Evidence map›Paper›PMID 36139512›Full record

ReviewCancers2022

Targeting the Metabolic Rewiring in Pancreatic Cancer and Its Tumor Microenvironment.

Keisuke Yamamoto, Dosuke Iwadate, Hiroyuki Kato, Yousuke Nakai, Keisuke Tateishi, Mitsuhiro Fujishiro

Abstract 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

  1. Review
  2. Article
  3. Fingerprinting the Metabolic and Lipidomic Landscapes of Pancreatic Ductal Adenocarcinoma with MALDI Imaging.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Personalizing DNA Cancer Vaccines.Journal of personalized medicine · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Molecular Imaging: Unveiling Metabolic Abnormalities in Pancreatic Cancer.International journal of molecular sciences · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. 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

6 authors.

Keisuke YamamotoDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku 113-8655, Tokyo, Japan.ORCID 0000-0002-6323-9540
Dosuke IwadateDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku 113-8655, Tokyo, Japan.ORCID 0000-0002-0181-794X
Hiroyuki KatoDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku 113-8655, Tokyo, Japan.
Yousuke NakaiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku 113-8655, Tokyo, Japan.ORCID 0000-0001-7411-1385
Keisuke TateishiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku 113-8655, Tokyo, Japan.
Mitsuhiro FujishiroDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku 113-8655, Tokyo, Japan.

Funding

JSPS KAKENHI 21K20828JSPS KAKENHI 22H02898JSPS KAKENHI 22H03053
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with only a few effective therapeutic options. A characteristic feature of PDAC is its unique tumor microenvironment (TME), termed desmoplasia, which shows extensive fibrosis and extracellular matrix deposition, generating highly hypoxic and nutrient-deprived conditions within the tumor. To thrive in this harsh TME, PDAC undergoes extensive metabolic rewiring that includes the altered use of glucose and glutamine, constitutive activation of autophagy-lysosomal pathways, and nutrient acquisition from host cells in the TME. Notably, these properties support PDAC metabolism and mediate therapeutic resistance, including immune suppression. A deeper understanding of the unique metabolic properties of PDAC and its TME may aid in the development of novel therapeutic strategies against this deadly disease.

Indexed as

anabolic glucose metabolismautophagyglutamine metabolismglycolysishexosamine biosynthesis pathwayimmune checkpoint blockadeimmune evasionKRASlysosomemacropinocytosismetabolic rewiringMHC-Ipancreatic ductal adenocarcinomapentose phosphate pathwayserine biosynthesis pathwaytumor microenvironment

Identifiers

PMID36139512
PMCPMC9497173

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.