Evidence map›Paper›PMID 35053615›Full record

ReviewCancers2022

CD26/DPP4 as a Therapeutic Target in Nonalcoholic Steatohepatitis Associated Hepatocellular Carcinoma.

Sohji Nishina, Keisuke Hino

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. EGFR-TKIs Induced DPP4 Drives Metabolic Reprogramming of Persister Cells in Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Incretin-Based Therapies and Cancer: What's New?Medicina (Kaunas, Lithuania) · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. CD26 and Cancer.Cancers · 2022
    Article
  17. Review
  18. Review
  19. Potential Effect of DPP-4 Inhibitors Towards Hepatic Diseases and Associated Glucose Intolerance.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022
    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

2 authors at 1 institution in 1 country.

Sohji NishinaDepartment of Hepatology and Pancreatology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan.
Keisuke HinoDepartment of Hepatology and Pancreatology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan.ORCID 0000-0002-3297-1720
Kawasaki Medical School · JP

Funding

Japan Society for the Promotion of Science 18K07923Japan Society for the Promotion of Science 19H03644
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is generally considered an "immune-cold" cancer since T cells are not observed abundantly in HCC tumor tissue. Combination therapy with immune checkpoint inhibitors and vascular endothelial growth factor (VEGF) inhibitors is currently recognized as a first-line systemic treatment for advanced-stage HCC. Immunologically, immune checkpoint inhibitors influence the recognition of cancer cells by T cells, and VEGF inhibitors influence the infiltration of T cells into tumors. However, no drugs that facilitate the trafficking of T cells toward tumors have been developed. Chemokines are promising agents that activate T cell trafficking. On the other hand, metabolic factors such as obesity and insulin resistance are considered risk factors for HCC development. CD26/dipeptidyl peptidase 4 (DPP4) functions as a serine protease, selectively cleaving polypeptides with a proline or alanine at the penultimate N-terminal position, such as chemokines. Recently, CD26/DPP4 has been reported to attenuate anticancer immunity via chemokine cleavage and to promote insulin resistance and inflammation in the liver and/or adipose tissue via dysregulation of macrophage M1/M2 polarization. In this review, we discuss the promotive roles of CD26/DPP4 in HCC development and progression and the potential of DPP4 inhibitors as therapeutic agents for HCC.

Indexed as

chemokineDPP4 inhibitoreosinophilimmunomodulationinsulin resistancemacrophage polarizationobesity

Identifiers

PMID35053615
PMCPMC8774170
OpenAlexW4205504872

What Socratic 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 Socratic graph.