Evidence map›Paper›PMID 31456946›Full record

ReviewFrontiers in oncology2019

Recent Insights Into the Multiple Pathways Driving Non-alcoholic Steatohepatitis-Derived Hepatocellular Carcinoma.

Kazuki Takakura, Tsunekazu Oikawa, Masanori Nakano, Chisato Saeki, Yuichi Torisu, Mikio Kajihara, Masayuki Saruta

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–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

27 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Hepatocellular carcinoma in patients without cirrhosis.World journal of gastroenterology · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Cell Autophagy in NASH and NASH-Related Hepatocellular Carcinoma.International journal of molecular sciences · 2022
    Review
  12. Smad3 Phospho-Isoform Signaling in Nonalcoholic Steatohepatitis.International journal of molecular sciences · 2022
    Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

7 authors.

Kazuki TakakuraDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
Tsunekazu OikawaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
Masanori NakanoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
Chisato SaekiDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
Yuichi TorisuDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
Mikio KajiharaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
Masayuki SarutaDivision of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of metabolic syndrome with fatty liver is spreading on a worldwide scale. Correspondingly, the number of patients with the hepatic phenotype of metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), and in its advanced states, non-alcoholic steatohepatitis (NASH), and the subsequent hepatocellular carcinoma (HCC) derived from NASH (NASH-HCC) is increasing remarkably. A large-scale epidemiological study revealed that obesity can be a risk factor of such cancers as HCC. Moreover, despite the ongoing trends of declining cancer incidence and mortality for most cancer types, HCC has experienced a markedly increased rate of both. Considering the differences in liver-related mortality among NAFLD patients, NASH, and NASH-HCC should be included in the objectives of initiatives to manage NAFLD patients and their progression to the advanced stages. Unfortunately, research has yet to make a crucial drug discovery for the effective treatment of NASH and NASH-HCC, although it is urgently needed. The latest widespread concept of the "multiple parallel hits hypothesis," whereby multiple factors contribute concurrently to disease pathogenesis has led to advances in the elucidation of hepatic and systemic molecular mechanisms driving NASH and the subsequent NASH-HCC progression; the results are not only extensive but promising for therapeutics. Here, we have summarized the myriad landmark discoveries of recent research into the pathogenic processes underlying NASH-HCC development and with the greatest possibility for a new generation of pharmaceutical products for interference and treatment.

Indexed as

dysbiosishepatocellular carcinomanon-alcoholic fatty liver diseasenon-alcoholic steatohepatitissignal transducer and activator of transcriptiontumor necrosis factor

Identifiers

PMID31456946
PMCPMC6700399

What OpenQuestion holds

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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.