ArticleDiscover oncology2025
Response to crizotinib in advanced intrahepatic cholangiocarcinoma with ZKSCAN1-MET fusion and MET amplification: case reports and literature review.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Histopathologic, molecular, and clinical associations of fusion-positive gastrointestinal carcinomas.Journal of gastrointestinal oncology · 2026Article
- Immunohistochemistry in intrahepatic cholangiocarcinoma: histological subtyping and drug selection.Frontiers in oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intrahepatic cholangiocarcinoma (ICC) is the second most prevalent liver cancer after hepatocellular carcinoma and is characterized by high malignancy and poor prognosis. Gemcitabine combined with cisplatin is the standard first-line therapy for metastatic or unresectable ICC. The combination of immunotherapy and targeted therapy represents a promising new direction for ICC treatment. Common genetic mutations in ICC include those in TP53, FGFR2, IDH1/2, and KRAS. MET alterations such as fusions and amplifications are rare in ICC. However, limited research has been conducted on the efficacy of specific MET inhibitors. We present two cases: the first with refractory ICC treated with a combination of immunotherapy and targeted therapy, harboring a ZKSCAN1-MET fusion and the second with a metastatic ICC with MET amplification. Both patients demonstrated a significant clinical response to crizotinib, a MET-specific tyrosine kinase inhibitor.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.