Evidence map›Paper›PMID 28260136›Full record

ReviewSurgery today2018

Cells of origin of pancreatic neoplasms.

Junpei Yamaguchi, Yukihiro Yokoyama, Toshio Kokuryo, Tomoki Ebata, Masato Nagino

Abstract readReview
PubMed Publisher
In one paragraph

Review in Surgery today, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Proteomics in pancreatic cancer.Biomarker research · 2025
    Review
  4. Article
  5. Methylation ofJournal of translational internal medicine · 2024
    Article
  6. Article
  7. Clinical and Molecular Attributes and Evaluation of Pancreatic Cystic Neoplasm.Biochimica et biophysica acta. Reviews on cancer · 2023
    Review
  8. Review
  9. Review
  10. Article
  11. Loss ofLife science alliance · 2021
    Article
  12. Review
  13. Genetically Engineered Pigs to Study Cancer.International journal of molecular sciences · 2020
    Review
  14. Cellular Plasticity in Cancer.Cancer discovery · 2019
    Review
  15. DuctalAnnals of pancreatic cancer · 2019
    Article
  16. Article
  17. Review
  18. Review
  19. 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

5 authors at 1 institution in 1 country.

Junpei YamaguchiDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8560, Japan. jumpei@med.nagoya-u.ac.jp.
Yukihiro YokoyamaDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8560, Japan.
Toshio KokuryoDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8560, Japan.
Tomoki EbataDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8560, Japan.
Masato NaginoDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi, 466-8560, Japan.
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignant disease associated with poor prognosis, despite recent medical advances. It is of great importance to understand the initial events and cells of origin of pancreatic cancer to prevent the development and progression of PDAC. There are three distinct precursor lesions that develop into PDAC: pancreatic intraepithelial neoplasms (PanINs), intraductal papillary mucinous neoplasms (IPMNs), and mucinous cystic neoplasms (MCNs). Studies on genetically engineered mouse models have revealed that the initiation and development of these lesions largely depend on genetic alterations. These lesions originate from different populations in the pancreas. PanIN development seems to be the result of the transdifferentiation of acinar cells, whereas IPMNs most likely arise from the progenitor niche of the pancreatic ductal epithelium. Pancreatic carcinogenesis is dependent on various events, including gene alterations, environmental insults, and cell types. However, further studies are needed to fully understand the initial processes of pancreatic cancer.

Indexed as

Acinar CellsAdenocarcinoma, MucinousAnimalsCarcinoma in SituCarcinoma, Pancreatic DuctalCell TransdifferentiationCell Transformation, NeoplasticDisease Models, AnimalDisease ProgressionEpithelial CellsHumansMicePancreatic DuctsPancreatic NeoplasmsStem CellsCell of originIPMNPancreatic cancerPanINProgenitors

Identifiers

PMID28260136
OpenAlexW2592176391

What OpenQuestion holds

Textmetadata
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.