Evidence map›Paper›PMID 28389139›Full record

ReviewJournal of hepatology2017

Emerging molecular therapeutic targets for cholangiocarcinoma.

Sumera I Ilyas, Gregory J Gores

Open access · greenAbstract readReview
In one paragraph

Review in Journal of hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 1 pooled it
19.1field-weighted citation impact, top 1% of its field
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

111 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Review
  7. Cholangiocytes' primary cilia regulate DNA damage response and repair.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Article
  8. The diverse roles of circular RNAs in cholangiocarcinoma.Medical oncology (Northwood, London, England) · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Actin-Like Protein 6A as an Oncogene and Therapeutic Target in Cancer.International journal of medical sciences · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Albumin promoter-driven FlpO expression induces efficient genetic recombination in mouse liver.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  19. Review
  20. Article

51 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Sumera I IlyasDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA.
Gregory J GoresDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA. Electronic address: gores.gregory@mayo.edu.
Mayo Clinic in Arizona · US

Funding

PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI Nicholas F. LaRusso · 2009 to 2026
$22.2M
Mechanisms of Carcinogenesis in Biliary EpitheliaR01DK059427 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2001 to 2016
$4.3M
Mechanisms of Carcinogenesis in Biliary EpitheliaR56DK059427 · NIDDK · MAYO CLINIC ROCHESTER · PI GORES, GREGORY J. · 2006 to 2006
$243k
NIDDK NIH HHS P30 DK084567NIDDK NIH HHS R01 DK059427NIDDK NIH HHS R56 DK059427
6 · The paper itself

Abstract

Cholangiocarcinomas (CCAs) are diverse epithelial tumors arising from the liver or large bile ducts with features of cholangiocyte differentiation. CCAs are classified anatomically into intrahepatic (iCCA), perihilar (pCCA), and distal CCA (dCCA). Each subtype has distinct risk factors, molecular pathogenesis, therapeutic options, and prognosis. CCA is an aggressive malignancy with a poor overall prognosis and median survival of less than 2years in patients with advanced disease. Potentially curative surgical treatment options are limited to the subset of patients with early-stage disease. Presently, the available systemic medical therapies for advanced or metastatic CCA have limited therapeutic efficacy. Molecular alterations define the differences in biological behavior of each CCA subtype. Recent comprehensive genetic analysis has better characterized the genomic and transcriptomic landscape of each CCA subtype. Promising candidates for targeted, personalized therapy have emerged, including potential driver fibroblast growth factor receptor (FGFR) gene fusions and somatic mutations in isocitrate dehydrogenase (IDH)1/2 in iCCA, protein kinase cAMP-activated catalytic subunit alpha (PRKACA) or beta (PRKACB) gene fusions in pCCA, and ELF3 mutations in dCCA/ampullary carcinoma. A precision genomic medicine approach is dependent on an enhanced understanding of driver mutations in each subtype and stratification of patients according to their genetic drivers. We review the current genomic landscape of CCA, the potentially actionable molecular aberrations in each CCA subtype, and the role of immunotherapy in CCA.

Indexed as

Molecular Targeted TherapyBile Duct NeoplasmsCholangiocarcinomaHepatocyte Growth FactorHistone Deacetylase InhibitorsHumansImmunotherapyIsocitrate DehydrogenasePhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-metReceptors, Fibroblast Growth FactorHepatocyte Growth FactorHistone Deacetylase InhibitorsIsocitrate DehydrogenasePhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-metReceptors, Fibroblast Growth FactorDistal cholangiocarcinomaImmunotherapyIntrahepatic cholangiocarcinomaPerihilar cholangiocarcinomaTargeted therapy

Identifiers

PMID28389139
PMCPMC5563275
OpenAlexW2604648767

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.