Evidence map›Paper›PMID 30221358›Full record

ReviewAnnals of the New York Academy of Sciences2019

Generic chemoprevention of hepatocellular carcinoma.

Sai Krishna Athuluri-Divakar, Yujin Hoshida

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Annals of the New York Academy of Sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Omics-derived hepatocellular carcinoma risk biomarkers for precision care of chronic liver diseases.Hepatology research : the official journal of the Japan Society of Hepatology · 2020
    Review
  11. Article
  12. Review
  13. Article
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.

Sai Krishna Athuluri-DivakarLiver Tumor Translational Research Program, Simmons Comprehensive Cancer Center, Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Yujin HoshidaLiver Tumor Translational Research Program, Simmons Comprehensive Cancer Center, Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
The University of Texas Southwestern Medical Center · US

Funding

Molecular Prognostic Indicators in Liver Cirrhosis and CancerR01DK099558 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HOSHIDA, YUJIN · 2013 to 2016
$2.6M
(PQB6) Accurate Comparative Genome-wide Analysis of Primary Tumors and MetastasesR21CA180016 · NCI · UNIVERSITY OF VIRGINIA · PI PEMBERTON, LUCY F, WOTTON, DAVID · 2013 to 2014
$373k
Cancer Prevention and Research Institute of Texas RR180016European Research Council 671231European Union ERC-2014-AdG-671231 HEPCIRNIDDK NIH HHS R01 DK099558U.S. Department of Defense W81XWH-16-1-0363
6 · The paper itself

Abstract

Chronic fibrotic liver disease caused by viral or metabolic etiologies is a high-risk condition for developing hepatocellular carcinoma (HCC). Even after curative treatment of early-stage HCC tumor, the carcinogenic microenvironment persists in the remnant diseased liver and supports the development of de novo HCC tumors (de novo HCC recurrence). Therefore, prevention of HCC development in patients at risk of not only first-primary but also second-primary HCC tumors is theoretically the most impactful strategy to improve patient prognosis. However, no such therapy has been established to date. One major challenge is the identification of clinically relevant targets that can be achieved by utilizing the reverse-engineering strategy of chemoprevention discovery, which integrates omics information from clinical cohorts with completed follow-up for cancer development. Clinical and experimental studies have suggested etiology-specific and generic candidate HCC chemoprevention strategies, including statins, antidiabetic drugs, selective molecular targeted agents, and dietary and nutritional substances. Clinical testing of the candidate compounds can be cost-effectively performed by combining it with HCC risk biomarker evaluation to specify the target patient population most likely to benefit from the therapy. Nontoxic, generic agents will have broad clinical applicability across the diverse HCC etiologies and clinical contexts and are expected to substantially improve the still dismal prognosis of HCC.

Indexed as

Anti-Inflammatory AgentsCarcinoma, HepatocellularChemopreventionDietHumansLife StyleLiver CirrhosisLiver NeoplasmsMetabolic DiseasesMolecular Targeted TherapyAnti-Inflammatory Agentschemopreventioncirrhosishepatocellular carcinomaprecision medicinerecurrence

Identifiers

PMID30221358
PMCPMC6420365
OpenAlexW2892082254

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.