Evidence map›Paper›PMID 28854942›Full record

ReviewMolecular cancer2017

The biology of Hepatocellular carcinoma: implications for genomic and immune therapies.

Galina Khemlina, Sadakatsu Ikeda, Razelle Kurzrock

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 263 papers.

0numbers the graph read from it
0cells of the map it votes in
263citing papers in PubMed
17.2field-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

263 citing papers in PubMed, 498 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Targeting cuproptosis in liver cancer: Molecular mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

203 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

3 authors at 3 institutions in 2 countries.

Galina KhemlinaDepartment of Geriatrics, University of California, UC San Diego, 9500 Gilman Drive, #9111, La Jolla, CA, 92093-9111, USA. gkhemlina@ucsd.edu.
Sadakatsu IkedaDepartment of Medicine, Division of Hematology/Oncology, and Center for Personalized Cancer Therapy, University of California, Moores Cancer Center, San Diego, USA.
Razelle KurzrockDepartment of Medicine, Division of Hematology/Oncology, and Center for Personalized Cancer Therapy, University of California, Moores Cancer Center, San Diego, USA.
Moores Cancer CenterTokyo Medical and Dental University · JPUniversity of California, San Diego · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC), the most common type of primary liver cancer, is a leading cause of cancer-related death worldwide. It is highly refractory to most systemic therapies. Recently, significant progress has been made in uncovering genomic alterations in HCC, including potentially targetable aberrations. The most common molecular anomalies in this malignancy are mutations in the TERT promoter, TP53, CTNNB1, AXIN1, ARID1A, CDKN2A and CCND1 genes. PTEN loss at the protein level is also frequent. Genomic portfolios stratify by risk factors as follows: (i) CTNNB1 with alcoholic cirrhosis; and (ii) TP53 with hepatitis B virus-induced cirrhosis. Activating mutations in CTNNB1 and inactivating mutations in AXIN1 both activate WNT signaling. Alterations in this pathway, as well as in TP53 and the cell cycle machinery, and in the PI3K/Akt/mTor axis (the latter activated in the presence of PTEN loss), as well as aberrant angiogenesis and epigenetic anomalies, appear to be major events in HCC. Many of these abnormalities may be pharmacologically tractable. Immunotherapy with checkpoint inhibitors is also emerging as an important treatment option. Indeed, 82% of patients express PD-L1 (immunohistochemistry) and response rates to anti-PD-1 treatment are about 19%, and include about 5% complete remissions as well as durable benefit in some patients. Biomarker-matched trials are still limited in this disease, and many of the genomic alterations in HCC remain challenging to target. Future studies may require combination regimens that include both immunotherapies and molecularly matched targeted treatments.

Indexed as

AnimalsBiomarkers, TumorCarcinoma, HepatocellularCell Transformation, NeoplasticGene Expression Regulation, NeoplasticGenetic VariationGenomicsHumansImmunotherapyLiver NeoplasmsSignal TransductionBiomarkers, TumorHepatocellular carcinomaMolecular targeted therapygNext-generation sequencing

Identifiers

PMID28854942
PMCPMC5577674
OpenAlexW2752067270

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.