 5 cm or smaller, without vascular invasion |
| T1b | Solitary tumour larger than 5 cm, without vascular invasion |
| T2 | Solitary tumour with intrahepatic vascular invasion, or multiple tumours with or without vascular invasion |
| T3 | Tumour perforating the visceral peritoneum |
| T4 | Tumour directly invading local extrahepatic structures |
| N1 | Regional lymph node metastasis (adequate staging requires 6 or more nodes) |
| M1 | Distant metastasis |
| Stage groups: IA = T1a N0; IB = T1b N0; II = T2 N0; IIIA = T3 N0; IIIB = T4 N0 or any T with N1; IV = any M1 | |
Structured reporting checklist
- Size of the dominant lesion (the 5 cm threshold separates T1a from T1b) and number of lesions, including satellites.
- Segmental location and relation to the hepatic veins, portal bifurcation and the future liver remnant.
- Vascular invasion — encasement, narrowing or occlusion of portal or hepatic veins and the hepatic artery. This determines T2.
- Biliary involvement — level of obstruction, longitudinal ductal extent, whether both hepatic ducts are involved.
- Capsular or peritoneal breach (T3) and invasion of adjacent organs or diaphragm (T4).
- Nodes by station, since regional nodal disease upstages to IIIB and changes candidacy for upfront resection.
- Estimated future liver remnant volume and background parenchymal disease.
- Subtype prediction — comment on infiltrative contour, absent arterial hyperenhancement, diffuse biliary dilatation and vascular invasion, which together favour the large-duct type and a worse outcome.
- A biopsy target — nominate the enhancing peripheral rim, not the fibrotic core, and flag if percutaneous access risks tract seeding in a potential transplant candidate.
Management in 2026
Surgery remains the only curative option, but only about 20 percent of patients are resectable at diagnosis. Adjuvant capecitabine for 6 months is the standard after macroscopically complete resection, on the basis of the BILCAP trial (median overall survival 51.1 versus 36.4 months in the intention-to-treat analysis, and 53 versus 36 months per protocol, hazard ratio 0.75).
Liver transplantation, historically an absolute contraindication in iCCA, is being revisited for very early disease. In an international multicentre series, patients with cirrhosis and a single iCCA of 2 cm or less found incidentally at explant had 5-year cumulative recurrence of 18 percent and 5-year survival of 65 percent, versus 61 percent and 45 percent for larger or multifocal tumours. That 2 cm figure is a radiological measurement, which is one more reason to be precise about lesion size in a cirrhotic liver.
First-line systemic therapy for advanced disease is no longer gemcitabine and cisplatin alone. Two phase 3 trials added a checkpoint inhibitor to that backbone and both improved survival: TOPAZ-1 (durvalumab; updated median overall survival 12.9 versus 11.3 months, hazard ratio 0.76, with 24-month survival roughly doubled) and KEYNOTE-966 (pembrolizumab; 12.7 versus 10.9 months, hazard ratio 0.83).
The bigger change for radiologists is molecular profiling. ESMO recommends profiling when first-line systemic therapy is started in locally advanced or metastatic disease. Because the actionable alterations cluster in small-duct iCCA, the biopsy the radiologist performs is now expected to yield enough tissue for next-generation sequencing, not just a diagnosis.
| Alteration | Approximate frequency in iCCA | Agent | Key result |
|---|---|---|---|
| FGFR2 fusion or rearrangement | 10 to 15 percent | Futibatinib; pemigatinib | Futibatinib objective response 42 percent, median progression-free survival 9.0 months, median overall survival 21.7 months; pemigatinib response 35.5 percent |
| IDH1 mutation | 10 to 15 percent | Ivosidenib | Median overall survival 10.3 versus 7.5 months (5.1 months adjusted for crossover); progression-free survival 2.7 versus 1.4 months |
| HER2 amplification or overexpression | 5 to 20 percent of biliary tract cancers | Zanidatamab; trastuzumab deruxtecan; tucatinib plus trastuzumab | Zanidatamab objective response 41.3 percent, median duration of response 12.9 months |
| BRAF V600E | About 5 percent | Dabrafenib plus trametinib | Objective response 53 percent |
| MSI-H or dMMR | 1 to 3 percent | Pembrolizumab; dostarlimab | Tumour-agnostic indication |
| NTRK or RET fusion | Under 1 percent | Larotrectinib, entrectinib, repotrectinib; selpercatinib | Tumour-agnostic indications |
Clinical features and risk factors
- Demographics: typically the sixth to seventh decade, slight male predominance. FGFR2-fusion tumours skew younger and female.
- Presentation: silent early. Late symptoms are abdominal pain, weight loss, and — when large ducts are involved — jaundice, pruritus, pale stool and dark urine. Intrahepatic mass-forming tumours often reach a large size before causing jaundice.
- Laboratory: cholestatic liver enzymes, raised CA 19-9 and CEA. CA 19-9 is unreliable in cholangitis, biliary obstruction and Lewis-antigen-negative individuals.
- Risk factors: primary sclerosing cholangitis, hepatolithiasis and recurrent pyogenic cholangitis, liver fluke infection (Opisthorchis viverrini, Clonorchis sinensis), choledochal cyst and Caroli disease, chronic hepatitis B and C, cirrhosis of any cause, metabolic dysfunction-associated steatotic liver disease, diabetes, obesity, biliary-enteric drainage procedures, and toxins including thorotrast, dioxin and polyvinyl chloride.
Quiz
All the following are common features of mass-forming cholangiocarcinoma EXCEPT?
- Gradual centripetal enhancement
- Dilated bile ducts
- Liver capsular retraction
- Tumour thrombus
Click here for the answer
Answer: 4. Tumour thrombus. Vascular encasement by mass-forming cholangiocarcinoma is common, but gross intravascular tumour thrombus is rare and is the key differentiating feature from hepatocellular carcinoma.
Frequently asked questions
What are the CT features of cholangiocarcinoma?
On contrast-enhanced CT, mass-forming intrahepatic cholangiocarcinoma is a hypoattenuating hepatic mass with an irregular lobulated margin that shows irregular rim enhancement in the arterial phase and progressive centripetal fill-in on portal venous and delayed images. Supporting findings are capsular retraction, peripheral biliary dilatation, segmental atrophy, satellite nodules and vascular encasement without gross tumour thrombus. The delayed phase is essential; without it the diagnostic enhancement pattern is not seen.
How do you differentiate cholangiocarcinoma from hepatocellular carcinoma on imaging?
Hepatocellular carcinoma shows non-rim arterial hyperenhancement with non-peripheral washout, an enhancing capsule and a tendency to form gross tumour thrombus. Mass-forming cholangiocarcinoma shows rim arterial enhancement, peripheral washout, delayed central enhancement, capsular retraction and peripheral biliary dilatation, and encases vessels rather than growing into them. CA 19-9 is typically raised and AFP is normal. In a cirrhotic liver these features place the lesion in LI-RADS category LR-M, which requires biopsy rather than imaging-only diagnosis.
Why is intrahepatic cholangiocarcinoma classified as LR-M?
LR-M means probably or definitely malignant but not specific for hepatocellular carcinoma. Its targetoid features — rim arterial hyperenhancement, peripheral washout, delayed central enhancement, targetoid diffusion restriction and targetoid transitional or hepatobiliary phase appearance — are typical of cholangiocarcinoma, so assigning LR-M keeps these tumours out of LR-5 and preserves the specificity of an imaging-only hepatocellular carcinoma diagnosis. LR-M is not synonymous with cholangiocarcinoma: pooled data show 96 percent of LR-M observations are malignant, but 29 percent are hepatocellular carcinoma.
What is the difference between small-duct and large-duct intrahepatic cholangiocarcinoma?
The WHO 5th edition separates them by cell of origin. Small-duct tumours arise peripherally from small ducts and ductules, usually in chronic hepatitis or cirrhosis, are almost always mass-forming, often show rim arterial hyperenhancement and targetoid diffusion restriction without biliary dilatation, and carry IDH1 mutations and FGFR2 fusions. Large-duct tumours arise near the hilum from large ducts and peribiliary glands, associate with hepatolithiasis and primary sclerosing cholangitis, show infiltrative margins, absent arterial hyperenhancement and diffuse biliary dilatation, carry KRAS mutations and have a worse prognosis.
Does capsular retraction always mean cholangiocarcinoma?
No. Capsular retraction reflects fibrosis and also occurs in confluent hepatic fibrosis, epithelioid haemangioendothelioma, treated metastases, sclerosed haemangioma and scirrhous hepatocellular carcinoma. It becomes strongly suggestive of cholangiocarcinoma only when combined with a rounded mass, targetoid delayed enhancement, restricted diffusion at the periphery and peripheral biliary dilatation.
Which MRI sequence is most useful for cholangiocarcinoma?
No single sequence is sufficient, but diffusion-weighted imaging combined with a delayed post-contrast phase carries the most weight. Targetoid diffusion restriction with a bright peripheral rim, together with delayed central enhancement, is the combination that separates cholangiocarcinoma from abscess, haemangioma and most metastases. MRCP is added to map the biliary tree before surgery.
Why does molecular profiling matter to the radiologist?
Approved targeted agents exist for FGFR2 fusions, IDH1 mutations, HER2 amplification, BRAF V600E and mismatch repair deficiency, and these alterations cluster in small-duct intrahepatic tumours. Guidelines recommend profiling when first-line systemic therapy begins, so an image-guided biopsy must yield enough viable tissue for next-generation sequencing. Sampling the enhancing peripheral rim rather than the fibrotic centre is what makes that possible.
References
- European Association for the Study of the Liver. EASL-ILCA Clinical Practice Guidelines on the management of intrahepatic cholangiocarcinoma. J Hepatol. 2023;79(1):181-208. PMID: 37084797
- Kang JG, Chung T, Kim DK, Rhee H. Imaging findings of intrahepatic cholangiocarcinoma for prognosis prediction and treatment decision-making: a narrative review. Ewha Med J. 2024;47(4):e66. PMID: 40703995
- Park S, Lee Y, Kim H, et al. Subtype classification of intrahepatic cholangiocarcinoma using liver MR imaging features and its prognostic value. Liver Cancer. 2022;11(3):233-246. PMID: 35949291
- Chernyak V, Fowler KJ, Kamaya A, et al. Liver Imaging Reporting and Data System (LI-RADS) version 2018: imaging of hepatocellular carcinoma in at-risk patients. Radiology. 2018;289(3):816-830. PMID: 30251931
- Shin J, Lee S, Hwang JA, et al. MRI-diagnosis of category LR-M observations in the Liver Imaging Reporting and Data System v2018: a systematic review and meta-analysis. Eur Radiol. 2022;32(5):3319-3326. PMID: 35031839
- Low G, Pfanner T, Qian XJ, et al. LR-M for CT/MRI on LI-RADS v2018: a review of imaging criteria, performance, challenges and future directions from an end-user perspective. Abdom Radiol (NY). 2026;51(3):1332-1346. PMID: 40810812
- Chung YE, Kim MJ, Park YN, et al. Varying appearances of cholangiocarcinoma: radiologic-pathologic correlation. Radiographics. 2009;29(3):683-700. PMID: 19448110
- Mantripragada S, Chawla A. Cholangiocarcinoma – part 2, tumoral and nontumoral mimics and imaging features helpful in differentiation. Curr Probl Diagn Radiol. 2022;51(3):362-374. PMID: 33627221
- Hu JH, Tang JH, Lin CH, et al. Preoperative staging of cholangiocarcinoma and biliary carcinoma using 18F-fluorodeoxyglucose positron emission tomography: a meta-analysis. J Investig Med. 2018;66(1):52-61. PMID: 28912249
- Sapisochin G, Facciuto M, Rubbia-Brandt L, et al. Liver transplantation for “very early” intrahepatic cholangiocarcinoma: international retrospective study. Hepatology. 2016;64(4):1178-1188. PMID: 27481548
- Primrose JN, Fox RP, Palmer DH, et al. Capecitabine compared with observation in resected biliary tract cancer (BILCAP): a randomised, controlled, multicentre, phase 3 study. Lancet Oncol. 2019;20(5):663-673. PMID: 30922733
- Oh DY, He AR, Bouattour M, et al. Durvalumab or placebo plus gemcitabine and cisplatin in participants with advanced biliary tract cancer (TOPAZ-1): updated overall survival from a randomised phase 3 study. Lancet Gastroenterol Hepatol. 2024;9(8):694-704. PMID: 38823398
- Kelley RK, Ueno M, Yoo C, et al. Pembrolizumab in combination with gemcitabine and cisplatin compared with gemcitabine and cisplatin alone for patients with advanced biliary tract cancer (KEYNOTE-966): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet. 2023;401(10391):1853-1865. PMID: 37075781
- Goyal L, Meric-Bernstam F, Hollebecque A, et al. Futibatinib for FGFR2-rearranged intrahepatic cholangiocarcinoma. N Engl J Med. 2023;388(3):228-239. PMID: 36652354
- Abou-Alfa GK, Sahai V, Hollebecque A, et al. Pemigatinib for previously treated, locally advanced or metastatic cholangiocarcinoma: a multicentre, open-label, phase 2 study. Lancet Oncol. 2020;21(5):671-684. PMID: 32203698
- Zhu AX, Macarulla T, Javle MM, et al. Final overall survival efficacy results of ivosidenib for patients with advanced cholangiocarcinoma with IDH1 mutation: the phase 3 randomized clinical ClarIDHy trial. JAMA Oncol. 2021;7(11):1669-1677. PMID: 34554208
- Harding JJ, Fan J, Oh DY, et al. Zanidatamab for HER2-amplified, unresectable, locally advanced or metastatic biliary tract cancer (HERIZON-BTC-01): a multicentre, single-arm, phase 2b study. Lancet Oncol. 2023;24(7):772-782. PMID: 37276871
- Vogel A, Bridgewater J, Edeline J, et al. ESMO Clinical Practice Guideline interim update on the management of biliary tract cancer. ESMO Open. 2025;10(1):104003. PMID: 39864891
Co-Authors: Dr. Mansi Sarmalkar and Dr. Bhargavi Sovani (illustration).
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