Evidence map›Paper›PMID 30450847›Full record

ReviewYonsei medical journal2018

Cancer Metabolism as a Mechanism of Treatment Resistance and Potential Therapeutic Target in Hepatocellular Carcinoma.

Misu Lee, Haeyong Ko, Mijin Yun

Open access · goldAbstract readReview
In one paragraph

Review in Yonsei medical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 22% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Genetic Variants ofJournal of hepatocellular carcinoma · 2025
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Exploring the efficacy ofAbdominal radiology (New York) · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Characterization of metabolic landscape in hepatocellular carcinoma.World journal of gastrointestinal oncology · 2021
    Review
  19. CircRNA has_circ_0001806 promotes hepatocellular carcinoma progression via the miR-193a-5p/MMP16 pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Article
  20. Review
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 2 institutions in 1 country.

Misu LeeDepartment of Nuclear Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Haeyong KoDepartment of Nuclear Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Mijin YunDepartment of Nuclear Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea. yunmijin@yuhs.ac.ORCID https://orcid.org/0000-0002-1712-163X
Yonsei University · KRIncheon National University · KR

Funding

Incheon National UniversityNational Research Foundation of Korea NRF-2015R1D1A1A01057737National Research Foundation of Korea NRF-2016R1E1A1A01943303
6 · The paper itself

Abstract

Various molecular targeted therapies and diagnostic modalities have been developed for the treatment of hepatocellular carcinoma (HCC); however, HCC still remains a difficult malignancy to cure. Recently, the focus has shifted to cancer metabolism for the diagnosis and treatment of various cancers, including HCC. In addition to conventional diagnostics, the measurement of enhanced tumor cell metabolism using F-18 fluorodeoxyglucose (18F-FDG) for increased glycolysis or C-11 acetate for fatty acid synthesis by positron emission tomography/computed tomography (PET/CT) is well established for clinical management of HCC. Unlike tumors displaying the Warburg effect, HCCs vary substantially in terms of 18F-FDG uptake, which considerably reduces the sensitivity for tumor detection. Accordingly, C-11 acetate has been proposed as a complementary radiotracer for detecting tumors that are not identified by 18F-FDG. In addition to HCC diagnosis, since the degree of 18F-FDG uptake converted to standardized uptake value (SUV) correlates well with tumor aggressiveness, 18F-FDG PET/CT scans can predict patient outcomes such as treatment response and survival with an inverse relationship between SUV and survival. The loss of tumor suppressor genes or activation of oncogenes plays an important role in promoting HCC development, and might be involved in the "metabolic reprogramming" of cancer cells. Mutations in various genes such as

Indexed as

AcetatesAdultAgedBiomarkers, TumorCarbonCarcinoma, HepatocellularFemaleFluorodeoxyglucose F18HumansLiver NeoplasmsMaleMiddle AgedPositron-Emission TomographyPositron Emission Tomography Computed TomographyRadiopharmaceuticalsAcetatesBiomarkers, TumorCarboncarbon-11 acetateFluorodeoxyglucose F18Radiopharmaceuticalscancer metabolismdrug resistanceHepatocellular carcinomapositron emission tomography/computed tomography (PET/CT)

Identifiers

PMID30450847
PMCPMC6240564
OpenAlexW2901287409

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.