Evidence map›Paper›PMID 33665585›Full record

ReviewJHEP reports : innovation in hepatology2021

Cell of origin in biliary tract cancers and clinical implications.

Agrin Moeini, Philipp K Haber, Daniela Sia

Abstract readReview
In one paragraph

Review in JHEP reports : innovation in hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Agrin MoeiniCancer Inflammation and Immunity Group, Cancer Research UK Manchester Institute, The University of Manchester, Alderley Park, Manchester, UK.
Philipp K HaberLiver Cancer Program, Division of Liver Diseases, Department of Medicine, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, USA.
Daniela SiaLiver Cancer Program, Division of Liver Diseases, Department of Medicine, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Biliary tract cancers (BTCs) are aggressive epithelial malignancies that can arise at any point of the biliary tree. Albeit rare, their incidence and mortality rates have been rising steadily over the past 40 years, highlighting the need to improve current diagnostic and therapeutic strategies. BTCs show high inter- and intra-tumour heterogeneity both at the morphological and molecular level. Such complex heterogeneity poses a substantial obstacle to effective interventions. It is widely accepted that the observed heterogeneity may be the result of a complex interplay of different elements, including risk factors, distinct molecular alterations and multiple potential cells of origin. The use of genetic lineage tracing systems in experimental models has identified cholangiocytes, hepatocytes and/or progenitor-like cells as the cells of origin of BTCs. Genomic evidence in support of the distinct cell of origin hypotheses is growing. In this review, we focus on recent advances in the histopathological subtyping of BTCs, discuss current genomic evidence and outline lineage tracing studies that have contributed to the current knowledge surrounding the cell of origin of these tumours.

Indexed as

ARID1A, AT-rich interactive domain-containing protein 1ABAP1, BRCA1-associated protein 1Biliary tract cancersBRAF, v-Raf murine sarcoma viral oncogene homolog BBTC, biliary tract cancerCCA, cholangiocarcinomaCDKN2A/B, cyclin-dependent kinase inhibitor 2A/BCell of originCholangiocarcinomaCK, cytokeratinCLC, cholangiolocarcinomaCoH, Canal of HeringdCCA, distal cholangiocarcinomaDCR, disease control rateeCCA, extrahepatic cholangiocarcinomaERBB2/3, Erb-B2 Receptor Tyrosine Kinase 2/3ER, estrogen receptorFGFR2, Fibroblast Growth Factor Receptor 2FGFR, fibroblast growth factor receptorGBC, gallbladder cancerGEMM, genetically engineered mouse modelsGenomicsHCC, hepatocellular carcinomaHPCs, hepatic progenitor cellsiCCA, intrahepatic cholangiocarcinomaIDH, isocitrate dehydrogenaseKRAS, Kirsten Rat Sarcoma Viral Oncogene HomologLineage tracingMET, Hepatocyte Growth Factor Receptormo, monthsMST1, Macrophage Stimulating 1NAFLD, non-alcoholic fatty liver diseaseNA, not applicableNASH, non-alcoholic steatohepatitisNGS, next-generation sequencingNR, not reportedNTRK, Neurotrophic Receptor Tyrosine Kinase 1ORR, objective response rateOS, overall survivalPBG, peribiliary glandpCCA, perihilar cholangiocarcinomaPersonalized therapyPFS, progression- free survivalPIK3CA, Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit AlphaPLC, primary liver cancerPRKACA/B, Protein Kinase CAMP-Activated Catalytic Subunit Alpha/BetaPROM1, Prominin 1PSC, primary sclerosing cholangitisRNF43, Ring Finger Protein 43SMAD4, SMAD Family Member 4TBG, thyroid binding globulinTP53, Tumor Protein P53WHO, World Health Organization

Identifiers

PMID33665585
PMCPMC7902553

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Registered trials

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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.